Dermatology

A man who had been taking prescribed methadone for many years presented with a desquamating rash (predominantly affecting the hands and feet) complicated by cellulitis of the right leg. There have now been multiple reports of a similar rash among methadone users in Sydney. The cause remains unknown. We report a man attending a methadone program in south-east Sydney who presented with a distinctive rash complicated by lower-leg cellulitis. This case adds to the widespread reports of a similar rash in methadone users around Sydney. The cause is under investigation by the New South Wales Department of Health. Clinical record In October 2004, a middle-aged man was referred to a hospital in south-east Sydney with a 14-day history of a painful, swollen, erythematous right lower leg and fever. Two days before onset of the leg symptoms, he had noticed a non-pruritic rash which started on his legs and feet and spread to abdomen and arms; it was accompanied by swelling, and then desquamation of the hands and feet. He had been diagnosed with cellulitis of the right lower leg 7 days before presentation and was prescribed oral flucloxacillin, but his condition did not improve significantly. Duplex ultrasound examination of the right leg 2 days before presentation excluded deep vein thrombosis. He was admitted to hospital for intravenous antibiotic treatment. The patient was a former intravenous heroin user and had been in a methadone program at a local pharmacy for the previous 8 years. He denied recreational drug use or injecting or sharing the oral methadone. His past medical history included previous right-leg deep vein thrombosis, chronic hepatitis B and C infection, gastro-oesophageal reflux, as well as melanoma excision several years before, and cholecystectomy a month previously. He had been taking griseofulvin for about 3 months for onychomycosis. He was taking methadone syrup (160 mg daily), griseofulvin (500 mg daily) and, when required, diazepam (5 mg three times daily), codeine/paracetamol (30/500 mg three times daily) and oxycodone (40 mg twice daily). He had recently started using, when required, cyproheptadine (4 mg at night), hyoscine (20 mg four times daily) and triamcinolone acetonide (0.02% cream topically) for the rash, and metoclopramide (10 mg three times daily) for mild nausea. On physical examination, the patient was haemodynamically stable and looked well. His temperature was 37.2°C. There was erythema, tenderness and warmth below the right knee, consistent with cellulitis. There was desquamation of the skin of both his lower legs, soles of feet (Box, a) and palms and fingers (Box, b), as well as non-pitting oedema of the feet and hands. There was hyperkeratosis of the soles, with xerosis and an erythematous maculopapular rash of the arms. The skin condition did not appear typical of disorders causing hyperkeratosis and desquamation, which usually do not present concurrently. He had no mucosal ulceration. Differential diagnoses included the early phase of an exfoliative erythroderma, psoriasis triggered by infection, early pityriasis rubra pilaris, bacterial toxin-mediated exfoliation, viral exanthem, sarcoidosis and syphilis. Rash in a patient who used oral methadone A: Hyperkeratosis and desquamation of the soles of the feet. B: Desquamation of the palms. C: Biopsy specimen from the maculopapular rash on the left arm, showing a slightly thickened epidermis with focal parakeratosis (P), and mild perivascular lymphocytic infiltrate (I). (Original magnification, × 20; haematoxylin–eosin stain.) Measurement of serum electrolyte, urea and creatinine levels and liver function tests all gave normal results. A full blood count revealed haemoglobin level of 125 g/L (reference range [RR], 130–180 g/L) and slight eosinophilia (0.48 × 10 9/L; RR, 0.04–0.44 × 10 9/L), but total white cell count was within the reference range (6.2 × 109/L; RR, 3.5–11.0 × 10 9 /L). Erythrocyte sedimentation rate was 10 mm/h (RR, 1–10 mm/h) and C-reactive protein level was 24 mg/L (RR, < 3 mg/L). Blood cultures showed no growth. A test for Treponema pallidum antibody was negative. Chest x-ray was normal, and HIV antibody test negative. Skin biopsy of the red macules on his left arm (Box, c) and the right-leg biopsy revealed non-specific histological changes, suggestive of chronic dermatitis. Periodic acid–Schiff staining for fungi was negative. Empirical treatment was begun with mometasone cream (0.1%), calcipotriol ointment (0.005%) and sorbolene cream twice daily to affected areas, and coal tar (5%) and salicylic acid (5%) in sorbolene base cream at night to the feet. Intravenous cephazolin (1 g three times daily) and oral clindamycin (300 mg four times daily) were begun for the cellulitis. The patient was discharged on Day 4 with the above topical preparations and oral cephalexin (500 mg three times daily), after both the rash and right-leg cellulitis abated significantly. He failed to attend a follow-up appointment, but reported by telephone that the rash had gradually resolved over several weeks. Discussion This case raises the alert to a possible adverse reaction to a methadone preparation. The cause may be methadone itself, another component of the preparation, or a contaminant. Previously reported cutaneous reactions to methadone include angioedema, facial oedema, flushing, pruritus, purpura, rash and urticaria.1 To our knowledge, no cases have been reported of a desquamating rash associated with methadone or other opioids. The cause of the rash in our patient did not appear infectious. He had no clinical evidence of staphylococcal toxic shock syndrome; he remained clinically well and did not develop the diffuse confluent erythema typical of this syndrome. Nor was the rash typical of a viral exanthem, in which a widespread morbilliform eruption predominates, without confluent erythema (as occurred on the lower legs), hyperkeratosis or desquamation. A reaction to a medication other than methadone seems less likely, as there had been no recent change. We are aware of other patients with a similar rash, oedema and desquamation of the hands and feet, all taking methadone: six patients in a methadone program at the same pharmacy as our patient, 20 from a local methadone clinic, and others at other methadone centres in Sydney (Mary Anne Ford, Registered Nurse, Bayside Clinic, Sydney, NSW, personal communication). We know of no patient with a similar rash who is not using methadone, and we believe all affected patients were taking the same brand and formulation of the drug. Most cases have been mild, and close contacts have not been affected. All patients appear to have continued using methadone from their usual dispensing clinic, and the rash has resolved over several weeks. The cause of the reaction remains unknown, and is possibly even an illicit drug available on the street. However, as all affected patients appear to have been taking methadone, this is perhaps the most likely agent. Marijuana has been reported, albeit rarely, to cause allergic reactions, and occasionally becomes contaminated with biological or chemical substances that might cause a reaction.2 -4 However, in that situation, one would expect cases to be more widely distributed outside the methadone-using population. In addition, at least one client with this rash from the local methadone clinic had a negative urine test for cannabinoids (Mary Anne Ford, as above, personal communication). Further investigation of these cases is required to determine the aetiology. Variables to be considered include the brand and batch of methadone used, storage, dose, mixing of batches in the dispensing pump, and other solutions included in the preparation to increase palatability. Pharmacists often mix batches of methadone and are not required to record the batch number dispensed to each patient, which makes tracing difficult. Also important to consider are any other prescription or non-prescription medications taken by patients, illicit drugs used, and sharing of methadone between patients from different methadone clinics. Many more cases may have been unreported and unrecognised, as most affected patients have had relatively mild and self-limiting symptoms. An investigation is now under way by the New South Wales Department of Health. Methadone clinics, pharmacists, dermatologists, general practitioners and emergency medicine staff need to be aware of the possibility of these reactions.

Natalie Kordjian BPharm, MB BS · Annabelle D Donaldson MB ChB · Steven A Krilis PhD, FRACP · Dedee F Murrell MA, BM BCh, FAAD(USA)

Arc welding produces the full spectrum of ultraviolet radiation (UVR). It is possible that welders are at greater risk of developing skin cancer than the general population, but there is a dearth of well designed studies in this area. The only major study of the relationship between arc welding and skin cancer risk did not reveal an increased incidence of skin cancer in welders. As the welders examined were all well protected and the length-of-exposure period was limited, the findings cannot be generalised to all welders. Studies have demonstrated that welding increases the risk of ocular melanoma. Just as we urge the public to protect themselves from UVR, we need to consider similar advice for arc welders.

Anthony J Dixon FACRRM · Brian F Dixon PhD

Alex J Chamberlain,* John W Kelly† * Registrar, † Head, Victorian Melanoma Service, The Alfred, Prahran, VIC. alex_chamberlainAThotmail.com To the Editor: Janda and colleagues’ survey of skin screening by general practitioners in regional Queensland1 demonstrated that only 20% of participants had undergone a total-body skin examination in the previous 3 years and that examination rates were slightly lower for patients 50 years of age and older. They conclude that those at greatest risk (older people, especially men) will need to be targeted if screening programs are to reduce melanoma mortality. In the same issue of the Journal, a study by English and colleagues of excisional biopsies of pigmented lesions by Perth GPs showed that the excision rate for patients under the age of 50 years (62%) is nearly twice that for patients over 50 years (38%), and that in the younger cohort this is primarily harvesting benign naevi.2 They conclude by encouraging GPs to increase their suspicion and lower their biopsy threshold in older patients in order to detect more melanomas. These studies serve to remind us that it is predominantly older people (and especially men) who are at greatest risk of thick (and potentially lethal) melanoma.3 The evidence provided by these studies of mismatch between skin cancer risk and resource allocation to surveillance and excisional surgery might help explain why recent advances in early detection seem to have bypassed elderly men. It is of continuing concern that despite the fact that melanomas are currently diagnosed at an earlier stage when compared with 20 or 30 years ago, the background incidence of thick melanoma has remained stable, both in Australia and around the world. In a recent study conducted in Victoria,4 we found that thick melanomas (≥ 3 mm) were predominantly nodular melanomas, primarily affecting people over 50 years of age and especially men. This elusive subtype frequently fails to fulfil the “ABCD” (asymmetry, border, colour, diameter) diagnostic criteria in that they are more often uniform in colour, symmetric in shape and predominantly amelanotic.5 A possible aide-mémoire that we have suggested elsewhere for identifying nodular melanoma is the addition of “EFG” (“elevated, firm, growing for more than 1 month”) criteria.6 The observation that nodular melanomas grow quickly, leading to deep invasion within a few months, poses a significant obstacle to the potential success of community-based screening programs.1 It is likely that many nodular melanomas will escape early detection by such programs, as they will evolve significantly in the interval between screening examinations.4,5 It is important that all clinicians recognise this subtype if we hope to reduce melanoma mortality in Australia.

Alex J Chamberlain · John W Kelly

Objective: To establish the prevalence and predictors of skin screening by general practitioners in regional Queensland.Design: Questionnaire administered to participants by professional interviewers via telephone.Participants and setting: Participants were 3100 adults aged ≥ 30 years (66.9% overall response rate), selected from residents of 18 regional Queensland communities with populations of between 2000 and 10 000 (as recorded in the 1996 Australian census). Within the last 10 communities surveyed, an additional telephone survey of 727 participants evaluated mole density. The survey was conducted between January and October 1998.Main outcome measure: Prevalence of whole-body skin examinations by GPs.Results: 11% of participants reported a whole-body skin examination by a GP during the previous 12 months, and 20% during the previous 3 years. Men and women reported a similar prevalence of whole-body skin examinations. Factors associated with a significantly increased likelihood of having had a whole-body skin examination within the previous 3 years included a positive attitude towards skin screening, a personal history of non-melanoma skin cancer, a tendency to burn, and having more than four moles on the right upper arm.Conclusions: A substantial proportion of Queenslanders undergo skin screening. Those at highest risk for skin cancer are more likely to be screened.

Monika Janda PhD · Philippa H Youl MPH · Joanne F Aitken PhD · Mark Elwood MD · Ian T Ring FAFPHM · David W Firman MMath · John B Lowe DrPH

Objective: To identify doctor and patient characteristics associated with excision of benign versus malignant pigmented skin lesions.Design, setting and participants: Retrospective audit of data on 4741 pigmented skin lesions excised from November 1998 to February 2000 by 468 general practitioners (39% response rate) from 223 practices in Perth, WA. (The data used were from the baseline period of a randomised controlled trial of a diagnostic aid for pigmented skin lesions.)Main outcome measure: The number needed to treat (NNT), defined as the number of pigmented lesions needed to be excised to identify one melanoma, in relation to demographic characteristics of GPs and patients.Results: Relatively more benign lesions were excised per melanoma (NNT = 83) in the youngest patients (aged 10–19 years) compared with the oldest (aged ≥ 70) (NNT = 11) (P [trend] < 0.001), in females (NNT = 37) compared with males (NNT = 23) (P = 0.02), and in the most socioeconomically disadvantaged (NNT = 60) compared with the least disadvantaged group (NNT = 20) (P [trend] < 0.001). The most recently graduated GPs excised more benign lesions for each melanoma (NNT = 59) than the least recently graduated (NNT = 22) (P [trend] = 0.01).Conclusions: GPs could raise their threshold for excising pigmented lesions in patients who are young, female, or from areas of low socioeconomic status, or if the GPs themselves are recent graduates.

Dallas R English PhD · Chris Del Mar MD · Robert C Burton MD, PhD

Using Botulinum toxins cosmetically. Jean Carruthers, Alastair Carruthers. London: Martin Dunitz, 2003 (v + 81 pp + CD-ROM). ISBN 1 84184 217 6. Botulinum toxin is mainly known in Australia as Botox, one of its popular trade names. It has become a household word, not so much for its use as an exciting drug in almost every field of medicine, but as a deadly poison that has been somehow transformed into a softener of facial expression lines. This book on its cosmetic uses is a timely work indeed. Jean and Alastair Carruthers are the mother and father of the aesthetic use of botulinum toxin. Jean, an ophthalmologist, and Alastair, a dermatologist, first noted the softening of expression lines in some patients being treated for oculospasm in the 1980s. From then on, through their relentless application of science and artistry, they have steered the course for the safe treatment of expression lines, initially of the upper face, and more recently those of the mid and lower face and neck. Botulinum toxin injected in doses used for cosmetic enhancement appears to be a very safe treatment without much risk to the patient’s general health. However, there may be local effects, and the emphasis of this book is very much "safety first" through optimal dosing and careful injection placement. This short text presents the most up-to-date factual information that I have seen, and the accompanying procedural CD-ROM is a most interesting and highly effective teaching aid. Even the most experienced injector will learn tips and tricks from this work. This book simply and succinctly acts as a step-by-step guide to the injector, but I feel it is being directed to those with some experience, rather than the complete novice — it should not substitute for mentoring and formal training. I would have liked to see the patients in the CD-ROM after their treatment, so the attempted outcomes and their subtleties could have been shown, but otherwise it is a wonderful instructional aid. Gregory J GoodmanDermatologistSkin and Cancer Foundation, Toorak, VIC

Gregory J Goodman

Clinical records Patient 1 An 88-year-old man gave a 12-month history of seeing insects attacking his legs and crawling along the floor of his house. He described these insects as 4 cm long, black and white bugs with beaks, which pecked at his legs, causing wounds. He often felt a sharp stinging sensation heralding their presence. He also had burning pain in both legs below the knees. He had had his house fumigated twice in the previous year and put various chemicals across his doorways and bed to ward off the bugs. He described no other hallucinations or delusions. He was not using any regular medications and had never been a consumer of alcohol. He lived alone and managed all activities of daily living independently. His home was clean, and he had no pets. Score on Folstein Mini Mental State Examination was 28/30. Neurological examination revealed signs of peripheral neuropathy of the lower limbs. His visual acuity was poor. During the examination, he pointed to several “bugs” on his legs, which were actually pieces of skin peeling from superficial ulcers. Nerve conduction studies confirmed peripheral neuropathy. Computed tomography and magnetic resonance imaging of the brain showed ischaemic changes. Magnetic resonance angiography showed severe stenosis of the left internal carotid artery. Septic screen and serological tests for syphilis gave negative results. The patient’s symptoms were thought to be due to neuropathic pain. He was prescribed carbamazepine (100 mg twice daily) to alleviate the sensory stimuli, and risperidone (0.5 mg in the morning, 1 mg at night). After 2 weeks, the pain and delusions had decreased substantially. Diagnosis: Delusional parasitosis associated with medical conditions — neuropathy and poor visual acuity. Patient 2 A 72-year-old woman had a 20-year history of the delusion of worms crawling throughout her body, especially around a scar on her hip. She was convinced that the scar should be surgically explored. Past medical history included type 2 diabetes mellitus, normal pressure hydrocephalus with shunt insertion, ischaemic heart disease and fractured right neck of femur. She lived in a hostel. Her cognition was normal, and clinical examination found no abnormalities. She was treated briefly with thioridazine (40 mg daily), which provided some benefit but caused drowsiness. She was then treated with pimozide (2 mg twice daily), which was changed to olanzapine (2.5 mg in the morning, 5 mg at night) because of continuing agitation, paranoid ideation about her neighbours and “intruders”, and aggression to neighbours and hostel staff. Her symptoms decreased but did not resolve, and compliance was poor. Diagnosis: Paranoid schizophrenia with major psychotic symptom related to infestation. Patient 3 An 81-year-old woman was referred with a persistent belief that she had scabies and lice infestation of her eyes, nose, arms and anus. This resulted in her persistently washing her clothes and herself and reporting the retirement village where she lived to the Health Department. She had received anti-scabies treatment empirically. She had a long history of severe depression after the death of her husband, for which she took doxepin. She had paranoid ideation about her neighbours and saw things crawling down the walls, and had moved residences several times to avoid these problems. Other medical problems included treated hyperthyroidism, oesophageal stricture and partial pneumonectomy. She did not drink alcohol. Score on Folstein Mini Mental State Examination was 28/30. She was prescribed haloperidol (0.5 mg twice daily) and continued taking doxepin. The delusions of scabies subsided. Four years later, she developed new thoughts that dirt was being deposited in her unit by builders working nearby. She had stopped taking haloperidol in the interim. She became agitated, covering her furniture and closing all gaps around doors and windows. She was prescribed olanzapine (2.5 mg at night). Diagnosis: Delusional parasitosis in conjunction with depressive illness. Patient 4 A 74-year-old woman was referred for assessment of tactile hallucinations. She had a 2-month history of presumed worm infestation and persistent complaints of anal and vaginal pruritus despite multiple courses of an anthelminthic. She had complained previously of feeling head and body lice. Her past medical history included chronic airways limitation, trigeminal neuralgia, which was treated with sodium valproate, and temporal arteritis, which had responded previously to corticosteroid therapy. She lived alone and was previously active, but had became depressed and isolated because of these delusions. No abnormalities were found on physical examination. Examination of a skin specimen, which the patient thought contained worms, showed cotton threads. Full blood count was normal, with no eosinophilia and normal erythrocyte sedimentation rate. Sigmoidoscopy found no abnormalities, while computed tomography of the head showed a previous left parietal infarct. She was prescribed pimozide (2 mg daily), with complete resolution of the worm sensation. Diagnosis: Isolated delusional parasitosis. An older person requesting treatment for an infestation may not seem unusual. However, when the complaint persists despite repeated treatments for lice, scabies and other parasites, and examination shows no evidence of an infestation, the differential diagnosis includes delusional parasitosis. Management of this condition is challenging but rewarding, as it may cause severe emotional, social and physical disability in both the afflicted individuals and those around them. We describe four patients with delusional parasitosis who were managed in our department of geriatric medicine (see Clinical records). Delusional parasitosis, named in 1946,1 is a chronic psychiatric disorder in which patients have a false and fixed belief that they are infested by parasites. It is not a phobia.2 The core of the disease is the delusion of infestation and, although it is a psychiatric disorder, patients usually seek help from dermatologists. Its onset is insidious, and the delusion is typically preceded by a primary tactile experience, such as pruritus or paraesthesia, or tactile hallucination, which precipitates the secondary delusion of infestation. The condition may occur as an isolated thought disorder in a person whose psyche is otherwise intact, as illustrated by Patient 4. This has also been termed monosymptomatic hypochondriacal psychosis3 and “primary” delusional parasitosis.4 When associated with a psychiatric condition, such as schizophrenia (Patient 2) or depression (Patient 3), delusional parasitosis has been termed “secondary functional”, and, when caused by a medical illness (eg, diabetes, malignancy or nutritional deficiency), medication or substance misuse, it has been termed “secondary organic”5 (Patient 1). In the classification system of the Diagnostic and statistical manual of mental disorders (DSM-IV), primary delusional parasitosis corresponds to “delusional disorder, somatic type”, while the secondary organic type corresponds to “psychotic disorder due to general medical condition”.6 The prevalence of delusional parasitosis is unknown, but our literature review identified several hundred cases reported by dermatologists and entomologists.2,3,5,7,8 It can occur at any age, the average being in the fifth decade. In the older age group, women are more often affected than men.2,7 Mean duration of symptoms before attending tertiary care was 1.3 years in one study.8 Patients with no precipitating medical problems or psychiatric illness often have a personality disorder and isolate themselves, but function well in other aspects of their day-to-day living.3 Patients provide incredibly detailed descriptions of the “bugs” and explanations about why they are not visible on examination. They often bring in “specimens” in a small container, which are actually pieces of skin, lint or hair (“the matchbox sign”), or may identify “bugs” during examination by probing into skin until they are able to pick up a small piece of tissue. This may produce traumatic ulcers of varying size, typically on areas the patient can reach, in an asymmetrical distribution corresponding to the dominant hand. Secondary dermatitis may develop as a result of repeated washing and application of chemical preparations.2 Management involves first excluding a real infestation and any underlying condition, including psychiatric disorders, medical conditions with altered sensation, use of drugs (prescribed and illicit) or withdrawal from alcohol or cocaine. Mental state, including cognition, needs to be assessed. Other investigations may include examination of skin scrapings and skin biopsies. In therapy, the most important step is to establish a trusting doctor–patient relationship. An empathic approach is required, acknowledging the reality of patients’ symptoms without challenging or confirming their views about the cause. Samples of any alleged parasites presented must be examined. Ideally, patients should be referred to a psychiatrist, but many resist this. Consequently, medication with an antipsychotic should be initiated by the doctor who makes the diagnosis. Treatments include pimozide2,3,5,7 and the newer atypical antipsychotics, such as risperidone.9 Medication compliance can be a problem. There have been some reports that tricyclic antidepressants and anxiolytic agents alleviate the reactive component of the condition without much effect on the delusions.2,7 Doxepin has strong antihistamine and anxiolytic effects, in addition to its antidepressant effect, and, based on its effectiveness in chronic neurotic excoriation,10 may be useful in patients who frequently experience intense pruritus, anxiety and agitation as well as depressive symptoms. Corticosteroid creams and lotions may be helpful adjuncts to alleviate skin symptoms. Lessons from practice Delusions of parasitosis may occur alone or in association with medical or psychiatric illness. Antipsychotic agents are the mainstay of medical management. Empathy and a good doctor–patient relationship are required to optimise outcome.

Linda Le BM BS, DCH · Peter N Gonski BMedSc, FRACP

Trial: Lipozencic J, Skerlev M, Orofino-Costa R, et al, and the Tinea Capitis Study Group. 2002; 146: 816-823.

Chris Commens FACD

A 71-year-old man with a past history of right-sided, renal cell carcinoma presented with a recurrent, right upper eyelid lesion (Box, Figure A). The initial biopsy showed Bowen's disease, but review after Mohs micrographic surgery revealed focal sebaceous differentiation suggestive of in-situ sebaceous carcinoma. A diagnosis of Muir–Torre syndrome was suspected, and the patient was referred for genetic counselling and targeted cancer surveillance. This led to the discovery of multiple dysplastic colonic adenomas and a left renal cell carcinoma (Box, Figure B). Muir–Torre syndrome is an autosomal-dominant genodermatosis characterised by cutaneous sebaceous neoplasia and one or more visceral malignancies. Diagnostic criteria include at least one sebaceous gland adenoma, epithelioma, or carcinoma, and at least one internal malignancy. The diagnosis of sebaceous carcinoma can be difficult, particularly in the periocular region, where it often masquerades clinically as blepharoconjunctivitis or recurrent chalazia. Furthermore, sebaceous carcinoma often displays only focal differentiation and, as seen in our patient, may be histologically misdiagnosed as squamous-cell or basal-cell carcinoma. A history of internal malignancy in patients presenting with sebaceous gland carcinoma should raise the possibility of Muir–Torre syndrome. Correct diagnosis in this case enabled early detection of dysplastic colonic polyps and renal cell carcinoma. A: Clinical photograph showing induration and ulceration of the central right upper eyelid margin. B: Computerised tomography scan showing a left renal mass (arrow) confined to the capsule.

Celia S Chen MB BS · Lindy Loweinstein · Shyamala C Huilgol FACD · Dinesh Selva FRANZCO · Craig James FACPA

Palmar erythema is a very unusual manifestation of sarcoidosis. We report on a patient whose presenting features of sarcoidosis were palmar erythema and a hoarse voice. The diagnosis was confirmed by palmar skin biopsy and the patient responded well to treatment with prednisolone. Sarcoidosis is a disease of unknown aetiology that can affect almost any organ of the body. Cutaneous involvement, occurring in up to 25% of cases of systemic sarcoidosis, is well recognised.1 However, palmar erythema is a very unusual skin manifestation of sarcoidosis — to our knowledge, it has been reported only once before in the literature.2 We describe a patient with palmar erythema and a hoarse voice who was subsequently shown to have sarcoidosis. Clinical recordA 58-year-old man presented complaining of increasing hoarseness of voice of three weeks' duration. The patient had also noticed increasing redness and a burning sensation over both palms. He had no history of any drug intake, fever, cough, breathlessness, chest pain, dysphagia, weight loss or anorexia. The patient was a non-smoker and did not consume alcohol. On examination, he had a confluent, non-blanching, macular, erythematous rash on both palms (Box 1), but no other skin rash elsewhere on the body. There was no thyromegaly or peripheral lymphadenopathy, and there were no abdominal, cardiovascular, respiratory or nervous system abnormalities. Ophthalmological examination was suggestive of episcleritis. Results of routine tests (including biochemical, haematological and liver function tests) were all normal except for a raised erythrocyte sedimentation rate (65 mm/hour). Indirect laryngoscopy performed to investigate the hoarseness revealed paralysis of the right vocal cord with no other local abnormality. The palate showed normal mobility and the bilateral gag reflex was normal. A chest x-ray showed clear lungs, with some mediastinal widening. A computed tomography scan of the thorax revealed enlarged mediastinal lymph nodes (Box 2). A Mantoux test was non-reactive. The serum level of angiotensin-converting enzyme was 76.2 U/L (normal range, 8–52 U/L). A skin biopsy taken from the palmar rash revealed non-caseating granulomas with multinucleated giant cells (Box 1). No acid-fast bacilli or fungal hyphae were detected on direct staining or subsequent culture of sputum and skin biopsy specimens. The histological features were thus suggestive of sarcoidosis. After two weeks' treatment with prednisolone 1 mg/kg per day, the patient's rash had resolved completely and the hoarseness was markedly reduced. A repeat computed tomography scan of the chest done after four weeks of treatment showed that the mediastinal lymph nodes had decreased in size. The patient has remained asymptomatic over seven months of follow-up. DiscussionSarcoidosis may involve any organ of the body and can have protean clinical manifestations, including skin lesions. Skin manifestations can be in the form of erythema nodosum (the most common), subcutaneous nodules, plaques, lupus pernio or maculopapular eruptions.3 Palmar erythema may be the presenting feature of a number of skin diseases such as eczema, psoriasis, tinea and pityriasis rubra pilaris.4 Isolated palmar erythema is commonly seen in pregnancy and liver diseases, and may occasionally occur in rheumatoid arthritis.5 However, as a manifestation of sarcoidosis, it is extremely rare.2 Interestingly, the only other reported patient presenting with palmar erythema was also of Indian origin. The diagnosis of cutaneous sarcoidosis is based on three features: clinical or radiological evidence of multisystem involvement; presence of non-caseating granulomas on histological examination; and failure to detect acid-fast bacilli or fungae by sputum or skin culture or in stained tissue sections. In our patient, all three features were present. An interesting feature was the patient's hoarse voice. Hoarseness in sarcoidosis may be caused by direct infiltration of the larynx,6 infiltration of the cranial nerves (especially IX and X),7,8 or compression of the recurrent laryngeal nerve by enlarged mediastinal lymph nodes, leading to vocal cord palsy.9 As indirect laryngoscopy did not show any local cause for the vocal cord palsy, the hoarseness in the present case was likely to be due to the third cause. A few series of cases of sarcoidosis have been reported from India.10-12 The clinical presentation in most of these cases included fever, weight loss, cough, breathlessness or hepatosplenomegaly. Skin lesions were reported in very few of the cases, and palmar erythema in none. Our patient was also somewhat atypical in having mediastinal lymphadenopathy, which is reported to be less common in India (28%) than in Western countries (70%).13 To our knowledge, sarcoidosis presenting as a combination of palmar erythema and hoarseness of voice has not previously been reported. Our case thus highlights the diverse clinical manifestations of this disease and emphasises the fact that palmar erythema may be the only visible sign of sarcoidosis. 1: Palmar erythema associated with sarcoidosis A: Diffuse erythematous macular rash seen on the palmar surface (biopsy site arrowed). B: Skin biopsy, showing non-caseating granulomas. C: Skin biopsy, showing multinucleated giant cell (arrowed). 2: Computed tomography scan of the thorax, showing right paratracheal lymphadenopathy

Ravinder P S Makkar MB BS, MD · Surabhi Mukhopadhyay MB BS, MD · Amitabh Monga MB BS, MD · Anju Arora MB BS, MD · Ajay K Gupta MB BS, MD

Treatment of skin disease. Comprehensive therapeutic strategies. Mark Lebwohl, Warren R Heyman, John Berth-Jones, Ian Coulson (editors). London: Mosby, 2002 (xxiv + 693 pp). ISBN 0 7234 3198. The treatment of skin disease has often been viewed as simply deciding whether a rash is “dry” or “wet” and then choosing between a range of creams, ointments and lotions. This book should help to change this misperception by demonstrating that progress has been made; current therapeutic options have been analysed in relation to levels of evidence, thus elevating the status of dermatological therapy. The editors have invited over 200 dermatologists from around the world to summarise and assign current skin therapy for 213 separate conditions. Levels of evidence have had to be modified, as, at present, there are insufficient double-blind controlled trials for most treatments to follow the Cochrane Collaboration’s levels of evidence. By using this modification, the review of available treatments can be stratified. The format adopted for each topic is outstanding. It consists of a representative colour photograph of the condition, a brief clinical description, management strategy, specific investigations and three separate levels of treatments — first, second and third choices. Pertinent references are included within the text and there is a succinct one- to two-line summary. The inclusion of some references to what may appear to be anecdotal reports of successful treatments may serve to stimulate larger controlled studies. Most of the authors have been chosen for their recognised expert knowledge in their fields and each section is a distillation of their individual experience and assessment of current treatments. This book is a useful reference for both general practitioners and specialists, as it deals with most common skin conditions, such as dermatitis, skin infections, skin cancers, as well as rarer conditions such as Fox–Fordyce disease. The book is ideal for the busy practitioner, as each section is short, structured and packed with useful information. Almost all the treatments included are currently available in Australia. The book is a handy guide for all who treat skin diseases. Steven KossardAssociate Professor of Dermatology Skin and Cancer Foundation Australiaand St Vincent’s Hospital, NSW

Steven Kossard

Any new patient with suspected genital herpes should have diagnostic testing with virus identification. Type-specific serological tests that distinguish between antibodies for type 1 and type 2 herpes simplex virus (HSV) may be useful to determine previous exposure but cannot be used to diagnose recurrences of genital herpes. Initial episodes of genital herpes usually require antiviral therapy, while recurrences may be treated with continuous antiviral suppression (if frequent) or episodic therapy; patient counselling and education (including how to recognise lesions) are essential. Topical or systemic therapy is available for initial and recurrent non-genital herpes simplex. Primary varicella infection (chickenpox) and herpes zoster (shingles) are usually diagnosed clinically, but can be confirmed by detection of varicella–zoster virus antigens or nucleic acid from swabs of lesions or by antibody tests. Antiviral therapy should be considered in chickenpox if disease is complicated or the patient is immunocompromised. In herpes zoster, antiviral therapy should be given within 72 hours of onset to patients aged over 50 years or with severe pain or neurological abnormalities to reduce the likelihood and duration of postherpetic neuralgia.

Dominic E Dwyer MD, FRACP, FRCPA · Anthony L Cunningham MD, FRACP, FRCPA

An atlas of surface microscopy of pigmented skin lesions: dermoscopy. Scott W Menzies, Kerry A Crotty, Christian Ingvar, William H McCarthy. Sydney: McGraw-Hill, 2003 (vii + 175pp). ISBN 0 07 471102 4. All medical practitioners who examine patients should be able to diagnose early melanoma. The diagnostic algorithm involves ascertaining how long the lesion has been present and whether it has been undergoing change. Examination includes not only observation of the specific morphology of the pigmented lesion in question, but also considering the lesion in the context of other skin lesions that the patient may have. This book on surface microscopy focuses specifically on the diagnosis of pigmented skin lesions based upon their morphology and, in particular, their morphology when examined with a hand held surface microscope. The authors have data to show that general practitioners achieve a 39% improvement in the sensitivity for the diagnosis of melanoma when using this Atlas. This cannot be specifically interpreted as meaning that fewer melanomas are missed when using this book, but it may translate to fewer benign naevi being excised unnecessarily. Nevertheless, any book that improves diagnostic accuracy has to be welcomed, and this book certainly does that. Examination of pigmented lesions using surface microscopy is a double-edged sword. To the uninitiated, hand held microscopes are confusing and may actually diminish diagnostic accuracy. As such, no general practitioner should pick up a hand held surface microscope without first having read this book. This excellent book is simply written and beautifully illustrated. It is the best of its type in the discipline and the first edition has been widely used by dermatologists and dermatology trainees. The steps to diagnosis are clear and constructive, and the quiz on the CD-ROM that accompanies the book is also very useful. At $94.95, including a CD-ROM, it is excellent value and I recommend it to all general practitioners contemplating the use of a hand held surface microscope. Rodney D SinclairDermatologistMelbourne, VIC Invasive melanoma - clinical view (a) and surface microscopy (b). Reproduced with permission. Order this book

Rodney D Sinclair

Dermatology, although a small specialty, has made great leaps forward in prevention, diagnosis and treatment in the past five years. Prevention. Skin cancer is the number one malignancy in Australia, and we lead the world in skin cancer control programs, which have now been running for over two decades. However, it is only within the past five years that we have been able to record a turnaround — not only in melanoma deaths but also in the incidence of both melanoma and basal cell carcinoma — in Australians young enough to have been influenced by these programs. Intervention. Major changes are coming in the treatment of some non-melanoma skin cancers. Topical imiquimod cream is the first of a new generation of immune modulators, which results in local cutaneous induction of interferon α and interleukin 12. Cure rates of almost 90% for superficial basal cell carcinomas have been recorded after six weeks of daily application.1 This topical treatment applied by the patient also shows promise for nodular basal cell carcinoma, solar keratosis and Bowen's disease (squamous cell carcinoma in situ). Research into the biology of ultraviolet (UV) radiation causing skin cancer has enhanced our awareness of its potential in treatment of skin disease. New techniques, such as photodynamic therapy, are being developed to treat many epithelial tumours, including those of the skin. The cosmetic results can be equal to or better than other treatment modalities.2 The role of photodynamic therapy in the treatment of solar keratoses, basal cell carcinoma, in-situ and invasive squamous cell carcinoma, cutaneous T cell lymphoma, and Kaposi's sarcoma is being delineated. Narrowband UVB therapy has largely superseded PUVA and broadband UVB in the management of psoriasis and atopic dermatitis. Narrowband UVB has the advantage of being safe in pregnancy and childhood, and is thought to have a lower risk of inducing the development of cutaneous malignancies. It has also been used in the prophylactic management of photosensitive conditions such as polymorphic light eruption, actinic prurigo, solar urticaria and cutaneous porphyria. The horizons of laser therapy continue to expand. Vascular lasers are being used to treat lesions ranging from spider telangiectases through poikiloderma of Civatte (the common sunlight-related pigmentation on the neck in women) to port wine stains. Short-pulse lasers are now the preferred method of treatment for tattoo removal. Disorders of cutaneous pigmentation, such as naevus of Ota, solar lentigines, café au lait macules, freckles, melasma and postinflammatory pigmentation, have been successfully treated with Q-switched ruby, Nd: YAG and alexandrite lasers. Laser-assisted epilation is not considered a permanent method of hair removal, but some patients achieve a long term reduction in hair density after a single treatment. Immunomodulatory drugs are increasingly used in dermatology for life-threatening diseases such as pemphigus vulgaris (100% mortality without treatment), pyoderma gangrenosum and vasculitis, as well as for patients with severe and intractable inflammatory diseases with an immunological component, such as psoriasis and atopic dermatitis. Mycophenolate mofetil and tacrolimus are now well established in the treatment of refractory immunobullous diseases, and newer agents such as rapomycin, infliximab and leflunomide all show promise, with enhanced efficacy and side effect profiles compared with conventional systemic therapies such as prednisolone, azathioprine and cyclosporin.3 Diagnosis. Genetic identification of dermatological diseases inherited as single-gene disorders has led to greater understanding of their mechanism, improved diagnosis (including antenatal testing) and classification, as well as genetic counselling.4 Some examples include porphyria, epidermolysis bullosa, Darier's and Hailey–Hailey diseases, xeroderma pigmentosum, and a variety of familial multiple tumour syndromes, such as neurofibromatosis and Gardner's, Gorlin's (multiple basal cell naevus) and Cowden's (multiple haematomas) syndromes. As our understanding of virology has increased, we have been finding more cutaneous diseases that appear to be caused by a viral infection. Examples include pityriasis rosea, a common disease in young people, and also Kaposi's sarcoma, both now being attributed to infection with human herpesviruses 7 and 8, respectively. Educating future generations. An atlas of common skin diseases has been published which is based on epidemiology studies looking at the frequency, morbidity and treatment in Australia of conditions such as acne, eczema, tinea, warts, and nappy rash.5 No other country has been able to map out in detail the frequency and morbidity of these conditions. As a result, education programs similar to those used for skin cancer control are being developed in Victoria and introduced into all schools and the Maternal and Child Health network. This is another world first for public health in Australia, a country which has an international reputation for this approach to disease control.

Robin Marks MB BS, MPH, FRACP, FACD · Peter A Foley MB BS, BMedSc, MD, FACD · Rodney D Sinclair MB BS, FACD

Bites and stings Outbreak of caterpillar dermatitis caused by airborne hairs of the mistletoe browntail moth (Euproctis edwardsi) Caterpillars may be an under-recognised cause of skin and eye reactions. We report a four-month outbreak of recurrent papulourticarial rash among staff and visitors at a community centre. The cause was eventually diagnosed as airborne hairs from caterpillars of the mistletoe browntail moth (Euproctis edwardsi), which infested a eucalypt tree growing in front of the centre. To our knowledge, this is the first clear case of airborne caterpillar hairs causing dermatitis in an indoor environment. Corrine R Balit, Helen C Ptolemy, Merilyn J Geary, Richard C Russell and Geoffrey K Isbister MJA 2001; 175: 641-643 Clinical records - Discussion - Acknowledgements - References - Authors' details - - - More articles on Informatics and computers Lepidopterism refers to adverse effects from moths and butterflies (Lepidoptera), the most common arising from skin and eye contact with caterpillar hairs or spines.1 The pattern of reaction varies between caterpillar types.2 Caterpillar dermatitis can result not only from direct contact with the caterpillar, but also from airborne caterpillar hairs.3,4 Caterpillar dermatitis is probably far more common than previously realised.1,3,5-10 Patients often present with a rash of unknown origin, and the association with caterpillar exposure is often not recognised. We report an outbreak of caterpillar dermatitis related to an infestation of the caterpillar Euproctis edwardsi (Family: Lymantriidae), commonly known as the mistletoe browntail moth. The infestation occurred at a community centre, where staff and visitors experienced dermatitis and skin irritation for several months before caterpillar dermatitis was diagnosed. To our knowledge, these are the first clear cases of dermatitis caused by airborne caterpillar hairs in an indoor environment. Clinical records In February 2001, the Wentworth Public Health Unit, Sydney, NSW, was contacted about a local community centre where both staff and clients had been experiencing skin reactions and irritation. Seven of the 14 employees of the centre were affected, as were about 5% of clients seen at the centre. The reactions began in November 2000 and appeared while people were at the centre. They would settle or resolve while people were away from the centre on weekends and holidays and recur on their return to work. The skin reactions comprised a papulourticarial rash. Clinical effects in six patients are shown in Box 1, and further details of one patient in Box 2. The centre had been sprayed against a variety of pests on several occasions, without benefit. Each time, the pest control company reported no visible evidence of insects in the centre. Many staff sought medical advice, and various treatments were prescribed, including topical corticosteroids and oral antihistamines, with no benefit. The site was inspected by the Environmental Health Officer of the Population Health Unit (H C P). In front of the centre was an ironbark tree (Eucalyptus sideroxylon) which contained a mistletoe plant and, at its base, a large clump of caterpillars (pictured above). The tree was growing adjacent to the mail box, about 3 m from the front door of the centre and the window of the upstairs lunchroom, and 10 m from the intake vent of the air-conditioning system. Caterpillar samples were identified at the Department of Medical Entomology, Westmead Hospital, Sydney, as E. edwardsi, commonly known as the mistletoe browntail moth. Caterpillar-like hairs were also identified in samples of dust from inside the centre. Based on reports of successful use of sticky tape to sample affected areas for nematocysts in jellyfish stings,11 this method was tried on three affected individuals. Transparent sticky tape was applied to the affected area and then placed onto a glass slide. Caterpillar-like hairs were identified from two of the three people thus tested (Box 3). The caterpillars were treated with insecticide and removed along with the mistletoe, according to the recommendations of the environmental health officer. Although the officer also recommended re-inspection of the tree and removal of any mistletoe regrowth the following spring, the centre eventually removed the tree completely. The building was thoroughly cleaned to remove all caterpillar hairs. Follow-up of people at the centre a month later showed significant improvement in their conditions. Occasional episodes of skin irritation in two people were successfully treated by immediate application of sticky tape to the affected areas. Follow-up after six months revealed no further reports of irritation. Discussion This is the first case series that clearly demonstrates dermatitis resulting from airborne caterpillar hairs in an indoor environment. Although the cause of the dermatitis was not identified for months, once found treatment was straightforward — removal of the caterpillars and their food source to prevent re-exposure. We also demonstrated the usefulness of the sticky-tape technique in diagnosing, as well as treating, caterpillar dermatitis by removing caterpillar hairs from the skin.1E. edwardsi is reported to be the most important cause of caterpillar dermatitis in Australia.1 It occurs from Queensland to South Australia and is widely distributed in south-eastern Australia.12 Its food source is usually Amyema species of mistletoes.1 The incidence of caterpillar dermatitis peaks between December and March,3 with two generations of the moth each year, in early summer and autumn.1 The fully grown caterpillar is about 4 cm long and has golden tufts of spicules on its back. These spicules easily separate from the caterpillar, causing irritation on skin contact. The most common reaction is a papulourticarial rash, usually on exposed skin, but possibly more extensive if clothing is contaminated.1 The hairs are small enough to become airborne and affect people without direct contact with the caterpillar. In patients presenting with skin reactions and dermatitis of unknown cause, particularly recurrent rash, a careful history of location and seasonality is required. Caterpillar dermatitis should be considered in the differential diagnosis and can be confirmed by identifying the source of the caterpillar or its hairs. Microscopy of sticky-tape samples from the affected area may aid diagnosis. The use of sticky tape has been reported previously as a treatment option in caterpillar exposures, to remove fine hairs that may cause ongoing symptoms.5 This is the first report demonstrating the use of sticky tape as a simple and effective diagnostic tool. Once the source of exposure has been removed, treatment of caterpillar dermatitis is essentially symptomatic and supportive. Patient 1 allowed several treatment options to be assessed. Most effective was topical aspirin paste, with improvement within hours. Topical aspirin has previously been reported to be effective for histamine-induced rash.13 The paste is made by adding a few drops of water to a soluble aspirin tablet and applying it to the affected area. A topical preparation containing lignocaine offered some symptomatic relief but did not shorten the duration of symptoms. A topical hydrocortisone cream produced no noticeable change. Outbreaks of caterpillar dermatitis are not uncommon and may be difficult to diagnose. Sticky-tape sampling of the affected area may aid diagnosis. Topical aspirin paste appears an effective treatment, and topical lignocaine preparations and oral antihistamines may provide partial symptomatic relief. Acknowledgements We thank Dr James Isbister (Royal North Shore Hospital, Sydney, NSW) for providing digital images of the sticky tape slides and Mr Stephen Doggett (Department of Medical Entomology, ICPMR, Westmead Hospital) for taking the clinical photograph. We also thank Judith Kirby and all the staff at the NSW Poisons Information Centre for their support and assistance. References Southcott RV. Lepidopterism in the Australian region. Records of the Adelaide Children's Hospital 1978; 2: 87-173. Isbister GK, Whelan PI. Envenomation by the billygoat plum stinging caterpillar (Thosea penthima). Med J Aust 2000; 173: 654-655. Thompson JI. Mistletoe brown tail moth - a skin irritation caterpillar. AGFACTS. Sydney: NSW Department of Agriculture, 1984. Southcott RV. Some harmful Australian insects. Med J Aust 1988; 149: 656-662. Dunlop K, Freeman S. Caterpillar dermatitis. Australas J Dermatol 1997; 38: 193-195. Scholz A, Russell R, Geary M. Investigation of caterpillar dermatitis in school children. NSW Public Health Bull 1993; 4: 65-66. Blair CP. The browntail moth, its caterpillar and their rash. Clin Exp Dermatol 1979; 4: 215-222. Cleland JB. Papulo-urticarial rashes caused by the hairlets of caterpillars of the moth (Euproctis edwardsi Newm.). Med J Aust 1920; 1: 169-170. McKeown KC. Australian insects. An introductory handbook. Sydney: Royal Zoological Society of NSW, 1942. Lee D. Arthropod bites and stings and other injurious effects. Sydney: School of Public Health and Tropical Medicine, University of Sydney, 1975. Currie BJ, Wood YK. Identification of Chironex fleckeri envenomation by nematocyst recovery from skin. Med J Aust 1995; 162: 478-480. Musgrave A. Harmful moth caterpillars. Aust Museum Mag 1941; 7: 391-396. Yosipovitch G, Ademola J, Lui P, et al. Topically applied aspirin rapidly decreases histamine-induced itch. Acta Derm Venereol 1997; 77: 46-48.(Received 14 Jun, accepted 27 Sep, 2001) Authors' details NSW Poisons Information Centre, The Children's Hospital, Sydney, NSW. Corrine R Balit, BPharm, Pharmacist. Wentworth Population Health Unit, Sydney, NSW. Helen C Ptolemy, BAppSci, Environmental Health Officer. Department of Medical Entomology, ICPMR, Westmead Hospital, Sydney, NSW. Merilyn J Geary, DipAppSci, PestContCert, Laboratory Manager; Richard C Russell, MSc, PhD, Director, and Associate Professor, University of Sydney, NSW. Department of Clinical Toxicology and Pharmacology, Newcastle Mater Misericordiae Hospital, Newcastle, NSW. Geoffrey K Isbister, BSc, MB BS, Toxicology Registrar. Reprints will not be available from the authors. Correspondence: Ms Corrine R Balit, NSW Poisons Information Centre, The Children's Hospital, Locked Bag 4001, Westmead, NSW 2145. CorrineBATchw.edu.au Make a comment 1: Details of six people who developed a papulo-urticarial rash at the community centre Patient (sex, age in years) Affected areas Duration of rash Sticky tape sample 1. Staff (M, 24) Arms, legs Recurrent, Nov-Feb Positive 2. Staff (F, 26) Face, legs, hands, stomach Recurrent, Nov-Feb Negative 3. Staff (F, 38) Arms, chest, neck Recurrent, Nov-Feb Positive 4. Staff (F, late 30s) Arm, chest, face Recurrent, Nov-Feb Not available 5. Visitor (F, 23) Neck, chest, face, arms 5 days Not available 6. Visitor (F, 32) Neck, chest 24 hours Not available F = female. M = male. Back to text 2: Severe reaction to caterpillar hairs (Patient 5) A 23-year-old woman developed a moderately severe reaction after visiting the community centre for an hour. She had a past history of atopy, asthma and mild atopic dermatitis. On examination, exposed areas were affected, including the forehead, face, neck, upper chest and lower arms. The reaction began as an itchy red area within six hours of exposure, and over the next 24 hours developed into a papulourticarial rash with intense pruritus (pictured 24 hours after exposure). Initial dizziness and light-headedness were the only systemic effects. A number of treatments were tried in different affected areas, including topical hydrocortisone (1%), a topical combination of lignocaine, bufexamac and chlorhexidine, topical aspirin paste, and sedating and non-sedating antihistamines. Areas treated with aspirin paste showed marked improvement over four hours. Topical lignocaine and sedating antihistamines provided symptomatic relief, but other treatments produced minimal responses. The rash cleared completely over five days. Back to text 3: Caterpillar hairs from Patient 1 Sticky-tape sample from an area of papulourticarial rash in Patient 1, showing a human hair (centre) surrounded by numerous smaller, caterpillar-like hairs (original magnification, x 20). Inset shows a control slide of hairs from the caterpillar Euproctis edwardsi (original magnification, x 40). Back to text

Corrine R Balit · Helen C Ptolemy · Merilyn J Geary · Richard C Russell · Geoffrey K Isbister

Research Use of fake tanning lotions in the South Australian population Kerri R Beckmann, Barbara A Kirke, Kieran A McCaul and David M Roder MJA 2001; 174: 75-78 Abstract - Methods - Results - Discussion - Conclusions - References - Authors' Details - - More articles on Public and environmental health Abstract Objective: To explore the relationship between the use of fake tanning lotions and repeated sunburn among South Australian adults, with a view to informing the Anti-Cancer Foundation of South Australia's (ACFSA) policy on fake tanning products. Study design: Population survey. Participants: 2005 South Australians aged 18 years or older, selected randomly from the electronic White Pages. Main outcome measures: Self-reported use of fake tanning lotions in the past 12 months; frequency of sunburn over summer; and various sun-protective behaviours. Results: 2005 of the 2536 eligible participants (79%) were surveyed by telephone. Fake tan use was most prevalent among women (15.9%), people aged 18-24 years (15.4%), and people with household incomes above $40 000 per year (11.9%). Fake tan users were more likely than non-users to use sunscreens (81.3% v 56.5%; P < 0.001), but less likely to take other precautions such as wearing hats (40.9% v 51.0%; P = 0.04) and protective clothing (22.3% v 34.1%; P = 0.005). They were also more likely to report having been burnt more than once over summer (26.2% v 16.5%; P = 0.025). Multivariate analysis indicates a statistically significant association between fake tan use and repeated sunburn (odds ratio, 2.07; 95% confidence interval, 1.17-3.69), which was independent of age, sex, skin type and sun-protection practices. Conclusion: Users of fake tanning products may be at greater risk of repeated sunburn. The ACFSA sees no justification at this stage for altering its present policy position of not actively promoting the use of fake tanning lotions as a means of reducing sunburn. Anticancer organisations in Australia have been conducting programs aimed at reducing Australia's high rate of skin cancer for over two decades.1 The main objective of these programs is to encourage people to reduce their exposure to solar ultraviolet radiation, the major contributing factor to the development of skin cancer.2In Australia public awareness about the dangers of overexposure to the sun is generally high. In spite of this, a suntan is still desired by some sectors of the community -- in particular, young, fashion-conscious people.3,4 Skin cancer prevention programs have attempted to change attitudes that value tanned skin as attractive and healthy with such messages as "there is no such thing as a safe tan" and "a tan is a sign of skin damage". Last year, Chapman challenged anticancer organisations to consider the role that fake tanning lotions might play in reducing sun exposure, suggesting that they should be assessed as a potential harm-reduction strategy.5 The Anti-Cancer Foundation of South Australia (ACFSA) has, for a number of years, provided information on fake tanning lotions. While not actively encouraging their use, the information suggests that, for those desiring a tan, using fake tanning lotions is preferable to exposure to artificial or solar ultraviolet radiation. In October 1999, the ACFSA included a question on the use of fake tanning lotions in a Health Monitor Survey along with questions on skin type, experience of sunburn and frequency of wearing hats, cover-up clothing, applying sunscreen and seeking shade. This article reports the findings of that survey and discusses them in relation to the position taken by the ACFSA regarding fake tanning lotions. Methods Questions relating to sun exposure and ultraviolet radiation protective behaviours, including one relating to the use of fake tanning lotions, were asked of a random sample of South Australians, by computer-assisted telephone interviewing. These questions (Box 1) were part of a larger health-related survey organised and conducted by the Department of Human Services, South Australia, in October 1999. Except for the question relating to fake tan use, these questions have been used routinely in monitoring sun-protection behaviours in South Australia and were originally validated as written questions in a national Secondary School Children's Survey conducted triennially since 1990.6 The question on fake tan use is a slightly modified version of a question asked in Victorian surveys in 1993 and 1995.7,8Ethical approval for the survey that incorporated the questions used in this study was obtained through the Department of Human Services, with legal authorisation under section 64d of the South Australian Health Commission Act (1976). A sample of 3400 residences from rural and metropolitan areas within South Australia was drawn from the electronic White Pages. One adult from each household (the person whose birthday was the most recent) was invited to participate. Two thousand and five interviews were conducted from the 2536 households that could be contacted after six callback attempts, giving a participation rate of 79.1%. All data were weighted by age, sex and region, and on the probability of selection within the household. The population profile for weighting was obtained from the Australian Bureau of Statistics' estimated population for South Australia, 1997. Geographical region was defined as either metropolitan or country region. Both descriptive analysis of the survey data and logistic regression modelling were undertaken using STATA version 6,9 as this software allows calculation of robust estimates of standard error using methods devised by Huber10 and White.11 Consequently, variance estimates are adjusted for the data weighting. The relationship between fake tan use and reported sunburn over summer was examined using logistic regression modelling, allowing adjustment for age, sex, skin type and sun-protective behaviours. We first constructed a model containing known risk factors for sunburn and then added fake tan use to this model to establish if this improved the fit of the model. "Having been burnt two or more times during the previous summer" was the dependent (outcome) variable. For each of the sun protective behaviour questions, respondents were coded as regular users if they indicated that they "usually, almost always, or always" took such precautions when out in the sun for an hour or more, and were coded as irregular users if they indicated that they "never, rarely or sometimes" took these measures. Results Based on results from this survey, the estimated prevalence of fake tanning lotion use during the past 12 months among South Australians aged 18 years or more was 8.7% (95% confidence interval [CI], 7.3%-10.5%). The prevalence of fake tan use among various subgroups of the population is shown in Box 2. The use of fake tanning lotions is most common among younger people, particularly women, with the peak prevalence being 28% among young women aged 18-24 years. Fake tan use is also more common among those who report that their skin burns before tanning, compared with those whose skin just tans or just burns. Fake tan use also appears to be related to household income, with those with relatively high household incomes (above $40 000 per year) more likely to use fake tanning lotions. Individuals who had used fake tanning lotions in the past year were more likely to report regularly using sunscreen with a sun protection factor (SPF) of 15+ or higher when in the sun than non-users (81% v 57%; P < 0.001). However, they were less likely to report regularly wearing hats (41% v 51%; P = 0.04) or protective clothing (22% v 34%; P = 0.005). They reported seeking shade at levels similar to those who had not used fake tanning lotions (80% v 76%, P = 0.4). Those who had used fake tanning lotions were also more likely to report having been burnt two or more times during the previous summer (26% v 17%; P = 0.025) (Box 3). Factors such as age, skin type, sex and regular sun-protective behaviours are likely to confound the association between fake tan use and risk of burning. Results of logistic regression modelling, which takes into account the effects of these potential confounders, indicate an increased risk among fake tan users of having been sunburnt more than once (odds ratio [OR], 2.07; 95% CI, 1.17-3.69), as shown in Box 4. As the use of fake tanning lotions was much more prevalent among women than men, we also undertook regression analyses for women and men separately. No association between fake tan use and sunburn was found among men (OR, 0.90; 95% CI, 0.14-5.97). This was most probably owing to the fact that only 12 men reported using fake tanning lotions. There was, however, a strong association between using fake tanning lotions and repeated sunburn among women (OR, 2.47; 95% CI, 1.38-4.42). Discussion While the overall prevalence of fake tan use among adult South Australians is low (8.7%; 95% CI, 7.3%-10.5%), the use of fake tanning lotions is fairly common in younger women, with more than one in four women aged 18-24 years reporting having used fake tanning lotions in the past year. These findings are consistent with the reported prevalence of use in Victoria.7,8Respondents who reported using fake tanning lotions were more likely to report regularly using SPF 15+ or higher sunscreen when out in the sun during summer, but were less likely to report wearing hats or protective clothing. Fake tan users were more likely to report being sunburnt two or more times over the past summer. When other known risk factors were taken into account, fake tan users had twice the risk of repeated sunburn over summer compared with non-users. The only previously reported findings in relation to the association between fake tan use and sunburn are from two surveys conducted in Victoria, one in 19937 and one in 1995.8 The first of these surveys found a higher prevalence of sunburn among fake tan users (66% v 46%), while the latter survey found no difference (39% v 40%). The inconsistency of these two reports may have been owing to the relatively small sample size of each survey (n < 700). Owing to the limited nature of the questions in this survey, we were unable to determine whether fake tanning lotions were used just at the start of the season to give a tanned look before a sun-induced tan could be achieved, or throughout the summer as a substitute for sunbathing. Given the timing of the survey (ie, spring), there may be some inaccuracy in people's recall of sunburn in the previous summer. However, it seems unlikely to us that one group would have been more or less likely to under-report having been sunburnt, so any recall effect would have been equivalent in both groups. Another limitation in relation to the timing and cross-sectional nature of the survey is the inability to establish a temporal relationship. In some cases, sunburn may have preceded the use of fake tanning lotions. We can not conclude that fake tan use contributes directly to an increased risk of sunburn. We can only suggest that the behaviours of fake tan use and sun exposure may be linked. A further limitation of this study is that we did not ask about the reason for or frequency of use. We do not know whether there are differences in the risk of sunburn among those who use fake tanning lotions only on special occasions (eg, theatrical performances) compared with those who use such products regularly to maintain a tanned appearance. This lack of detail does not negate the finding that, as a whole, those who use fake tanning lotions are at greater risk of sunburn. Regardless of when and why people use fake tanning lotions, the results of this survey do not offer any evidence that use of fake tanning lotions, as currently practised, protects against sunburn. However, since this is an observational study, we can not rule out the possibility that the use of fake tanning lotions may actually offer some protection. It is conceivable that, had users not been applying fake tanning lotions, sunburn levels could have been even higher in this group. Further clarification of this issue would require a longitudinal (experimental) study design. Our results suggest that, rather than reducing their sun exposure, fake tan users are more likely to be exposing their skin to damaging levels of ultraviolet radiation than non-users. The evidence also suggests that, in general, fake tan users take fewer precautions to protect their skin from the sun. While fake tan users are more likely to report using sunscreens, they appear to rely on sunscreens alone for sun protection rather than using multiple strategies, as recommended by the Anti-Cancer Foundation. Some fake tan users may believe that the tanned effect provided by fake tanning lotions offers protection against the sun. Further confusion may arise in cases where their chosen brand of tanning lotion contains sunscreen. An inspection of fake tanning lotions currently available in South Australia showed that most brands do not include a sunscreen, and many state on the label that the fake tan does not provide protection against solar ultraviolet radiation. Some brands also include the advice to use a regular SPF 30+ sunscreen when going into the sun. However, a few brands of fake tanning lotions do contain sunscreen, varying in their sun protection factor from 4 to 15. One commonly available product with an SPF 4 rating states on its label, "UV Protection: Protects you in the sun, providing 4 times your natural sunburn protection". While technically correct, the protection would apply only to the period immediately after application and not for the time that the tan remains visible on the skin. Such claims are obviously very misleading. Anticancer organisations advise that sunscreens need to be reapplied regularly, ideally two-hourly, to maintain adequate protection. If such advice was followed when using a fake tanning lotion containing a sunscreen, the colour of the tan would deepen with each application. Also, it may take up to four hours for the tan colour to fully develop. Most products recommend removal of dry or flaky skin before applying the fake tanning lotion. The need to do this and the effect of repeated applications on tan colour are likely to preclude regular reapplication of fake tanning lotions, thereby increasing the likelihood of users risking sunburn if they rely on the protection offered by one application. In our view, including a sunscreen in a fake tanning lotion offers no obvious benefit. On the contrary, it has the potential to generate a false sense of protection which may lead to sunburn in fake tan users. Conclusions In response to the discussion posed by Chapman5 in relation to the use of fake tanning lotions as a "harm minimisation" approach, the ACFSA was prompted to review its policy in relation to the promotion and sale of fake tanning lotions. The results of this study do not point to a reduced risk of harmful sun exposure among fake tan users. Rather, they suggest an elevated risk of sunburn. In the light of these findings, the ACFSA sees no justification for altering its current position on the use of fake tanning lotions. The use of fake tanners is not actively promoted by the ACFSA. However, where there is a strong desire for a tan, people are advised that the use of fake tanning lotions is a better alternative than sunbathing or using a solarium. They are also advised that a fake tan does not provide protection against the sun and are warned about the limited protection offered by products that contain a sunscreen. More in-depth investigation of why and when fake tanning lotions are used, and the extent to which fake tan users believe they are protected from the harmful effects of the sun while using such products, is needed to inform education strategies and guide any policy change by organisations such as the ACFSA. The potential of the labelling of fake tan products containing sunscreens to be misleading needs to be brought to the attention of the relevant authorities. References Gray N. Report of the Chairman of the Education Committee. Australian Cancer Society Annual Report, 1979. Sydney: ACS, 1979: 9. Armstrong BK. Stratospheric ozone and health. Int J Epidemiol 1994; 23: 873-885. Arthey S, Clarke V. Suntanning and Sun protection: A review of the psychological literature. Soc Sci Med 1995; 40 (2): 265-274. Clarke V, Williams T, Arthey S. Skin type and optimistic bias in relation to the sun protection and suntanning behaviors of young adults. J Behav Med 1997; 20: 207-222. Chapman S. Faking it: should cancer control agencies promote fake tanning lotions? Med J Aust 1999; 170: 603-604. Broadstock M, Borland R, Hill D. Knowledge, attitudes and reported behaviours relevant to sun protection and suntanning in adolescents. Psychol Health 1996; 11: 527-539. Purchase M, Borland R. Public reaction to the 1992/93 SunSmart campaign: results from a representative survey of Victorians. SunSmart Evaluation Studies 3. Melbourne: Anti-Cancer Council of Victoria, 1994: 93. Dixon H, Cappiello M, Borland R. Reaction to the 1994/95 SunSmart campaign: results from a representative household survey of Victorians. SunSmart Evaluation Studies 5. Melbourne: Anti-Cancer Council of Victoria, 1997: 64. Stata version 6 [computer program]. College Station, TX: Stata Corporation, 1999. Huber PJ. The behavior of maximum likelihood estimates under non-standard conditions. Proceedings of the Fifth Berkeley Symposium on Mathematical Statistics and Probability 1967; 1: 221-233. White H. A heteroskedasticity-consistent covariance matrix estimator and direct test for heteroskedasticity. Econometrica 1980; 48: 817-830. (Received 21 Mar, accepted 31 Jul, 2000) Authors' Details Anti-Cancer Foundation of South Australia, Adelaide, SA. Kerri R Beckmann, BSc(Hons), MPH, Program Evaluation Officer; Barbara A Kirke, DipN, MPHC, Skin Cancer Prevention Project Officer. Collaborative Research Centre for Asthma, University Department of Medicine, Sir Charles Gairdner Hospital, Perth, WA. Kieran A McCaul, BSc, MPH, Biostatistician. Epidemiology Branch, South Australian Department of Human Services, Adelaide, SA. David M Roder, AM, MPH, DDSc, Director. Reprints will not be available from the authors. Correspondence: Ms K R Beckmann, Anti-Cancer Foundation of South Australia, PO Box 929, Unley, SA 5061. kbeckmannATcancersa.org.au Make a comment Back to text Back to text Back to text 4: Factors associated with being burnt more than once over summer All respondents Women only Adjusted Adjusted odds ratio 95% CI P odds ratio 95% CI P Fake tan use Non-users Users 1.00 2.07 - 1.17-3.69 0.013 2.47 1.38-4.42 0.002 Sex Female Male 1.00 2.99 - 2.09-4.29 - - - Age (group years) 65+ 18-24 25-34 35-44 45-54 55-64 1.00 13.70 5.83 4.72 2.46 1.27 - 7.00-26.78 3.19-10.65 2.66-8.38 1.34-4.53 0.61-2.66 0.004 0.529 15.46 4.40 5.12 3.56 0.40 5.34-44.77 1.71-11.34 2.04-12.86 1.37-9.23 0.09-1.65 0.002 0.001 0.009 0.203 Skin type Just tan Burn then tan Just burn 1.00 2.07 2.47 - 1.20-3.56 1.47-4.16 0.009 0.001 1.86 2.12 0.69-5.01 0.83-5.39 0.222 0.117 Sunscreen use Irregular Regular 1.00 1.03 - 0.72-1.48 0.876 0.82 0.44-1.49 0.509 Hat wearing Irregular Regular 1.00 0.69 0.48-0.98 0.038 0.91 0.52-1.59 0.746 Protective clothing Irregular Regular 1.00 0.63 - | 0.44-0.91 0.014 0.95 0.56-1.61 0.856 Shade seeking Irregular Regular 1.00 0.91 - 0.62-1.32 0.604 0.55 0.30-1.01 0.056 *Logistic regression modelling using forced entry of all variables. Separate models for all respondents and women only. Back to text

Kerri R Beckmann · Barbara A Kirke · Kieran A McCaul · David M Roder

Letters Chromomycosis MJA 2000; 173: 656 To the Editor: A 38-year-old man presented with a hyperkeratotic, crusting lesion on his right knee which had been present for 17 years and had not responded to treatment (Box 1). The lesion developed in 1983 after he knelt on wood chips while cutting wood in scrub country to the west of Mackay in Queensland. The lesion had slowly increased in size and persisted despite various attempts at therapy. When it was about 1 cm in diameter, local excision was offered, but, as the surgeon was not able to guarantee the lesion would not recur, excision was not performed. In January 1996 a biopsy was taken. The report read "pseudoepitheliomatous hyperplasia" of the epidermis. In the dermis there was a "granulomatous inflammatory reaction in which there were collections of pigmented yeast bodies". The histological diagnosis was chromomycosis (chromoblastomycosis) (Box 2). Chromomycosis organisms are round, thick-walled brown cells, 5-12 mm in diameter, usually occurring in dermal microabscesses. After one month's culture, Cladophialophora carrionii (also known as Cladosporium carrionii) was isolated. By 1999, when the patient presented, he had been treated sequentially, without success, with ketoconazole (200 mg daily for six months), fluorocytosine (dose unknown) and terbinafine (250 mg daily). In October 1999, he was given itraconazole 100 mg daily. This dose was increased to 100 mg twice daily in November 1999 and was continued until May 2000, by which time the total dose of itraconazole administered was 54 g. (The patient was 179 cm tall and weighed 114 kg.) The drug has been well tolerated, with no abnormality of blood film or liver function. There has been a slow but steady healing of the knee lesion (Box 3). Chromomycosis (chromoblastomycosis) is a chronic mycotic infection of the cutaneous and subcutaneous tissues. It is diagnosed by the presence in the tissue of phaeoid (Greek phaeios, "dusky") muriform cells and by isolation and identification of the pathogenic fungus. The muriform cells represent an intermediate vegetative fungal form arrested between yeast and hyphal development. The dusky colour of these muriform cells results from a melanin pigment.1 The lesions produced by the infection are nodulo-verrucous. The fungal genera that can cause this infection (Cladophialophora, Fonsecaea, Phialophora, Rhinocladiella) live as saprophytes in soil and in decaying wood and vegetation. Infection is caused by inoculation, but the injury may be so minor as to go unnoticed and may have occurred years before the slow-growing lesion is noticed. It occurs most commonly on the feet or legs, but, in Australia, the upper limbs are more commonly involved. Cladophialophora carrionii infection is a common cause of chromoblastomycosis and, although the infection can be contracted from many environments, it is particularly prevalent in arid and semi-arid areas, most often in tropical and subtropical zones. It has been reported from North, Central and South America, Cuba, Jamaica, Martinique and many other countries, including India, South Africa, and Madagascar, as well as Australia and Northern Europe. It has occurred as an imported infection in the United Kingdom.2 Chromoblastomycosis is frustratingly difficult to treat, but it is becoming increasingly evident that itraconazole is the treatment of choice, at least for infections with Cladophialophora spp., partly because itraconazole accumulates in the skin and subcutaneous tissues owing to its lipophilicity.3 In adults the dose of itraconazole is 200 mg or more per day for as long as required (the dose is continued for a period two to three times longer than that required to obtain negative culture results).4 George R Crowe Plenary Physician, Pioneer Valley Private Hospital PO Box 8877, Mount Pleasant, QLD 4740 Michael Martin Pathologist, Central Queensland Pathology Laboratory Mackay, QLD Acknowledgements: Dr Brian Reid, Dermatologist, Townsville; Dr Andrew O'Neill, Mackay; Mr John Atkinson, Librarian, Mackay Base Hospital; and Ann James, Janssen-Cilag Australia. Guerrant RL, Walker DH, Weller PF. Tropical infectious diseases: priciples, pathogens and practice. London: Churchill Livingstone, 1999: 621-623. Champion RH, Burton JL, Ebling FJG. Textbook of dermatology. 5th ed. Oxford: Blackwell Scientific Publications, 1992: 1205-1206. Strickland GT. Hunter's tropical medicine. 8th ed. Philadephia: WB Saunders, 1999: 573. Borelli D. A clinical trial of itraconazole in the treatment of deep mycoses and leishmaniasis. Rev Infect Dis 1987; 9 Suppl 1: S57-S63. 1: The lesion The lesion on the knee when the patient presented in 1999. The lesion first developed in 1983 after the patient knelt on wood chips. Back to text 2: Chromomycosis organisms Photomicrograph (haematoxylin-eosin, original magnification x400) of skin biopsy in 1996, showing two Cladophialophora spores in a microabscess (arrow). Back to text 3: Healing after 17 years Treatment with itraconazole in late 1999 resulted in steady healing of the lesion. Back to text

>Advances in technology and well documented clinical studies continue to expand the list of disorders amenable to laser therapy. In this issue, Tan and Vinciullo report their study of 186 children and adults with port-wine stains (capillary malformations) treated with a flashlamp-pumped tunable dye laser in Perth, Western Australia. They confirm reports from other countries of its efficacy and safety. Preferential uptake of yellow laser light (wavelength, 585 nm) by haemoglobin, combined with very short (450-µs) laser pulses, ensures maximum damage to small blood vessels with minimum heat transfer to surrounding tissue (selective photothermolysis).1 Good-to-excellent responses were seen in 78% of patients. The results are similar to those of a recent study at Royal Prince Alfred Hospital (RPAH), Sydney, and Flinders Medical Centre, Adelaide.2 Treatment failures may be related to depth and diameter of blood vessels, as the laser beam penetrates only about 1 mm. Given the well documented, sometimes severe but often hidden, psychological impact of a disfiguring port-wine stain, its potential complications and the lack of significant therapeutic alternatives, these results are impressive. However, critical issues apart from efficacy and safety include cost and access to treatment. The RPAH/Flinders study estimated the cost of treating a port-wine stain involving one cheek to be about $700-$1800 in an adult. This cost includes staff and topical or local anaesthesia, but not general anaesthesia, which is needed for most children. We must also add the laser capital costs (currently $150 000-$200 000) and substantial running costs. Will all patients with port-wine stains have access to a treatment now proven to be efficacious and safe? Ideally, all affected patients should be assessed at or soon after birth and treatment begun in the first two years of life and completed before the potential psychological impact of being a "marked child"3 has developed. Until recently at RPAH the estimated time to completion of treatment for children after assessment was 3.5 years. The service has been advertised only to dermatologists, because resources are too limited to treat the estimated potential number of patients, although the recent purchase of a third generation laser may increase the number able to be treated. Public hospital dermatological laser services vary between States and generally range from severely restricted to non-existent. Now that Australian studies have addressed issues of efficacy and cost, it is up to State Governments and the Federal Government to urgently establish appropriate funding arrangements. There is a large backlog of older children and adults who would benefit greatly from treatment. In the medium to long term, even with current technology, these patients could be treated, leaving a steady-state situation with only children in their first 2-4 years needing treatment. Treatment with the yellow-light laser is not confined to port-wine stains, but can be used for many other conditions characterised by a real or apparent excess of small blood vessels close to the surface of the skin. Proliferating or ulcerating capillary haemangiomas that affect vital structures (e.g., eyes, nose, mouth, pharynx and genitalia) in babies and young children have been shown in both Australia and other countries to respond to treatment with the flashlamp-pumped dye laser. This treatment is often urgent or semiurgent, depending on the rate of proliferation of the haemangioma or rate of ulceration and tissue destruction. Has technology in this area gone as far as it can? The answer is no. Newer lasers are now available that are able to operate several times faster than the initial pumped dye lasers and may require less maintenance. We await lasers that are more portable, cheaper and able to treat at a deeper skin level than current technology allows. Timely and affordable access to treatment for any patient, young or old, affected with a port-wine stain is the goal. Whether this is realised depends on a commitment by State and federal health funding bodies to recognise the extent of the problem, acknowledge the long term benefits of early treatment and provide an adequate funding mechanism. Margaret M Stewart Visiting Medical Officer, Department of Dermatology Royal Prince Alfred Hospital, Sydney, NSW Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220: 524-527. Stewart M, Hailey D, Angel A. Yellow light lasers in dermatology. Canberra: Australian Institute of Health and Welfare, 1995: 1-43. Lanigan SW, Cotterill JA. Psychological disabilities amongst patients with port wine stains. Br J Dermatol 1989; 121: 209-215.

Margaret M Stewart

Editorial Acne and acne scarring: why should we treat? Reasons for early medical intervention, and options for treatment of scarring MJA 1999; 171: 62-63 Acne is so common that one could argue that it is a normal occurrence in human development. Its prevalence has been estimated at 95%-100% in 16-17-year-old boys and 83%-85% in 16-17-year-old girls.1 The initial presentation is usually comedonal acne, progressing to inflammatory lesions within 2-3 years,2 then rising in incidence and severity to reach its most serious stage between the ages of 14 and 17 years in girls and 16 and 19 years in boys.1 Development of comedonal acne at an early age, in girls at least, appears predictive of more severe disease in later years.3 Acne will mostly resolve by the age of 23-25 years; nevertheless, 1% of men and 5% of women still bear acne lesions at 40 years of age.4So, is acne a disease worthy of treatment, or a normal occurrence that should be ignored, as it will eventually cease to be a problem for most affected individuals? Concern about acne is one of the commonest reasons for young patients to consult a medical practitioner, so the direct cost of consultations and of the diversion of medical services needs to be taken into account in any assessment of the value of treating this apparently "normal" life event. Added to this, we are seeing the development of increasing antibiotic resistance in Propionibacterium acnes,5 a problem exacerbated by long term and widespread use of often suboptimal doses of antibacterial agents. So how can one justify treatment? Firstly, acne as a condition is aesthetically and sometimes physically unpleasant. Severe cystic acne causes pain, recurrent bleeding and purulent discharge. In rare instances, patients with acne develop severe systemic toxicity and require treatment in hospital. Before isotretinoin was introduced, such patients were extremely difficult to treat. Secondly, it can cause great distress in adolescents at a time when they are probably least able to deal psychologically and socially with the unsightliness of active acne. Being so readily visible (affecting the face in 99% of cases6), acne can reduce employment prospects7 and create interpersonal difficulties.8 Affected adolescents report more social isolation and self-consciousness than their unaffected peers8 and experience more embarrassment, social inhibition, unhappiness, anxiety, and dissatisfaction with their facial appearance.9 Finally, acne scarring can cause devastating long term psychic trauma for the sufferer and it has been suggested that such scarring may be a risk factor for suicide, particularly in men.10As current treatments for acne are very effective, scarring could be avoided in many cases by adequate medical intervention early in the course of the disease. Successful treatment of cystic acne with isotretinoin appears to reduce anxiety and depression in patients.11 Anti-androgen hormonal treatments such as cyproterone acetate and spironolactone, topical preparations such as adapalene, azelaic acid, topical antibiotics and retinoic acid may help to replace or augment long term antibiotic therapy, ensuring a sufficient armamentarium to keep the incidence of acne scarring to a minimum. Unfortunately, scarring may affect up to 95% of patients with acne. The degree of scarring is related to the severity and duration of acne before adequate therapy is instituted. One study found that a time delay of up to three years between acne onset and adequate treatment was sufficient to cause facial scarring in either sex, although keloidal or hypertrophic truncal scarring was more common in men.12 The same study established that superficial inflamed papular acne and cystic acne could both produce scarring, a finding with important implications for our healthcare system, which subsidises isotretinoin for failed therapy in nodulocystic disease only. If hypertrophic scarring occurs it should be dealt with by such measures as intralesional steroids, silicone sheeting or vascular laser treatment, as required. However, most scarring in acne is atrophic rather than hypertrophic in nature, with destruction and dissolution of supporting tissues. In the young, most scars will initially improve, the erythema will subside and the scars mature over the first two to three years. After this initial improvement the scarring is quiescent, but, over time, as facial tone declines and facial fat stores are resorbed, the scars will become more noticeable. With ageing, the facial skin starts to sag and seems to literally hang on the scars. The inelastic strands of scars bind the skin, giving it an uneven, cascading appearance. This is amplified by other age-related changes such as the resorption of skeletal and soft tissues. Remedial approaches to acne scarring have improved over the years. The older, less successful treatments such as dermabrasion and chemical peeling have been replaced by the use of resurfacing infrared lasers such as CO2 lasers13 and, more recently, erbium lasers14 to better remove and tighten the skin. An understanding that replacement of the atrophied structures in the dermis and subcutaneous tissues is necessary in severe cases of acne scarring has led to the development of superior dermal and subcutaneous augmentation techniques. Dermal and subcutaneous augmentation is possible by a number of autologous techniques, including dermal grafting,15 lipocytic dermal augmentation,16 fat transfer17 and, more recently, the implantation of autologous collagen and cultured and expanded autologous fibroblasts. Non-autologous augmentation is also possible by way of injections of bovine collagen, fibrin foam, hyaluronic acid or polymethylmethacrylate microspheres. For "punched out" ("ice pick") scars, none of these methods is useful. For these a range of punch techniques is used, involving coring out of scars with an appropriately sized cylindrical instrument, followed by suturing or graft application. Punch techniques can be used to treat many scars at a single operation, and may be combined with resurfacing techniques such as infrared laser treatment.18 Subcision (dermal scarification) is another helpful technique, in which dermal undermining of scars is used to improve the scar tissue by two mechanisms: (i) direct breaking of scar attachments, and (ii) intentional injury of the dermis to induce laying down of new collagen.19 All of these techniques are valuable tools for practitioners seeking to improve the outcome of treating acne scarring, but it would be better still if the problem never arose. A preventable condition such as postacne scarring should be one deserving of the earliest, best and most effective treatment. Gregory J Goodman President, Skin and Cancer Foundation Melbourne, VIC Burton JL, Cunliffe WJ, Stafford I, Shuster S. The prevalence of acne vulgaris in adolescence. Br J Dermatol 1971; 85: 119-126. Lucky AW, Biro FM, Huster GA, et al. Acne vulgaris in early adolescent boys: correlations with pubertal maturation and age. Arch Dermatol 1991; 172: 210-216. Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study. J Pediatr 1997; 130: 30-39. Cunliffe WJ, Gould DJ. Prevalence of facial acne vulgaris in late adolescence and in adults. BMJ 1979; 1: 1109-1110. Cooper AJ. Systematic review of Propionibacterium acnes resistance to systemic antibiotics. Med J Aust 1998; 169: 259-261. Cunliffe WJ. The acnes. London: Dunitz, 1989. Cunliffe WJ. Unemployment and acne. Br J Dermatol 1986; 115: 386. Schachter RJ, Pantel ES, Glassman GM, Zweibelson I. Acne vulgaris and psychologic impact on high school students. N Y State J Med 1971; 24: 2886-2890. Wu SF, Kinder BN, Trunnell TN, Fulton JE. Role of anxiety and anger in acne patients: a relationship with the severity of the disorder. J Am Acad Dermatol 1988; 18: 325-333. Cotterill JA, Cunliffe WJ. Suicide in dermatological patients. Br J Dermatol 1997; 137: 246-250. Rubinow DR, Peck GL, Squillace KM, Gantt GG. Reduced anxiety and depression in cystic acne patients after successful treatment with isotretinoin. J Am Acad Dermatol 1987; 17: 25-32. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne scarring and its incidence. Clin Exp Dermatol 1994; 19: 303-308. Goodman GJ. Facial resurfacing using a high-energy, short-pulse carbon dioxide laser. Australas J Dermatol 1996; 37: 125-131. Stuzin JM, Baker TJ, Baker TM. CO2 and erbium:YAG laser resurfacing: current status and personal perspective. Plast Reconstr Surg 1999; 103: 588-591. Goodman GJ. Laser assisted dermal grafting for the correction of cutaneous contour defects. Dermatol Surg 1997; 23: 95-99. Coleman WP 3d. Lipocytic dermal augmentation. In: Klein AW, editor. Tissue augmentation in clinical practice. Procedures and techniques. New York: Marcel Dekker, 1998: 49-62. Coleman SR. Long-term survival of fat transplants: controlled demonstrations. Aesthetic Plast Surg 1995; 19: 421-425. Johnson WC. Treatment of pitted scars: punch transplant technique. J Dermatol Surg Oncol 1986; 12: 260-265. Orentreich DS. Subcutaneous incisionless (subcision) surgery for the correction of depressed scars and wrinkles. Dermatol Surg 1995; 21: 543-549.

Gregory J Goodman

Photo Essay Practising dermatology in the South Pacific Two dermatologists describe their working visits to Samoa and Vanuatu Anthony D White and Ross StC Barnetson MJA 1998; 169: 659-662 Introduction - Diagnoses - Teaching - Problems - Discussion - Acknowledgements - References - Authors' details - - More articles on Dermatology Introduction In 1996 and 1997, we conducted a series of dermatology clinics in Samoa and Vanuatu -- countries which lack resident dermatologists -- under the aegis of the Pacific Islands Project. This three-year project was an undertaking of the Australian Agency for International Development (AusAID) to increase tertiary health service capacities in Pacific Island countries with a shortage of trained specialists. The project was implemented by the Royal Australasian College of Surgeons and covered, in addition to dermatology, anaesthesiology, general medicine, neurology/neurosurgery, ophthalmology, orthopaedic surgery, otolaryngology, paediatric surgery, plastic and reconstructive surgery and radiology. Major aims were to educate local health workers and to use inexpensive treatments which would be available long-term in the country. We describe our experience during four separate two-week visits to Samoa and Vanuatu in 1996 and 1997, and our resulting recommendations. Diagnoses We saw 1072 patients at clinics in local hospitals in Apia and Savaii in Samoa (765 patients), and in Port Vila, Espiritu Santo and Tanna in Vanuatu (307 patients). The clinics were advertised on local radio, and there was prior liaison with hospital doctors. Patients were therefore probably those with severe skin diseases, who were able to travel to the clinics. Diagnoses are shown in the Box. The vast majority of patients had common skin conditions, often in severe or extensive forms, rather than rare, exotic diseases. Fungal infection: This was the most common condition, affecting almost 40% of patients. Tinea (ringworm) was found in a quarter of patients and was often extensive, involving up to 20% of the body surface (Figure 1). Tinea (pityriasis) versicolor, caused by the yeast Malassezia furfur, affected a further 13% of patients (Figure 2), while some patients had both types of infection (Figure 3). The main contributing factors to the prevalence and extent of fungal infections appeared to be the hot, humid climate, occlusive clothing and inadequate treatment. There is a culturally determined tendency to wear multiple layers of clothing, particularly in Samoa. Antifungal drugs, even when available, were often out of patient reach because of cost. Dermatitis: 21% of patients had contact, atopic or seborrhoeic dermatitis. A predisposing factor is the tendency, despite the high ambient humidity, for Polynesian and Melanesian skins to be dry. Among Samoans, this dryness is often aggravated by overuse of soap and water and the practice of scrubbing the skin with a ball of plant fibre. Photosensitivity dermatitis was seen in six patients, all of whom had used a soap containing trichlorocarbanilide, an antiseptic known to cause a photosensitive rash. Scabies: Each year all Samoans over the age of 12 months are treated with oral diethylcarbamazine as part of a national filariasis eradication campaign. In 1997, ivermectin was added to the regimen. This drug is also active against scabies, and during the clinic visit a month after the campaign many patients were seen with the stigmata of resolving scabies. The few patients with active scabies were infants (who are excluded from the drug program) and an adult who had refused treatment. Pigmentary disorders: These included melasma, vitiligo, postinflammatory hyperpigmentation and pityriasis alba. Striking depigmentation was also the presenting symptom in two patients with chronic discoid lupus erythematosus (Figure 4). Pigmentary disorders are a greater cosmetic problem in dark-skinned than in white-skinned people, because of the greater contrast between affected and unaffected skin. Other skin disorders: Acne was surprisingly infrequent in both countries, while psoriasis was common (Figure 5). Other notable conditions which affected small numbers of patients included epidermolytic hyperkeratosis, leprosy, and lichen amyloidosis (Figures 6-8). One skin cancer was seen, in a 60-year-old Vanuatu Melanesian man. It presented as an eroded 8 cm plaque on the shoulder; biopsy showed it to be basal cell carcinoma, a condition never previously encountered by local physicians on black skin. Teaching Every opportunity was taken to discuss diagnosis and management of skin disease with interested local health workers, using clinic patients as subjects. During one visit to Samoa, one of us (R StC B) was accompanied by an indigenous physician, providing an opportunity to discuss local dermatological problems and solutions. This was not possible during other visits because of the shortage of available medical personnel. Four lectures on skin diseases were given to hospital staff. Problems The main clinical difficulties we encountered were poor conditions for examination, lack of diagnostic facilities and inadequate pharmaceutical supplies. Skin specimens were returned to Australia for histopathological examination or fungal culture, as neither Samoa nor Vanuatu had facilities for these procedures. Discussion and recommendations The spectrum of infectious skin diseases encountered in Samoa and Vanuatu was similar to that seen in Australian clinics,3 although these diseases tended to have a more severe and extensive course. In contrast, skin cancer and precancer were virtually absent. Few diseases were exotic or "tropical". Inadequate treatment because of the lack of availability or high cost of antifungal drugs was probably a contributing factor to the severity of fungal infections. Topical antifungal creams were available in impracticably small volumes. For example, clotrimazole must be applied for four weeks, but the standard 20 g tube is sufficient to treat extensive disease for only a day. The standard oral fungistatic drug, griseofulvin, needs to be taken for four weeks, but is usually prescribed in Samoa and Vanuatu for only seven days. An alternative treatment, oral terbinafine, is fungicidal and may be adequate in a seven-day course.4 The manufacturer of terbinafine, Novartis, has been approached officially to provide this drug as a humanitarian service to these countries. Inadequate treatment probably also contributed to the prevalence and extent of dermatitis. Topical steroids were available, in both countries, but only in 15 g tubes (30 g of cream/ointment is needed for one total body application). Scabies was common. It requires community-based rather than individual treatment, as repeated re-infestation occurs from untreated individuals. In Samoa, it should now be possible to capitalise on the fortuitous scabicidal effect of ivermectin (used in the filariasis eradication campaign), which is an ideal treatment in populations with high endemic rates of infestation.5 However, this needs to be backed up by topical antiscabetic treatment for those who are ineligible for ivermectin or who become re-infested. Unfortunately, no topical antiscabetic agents were available in Samoa at the time of the 1997 campaign, and an opportunity to eradicate scabies was lost. Although leprosy is endemic in Samoa and Vanuatu, only one new case was seen. This condition is well managed by the World Health Organization, which undertakes treatment, contact tracing and follow-up. Public education about preventing skin disease could be beneficial. It should define simple hygiene but explain that excessive washing, scrubbing of the skin and use of germicidal soaps, although customary, are unnecessary and often injurious. In addition, occlusive clothing is inappropriate for a hot, humid climate and encourages skin disease, particularly fungal infection. Effort is also needed to overcome the enormous stigma attached to skin disease, which delays or prevents presentation and increases individual suffering and the prevalence of infectious disease in the community. With adequate resources, most of the conditions we saw are treatable and many are preventable. Because half a dozen diseases account for two-thirds of patients presenting, it should be possible to educate primary carers to diagnose and treat most cases. We are currently preparing an illustrated booklet describing the clinical features, prevention and treatment of the main diseases. However, the need for affordable, effective treatments remains. The dermatological contribution to the Pacific Islands Project was valuable in defining the main problems, formulating solutions, educating local health workers and providing treatment in two of Australia's less-developed neighbours. We hope that the program will continue and expand to assist other countries in the area. Acknowledgements We are very grateful to Associate Professor Steven Kossard (Skin Cancer Foundation, Sydney, NSW) and Dr Andrew Gal (Sydney, NSW) for histopathological examinations, to pharmaceutical companies for generous donation of drugs, and to the Department of Microbiology, Royal Prince Alfred Hospital, for fungal cultures. We also thank our patients for allowing publication of their photographs. References Manzano-Gayosso P, Mendez-Tovar LJ, Hernandez-Hernandez F, et al. Dermatophytoses in Mexico City. Mycoses 1994; 37: 49-52. Khosravi AR, Aghamirian MR, Mahmoudi M. Dermatophytoses in Iran. Mycoses 1994; 37: 43-48. Kilkenny MF, Marks R. The frequency and nature of skin conditions seen in a private dermatology practice in central Victoria. Aust J Dermatol 1996; 37: S50-S53. Barnetson R StC, Marley J, Bullen M, et al. Comparison of one week of oral terbinafine (250 mg/day) with four weeks of treatment with clotrimazole 1% cream in interdigital tinea pedis. Br J Dermatol 1998; 139: 675-678. Meinking TL, Taplin D, Hermida JL, et al. The treatment of scabies with ivermectin. N Engl J Med 1995; 333: 26-30. (Received 22 Jul, accepted 7 Oct, 1998) Authors' details Department of Dermatology, Royal Prince Alfred Hospital, Sydney, NSW. Anthony D White, FRACP, FACD, Consultant Dermatologist; Ross StC Barnetson, MD, FRACP, FACD, Head of Department, and Professor of Dermatology, Sydney University, Sydney, NSW. Reprints will not be available from the authors. Correspondence: Professor R StC Barnetson, Department of Dermatology, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050. Email: rossATcanc.rpa.cs.nsw.gov.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Anthony D White

Factors involved in presentation of older people with thick melanoma Pauline F Hanrahan, Peter Hersey and Catherine A D'Este MJA 1998; 169: 410-414 For editorial comment, see Kelly Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Oncology - ©MJA1998 Abstract Objective: To examine whether presentation of older people with thick melanoma is a result of the site and histological type or of their reduced ability to identify melanoma. Design and setting: Retrospective analysis of the Newcastle Melanoma Unit patient database. Patients: 2154 patients with melanoma for whom complete data (histological type, thickness and site of melanoma) were available and who presented from February 1981 to April 1997. Main outcome measures: Histological type and site of melanoma in older (≥50 years) versus younger men and women; frequency with which these groups identified melanoma and the first changes of melanoma that were noticed. Results: Patients aged ≥50 years, particularly men, were more likely to present with thicker lesions. Older men and, to a lesser extent, older women were more likely to present with nodular melanoma, which were more frequent on the scalp and face in older, compared with younger, men, and scalp and back in older men compared with older women. Failure to identify melanoma was associated with older age, sites on the scalp and back and histological type of the lesion, but was independent of sex once histological type, age, site and thickness were taken into account. Multivariate analysis indicated that the association of older age of patients with failure to identify melanoma applied irrespective of the site, type and thickness of their melanoma. Conclusion:. The higher frequency of thick melanoma in older people is accounted for by an increased proportion of nodular melanoma and decreased ability to recognise the changes of melanoma. These findings have important implications for examination of older patients by doctors and for design of strategies for early detection of melanoma in this age group. Introduction Survival from melanoma is related to thickness of the tumour. Ninety-six per cent of patients whose lesions are detected early (< 0.75 mm thick) will survive to 10 years,1,2 but this decreases to 50% for patients with lesions 4 mm or greater.3,4 Previous studies have shown that most patients who present with thick lesions are men aged over 50 years.5-7 In New South Wales over 50% of deaths from melanoma involve men over 50, even though this group comprises only 12%-14% of the population.8 Clearly, strategies that facilitate early detection of melanoma in older men may markedly reduce the death rate from this cancer. We have previously investigated the ability of older men to distinguish between benign and malignant pigmented skin lesions in photographs and whether an educational brochure assists this ability;9 the brochure increased knowledge of melanoma, but did not help participants distinguish between benign and malignant pigmented skin lesions. We then investigated whether this age group had inherent difficulties in recognising the changes of melanoma and found that all age groups had difficulty in recognising the appearance of new pigmented lesions and changes in lesions over time.10,11 Older people were no less able than younger people to identify change, but falsely identified changes in unchanged lesions more frequently. In this study we sought to examine factors associated with failure of patients to identify their melanoma and the importance of this in presentation of older patients with thick melanoma. Methods Information for the study was obtained from the database in the Newcastle Melanoma Unit (NMU), which was established in 1981 and is a referral centre for patients from the Hunter region of New South Wales. Over 90% of patients with melanoma in the Hunter region attend the unit. The database contains information obtained by experienced oncology nurses who interview patients, asking questions about changes they had noticed leading to diagnosis of melanoma, for how long they had noticed the changes and whether these were in a pre-existing or new lesion. The age and sex of patients, site of their primary lesion, its histological type and thickness were also recorded. Histological investigation of the lesions was reviewed by at least two pathologists and reported as described previously.12 Patient clinical data were entered into a program developed jointly by the Sydney Melanoma Unit and the Macquarie University using Clinical Reporting Systems software (Brisbane Road, Castle Hill, NSW). We included data for all patients presenting to the NMU between February 1981 and April 1997. The data were categorised for statistical analysis as follows. Patients were divided into two groups by age (< 50 and ≥50). As in a previous study,5 thickness of primary lesions was categorised as < 3 mm, or ≥3 mm. Data on the site of the primary melanoma were divided into seven categories (scalp, face, neck, back, anterior trunk, arm and leg). Melanomas were categorised into seven histological types (superficial spreading melanoma [SSM], nodular melanoma [NM], lentigo maligna [LM], in-situ melanoma, desmoplastic melanoma, unknown, and unclassified) of which we included only the first three relatively common types. Categories for types of changes were: unidentified (including instances where patients were uncertain whether a change had occurred, or said that no change had occurred, but melanoma was detected by their general practitioners or other doctors); size and shape; colour; changes in sensation (eg, itching, tingling); and bleeding. Statistical analysis Data were analysed with SAS13 and STATA14 statistical software. Lesion characteristics (thickness, histological type and site of melanoma) were compared by age and by sex separately using chi-squared analyses. Lesion characteristics and age and sex were also compared for those who had, and had not, identified any changes. Logistic regression analyses were performed to examine factors associated with identification of any changes of melanoma, using any change versus no change, as the outcome variable. All five independent variables were tested for significance by forward stepwise regression analysis. After the final main effects model was obtained, all possible interactions were tested. The likelihood ratio statistic was used to assess statistical significance in the logistic regression analyses. We also tested (by chi-squared analysis) lesion characteristics, age and sex for association with type of changes noticed; 95% confidence intervals (CI) were calculated for each type of change. A significance level of 0.05 was used for all analyses. Subgroups were considered to differ significantly if 95% CIs did not overlap. Results The database included records for 3435 patients who attended the NMU during the study period. Exclusions included: 932 patients for whom there was incomplete data or for whom data could not be appropriately classified; 325 with uncommon, unknown, desmoplastic or unclassified histological types of melanoma; and 22 with melanoma at unusual sites (eg, mucosal regions, buttocks, groin). The final sample of 2154 patients comprised 1144 men (53%) and 1010 women (47%); 1142 patients (53%) were aged 50 years or over and 59% of the men in the study were in this age group, compared with 46% of the women. There were no significant differences in sex or age of patients excluded compared with those included (sex: chi-squared = 0.006, df = 1, P = 0.94; age: chi-squared = 1.7, df = 1, P = 0.18). The site and thickness of melanomas were similar in those excluded and included. Excluded patients had a different distribution of histological types (as this was part of the basis for their exclusion) and a higher proportion of unnoticed changes than those included. More detailed information about excluded patients is available from the authors. Lesion characteristics Thickness: Box 1 shows that patients aged 50 years or over (14.5%; 95% CI, 12%-16%) were significantly more likely to present with thick lesions than younger patients (4.7%; 95% CI, 3%-6%), and men (12%; 95% CI, 10%-14%) were more likely to have thick lesions than women (7%; 95% CI, 6%-9%). Site: Melanoma was found most often on the backs of male patients (47%; 95% CI, 45%-50% v. 24%; 95% CI, 22%-27% for women), whereas the leg was the predominant site in women (38%; 95% CI, 35%-41% v. 16%; 95% CI, 13%-18% for men). The incidence of melanoma on the scalp, face and neck was similar for men and women. Melanoma on the arms was more common in women (19%; 95% CI, 16%-21% v. 12%; 95% CI, 10%-13% for men), while melanoma on the face was more common in older patients and melanoma on the anterior trunk and leg was more common in younger men than older men. Melanomas were more common on the scalp and face in older, compared with younger, men and more common on the scalp and back of older men compared with older women (Box 1). Histological type: SSM was more common in younger patients of both sexes and NM was more common in older male patients. Most thin lesions (80%) were SSM and most thick lesions (72%) were NM. Thicknesses of the three histological types were: SSM, 0.02-10.5 mm (median, 0.63 mm; interquartile range [IQR], 0.4-1.0 mm); NM, 0.2-25 mm (median, 2.46 mm; IQR, 1.4-3.8 mm); and LM, 0.1-8.5 mm (median, 0.4 mm; IQR, 0.25-0.8 mm). Factors associated with failure to identify melanoma Many melanomas were not detected by patients, but were identified by their doctors. Sex and age: Men were more likely to fail to notice changes of melanoma than women (37%; 95% CI, 35%-49% v. 30%; 95% CI, 28%-32%) as were older, compared with younger, people (38%; 95% CI, 35%-41% v. 28%; 95% CI, 25%-31%). As shown in Box 2, a greater proportion of older men failed to identify changes in their lesions than younger men; the same trend was evident in women. Site: Patients most frequently failed to identify changes in lesions on the scalp (42%; 95% CI, 30%-52%) and back (41%; 95% CI, 37%-45%), but even among patients with a lesion on the face, 31% (95% CI, 26%-33%) did not identify it as melanoma. The anterior trunk was the least common site for unidentified change (24%; 95% CI, 20%-28%). Older patients failed to identify changes more often than younger patients for all sites except the face and scalp, where the reverse was the case (Box 2). However, numbers are very small for these groups and results should be interpreted with caution. Histological type: A greater proportion of patients with LM (47%; 95% CI, 40%-55%) failed to identify their melanoma than patients with SSM (33%; 95% CI, 31%-35%) or NM (29%; 95% CI, 25%-33%), although by the time they were detected the NM were much thicker. Older people were less likely than younger people to identify melanoma of all three histological types. Regression analyses: Age, thickness, histological type and site of lesion were significantly associated with identifying changes (Box 3). After these variables were included in the model, sex was no longer statistically significant. After adjustment for other variables in the model, the odds of older people identifying changes was two-thirds the odds of younger people identifying changes, and the odds of those with thicker lesions identifying changes was one-and-a-half times the odds of those with thinner lesions identifying changes. Those with LM had about half the odds of identifying changes as those with NM. As shown in Box 3, those with lesions on the face, arm, anterior trunk and leg had significantly higher odds of identifying changes than those with lesions on the back (reference group). Associations with thick melanoma (≥3 mm) As shown in Box 3, age and nodular melanoma were strongly associated with presentation with thick lesions. Changes of melanoma were more frequently identified in thick lesions, but as shown in Box 2, older people were less able to identify melanoma, irrespective of its thickness. It was also of interest that once the histological type of the lesion was taken into account, the site of the melanoma and sex of the patient were no longer related to thickness (ie, thick melanoma on the back and scalp in men appeared to result from the higher frequency of NM at these sites in men; see Box 3). Types of changes reported by patients Significantly fewer older than younger men reported changes in size and shape (21% v. 30%). The same was true for colour (20% v. 27%), and twice as many older men stated that the first change they were aware of in their skin lesion was bleeding (7% v. 3%). However, these differences were not statistically significant. Similarly, our findings that more younger than older women reported colour changes as the first change noticed (32% v. 25%) and (in contrast to men) older women reported changes in size and shape as the first change as frequently as younger women (30% v. 28%), were also not statistically significant. As shown in Box 4, patients with NM reported changes in colour significantly less frequently than those with SSM, change in sensation significantly more frequently than those with LM, and bleeding significantly more frequently than those with LM and SSM. Changes in size and shape were the most frequent changes reported in thick melanoma (34%), whereas changes in colour were more frequently reported in thin lesions (27%). Bleeding was reported as the first change significantly more frequently in thick than thin lesions (17% v. 4%). Reported changes in sensation were similar for thick or thin lesions. Discussion We excluded approximately one-third of the patients on the NMU database, mainly because of missing information about changes noticed or thickness measurements, or because they had melanoma of unusual histological type or location. However, the excluded patients appeared to have similar age and sex distribution, site and thickness measurements to patients in the study. Nonetheless, our results may not be generalisable to patients with the less common histological types of melanoma. Forty per cent of men and 34% of women aged over 50 failed to identify their melanoma. In contrast, younger patients of both sexes reported changes of melanoma in over 70% of cases. These findings were consistent with those of Koh et al15 who found that 38% of melanomas were not identified by men over the age of 60, compared with 23% in men less than 40 years of age. We also found that failure to detect melanoma was not only related to the age of the patient, but was associated with the site and type of the melanoma. Firstly, older men had lesions at sites which are more difficult to see, such as the back and scalp, with nearly 50% of melanoma in older men (compared with only 20% in older women) occurring on the back. Other series have reported similar differences in site distribution of melanoma between the sexes.16,17 Secondly, compared with younger people, older people, particularly men, had a higher proportion of NM, similar to that reported elsewhere.5,18 Patients also identified NMs when they were much thicker than SSMs (median, 2.46 mm v. 0.63 mm). The higher frequency of bleeding as the first change noted in patients with NM was consistent with this finding.19 The higher proportion of NM in older people and more frequent occurrence in "hard-to-see" sites could solely explain the presentation of older people with thicker melanomas. However, regression analysis indicated that for any given thickness and type of melanoma at a given site, older people were less able to recognise melanoma than younger people. In our examination of the first change that drew the attention of patients to their melanoma, we found that self-reporting of a change in colour was infrequent in patients with thick melanoma, and in patients with NM relative to those with SSM. These results were surprising, as previous studies have shown that changes in colour were one of the most frequent early changes of melanoma.20,21 Most of the thick melanoma were NM, which tend to be relatively homogeneous in colour compared with SSM. Thus, the different patterns of colour between NM and SSM may need to be emphasised in educational material directed at older patients. Bleeding was clearly associated with thick and nodular melanoma, but this is a late rather than an early sign.19 To the best of our knowledge this is the first study that has sought to identify reasons why older people present with thicker melanoma. The finding that older patients had lower ability to detect melanoma than younger people is consistent with our previous findings that older people had difficulty in discriminating early changes of melanoma in photographs of pigmented lesions.10,11 Previous studies have noted that younger people were more likely to rate change in skin lesions as extremely important in diagnosis of melanoma than older respondents.22 Older people may also not inspect their skin as frequently as younger people and this may contribute to their lower rate of detection of melanoma. Our findings raise questions about the likely effectiveness for older people of public health strategies that rely on self-detection of melanoma. It seems that that greater reliance will need to be placed on detection of melanoma in this age group by health professionals, who may need to be made aware of the high frequency of thick melanoma and characteristics of melanoma in this age group. Our previous studies have shown that recognition of change in existing lesions over time or the appearance of new pigmented skin lesions can be very difficult, but is assisted by whole-body photographs.10,11 The feasibility of using whole-body photographs to help general practitioners detect melanoma is currently under evaluation in a project funded by the National Health and Medical Research Council. Acknowledgements We thank the nursing sisters Sue Collins, Debbie Bradley, Donna Owens and Kathy Hall for collection of the data and Vicky Hunter for data entry. Dr Hanrahan was supported in part by the Hunter Melanoma Foundation. References Buttner P, Garbe C, Bertz J, et al. Primary cutaneous melanoma: optimized cutoff points of tumor thickness and importance of Clarks level for prognostic classification. Cancer 1995; 75: 2499-2506. Thorn M, Ponten F, Bergstrom R, et al. Clinical and histopathologic predictors of survival of patients with malignant melanoma: a population based study in Sweden. J Natl Cancer Inst 1994; 86: 761-769. Balch CM, Soong SJ, Shaw HM, et al. An analysis of prognostic factors in 8500 patients with cutaneous melanoma. In: Balch CM, Houghton AN, Milton GW, et al, editors. Cutaneous melanoma. Philadelphia: JB Lippincott Co.; 1992: 165-185. Breslow A. Tumor thickness, level of invasion and node dissection in stage 1 cutaneous melanoma. Ann Surg 1975; 182: 572-578. Hersey P, Sillar R, Howe CG, et al. Factors related to the presentation of patients with thick primary melanomas. Med J Aust 1991; 154: 583-587. McHenry PM, Hole DJ, Mackie RM. Melanoma in people aged over 65 in Scotland, 1979-89. BMJ 1992; 304: 746-749. Cohen HJ, Cox E, Manton K, Woodbury M. Malignant melanoma in the elderly. J Clin Oncol 1987; 5: 100-106. Coates M, Day P, McCredie M, Taylor R. NSW cancer incidence and mortality 1992. In: NSW Central Cancer Registry. Sydney: NSW Cancer Council; June 1995: 87, 97. Hanrahan P, Hersey P, Watson AB, Callaghan TM. The effect of an educational brochure on knowledge and early detection of melanoma. Aust J Public Health 1995; 19: 270-274. Hanrahan P, Hersey P, Menzies SW, et al. Examination of the ability of older people to identify early changes of melanoma in computer-altered pigmented skin lesions. Arch Dermatol 1997; 133: 301-311. Hanrahan P. Early detection of melanoma in older people [PhD thesis]. Sydney: University of NSW, 1998. McGovern VJ, Cochran AJ, Van Der Esch EP, et al. The classification of malignant melanoma, its histological reporting and registration: a revision of the 1972 Sydney classification. Pathology 1986; 18: 12-21. SAS for PC [computer program]. Version 6.11. Cary, NC: SAS Institute Inc., 1995. STATA [computer program]. Version 5.0. Houston, Tx: Stata Corp, 1997. Koh HK, Miller DR, Geler AC, et al. Who discovers melanoma? J Am Acad Dermatol 1992; 26: 914-919. Nguyen HL, Armstrong B, Coates M. Cutaneous melanoma in NSW 1983-1995. In: NSW Central Cancer Registry. Sydney: NSW Cancer Council; June 1997: 40. Green A, MacLennan R, Youl P, Martin N. Site distribution of cutaneous melanoma in Queensland. Int J Cancer 1993; 53: 232-236. Nguyen HL, Armstrong B, Coates M. Cutaneous melanoma in NSW 1983-1995. In: NSW Central Cancer Registry. Sydney: NSW Cancer Council; June 1997: 38. Fitzpatrick TB, Milton GW, Balch CM, et al. Clinical characteristics of primary melanoma. In: Balch CM, Houghton AN, Milton GW, et al, eds. Cutaneous melanoma. 2nd ed. Philadelphia: JB Lippincott Co.; 1992: 225-226. Mackie RM. Clinical recognition of early invasive melanoma. BMJ 1990; 301: 1005-1006. McGovern TW, Litaker MS. Clinical predictors of malignant pigmented lesions. J Dermatol Surg Oncol 1992; 18: 22-26. Baade PD, Balanda KP, Stanton WR, et al. Community perceptions about the important signs of early melanoma. J Am Acad Dermatol 1997; 36: 33-39. (Received 1 Sep 1997, accepted 14 May 1998) Authors' details John Hunter Hospital, Newcastle, NSW. Pauline F Hanrahan, BA, PhD, Research Officer, Newcastle Melanoma Unit and Division of Surgery; Peter Hersey, FRACP, D. Phil, Conjoint Professor of Oncology, Oncology and Immunology Unit, Division of Surgery. Centre for Clinical Epidemiology and Biostatistics, University of Newcastle, Newcastle, NSW. Catherine A D'Este, BMath, PhD, Lecturer in Biostatistics, Faculty of Medicine and Health Sciences. Reprints will not be available from the authors. Correspondence: Dr P Hersey, Room 443, David Maddison Clinical Sciences Building, Cnr King and Watt Streets, Newcastle, NSW 2300. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Pauline F Hanrahan · Peter Hersey · Catherine A D'Este

A tremendous amount of research has been done in the past decade into the pathogenesis and management of skin diseases. From this has come greater understanding of skin function and disease mechanisms, with the development of new drugs, new technology and new methods of treatment. Dermatologists have even started to subspecialise, into areas such as dermatopathology and dermatological surgery. Australians are no slouches when it comes to innovation and investigation, as evidenced by their contributions at the huge 19th World Congress of Dermatology in Sydney in June 1997. As editor of MJA Practice Essentials -- Dermatology, Robin Marks (one of only two professors of dermatology in Australia) has obtained contributions from those with international reputations as leaders in their fields. All contributors are excellent communicators who are very practical in their outlook. The book was first published as a series of articles in The Medical Journal of Australia. It was written with general practitioners in mind: after all (according to Professor Marks' introduction), nearly 13% of Australians suffer a skin (or subcutaneous tissue) disease, and over 17% of patient encounters with general practitioners are related to skin disorders. The general practitioner is the first, and sometimes only, port of call for most patients. Each chapter is set out in a very clear, structured way, with logical subheadings, helpful summaries, illustrated case histories and excellent colour photographs throughout. The update on the uses and capabilities of laser therapy is particularly interesting. This topic fascinates the media, and unfortunately it is very easy to create an environment of unrealistic expectations. Yet quite outstanding results are being achieved with some of the newer lasers.

Alan J Cooper

A high incidence of melanoma found in patients with multiple dysplastic naevi by photographic surveillance John W Kelly, Josephine M Yeatman, Cheryl Regalia, Grahame Mason and Amanda P Henham Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - ©MJA1997 Abstract Objectives: (1) To assess the incidence of melanoma in a cohort of patients with dysplastic melanocytic naevi (DMN) and the relationships between incident melanomas and preexisting naevi and between melanoma risk and numbers of DMN. (2) To examine the role of the patient versus the physician in detecting melanoma and the relative value of surveillance versus prophylactic excision. Design: Prospective cohort study. Patients and setting: Two hundred and seventy-eight adults, each with five or more DMN, were followed up for a mean period of 42 months in a private dermatology practice. DMN were clinically diagnosed. Results: Twenty new melanomas were detected in 16 patients, corresponding to an age-adjusted incidence of 1835/100 000 person-years, 46 times the incidence in the general population. Eleven were detected because of changes evident in comparison with baseline photographs and nine were detected by patients or their partners. Thirteen of the 20 melanomas arose as new lesions and only three from DMN. Melanoma risk rose with increasing numbers of DMN. Conclusions: Increasing numbers of DMN are associated with increasing melanoma risk. Surveillance (baseline photography and follow-up) enabled early diagnosis of melanoma and was very much more cost-effective in preventing life-threatening melanoma than prophylactic excision of DMN. MJA 1997; 167: 191-194 Introduction Eight case-control studies have indicated that dysplastic melanocytic naevi (DMN) are a strong and independent risk factor for the development of melanoma.1-8 Cohort studies show that individuals with DMN develop more melanomas than the general population.9-14 Only one cohort study has assessed the association of incident melanomas with preexisting naevi and the role of the patient versus the clinician in detection.10 None has examined an Australian cohort or addressed the relationship between DMN numbers and melanoma risk, the cost-effectiveness of surveillance compared with prophylactic excision or the occurrence of non-melanoma skin cancer in subjects with DMN. We followed a cohort of 278 Australian patients with DMN, using baseline skin surface photography to address these issues. Methods All patients who presented to the private dermatological practice of one of us (J W K) between March 1985 and November 1992 who required total body cutaneous examination were assessed for entry to the study. Any who had five or more clinically determined DMN and who were aged 18 years or more were offered baseline skin surface photography and follow-up on an annual basis. Over 80% had been referred for assessment of their atypical naevi or because of other melanoma risk factors, particularly a personal or family history of melanoma. In November 1993 all patients who had baseline photographs and had returned for at least one 12-month follow-up visit were entered in the study. The entry criterion of five DMN was based on the results of an earlier study that suggested to us that this number of DMN is associated with sufficient melanoma risk to justify entry to a screening program.2 A systematic set of 14 baseline photographs of the skin surface was used. A clinical photographer (A P H) worked with us in designing the views and did the photography, using anatomical site definitions to define standard views of recognisable body regions rather than using standard magnifications (Box 1). This reduced the number of views needed to cover the skin surface while providing adequate magnification. At entry to the study subjects were advised about their high risk of mela noma; three-monthly self-examination was recommended, the clinical features of early melanoma were discussed and appropriate sun protection measures were described. DMN were diagnosed clinically accor ding to published criteria.15 A naevus was considered clinically dysplastic if it had a macular component and showed at least three of the following five clinical features: ill-defined border, irregularly distributed pigmentation, background erythema, size greater than 5 mm, and irregular border. An exact count was made of the number of DMN and recorded in ranges 1-4, 5-10, 11-20, 21-50 and >50. The total number of MN was estimated and recorded in ranges <20, 21-50, 51-100 and 101-500. Patients were reviewed at 6- to 12- month intervals. Total body cutaneous examination was performed at each visit and the patient's pigmented lesions were compared with baseline photographs. Excisional biopsies were performed for any lesions that were clinically suggestive of melanoma and were not done routinely for histological confirmation of the presence of dysplastic naevi. All histo pathological specimens were examined at a single private pathology laboratory. All melanomas arising during the study were reviewed by one pathologist (G M). Melanomas detected at the initial visit were excluded from the analysis. Results The study enrolled 278 patients (162 women and 116 men). Mean age was 37 years (range, 18-67 years). Sixty-five patients (23%) had a family history of melanoma, 54 (19%) had a past history of melanoma, and 9 (3%) had both. None were from melanoma-prone families (as defined by a history of two or more affected first degree relatives). The mean period of follow-up was 42 months (range, 12-99 months). Twenty melanomas were detected in 16 patients over 955 person-years of follow-up. The age-adjusted incidence of melanoma in this group was 1835/100 000 person-years, 46 times the age-adjusted incidence of in-situ and invasive melanoma of 40/100 000 person-years for the population of Victoria in 1990 (G Giles, Anti-Cancer Council of Victoria, 1996, personal communication). The mean time from baseline to diagnosis of melanoma was 36 months (SD, 12 months; range, 11-75 months). Eleven of the 20 melanomas were detected at follow-up visits by comparison with the baseline photographs. These 11 patients were unaware of the changing lesion, and in most of these lesions the change would not have been apparent to the clinician without the use of photo graphs. Seven melanomas were detected by the patient as a change seen on self-examination and two were detected by patients' partners. Four were amelanotic melanomas that did not fulfil the normal diagnostic criteria for melanoma; nonetheless, one of these was detected by the patient. Detecting the 20 melanomas in these 278 patients required 1554 patient consultations (78 for each melanoma). Two hundred and ten biopsies were performed to assess changes observed during follow-up of 104 patients (10 biopsies for each melanoma detected). Not all changes in pigmented lesions led to a biopsy: if melanoma could be confidently ruled out on clinical examination and skin surface microscopy, the lesion was simply rephoto graphed. Histopathological results of these biopsies are shown in Box 3. Changing dysplastic naevi were the predominant source of clinically suspicious change; we do not know how many of these may have progressed to melanoma if they had not been removed. Nineteen non-melanoma skin cancers were detected during follow-up in this group of patients and removed: 16 basal cell carcinomas, one squamous cell carcinoma, one keratoacanthoma, and one Bowen's disease. Of the 16 patients who developed mela noma, five had a family history and seven had a past history of melanoma. Patients with melanoma were more likely to have had a previous melanoma (P = 0.001) and to have a family history of melanoma (P = 0.05) than those who had not. The percentage of patients in each risk group who developed melanoma is shown in Box 2. Boxes 4 and 5 show the incidence of melanoma in the study cohort in relation to the number of dysplastic naevi and total naevi. For an Australian population, the total numbers of naevi were not remarkable (61% had 100 naevi or less), but there were large numbers of DMN (59% had more than 10). Melanoma incidence correlated more closely with increasing numbers of DMN than with increasing total numbers of naevi. Subjects with 21 to 50 DMN developed melanomas at a rate of 3.3% per year. The 20 incident melanomas were all superficial spreading in type. Twelve were invasive and eight were in situ. All the invasive lesions were less than 0.6 mm thick and level II,16 except one amelanotic melanoma that showed a desmoplastic component and invaded to 1 mm in thickness and reached level IV.16 According to the criteria of Clark et al.,17 15 were classified as radial growth phase lesions and four as vertical growth phase; one was classified separately as desmoplastic. The melanomas were widely scattered over the skin surface, with six on the upper limbs, four on the upper back, four on the lower limbs, three on the chest, two on the abdomen, and one on the head. Seven melanomas showed histological evidence of an associated benign naevus (intradermal naevoid remnants in four and features of dysplastic naevi in three). Nine melanomas evolved as a change in a preexisting pigmented lesion that had been evident on baseline photos. In two of these nine the preexisting pigmented lesion was likely to have been a de novo melanoma. One of these patients had a stable pigmented lesion on the right side of her chest over six years. It was excised when it began to enlarge and darken and was found to be a level II, 0.6 mm thick melanoma without histological evidence of any associated naevus. A second patient had a tiny, 2 mm diameter lesion on his chest at his first visit. At his initial review visit, six months later, this had enlarged slightly and become more angular in shape. Histologically, this was a level I melanoma with no associated naevus. Discussion In this study the presence of five or more clinically determined DMN identified a group of patients with 46 times the general population incidence of melanoma. None of these patients came from melanoma-prone families, in whom Clark et al. originally described dysplastic naevi.18 Five cohort studies of patients with DMN who are not from melanoma-prone families have been published and all showed a very high rate of mela noma.9-13 These findings confirm those from case-control studies showing that DMN constitute a strong and independent risk factor for melanoma.1-8 Our age-adjusted incidence of mela noma of 1835/100 000 person-years is higher than that reported in other studies (692-709/100 000 person-years).9,11 This may be explained by the relatively large numbers of DMN in our patients (Box 4) and by the higher background rate of melanoma in Austra lia than in the United States and United Kingdom. We did not examine a cohort of control patients, but Marghoob et al. did.12 They found a 10-year cumulative risk of melanoma of 10.7% among 287 patients with at least one large naevus, one atypical naevus and 100 total naevi. This risk compared with a 0.62% 10-year risk among 831 controls selected from patients requiring annual dermatological follow-up for other reasons. We have intentionally continued to use the word "dysplastic" rather than "atypical". These naevi have been studied because they are believed to be associated with melanoma risk. There are other naevi that are clinically atypical and that are not linked with melanoma risk. Examples are naevus spilus, blue naevus and halo naevus. We prefer the term "dysplastic" because it clearly does not embrace these other atypical naevi. There are several definitions in the literature for syndromes associated with atypical or dysplastic naevi. One includes patients with a single atypical naevus, a large (>8 mm diameter) naevus and >100 total naevi.12 Another depends on distribution of atypical naevi on the anterior scalp, dorsa of the feet, iris or buttocks.19 DMN have been demonstrated to be independently associated with mela noma risk and are not always associated with large numbers of naevi or naevi in certain locations. We prefer not to include DMN in a syndrome definition but rather to consider them as a continuous numerical variable. There is evidence from this study (Box 2) and from two case-control studies of increasing risk with increasing numbers of DMN.2,11 The risk associated with a single DMN is likely to be small and insufficient to justify our follow-up regimen. It is also difficult to accurately diagnose a single naevus as being dysplastic or otherwise on clinical grounds, but much more easy to identify the patient with numerous DMN. It is also difficult to apply definitions of large numbers of naevi in different geographical locations. A recent Australian study reported a mean total count of naevi (>2 mm diameter) that approached 100 in 15-year-old adolescents, which is considered a large number in the United States and United Kingdom.20 The proportion of the Australian adult population with five or more dysplastic naevi has not been defined. One study of 1123 Australian schoolchildren aged 6-15 years showed that 2.7% had three or more dysplastic naevi according to the clinical definition applied here.21 Two-thirds of the incident melanomas in this study were de novo lesions. This finding is similar to those of studies that examine the histological frequency of associated naevi with melanoma, which suggest that 43%-77% of melanomas are new lesions.22-24 The predominance of de novo melanoma in these patients supports management by photographic surveillance rather than by attempts at prophylactic excision. If every one of the 5838 DMN present in our cohort of patients had been excised at the outset, only three of the incident melanomas would have been prevented. Ninety-three DMN were excised in the course of the study because of changes evident in comparison with photographs and because the possibility of melanoma could not be confidently excluded. These changing DMN would seem to be the most likely pigmented lesions to develop into melanoma, and it is possible that some would have progressed to melanoma had they been left in place. When consultations and biopsies are costed at the Australian Government's Medi care Schedule rates for 1997 and $100.00 is allowed per set of photo graphs, the cost of diagnosing each mela noma in this study is $5583. Prophy lactic excision of all dysplastic naevi would have cost $1118038 and would have prevented only three of 20 mela nomas, at a cost of $395038 each. The use of baseline photographs in patients with many floridly atypical pigmented lesions provided knowledge of the stability of many lesions that would otherwise have demanded excisional biopsy, and greatly reduced the number of excisions needed in managing such patients. Patients commonly presented with concern about a change in a particular pigmented lesion. Reference to the photographs usually revealed no change and the lesion remained under observation. Only 10 biopsies were necessary to detect each melanoma and less than one biopsy was necessary per subject in the course of this study. The melanomas incident in this study were detected at an earlier stage than other melanomas that were incident in the State of Victoria in 1990. In-situ melanomas comprised 45% of those seen in the DMN cohort and 33% of those seen in Victoria for 1990 (G Giles, Anti-Cancer Council of Victoria, 1996, personal communication). Median tumour thickness was 0.40 mm in our cohort and 0.77 mm for the State in 1990. Mean tumour thickness for invasive melanoma in the cohort was 0.44 mm compared with 1.40 mm (95% confidence interval, 1.29-1.51) for the State. It is possible that such close surveillance leads to the detection of some melanomas that would otherwise have remained undetected and may have regressed spontaneously or failed to progress and become life threatening. Such "harvesting" of early melanomas may contribute to the very high incidence observed. We conclude that numerous dysplastic naevi identify patients at high risk of melanoma. Baseline photography of the entire skin surface and 6-12-monthly surveillance provides an effective method for early detection of incident melanomas. As most new melanomas were de novo lesions, prophylactic excision of dysplastic naevi would not have provided a satisfactory alternative to follow-up and does not provide sufficient risk reduction to justify the cost and morbidity of the procedure. References Grulich AE, Bataille V, Swerdlow AJH, et al. Naevi and pigmentary characteristics as risk factors for melanoma in a high-risk population: a case-control study in New South Wales, Australia. Int J Cancer 1996; 67: 485-491. Holly EA, Kelly JW, Shpall SN, et al. Number of melanocytic nevi as a major risk factor for malignant melanoma. J Am Acad Dermatol 1987; 17: 459-468. Swerdlow AJ, English J, MacKie RM, et al. Benign melanocytic naevi as a risk factor for malignant melanoma. BMJ 1986; 292: 1555-1559. Augustsson A, Stierner U, Rosdahl I, et al. Common and dysplastic naevi as risk factors for cutaneous malignant melanoma in a Swedish population. Acta Derm Venereol (Stockh) 1990; 71: 518-524. Halpern AC, Guerry D, Elder DE, et al. Dysplastic nevi as risk markers of sporadic (nonfamilial) melanoma. Arch Dermatol 1991; 127: 995-999. Grob JJ, Gouvernet J, Aymar D, et al. Count of benign melanocytic naevi as a major indicator of risk for nonfamilial nodular and superficial spreading melanoma. Cancer 1990; 66: 387-395. Garbe C, Kruger S, Stadler R, et al. Markers and relative risk in a German population for developing malignant melanoma. Int J Dermatol 1989; 28: 517-523. Roush GC, Nordlund JJ, Forget B, et al. Independence of dysplastic nevi from total nevi in determining risk for nonfamilial melanoma. Preventive Medicine 1988; 17: 273-279. Mackie RM, McHenry P, Hole D. Accelerated detection with prospective surveillance for cutaneous malignant melanoma in high risk groups. Lancet 1993; 3421: 1618-1620. Rivers JK, Kopf A, Vinokur AF, et al. Clinical characteristics of malignant melanomas developing in persons with dysplastic naevi. Cancer 1990; 65: 1232-1236. Halpern AC, Guerry D, Elder DE, et al. A cohort study of melanoma in patients with dysplastic nevi. J Invest Dermatol 1993; 100: 346-349. Marghoob AA, Kopf AW, Bart RS, et al. Risk of cutaneous malignant melanoma in patients with "classic" atypical mole syndrome. Arch Dermatol 1994; 130: 993-998. Kang S, Barnhill RL, Mihm MC, et al. Melanoma risk in individuals with clinically atypical naevi. Arch Dermatol 1994; 130: 999-1001. Schneider JS, Moore DH, Sagebiel RW. Risk factors for melanoma incidence in prospective follow-up. The importance of atypical (dysplastic) nevi. Arch Dermatol 1994; 130: 1002-1007. Kelly JW, Crutcher WA, Sagebiel RW. Clinical diagnosis of dysplastic melanocytic nevi. J Am Acad Dermatol 1986; 14: 1044-1052. Clark WH Jr, From L, Bernadino EH, et al. Histogenesis and biological behaviour of primary human malignant melanoma of the skin. Cancer Res 1969; 29: 705-727. Clark WH, Elder DE, Guerry D, et al. Model predicting survival in stage I melanoma based on tumour progression. J Natl Cancer Inst 1989; 81: 1893-1904. Clark WH, Reimer RR, Greene M. Origin of familial malignant melanomas from heritable melanocytic lesions. Arch Dermatol 1978; 114: 732-738. Newton JA, Bataille V, Griffiths K, et al. How common is the atypical mole syndrome phenotype in apparently sporadic melanoma? J Am Acad Dermatol 1993; 29: 989-996. Kelly JW, Rivers JK, MacLennan R. Sunlight: a major factor associated with the development of melanocytic nevi in Australian school children. J Am Acad Dermatol 1994; 30: 40-48. Rivers JK, Maclennan R, Kelly JW, et al. The Eastern Australian childhood nevus study: prevalence of atypical nevi, congenital nevus-like nevi, and other pigmented lesions. J Am Acad Dermatol 1995; 32: 957-963. Marks R, Dorevitch AP, Mason G. Do all melanomas come from "moles"? A study of the histological association between melanocytic naevi and melanoma. Australas J Dermatol 1990; 31: 77-80. Sagebiel RW. Melanocytic nevi in histologic association with primary cutaneous melanoma of superficial spreading and nodular types: Effect of tumour thickness. J Invest Dermatol 1993; 100 Suppl: 322S-325S. Skender-Kalnenas TM, English DR, Heenan PJ. Benign melanocytic lesions: risk markers or precursors of cutaneous melanoma? J Am Acad Dermatol 1995; 33: 1000-1007. (Received 10 Dec 1996, accepted 10 Jun 1997) Authors' details Victorian Melanoma Service, Alfred Hospital, Melbourne, VIC. John W Kelly, MD BS, FACD, Head; Head of Dermatology Unit, Alfred Hospital; Clinical Associate Professor, Monash University Department of Medicine. Dermatology Unit, Alfred Hospital, Melbourne, VIC. Josephine M Yeatman, MB BS, GradDipEpi, Registrar. Cheryl Regalia, Medical student, University of California at San Diego; now MD. Dorevitch Laboratories, Melbourne Grahame Mason, MB BS, FRCPA, Pathologist. Department of Photography, Northern Territory University, Darwin, NT. Amanda P Henham, BAppSci(Photog), SRN, Lecturer. Reprints: Dr J W Kelly, Victorian Melanoma Service, Alfred Hospital, Commercial Road, Prahran, VIC 3181. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

John W Kelly · Josephine M Yeatman · Cheryl Regalia · Grahame Mason · Amanda P Henham

Systematic review of the diagnostic accuracy of dermatoscopy in detecting malignant melanoma Justine Mayer Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Data sources - Study selection and data extraction - Results - Design and validity of selected studies - Results of selected studies - Discussion - Acknowledgements - References - Authors' details - - ©MJA1997 Abstract Objective: To assess the evidence that dermatoscopy improves the accuracy of diagnosis of melanomas in clinical practice. Data sources: MEDLINE 1983-January 1997, EMBASE 1980-1996, and bibliographies of retrieved articles. Study selection and data extraction: Studies selected were original studies with formal methods and results sections comparing diagnostic accuracy of dermatoscopy for malignant melanoma with another clinical method; the criterion standard was excision biopsy with histopathological examination; and accuracy of dermatoscopic diagnosis was determined over a spectrum of stages of melanoma and skin lesions commonly confused with melanoma. Data were extracted by a single observer. Data synthesis: 579 articles were identified; six studies met the inclusion criteria. Positive likelihood ratios for dermatoscopy for diagnosis of melanoma ranged from 2.9 to 10.3. Dermatoscopy had 10%-27% higher sensitivity than clinical diagnosis in the two studies with the most clinically equivocal lesions. However, when sensitivity of clinical diagnosis was more than 84%, sensitivity of dermatoscopy was only slightly higher. One study of dermatologists with no training in dermatoscopy showed a significant decrease in sensitivity. Conclusions: Variability between studies in methods, observers and types of pigmented skin lesions and lack of studies in primary care make generalisation of results difficult. Dermatoscopy appeared not to improve the accuracy of diagnosis enough to alter the clinical management of most pigmented skin lesions. Further research with more explicit methods is needed. MJA 1997; 167: 206-210 Introduction Malignant melanoma is an important cause of morbidity and mortality in Australia. Public health strategies emphasise, in addition to reducing sun exposure, early diagnosis and treatment. It has been claimed that dermatoscopy improves the accuracy of diagnosis of malignant melanomas,1,2 but calls have also been made for a systematic review of the evidence3 (see Box 1 for description of dermatoscopy). An ideal diagnostic test achieves maximum levels of sensitivity and specificity. However, as sensitivity reflects a test's ability to identify individuals with the disease, most clinicians considering the diagnosis of melanoma would prefer a test with high sensitivity. Furthermore, diagnostic tests should be performed only if they have the potential to alter clinical management. For pigmented skin lesions, this means helping decide whether to excise the lesion. This review aimed to identify primary studies that researched the diagnostic accuracy of dermatoscopy compared with clinical diagnosis and to assess their implications for clinical practice. Methods The review followed current recommendations on systematic reviews of the accuracy of diagnostic tests.7,8 Data sources MEDLINE Express (Silverplatter Winspirs) on CD-ROM databases January 1983-January 1997 and Elsevier Science EMBASE Database 1980-1996 were searched. The Medline search was conducted with exploded MeSH headings "melanoma" or "skin neoplasms", combined with "sensitivity and specificity", and with text words "dermoscop*", "dermatoscop*", "skin surface microscop*", "epiluminesc*", or "incident light microscop*". Similar strategies were used to search EMBASE. Study selection and data extraction Abstracts of articles were reviewed by the author for studies that met the selection criteria: Original study with a formal methods and results section comparing the diagnostic accuracy of dermatoscopy for malignant melanoma with another method of clinical diagnosis; Excision biopsy with histopathological examination was the criterion standard; and The accuracy of dermatoscopic diagnosis was determined over a large range of pigmented skin lesions, including a spectrum of stages of melanoma and lesions commonly confused with melanoma. Articles describing studies that appeared to meet the criteria were retrieved for more detailed review (after translation if not in English). Bibliographies of articles retrieved were also checked for articles not listed or incorrectly indexed in MEDLINE or EMBASE. Articles that did not meet the selection criteria included those on the terminology of dermatoscopic techniques, development of criteria for diagnosing pigmented skin lesions, observer error of diagnosis, accuracy of diagnosis of a single type of pigmented skin lesion, and accuracy of digital imaging computer programs. Studies providing data on the sensitivity and specificity of dermatoscopy but with no comparison group were also excluded.9,10 Articles that met the selection criteria were reviewed for study validity and applicability to clinical practice.11 The methods section of each article was checked for explicit mention of the criterion standard of histopathological examination, blinding of observers, spectrum of pigmented skin lesions, study setting, patient demographics, prevalence of melanoma, sample size, intraobserver and interobserver error, and the proportion of pigmented skin lesions in which no dermatoscopic diagnosis could be made. Results Three hundred and thirty-six articles were identified from MEDLINE and 243 from EMBASE. Six articles met the inclusion criteria.4,12-16 All were indexed in MEDLINE and one in EMBASE and all were in English. No further articles meeting the inclusion criteria were found on review of the bibliographies of retrieved articles. Design and validity of selected studies The designs of the six studies are summarised in Box 2. Assessment of the studies' internal and external validity was hampered by lack of information. Only Binder et al.14 provided sufficient details of methods to enable the study to be repeated. All studies were set in specialist dermatology clinics, but none provided further details of the setting (i.e., whether a secondary or tertiary referral centre). They investigated selected groups of pigmented skin lesions, with melanomas comprising 15%-41%, but only one study explicitly stated how lesions were chosen for entry into the study.12 All appeared to include only lesions to be excised because of presumed risk of malignancy or, possibly, patient request. None commented on the suitability of the sample to detect clinically important differences in the diagnostic methods being evaluated, and none provided data on all presenting lesions or followed them up to calculate the true false negative rate. Although all studies used the criterion standard of histopathological examination, none commented on how the histological diagnosis was reached, although pathologists may vary in classifying pigmented skin lesions.24,.25 Only four studies provided objective data on melanoma diameter or Breslow depth.4,12,14,15 Five studies assessed dermatoscopy results in vivo and one, from photographic slides.14 Observers in the in vivo studies were assumed to be blinded to the histopathological results, but it was not apparent that clinical and dermatoscopic diagnoses were independent, despite the importance of history in the diagnosis of malignant lesions. Five studies did not provide the criteria used for clinical diagnosis, and only Binder et al. provided complete details of the method of non-dermatoscopic examination. The diagnostic criteria and method of surface microscopy used differed between the studies. Three studies used handheld monocular dermatoscopes with x 10 magnification,4,13,16 and two studies used binocular stereomicroscopes with magnification up to x 40.12,14 One study used both types of instrument, but did not clearly distinguish their results.15 No study remarked that a skin lesion was unable to be diagnosed by dermatoscopy. Results of selected studies Results of the six studies are shown in Box 2. Five of the studies compared dermatoscopy with clinical diagnosis or diagnosis by microscopy without oil. Likelihood ratios for a positive diagnosis of melanoma by dermatoscopy ranged from 2.9 to 10.3 (meaning that pigmented lesions diagnosed as melanoma by dermatoscopy were 2.9 to 10.3 times morelikely to be melanoma than not). Two studies found that dermatoscopy had higher sensitivity than non-dermatoscopic diagnosis,12,13 one found no difference,15 and one found that dermatoscopy increased sensitivity when performed by experts, but decreased it when performed by dermatologists without training in the technique.14 Pazzini et al. provided insufficient data to calculate sensitivity.16 Nachbar et al.4 compared two forms of dermatoscopy -- with explicit structured diagnostic criteria and without these criteria, but combined with clinical diagnosis. They found that dermatoscopy with structured ABCD criteria19,21 (specific for dermatoscopy and differing from the ABCDE criteria for clinical diagnosis) had higher sensitivity and specificity than dermatoscopy without such criteria. Clinical diagnosis varied widely in sensitivity and specificity between the studies, most likely because the lesions varied in their ease of diagnosis. Observers may also have varied in their ability to make the diagnosis. This variability prevented formal meta-analysis and estimation of a single summary statistic for the diagnostic benefit of dermatoscopy. The studies that provided results for handheld monocular dermatoscopes with x 10 magnification are most relevant to clinical practice.4,13 Cristofolini et al.13 found that dermatoscopy with pattern-analysis criteria had slightly higher sensitivity (88%) and specificity (79%) than clinical diagnosis with ABCDE criteria.18 However, the latter was already highly accurate (sensitivity, 85%; specificity, 75%). Nachbar et al. found that dermatoscopy with structured criteria had higher sensitivity (93% versus 84%) and specificity (91% versus 84%) than without such criteria.4 Interestingly, the studies that showed the greatest improvement in sensitivity for dermatoscopy were those that had the lowest baseline sensitivity for clinical diagnosis. Steiner et al.12 found that dermatoscopy increased sensitivity from 59% to 86% (an increase of 27%) compared to microscopy without oil. Binder et al.14 found dermatoscopy performed by experts increased sensitivity from 58% to 68% (increase of 10%) compared to clinical diagnosis. Both these studies appeared to include small difficult-to-diagnose lesions, suggesting that dermatoscopy may be most useful in these circumstances. In contrast, when clinical diagnosis was very accurate (as found by Soyer et al.15) dermatoscopy was of no benefit. This study also provided data on the accuracy of individual dermatoscopy criteria (not shown). The study by Binder et al. also examined two further important issues. They found that, although dermatoscopy had higher sensitivity than clinical diagnosis when performed by experts, it had lower sensitivity when performed by dermatologists with no formal training in the technique; these observers misdiagnosed more melanomas with dermatoscopy. Further, while experts showed moderate interobserver and intraobserver agreement (average k = 0.47 and 0.56, respectively), non-experts showed only fair agreement (average k = 0.29 and 0.36, respectively). This study used photographic slides and it may be problematic generalising these results to clinical practice. Discussion Despite the comprehensive search strategy used for this review, publication bias is still possible, and small studies of dermatoscopy with negative results may not have been submitted or accepted for publication. For dermatologists working within specialist clinics the evidence on dermatoscopy is: When sensitivity and specificity are low for clinical diagnosis of melanoma (50%-60%), both are improved by dermatoscopy performed by formally trained experts. However, when sensitivity and specificity are high for clinical diagnosis (84%-95%), dermatoscopy adds little or nothing to either. Improvement in diagnostic accuracy is most apparent for equivocal pigmented skin lesions and when using explicit structured criteria. However, as none of the studies were conducted in a primary care setting, the place of dermatoscopy in general practice is unknown. In addition, none of the studies commented that dermatoscopy improved the sensitivity and specificity of diagnosis enough to alter the clinical management of the pigmented skin lesion. In fact, dermatoscopy only increased the accuracy of diagnosis of equivocal lesions that were to undergo biopsy anyway. Given the low threshold clinicians already have for excision biopsy, the modest impact of dermatoscopy on likelihood ratios suggests it does not improve diagnostic accuracy enough to alter clinical management of most pigmented skin lesions. Further research is currently being undertaken using dermatoscopy to describe the sensitivities and specificities of individual features of pigmented lesions.6 This may prove to be more clinically relevant in the long term. In one study, the use of dermatoscopy by untrained dermatologists resulted in more melanomas being missed than with magnification alone. Non-experts also showed more interobserver and intraobserver variation. This suggests that the benefits of dermatoscopy depend on training and experience with its use. However, none of the studies commented on the type of training needed to develop competence. Two of the studies investigated the effect of using defined diagnostic criteria in diagnosing melanoma. Their results were consistent with the view that simple structured explicit criteria, such as ABCD criteria, either with or without dermatoscopy, result in a high sensitivity and specificity for diagnosis of melanoma. To provide better evidence on the value of dermatoscopy in Australian clinical practice, future research should be more explicit in the methods used and should select lesions representative of those seen in primary and secondary care in Australia. An investigation in clinical practice, where the prevalence of melanoma is low, is not practicable. However, it would be possible to compare the accuracy of diagnosis from dermatoscopic and standard magnified images of skin lesions by dermatologists and general practitioners. This type of study would also allow further assessment of intraobserver and interobserver variability and could be combined with assessment of the impact of training. This approach would allow the potential clinical benefits and limitations of dermatoscopy to be more clearly understood. Acknowledgements I gratefully thank Dr P S Morris (Menzies School of Health Research, Darwin, NT), Associate Professor L Piterman (Department of Community Medicine, Monash University, Melbourne, VIC), and three anonymous reviewers for helpful comments on an earlier draft of the manuscript; Mariella Stroschio and Antje Haase for translation of Italian and German articles; the RACGP Resource Centre librarians, Jane Ryan and Diane Horrigan, for their skills in searching Embase and hard work in locating the articles; the Royal Darwin Hospital library for use of Medline ; and the RACGP Research and Development Fund. References Kelly JW. Malignant melanomas -- how many have you missed? Med J Aust 1996; 164: 431-436. Kelly JW. Melanoma: detection and management. Aust Fam Phys 1994; 23: 801-812. Del Mar CB. How many melanomas have I missed? Is this the question? [letter]. Med J Aust 1996; 165: 456. Nachbar F, Stoltz W, Merckle T, et al. The ABCD rule of dermatoscopy. High prospective value in diagnosis of melanocytic lesions. J Am Acad Dermatol 1994; 30: 551-559. Kenet R, Kang S, Kenet BJ, Fitzpatrick TB. Clinical diagnosis of pigmented lesions using digital epiluminescence microscopy grading protocol. Arch Dermatol 1993; 129: 157-174. Menzies SW, Ingvar C, McCarthy WH. A sensitivity and specificity analysis of the surface microscopy features of invasive melanoma. Melanoma Res 1996; 6: 55-62. Irwig L, Toteson A, Gatsonis C, et al. Guidelines for meta-analyses evaluating diagnostic tests. Ann Intern Med 1994; 120: 667-676. Cochrane Methods Working Group on Systematic Review of Screening and Diagnostic Tests. The Cochrane methods working group on systematic review of screening and diagnostic tests: recommended method. [sighted 6 Oct 1996] < http://som.flinders.edu.au/FUSA/COCHRANE/cochrane/sadt.doc.html > > Nilles M, Boedeker RH, Schill WB. Surface microscopy of naevi and melanomas -- clues to melanoma. Br J Dermatol 1994; 130: 349-355. Carli P, De Georgi V, Donati E, et al. La microscopia a epilumescenza (ELM) riduce il rischio di asportare lesioni melanocitarie clinicamente sospette ma istologicamente comuni. Giornale Italiano Dermatologia e Venereologia 1994; 129: 599-605. Sackett DL, Haynes RB, Guyatt GH, et al. Clinical epidemiology: a basic science of clinical medicine. 2nd ed. Boston, Mass: Little, Brown and Company, 1991: 151-152. Steiner A, Pehamberger H, Wolff K. In vivo epiluminescence microscopy of pigmented skin lesions. 2. Diagnosis of small pigmented skin lesions and early detection of malignant melanoma. J Am Acad Dermat 1987; 17: 584-591. Cristofolini N, Zumiani G, Bauer P, et al. Dermatoscopy: usefulness in the differential diagnosis of cutaneous pigmentary lesions. Melanoma Res 1994; 4: 391-394. Binder N, Schwarz N, Winkler A, et al. Epiluminescence microscopy. A useful tool for the diagnosis of pigmented lesions for formally trained dermatologists. Arch Dermatol 1995; 131: 286-291. Soyer HP, Smolle J, Leitinger G, Kerl H. Diagnostic reliability of dermoscopic criteria for detecting malignant melanomas. Dermatology 1995; 190: 25-30. Pazzini C, Pozzi M, Betti R, et al. Improvement of diagnostic accuracy in the clinical diagnosis of pigmented skin lesions by epiluminescence microscopy. Skin Cancer 1996; 11: 159-161. Pehamberger H, Steiner A, Wolff K. In vivo epiluminescence microscopy of skin lesions. 1. Pattern analysis of pigmented skin lesions. J Am Acad Dermat 1987; 17: 571-583. McGovern TW, Litaker MS. Clinical predictors of malignant pigmented lesions. J Dermatol Surg Oncol 1992; 18: 22-26. Stoltz W, Holzel D, Riemann A, et al. Multivariate analysis of criteria given by dernatoscopy for the recognition of melanocytic lesions [abstract]. Abstracts of the Fiftieth Meeting of the American Academy of Dermatology; 1991; Dallas (TX). American Academy of Dermatology, 1991. Bahmer FA, Fritsch P, Kreusch J, et al. Terminology in surface microscopy. J Am Acad Dermat 1990; 23: 1159-1162. Stoltz W, Riemann A, Armand B, et al. ABCD rule of dermatoscopy: a new practical method for early recognition of malignant melanoma. Eur J Dermatol 1994; 4: 521-527. Lightstone A, Kopf A, Garfinkel L. Diagnostic accuracy -- a new approach to its evaluation: results in basal epitheliomas. Arch Dermatol 1965; 91: 497-501. Jaescheke R, Guyatt GH, Sackett DL. Users guide to the medical literature. 3. How to use an article about a diagnostic test: B. What are the results and will they help me in caring for my patients? JAMA 1994; 271: 703-707. Krieger N, Hiatt RA, Sagebiel RW, et al. Inter-observer variability among pathologists' evaluation of malignant melanoma: effects upon an analytic study. J Clin Epidemiol 1994; 47: 897-902. de Wit PEJ, van't Hof-Grootenboer B, Ruiter DJ. Validity of the histopathological criteria used for diagnosing dysplastic naevi. Eur J Cancer 1993; 29a: 831-839. (Received 14 Nov 1996, accepted 16 May 1997) Authors' details Danila Dilba Medical Service, Darwin, NT. Justine Mayer, FRACGP, General Practitioner; Master of Family Medicine Student (Monash University, Melbourne, VIC). Reprints will not be available from the author. Correspondence: Dr Justine Mayer, PO Box 538, Nightcliff, NT 0814. E-mail: jmayer@racgp.org.au ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Justine Mayer

AbstractObjective: To assess the effectiveness of the flashlamp-pumped pulsed dye laser in the treatment of port-wine stains. Design: A retrospective review of medical records and patients. Setting: Royal Perth Hospital (a tertiary referral hospital), August 1989 to December 1992. Subjects: 186 consecutive patients with port-wine stains treated with a flashlamp-pumped pulsed dye laser. Outcome measures: Degree of lesion fading; adverse reactions. Results: Of 131 patients who completed treatment, 78% had better than 50% fading of the lesion and only 9% had less than 25% fading. An average 3.4 treatments were needed to achieve more than 50% fading. The response was better in children than in adults, although the difference was not significant. Anaesthesia was needed for 44% of patients. Pigmentary change (usually transient) occurred in 6.1% of patients and permanent and significant adverse effects in only 4.6%. Conclusion: This study confirms the efficacy of the flashlamp-pumped pulsed dye laser in the treatment of port-wine stains in children and adults. Early treatment of port-wine stains should be encouraged to reduce the physical and psychological morbidity of disfiguring lesions. IntroductionPort-wine stains (now termed capillary malformations) are congenital vascular malformations characterised by ectatic vessels within the cutaneous superficial vascular plexus.1 They affect 0.3% of children at birth, with an equal sex distribution.2 Most port-wine stains are found on the head and neck, with 85% occurring in a unilateral, dermatomal distribution.3 Their natural history is to progress from a pink, macular lesion at birth to a dark red (or even purple), nodular, proportionately larger lesion in adulthood.1,4 Cosmetic disfigurement can cause considerable psychological morbidity, and be socially disadvantageous.5,6 Hypertrophic, nodular lesions may bleed, either spontaneously or after trauma, encroach on essential facial structures or even develop into pyogenic granulomas.7 All port-wine stains should be treated, preferably early in life, to prevent or reduce the potential physical and psychological complications. Before the development of laser technology, treatment for port-wine stains was often unsatisfactory.8 Earlier lasers, including ruby, carbon dioxide and argon lasers, improved the lesions in most patients, but, as they were non-selective in their effects on tissue, the frequency of side effects, such as scarring and pigmentary changes, was unacceptably high.9 The flashlamp-pumped pulsed dye laser (PDL) was the first laser to be based on selective photothermolysis;10 it produces vascular- specific damage without affecting surrounding dermal structures or the epidermis.11-13 Studies have confirmed its effectiveness in the treatment of port-wine stains in adults, children and infants, with an extraordinarily low incidence of side effects.14-19 The PDL is now regarded as the first-line treatment for port-wine stains whenever possible.8,9,20-22 In Australia, the PDL has been in use since the late 1980s for the treatment of cutaneous vascular lesions, especially port-wine stains. However, no Australian study of its effects has been published. Therefore, we undertook a retrospective clinical review of all patients with port-wine stains treated with PDL at Royal Perth Hospital between August 1989 and December 1992. MethodsThe study was a retrospective review of patient medical records. If response to treatment was not recorded, attempts were made to review the patient between January and December 1993. PatientsAll patients (adult and paediatric) with a port-wine stain treated with PDL at Royal Perth Hospital between August 1989 and December 1992 were eligible. Patients attended outpatient clinics, where the site and size of the port-wine stain and demographic data were recorded and the treatment procedure and its risks and benefits were explained. Patients were photographed before treatment by a professional photographer in a studio dedicated to medical photography, with efforts to use the same magnification, lighting and exposure. Laser and techniqueA flashlamp-pumped pulsed dye laser (Candela SPTL-1, Candela Corp, Wayland, Mass, United States) was used. It emitted yellow light at a wavelength of 585 nm, with a pulse duration of 450 µs and a 3 s pause between pulses. The laser beam was transmitted down a 1 mm fibre by a planoconvex lens and focused as a 5 mm spot beam. Energy densities were measured by an energy meter (Ophir, Jerusalem, Israel), calibrated to 10% accuracy. Both the physicians and the patients eyes were protected from laser light during treatment. Some patients had a small initial test patch treated, depending on patient anxiety and time of presentation (before 1991, most had a patch test). Otherwise, the entire lesion was treated at once, unless it involved a large surface area (> 100 cm2). Treatments were repeated at intervals of 23 months. The energy density used varied with the age of the patient and colour, nodularity and location of the lesion and was adjusted according to the degree of purpura produced and the patients response to the previous treatment. Pulses were overlapped by a maximum of 10% across the affected area. The anaesthetic varied according to the site and area to be treated and the level of patient cooperation. EMLA cream (eutectic mixture of 2.5% lignocaine and 2.5% prilocaine cream, Astra Pharmaceuticals, North Ryde, NSW) was used for topical anaesthesia, applied under occlusion for 60120 minutes before treatment. Local anaesthesia involved an injection of 1% lignocaine, either locally or as a regional nerve block. General anaesthesia was given to children who had extensive lesions or were uncooperative with topical or local anaesthesia. The treated area developed purpura within a few minutes, usually persisting for 710 days. No immediate postoperative care was necessary, except for an occasional ice pack to reduce oedema in those with large treatment areas. Postoperative instructions were to protect the area from trauma, avoid excessive exposure to sunlight and use a topical antiseptic cream for any scaling or crusting. Treatment evaluationEach port-wine stain was evaluated, either before the next treatment or 34 months after the final treatment. Lesional lightening was assessed as the percentage reduction in colour compared with the pretreatment photo (fading < 25%, poor; 25% to 50%, fair; > 50% to 75%, good; and > 75%, excellent) (Figures 1-4). Adverse effects, such as scarring and textural or pigmentary changes, were also noted. All patients were individually assessed by one or both investigators. The endpoint of treatment was assessed clinically. Data analysisData were analysed with the Statistical Analysis Systems software package.23 The chi-squared statistic was used to assess the difference in response between age groups. ResultsThere were 186 patients treated by PDL: 131 completed treatment (55 either did not complete treatment or were having ongoing treatment). Patients were either Caucasian or Asian and aged 8 months to 66 years (mean, 25.6 years). There were 59 males (32%) and 127 females (68%). Most of the treated lesions were present from birth (97%). Acquired lesions appeared most commonly between the ages of six and 12. Most lesions were on the face and neck (87%), with the rest distributed unilaterally on the arms (4%), legs (5%), back (2%) and chest (2%). The size of treated lesions ranged from 1 cm2 to 280 cm2 (mean, 42 cm2). All responded to energy fluences between 5 and 10 joules/cm2(mean, 6.7 joules/cm2). Sixty-two per cent of the patients had a patch test before treatment. Anaesthesia was used for 44% of patients (general anaesthesia by 20%, topical by 19% and local or regional block by 5%). Responses of patients who completed treatment are shown in the Box. A good-to-excellent response was achieved in 78% and a poor response in only 9%. An average 3.4 treatments per lesion were required to achieve a good-to-excellent response. Adverse side effects occurred in 11% of patients who completed treatment; all had some fading of the lesion. The most common adverse effect was pigmentary change (6.1%), which was usually transient and resolved in 23 months. Only 4.6% had significant permanent adverse effects; two had scarring (in both the port-wine stain was on the face and neck region). More children than adults had a good or excellent response, but the difference was not significant when compared with a 2 x 2 contingency table and chi-squared test (r = 0.60). Similarly, fewer children than adults had a poor response. DiscussionOur results compare favourably with those of other studies. A good-to-excellent response (more than 50% fading) was obtained in 78% of our patients (including both adults and children, with lesions on sites including the trunk and lower limbs), with an average 3.4 treatments required. Others have found more than 50% fading in 73%-95% of patients after 2.4-2.8 treatments.14-17,24,25 Response to treatment varies between sites: the periorbital area, temple, lateral aspect of the cheek, neck and chin have been observed to be more responsive18,25 and the centrofacial area and lower leg to be less responsive.18,19 We found that a poor response was more common in adults than in children (although the difference was not significant), possibly because port-wine stains become progressively hypertrophied and nodular in adults. We found a higher rate of adverse effects (11%) than in other studies. The most common (usually transient) adverse effect was pigmentary change (increase or decrease), possibly because of excessive sunlight exposure after treatment. This transient change may not have been recorded in other studies; when it was excluded from our figures, the rate of adverse reactions was reduced to less than 5%, which is comparable with that found in other studies. Scarring was seen in two of our patients, with lesions on the face and neck, where damage to dermal structures with fibrosis occurs when excessive energy fluence is used. A low energy fluence should be used initially when treating port-wine stains on the neck and anterior chest. The PDL is the first laser specifically designed for cutaneous vascular malformations. It is based on the theory of selective photothermolysis, which predicts selective destruction of blood vessels without damage to the surrounding tissues.10 Laser light emitted by the PDL is absorbed by oxyhaemoglobin in the dilated vessels of the lesion, producing agglutination of erythrocytes, thrombus formation and eventual destruction of the vessels.11 They are replaced by non-dilated superficial dermal blood vessels with a normal appearance.12 A recent comparison of PDL and the copper vapour laser showed that PDL produced significantly better fading of port-wine stains.22 The characteristics and degree of pain associated with PDL treatment have been well described.26 Initially, there is a sharp stinging pain, very similar to the snap of a rubber band against the skin. Accompanying this is a second distinct heat sensation that can be at least as unpleasant as the initial sting. Pain rapidly subsides but seems to build up if successive pulses are used for a moderately sized lesion. Our current practice is to give general anaesthesia to all children from four weeks of age, until they are able to co-operate with topical or local anaesthesia, usually at eight to 10 years. Young children undergoing multiple painful treatments with inadequate anaesthesia under restraint may develop phobic responses. Furthermore, a struggling child may compromise the clinicians ability to perform the procedure optimally. In conclusion, this study supports the contention that all port-wine stains should be treated with PDL, as it has a high therapeutic index with a low incidence of adverse effects. Patients should preferably be treated in infancy or childhood, under general anaesthesia, to minimise the potential psychological morbidity of disfiguring lesions. In addition, the response to treatment seems better in children than in adults, although the difference was not significant, possibly because of the relatively small sample size. Laser treatment of port-wine stains should no longer be considered just cosmetic, but a medical necessity for a problem that can cause psychological and physical morbidity. References Mulliken JB. Capillary (port-wine) and other telangiectatic stains. In: Mulliken JB, Young AE, editors. Vascular birthmarks -- haemangiomas and malformations. Philadelphia: W B Saunders, 1988: 179-195. Jacobs AH, Walton RG. The incidence of birthmarks in the neonate. Pediatrics 1976; 58: 218-222. Tallman B, Tan OT, Morelli JG, et al. Location of port-wine stains and the likelihood of ophthalmic and/or central nervous system complications. Pediatrics 1991; 87: 323-327. Barsky SH, Rosen S, Geer DE, Noe JM. The nature and evolution of port-wine stains: a computer-assisted study. J Invest Dermatol 1980; 74: 154-157. Lanigan SW, Cotterill JA. Psychological disabilities amongst patients with port wine stains. Br J Dermatol 1989; 121: 209-215. Pickering JW, Butler PH, Ring BJ, Walker EP. 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Authors detailsDepartment of Dermatology, Royal Perth Hospital, Perth, WA. Ernest Tan, MB BS, Dermatology Registrar; Carl Vinciullo, FACD, Visiting Dermatologist. No reprints will be available. Correspondence: Dr C Vinciullo, Department of Dermatology, Royal Perth Hospital, Wellington Street, WA 6000. E-mail: carlATdermlaser.com.au

Ernest Tan · Carl Vinciullo