Topics

Summary

Introduction

This article summarises the Cardiac Society of Australia and New Zealand position statement on coronary artery calcium (CAC) scoring. CAC scoring is a non-invasive method for quantifying coronary artery calcification using computed tomography. It is a marker of atherosclerotic plaque burden and the strongest independent predictor of future myocardial infarction and mortality. CAC scoring provides incremental risk information beyond traditional risk calculators such as the Framingham Risk Score. Its use for risk stratification is confined to primary prevention of cardiovascular events, and can be considered as individualised coronary risk scoring for intermediate risk patients, allowing reclassification to low or high risk based on the score. Medical practitioners should carefully counsel patients before CAC testing, which should only be undertaken if an alteration in therapy, including embarking on pharmacotherapy, is being considered based on the test result.

Main recommendations

CAC scoring should primarily be performed on individuals without coronary disease aged 45–75 years (absolute 5-year cardiovascular risk of 10–15%) who are asymptomatic.
CAC scoring is also reasonable in lower risk groups (absolute 5-year cardiovascular risk, < 10%) where risk scores traditionally underestimate risk (eg, family history of premature CVD) and in patients with diabetes aged 40–60 years.
We recommend aspirin and a high efficacy statin in high risk patients, defined as those with a CAC score ≥ 400, or a CAC score of 100–399 and above the 75th percentile for age and sex.
It is reasonable to treat patients with CAC scores ≥ 100 with aspirin and a statin.
It is reasonable not to treat asymptomatic patients with a CAC score of zero.

Changes in management as a result of this statement

Cardiovascular risk is reclassified according to CAC score.
High risk patients are treated with a high efficacy statin and aspirin.
Very low risk patients (ie, CAC score of zero) do not benefit from treatment.

1 Heart and Lung Institute, The Prince Charles Hospital, Brisbane, QLD
2 Centre for Advanced Imaging, University of Queensland, Brisbane, QLD
3 The George Institute for Global Health, Sydney, NSW
4 Westmead Hospital, Sydney, NSW
5 Royal Brisbane and Women's Hospital, Brisbane, QLD
6 St Vincent's Hospital, Melbourne, VIC
7 Cardiovascular Research Centre, Australian Catholic University, Melbourne, VIC
8 Griffith University, Gold Coast, QLD
9 Gold Coast Heart Centre, Gold Coast, QLD
10 University of Adelaide, Adelaide, SA
11 Epworth HealthCare, Melbourne, VIC

Correspondence: c.hamiltoncraig@uq.edu.au

Competing interests:

No relevant disclosures.

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18. Antithrombotic Trialists’ Collaboration; Baigent C, Blackwell L, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet 2009; 373: 1849-1860.
19. Berger JS, Roncaglioni MC, Avanzini F, et al. Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials. JAMA 2006; 295: 306-313.
20. Seshasai SR, Wijesuriya S, Sivakumaran R, et al. Effect of aspirin on vascular and nonvascular outcomes: meta-analysis of randomized controlled trials. Arch Intern Med 2012; 172: 209-216.
21. Miedema MD, Duprez DA, Misialek JR, et al. Use of coronary artery calcium testing to guide aspirin utilization for primary prevention: estimates from the multi-ethnic study of atherosclerosis. Circ Cardiovasc Qual Outcomes 2014; 7: 453-460.
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23. Raggi P, Callister TQ, Shaw LJ. Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy. Arterioscler Thromb Vasc Biol 2004; 24: 1272-1277.
24. Budoff MJ, Hokanson JE, Nasir K, et al. Progression of coronary artery calcium predicts all-cause mortality. JACC Cardiovasc Imaging 2010; 3: 1229-1236.

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Narrative review

Atopic dermatitis: the new frontier

Victoria R Harris and Alan J Cooper

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00463
Published online: 16 October 2017

ARTICLE
AUTHORS
REFERENCES

Topics

Immune system diseases

Pharmaceutical preparations

Skin and connective tissue diseases

Summary

Atopic dermatitis (AD) is the most common inflammatory skin condition in adults and children.
AD is a chronic disease that has a considerable negative impact on the quality of life of patients and their families.
Most cases of AD may be effectively treated with topical therapies that are directed at decreasing cutaneous inflammation and alleviating pruritus. These therapies include emollients, antihistamines, topical corticosteroids, topical calcineurin inhibitors and antimicrobial and antiseptic measures; more refractory cases may require additional oral immunosuppression (eg, cyclosporine, azathioprine, methotrexate and mycophenolate).
Improved understanding of the immune pathogenesis of AD, including the role of T helper cells and the inflammatory pathways involved, has led to breakthrough translational clinical research and treatment.
New targeted immunotherapies, such as inhibitors of interleukin (IL)-4, IL-13, IL-31, Janus associated kinase and phosphodiesterase, have had promising results from phase 2 and 3 trials for patients with moderate to severe AD.

Royal North Shore Hospital, Sydney, NSW

Correspondence: Victoria.harris@health.nsw.gov.au

Competing interests:

No relevant disclosures.

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Research

The prevalence of monogenic diabetes in Australia: the Fremantle Diabetes Study Phase II

Timothy ME Davis, Ashley E Makepeace, Sian Ellard, Kevin Colclough, Kirsten Peters, Andrew Hattersley and Wendy A Davis

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja16.01201
Published online: 16 October 2017

ARTICLE
AUTHORS
REFERENCES

Topics

Endocrine system diseases

Statistics, epidemiology and research design

Abstract

Objective: To determine the prevalence of monogenic diabetes in an Australian community.

Design: Longitudinal observational study of a cohort recruited between 2008 and 2011.

Setting: Urban population of 157 000 people (Fremantle, Western Australia).

Participants: 1668 (of 4639 people with diabetes) who consented to participation (36.0% participation).

Main outcome measures: Prevalence of maturity-onset diabetes of the young (MODY) and permanent neonatal diabetes in patients under 35 years of age, from European and non-European ethnic backgrounds, who were at risk of MODY according to United Kingdom risk prediction models, and who were then genotyped for relevant mutations.

Results: Twelve of 148 young participants with European ethnic backgrounds (8%) were identified by the risk prediction model as likely to have MODY; four had a glucokinase gene mutation. Thirteen of 45 with non-European ethnic backgrounds (28%) were identified as likely to have MODY, but none had a relevant mutation (DNA unavailable for one patient). Two patients with European ethnic backgrounds (one likely to have MODY) had neonatal diabetes. The estimated MODY prevalence among participants with diagnosed diabetes was 0.24% (95% confidence interval [CI], 0.08–0.66%), an overall population prevalence of 89 cases per million; the prevalence of permanent neonatal diabetes was 0.12% (95% CI, 0.02–0.48%) and the population prevalence 45 cases per million.

Conclusions: One in 280 Australians diagnosed with diabetes have a monogenic form; most are of European ethnicity. Diagnosing MODY and neonatal diabetes is important because their management (including family screening) and prognosis can differ significantly from those for types 1 and 2 diabetes.

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1 University of Western Australia, Perth, WA
2 Fiona Stanley Hospital, Perth, WA
3 Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, United Kingdom
4 Royal Devon and Exeter NHS Foundation Trust, Exeter, United Kingdom

Correspondence: tim.davis@uwa.edu.au

Acknowledgements:

We are grateful to patients who participated in the Fremantle Diabetes Study Phase II (FDS2), and FDS2 staff for help with collecting and recording clinical information. We thank the biochemistry department at Fremantle Hospital and Health Service for performing laboratory tests. FDS2 has been supported by the National Health and Medical Research Council (NHMRC; project grants 513781 and 1042231). Timothy Davis is supported by an NHMRC Practitioner Fellowship (1058260). The funders had no role in the design and conduct of the study, or in the preparation of the manuscript and the decision to submit it for publication.

Competing interests:

No relevant disclosures.

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2. Galler A, Stange T, Muller G, et al. Incidence of childhood diabetes in children aged less than 15 years and its clinical and metabolic characteristics at the time of diagnosis: data from the Childhood Diabetes Registry of Saxony, Germany. Horm Res Paediatr 2010; 74: 285-291.
3. Ledermann HM. Maturity-onset diabetes of the young (MODY) at least ten times more common in Europe than previously assumed? Diabetologia 1995; 38: 1482.
4. Shields BM, Hicks S, Shepherd MH, et al. Maturity-onset diabetes of the young (MODY): how many cases are we missing? Diabetologia 2010; 53: 2504-2508.
5. Karges B, Meissner T, Icks A, et al. Management of diabetes mellitus in infants. Nat Rev Endocrinol 2012; 8: 201-211.
6. Ellard S, Bellanné-Chantelot C, Hattersley AT; European Molecular Genetics Quality Network MODY Group. Best practice guidelines for the molecular genetic diagnosis of maturity-onset diabetes of the young. Diabetologia 2008; 51: 546-553.
7. Shields BM, McDonald TJ, Ellard S, et al. The development and validation of a clinical prediction model to determine the probability of MODY in patients with young-onset diabetes. Diabetologia 2012; 55: 1265-1272.
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14. Australian Bureau of Statistics. 4820.0.55.001. Diabetes in Australia: a snapshot, 2007–08. Sept 2011. http://www.abs.gov.au/ausstats/abs@.nsf/mf/4820.0.55.001 (accessed Jan 2017).
15. Sewell MF, Presley LH, Holland SH, Catalano PM. Genetic causes of maturity onset diabetes of the young may be less prevalent in American pregnant women recently diagnosed with diabetes mellitus than in previously studied European populations. J Matern Fetal Neonatal Med 2015; 28: 1113-1115.
16. Harron KL, Feltbower RG, McKinney PA, et al. Rising rates of all types of diabetes in south Asian and non-south Asian children and young people aged 0–29 years in West Yorkshire, UK, 1991–2006. Diabetes Care 2011; 34: 652-654.
17. Al-Sheyab F, Khamaiseh E, Halaweh MA, Khaul RW. Characterization of glucokinase polymorphisms associated with maturity-onset diabetes of the young (MODY2) in Jordanian population. Tsitol Genet 2009; 43: 58-63.
18. Ng MC, Cockburn BN, Lindner TH, et al. Molecular genetics of diabetes mellitus in Chinese subjects: identification of mutations in glucokinase and hepatocyte nuclear factor-1α genes in patients with early-onset type 2 diabetes mellitus/MODY. Diabet Med 1999; 16: 956-963.
19. Misra S, Shields B, Colclough K, et al. South Asian individuals with diabetes who are referred for MODY testing in the UK have a lower mutation pick-up rate than white European people. Diabetologia 2016; 59: 2262-2265.
20. Søvik O, Irgens HU, Molnes J, et al. Monogenic diabetes mellitus in Norway. Norsk Epidemiologi 2013; 23: 55-60.
21. Lindner TH, Cockburn BN, Bell GI. Molecular genetics of MODY in Germany. Diabetologia 1999; 42: 121-123.
22. Moises RS, Reis AF, Morel V, et al. Prevalence of maturity-onset diabetes of the young mutations in Brazilian families with autosomal-dominant early-onset type 2 diabetes. Diabetes Care 2001; 24: 786-788.
23. Chevre JC, Hani EH, Boutin P, et al. Mutation screening in 18 Caucasian families suggest the existence of other MODY genes. Diabetologia 1998; 41: 1017-1023.
24. Giuffrida FM, Reis AF. Genetic and clinical characteristics of maturity-onset diabetes of the young. Diabetes Obes Metab 2005; 7: 318-326.
25. Pearson ER, Starkey BJ, Powell RJ, et al. Genetic cause of hyperglycaemia and response to treatment in diabetes. Lancet 2003; 362: 1275-1281.
26. Grulich-Henn J, Wagner V, Thon A, et al. Entities and frequency of neonatal diabetes: data from the diabetes documentation and quality management system (DPV). Diabet Med 2010; 27: 709-712.

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Research

The incidence and multiplicity rates of keratinocyte cancers in Australia

Nirmala Pandeya, Catherine M Olsen and David C Whiteman

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00284
Published online: 16 October 2017

ARTICLE
AUTHORS
REFERENCES

Topics

Skin and connective tissue diseases

Neoplasms

Abstract

Objectives: To assess the incidence and multiplicity of keratinocyte cancers (basal cell carcinoma [BCC] and squamous cell carcinoma [SCC]) excised in Australia, and to examine variations by age, sex, state, and prior skin cancer history.

Design: Analysis of individual-level Medicare data for keratinocyte cancer treatments (identified by eight specific MBS item codes) during 2011–2014. Histological data from the QSkin prospective cohort study were analysed to estimate BCC and SCC incidence.

Setting: A 10% systematic random sample of all people registered with Medicare during 1997–2014.

Participants: People aged at least 20 years in 2011 who made at least one claim for any MBS medical service during 2011–2014 (1 704 193 individuals).

Main outcome measures: Age-standardised incidence rates (ASRs) and standardised incidence ratios (SIRs).

Results: The person-based incidence of keratinocyte cancer excisions in Australia was 1531 per 100 000 person-years; incidence increased with age, and was higher for men than women (SIR, 1.43; 95% CI, 1.42–1.45). Lesion-based incidence was 3154 per 100 000 person-years. The estimated ASRs for BCC and SCC were 770 per 100 000 and 270 per 100 000 person-years respectively. During 2011–2014, 3.9% of Australians had one keratinocyte cancer excised, 2.7% had more than one excised; 74% of skin cancers were excised from patients who had two or more lesions removed. Multiplicity was strongly correlated with age; most male patients over 70 were treated for multiple lesions. Keratinocyte cancer incidence was eight times as high among people with a prior history of excisions as among those without.

Conclusions: The incidence and multiplicity of keratinocyte cancer in Australia are very high, causing a large disease burden that has not previously been quantified.

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QIMR Berghofer Medical Research Institute, Brisbane, QLD

Correspondence: david.whiteman@qimrberghofer.edu.au

Acknowledgements:

We are grateful to Jonathan Davies and Archie De Guzman (QIMR Berghofer IT Department) for their help in obtaining and managing Medicare data and extracting the relevant subset for this analysis. This work is supported by the National Health and Medical Research Council (grant numbers 1073898, 1058522). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests:

No relevant disclosures.

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11. Whiteman DC, Thompson BS, Thrift AP, et al. A model to predict the risk of keratinocyte carcinomas. J Invest Dermatol 2016; 136: 1247-1254.
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Editorials

Whither melanoma in Australia?

B Mark Smithers, Jeff Dunn and H Peter Soyer

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00740
Published online: 16 October 2017

ARTICLE
AUTHORS
REFERENCES

Topics

Skin and connective tissue diseases

Neoplasms

To improve melanoma outcomes, the focus on prevention, early detection and new treatment strategies must continue

Over the past 5 years, we have seen a dramatic response to the intense biological research into late-stage, metastatic melanoma, with therapies targeting melanoma metastases and improving an individual’s immune response to the disease. This has led to an improvement in progression-free and overall survival in a group of patients who would have previously been treated with drugs that had little effect. Intense research and clinical trials continue with the aim of identifying patients most likely to respond, as well as exploring new combinations of therapies with this new paradigm for melanoma treatment.

1 University of Queensland, Brisbane, QLD
2 Princess Alexandra Hospital, Brisbane, QLD
3 Institute for Resilient Regions, University of Southern Queensland, Toowoomba, QLD
4 Cancer Council Queensland, Brisbane, QLD
5 Dermatology Research Centre, The University of Queensland Diamantina Institute, Brisbane, QLD

Correspondence: m.smithers@uq.edu.au

Competing interests:

No relevant disclosures.

1. Whiteman DC, Green AC, Olsen CM. The growing burden of invasive melanoma: projections of incidence rates and numbers of new cases in six susceptible populations through 2031. J Invest Dermatol 2016; 136: 1161-1171.
2. Green AC, Baade P, Coory M, et al. Population-based 20-year survival among people diagnosed with thin melanomas in Queensland, Australia. J Clin Oncol 2012; 30: 1462-1467.
3. Davis NC. Cutaneous melanoma: the Queensland experience. Curr Probl Surg 1976; 13: 1-63.
4. Gordon LG, Rowell D. Health system costs of skin cancer and cost-effectiveness of skin cancer prevention and screening: a systematic review. Eur J Cancer Prev 2015; 24: 141-149.
5. Ainger SA, Jagirdar K, Lee KJ, et al. Skin pigmentation genetics for the clinic. Dermatology 2017; 233: 1-15.
6. Janda M, Soyer HP. Greater precision in melanoma prevention. JAMA Dermatol 2017; 153: 18-19.
7. Janda M, Soyer HP. Automated diagnosis of melanoma. Med J Aust 2017; 207: 361-362.
8. Mar VJ, Chamberlain AJ, Kelly JW, et al. Clinical practice guidelines for the diagnosis and management of melanoma: melanomas that lack classical clinical features. Med J Aust 2017; 207: 348-350.
9. Pan Y, Adler NR, Wolfe R, et al. Nodular melanoma is less likely than superficial spreading melanoma to be histologically associated with a naevus. Med J Aust 2017; 207: 333-338.
10. Australian Institute of Health and Welfare. Skin cancer in Australia (AIHW Cat. No. CAN 96) Canberra: AIHW 2016.

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Perspectives

The rationale for action to end new cases of rheumatic heart disease in Australia

Rosemary Wyber, Judith M Katzenellenbogen, Glenn Pearson and Michael Gannon

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00246
Published online: 16 October 2017

ARTICLE
AUTHORS
REFERENCES

Topics

Cardiovascular diseases

Indigenous health

Closing the gap in cardiovascular health

On 25 November 2016, the Australian Medical Association (AMA) launched their annual Report Card on Indigenous Health entitled A call to action to prevent new cases of rheumatic heart disease in Indigenous Australia by 2031.1 In 14 years of AMA report cards, this is the first to focus on a single pathology. The choice of rheumatic heart disease (RHD) is telling: the disease is a striking marker of inequality, a novel lens for considering health systems and a feasible target for definitive disease control.

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1 Telethon Kids Institute, University of Western Australia, Perth, WA
2 Western Australian Centre for Rural Health, University of Western Australia, Perth, WA
3 Australian Medical Association, Canberra, ACT

Correspondence: rosemary.wyber@telethonkids.org.au

Acknowledgements:

The founding members of the END RHD Coalition are the END RHD CRE, the AMA (President Michael Gannon), the National Aboriginal Community Controlled Health Organisation (Chief Executive Officer [CEO] Patricia Turner), RHDAustralia (Director Bart Currie), Aboriginal Medical Services Alliance Northern Territory (CEO John Paterson) and the National Heart Foundation of Australia (CEO John Kelly).

Competing interests:

No relevant disclosures.

1. Australian Medical Association. AMA Report Card on Indigenous Health: a call to action to prevent new cases of rheumatic heart disease in Indigenous Australia by 2031. Canberra: AMA; 2016. https://ama.com.au/system/tdf/documents/2016-AMA-Report-Card-on-Indigenous-Health.pdf?file=1&type=node&id=45394 (accessed Aug 2017).
2. Carapetis J, Beaton A, Cunningham MW, et al. Acute rheumatic fever and rheumatic heart disease. Nat Rev Dis Primers 2016; 2: 15084.
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4. Roberts KV, Maguire GP, Brown A, et al. Rheumatic heart disease in Indigenous children in northern Australia: differences in prevalence and the challenges of screening. Med J Aust 2015; 203: 221. <MJA full text>
5. Australian Bureau of Statistics. 2075.0 — Census of population and housing. 2011 census counts: Aboriginal and Torres Strait Islanders peoples. Canberra: ABS; 2012. http://www.abs.gov.au/ausstats/abs@.nsf/Lookup/2075.0main+features32011 (accessed Aug 2017).
6. Australian Health Ministers’ Advisory Council. Aboriginal and Torres Strait Islander Health Performance Framework 2014 Report. Canberra: Commonwealth of Australia; 2015. https://www.pmc.gov.au/sites/default/files/publications/Aboriginal_and_Torres_Strait_Islander_HPF_2014%20-%20edited%2016%20June2015.pdf (accessed Aug 2017).
7. Australian Institute of Health and Welfare. Rheumatic heart disease and acute rheumatic fever in Australia: 1996–2012 (Cardiovascular Disease Series No.36). Canberra: AIHW; 2013. http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=60129542747 (accessed Aug 2017).
8. Roberts K, Maguire G, Brown A, et al. Echocardiographic screening for rheumatic heart disease in high low risk Australian children. Circulation 2014; 129: 1953-1961.
9. Smith MT, Zurynski Y, Lester-Smith D, et al. Rheumatic fever. identification, management and secondary prevention. Aust Fam Physician 2012; 41: 31-35.
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11. Watkins DA, Mvundura M, Nordet P, Mayosi BM. A cost-effectiveness analysis of a program to control rheumatic fever and rheumatic heart disease in Pinar del Rio, Cuba. PLoS One 2015; 10: e0121363.
12. Baker MG, McDonald A, Zang J, Howden-Chapman P. Infectious diseases attributable to household crowding in New Zealand: a systematic review and burden of disease estimate. Wellington, New Zealand: He Kainga Oranga/Housing and Health Research Programme, University of Otago; 2013. http://www.healthyhousing.org.nz/wp-content/uploads/2010/01/HH-Crowding-ID-Burden-25-May-2013.pdf (accessed Aug 2017).
13. Zühlke LJ, Karthikeyan G. Primary prevention for rheumatic fever: progress, obstacles, and opportunities. Glob Heart 2013; 8: 221-226.
14. Ministry of Health New Zealand. Progress on the Better Public Services rheumatic fever target: Ministry of Health New Zealand, 2017. http://www.health.govt.nz/about-ministry/what-we-do/strategic-direction/better-public-services/previous-bps-target-reduce-rheumatic-fever (accessed Apr 2017).

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Guideline summary

Clinical practice guidelines for the diagnosis and management of melanoma: melanomas that lack classical clinical features

Victoria J Mar, Alex J Chamberlain, John W Kelly, William K Murray and John F Thompson

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00123
Published online: 9 October 2017

ARTICLE
AUTHORS
REFERENCES

Topics

Skin and connective tissue diseases

General medicine

Abstract

Introduction: A Cancer Council Australia multidisciplinary working group is currently revising and updating the 2008 evidence-based clinical practice guidelines for the management of cutaneous melanoma. While there have been many recent improvements in treatment options for metastatic melanoma, early diagnosis remains critical to reducing mortality from the disease. Improved awareness of the atypical presentations of this common malignancy is required to achieve this. A chapter of the new guidelines was therefore developed to aid recognition of atypical melanomas.

Main recommendations: Because thick, life-threatening melanomas may lack the more classical ABCD (asymmetry, border irregularity, colour variegation, diameter > 6 mm) features of melanoma, a thorough history of the lesion with regard to change in morphology and growth over time is essential. Any lesion that is changing in morphology or growing over a period of more than one month should be excised or referred for prompt expert opinion.

Changes in management as a result of the guidelines: These guidelines provide greater emphasis on improved recognition of the atypical presentations of melanoma, in particular nodular, desmoplastic and acral lentiginous subtypes, with particular awareness of hypomelanotic and amelanotic lesions.

1 Victorian Melanoma Service, Alfred Health, Melbourne, VIC
2 Monash University, Melbourne, VIC
3 Peter MacCallum Cancer Centre, Melbourne, VIC
4 Melanoma Institute Australia, Sydney, NSW
5 University of Sydney, Sydney, NSW

Correspondence: victoria.mar@monash.edu

Acknowledgements:

We thank Laura Wuellner, Jutta von Dincklage and Jackie Buck from the Cancer Council Australia Clinical Guidelines Network for their assistance in this work. Development of the new Clinical Practice Guidelines for the Diagnosis and Management of Melanoma was funded by Cancer Council Australia and Melanoma Institute Australia, with additional support from the Skin Cancer College Australasia.

Competing interests:

No relevant disclosures.

1. Smithson SL, Pan Y, Mar V. Differing trends in thickness and survival between nodular and non-nodular primary cutaneous melanoma in Victoria, Australia. Med J Aust 2015; 203: 20. <MJA full text>
2. Baade PD, English DR, Youl PH, et al. The relationship between melanoma thickness and time to diagnosis in a large population-based study. Arch Dermatol 2006; 142: 1422-1427.
3. Criscione VD, Weinstock MA. Melanoma thickness trends in the United States, 1988-2006. J Invest Dermatol 2010; 130: 793-797.
4. Demierre MF, Chung C, Miller DR, Geller AC. Early detection of thick melanomas in the United States: beware of the nodular subtype. Arch Dermatol 2005; 141: 745-750.
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7. Tejera-Vaquerizo A, Mendiola-Fernandez M, Fernandez-Orland A, Herrera-Ceballos E. Thick melanoma: the problem continues. J Eur Acad Dermatol Venereol 2008; 22: 575-579.
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10. Chamberlain AJ, Fritschi L, Giles GG, et al. Nodular type and older age as the most significant associations of thick melanoma in Victoria, Australia. Arch Dermatol 2002; 138: 609-614.
11. Kelly JW, Chamberlain AJ, Staples MP, McAvoy B. Nodular melanoma. No longer as simple as ABC. Aust Fam Physician 2003; 32: 706-709.
12. Lin MJ, Mar V, McLean C, et al. Diagnostic accuracy of malignant melanoma according to subtype. Australas J Dermatol 2014; 55: 35-42.
13. Liu WD, Dowling JP, Murray WK, et al. Amelanotic primary cutaneous melanoma – clinical associations and dynamic evolution. Australas J Dermatol 2006; 47(Suppl 1): A1.
14. Menzies SW, Kreusch J, Byth K, et al. Dermoscopic evaluation of amelanotic and hypomelanotic melanoma. Arch Dermatol 2008; 144: 1120-1127.
15. Chamberlain AJ, Fritschi L, Kelly JW. Nodular melanoma: patients’ perceptions of presenting features and implications for earlier detection. J Am Acad Dermatol 2003; 48: 694-701.
16. Phan A, Dalle S, Touzet S, et al. Dermoscopic features of acral lentiginous melanoma in a large series of 110 cases in a white population. Br J Dermatol 2010; 162: 765-771.
17. McCormack CJ, Conyers RK, Scolyer RA, et al. Atypical Spitzoid neoplasms: a review of potential markers of biological behavior including sentinel node biopsy. Melanoma Res 2014; 24: 437-447.
18. Pizzichetta MA, Talamini R, Stanganelli I, et al. Amelanotic/hypomelanotic melanoma: clinical and dermoscopic features. Br J Dermatol 2004; 150: 1117-1124.
19. Menzies SW, Moloney FJ, Byth K, et al. Dermoscopic evaluation of nodular melanoma. JAMA Dermatol 2013; 149: 699-709.
20. Betti R, Martino P, Vergani R, et al. Nodular melanomas: analysis of the casistic and relationship with thick melanomas and diagnostic delay. J Dermatol 2008; 35: 643-650.
21. Richard MA, Grob JJ, Avril MF, et al. Delays in diagnosis and melanoma prognosis (II): the role of doctors. Int J Cancer 2000; 89: 280-285.
22. Richard MA, Grob JJ, Avril MF, et al. Delays in diagnosis and melanoma prognosis (I): the role of patients. Int J Cancer 2000; 89: 271-279.
23. Lin MJ, Mar V, McLean C, Kelly JW. An objective measure of growth rate using partial biopsy specimens of melanomas that were initially misdiagnosed. J Am Acad Dermatol 2014; 71: 691-697.
24. Liu W, Dowling JP, Murray WK, et al. Rate of growth in melanomas: characteristics and associations of rapidly growing melanomas. Arch Dermatol 2006; 142: 1551-1558.
25. Martorell-Calatayud A, Nagore E, Botella-Estrada R, et al. Defining fast-growing melanomas: reappraisal of epidemiological, clinical, and histological features. Melanoma Res 2011; 21: 131-138.
26. Tejera-Vaquerizo A, Barrera-Vigo MV, Lopez-Navarro N, Herrera-Ceballos E. Growth rate as a prognostic factor in localized invasive cutaneous melanoma. J Eur Acad Dermatol Venereol 2010; 24: 147-154.

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Narrative review

Diagnosis and management of irritable bowel syndrome: a guide for the generalist

Ecushla C Linedale and Jane M Andrews

Med J Aust 2017; 207 (7): . || doi: 10.5694/mja17.00457
Published online: 2 October 2017

ARTICLE
AUTHORS
REFERENCES

Topics

Digestive system diseases

General medicine

Summary

Irritable bowel syndrome (IBS) and other functional gastrointestinal disorders (FGIDs) are so prevalent they cannot reasonably have their diagnoses and management based within specialty care. However, delayed diagnosis, lengthy wait times for specialist review, overinvestigation and lack of clear diagnostic communication are common.
The intrusive symptoms of IBS and other FGIDs impair patient functioning and reduce quality of life, and come with significant costs to individual patients and the health care system, which could be reduced with timely diagnosis and effective management.
IBS, in particular, is no longer a diagnosis of exclusion, and there are now effective dietary and psychological therapies that may be accessed without specialist referral.
The faecal calprotectin test is widely available, yet not on the Medical Benefits Schedule, and a normal test result reliably discriminates between people with IBS and patients who warrant specialist referral.

1 University of Adelaide, Adelaide, SA
2 Royal Adelaide Hospital, Adelaide, SA

Correspondence: Jane.Andrews@sa.gov.au

Competing interests:

Jane Andrews has worked as a speaker, consultant and advisory board member for Abbott, AbbVie, Allergan, Celgene, Ferring Pharmaceuticals, Takeda Pharmaceuticals, MSD, Shire, Janssen, Hospira and Pfizer; and has received research funding from Abbott, AbbVie, Ferring Pharmaceuticals, MSD, Shire and Janssen.

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