Anatomy and physiology

To the Editor:Lichen planus is an autoimmune mucocutaneous inflammatory disorder. Diagnosis is often made clinically and confirmed on biopsy.1 Hypertrophic lichen planus is a distinct subtype characterised by pruritic, hyperkeratotic plaques. Histopathological findings may not have the typical features of lichen planus and can mimic squamous cell carcinoma (SCC).2 Distinguishing between hypertrophic lichen planus and SCC can be difficult for clinicians and pathologists. In our dermatology practice, we encountered three patients initially diagnosed with SCC, but on review, the cases were consistent with lichen planus. One patient was a 52-year-old woman presenting with asymmetrical, raised and violaceous lesions to her lower legs. She was referred to a skin cancer clinic that performed biopsies of these lesions, which were reported as well differentiated SCC. These lesions were excised, but they were recurrent and were excised again. The second patient was a 54-year-old man who presented with a one-year history of eruptive raised, violaceous lesions to his chest and legs. Biopsies were reported as SCC and multiple lesions were excised by a general surgeon. The third patient was a 77-year-old woman with a 2-year history of pruritic lesions to the lower legs (Box). Biopsies were reported as well differentiated SCC. Each of these patients underwent numerous excisions before being referred to our practice. The patients were reassessed and new biopsies taken, and the clinical picture was discussed with a dermatopathologist. Hypertrophic lichen planus was confirmed as the diagnosis in each of these patients, and they responded well to prednisone, acitretin and topical steroid treatment. SCC may arise in long-standing hypertrophic lichen planus, but it should be emphasised that cases of supposed SCC with atypical history should not be treated without consideration of the many mimics of SCC, including pseudoepitheliomatous hyperplasia, irritated seborrhoeic keratosis, coral reef granuloma, hypertrophic lupus erythematosus and hypertrophic lichen planus. Clinicians should provide clinical description and a list of potential differentials when referring to a pathologist. Adequate biopsy depth is important, as lichenoid activity may only be present at the tips of the rete ridges, which may be missed on a superficial biopsy. These cases highlight the difficulties in distinguishing hypertrophic lichen planus from SCC. In the cases we described, correct diagnosis was made after re-evaluation and clinicopathological correlation. Box – Figure showing violaceous hyperkeratotic patches on the patient’s lower leg, with original biopsies reported as squamous cell carcinoma (A). Histopathology showed a lichenoid inflammatory infiltrate confined to the tips of the rete processes (B)* * Infiltrate is composed of predominantly lymphocytes with few eosinophils and plasma cells. While these features are typical of hypertrophic lichen planus, superficial shave biopsies may not capture the lichenoid infiltrate at the rete processes.

Emily X Shao · Benjamin Carew · James Muir

To the Editor:The Editorial by Harvey and Diug1 on the value of food fortification as a public health intervention was prompted by demonstration of the effectiveness of mandatory iodine fortification in reducing iodine deficiency.2 Mandatory fortification of wheat flour for bread making was introduced in Australia at the same time to prevent neural tube defects. Harvey and Diug state that the two are conceptually different, as the former addresses a population iodine deficiency, whereas folic acid fortification is to compensate a presumed genetic defect that cannot be individually recognised, thus raising ethical questions about exposing the many for the benefit of the few. However, this is the case in almost all public health interventions. Using an example of Harvey and Diug, we expose the whole population to the mandatory fortification of flour with thiamine to prevent Wernicke–Korsakoff syndrome, a condition largely confined to people with a chronic alcohol problem. The concern they raise about mandatory folic acid fortification1 is exposure to unmetabolised folic acid, proposed as possibly increasing adverse effects, but which have not been clearly or conclusively shown. They refer to an Irish study reporting that seven of the 68 children in the study had detectable levels of unmetabolised folic acid in their blood.3 Ireland does not have mandatory folic acid fortification; the main sources of folic acid were voluntarily fortified breakfast cereals and fortified milk — products that are fortified with relatively high levels of folic acid. In Australia, breakfast cereals and other food products are also permitted to be fortified voluntarily — breakfast cereals often contain around 200–300 μg of added folic acid per 100 g (or about 100 μg per serve). This compares with mandatory fortification of flour of 200–300 μg per 100 g flour, or about 40 μg folic acid per slice of bread. While either source could lead to circulating unmetabolised folic acid, the higher doses in voluntarily fortified products are more likely to do so. With the introduction of mandatory fortification, there was a reduction in neural tube defects.4 Importantly, there has been a 68% reduction in previously higher rates of neural tube defects in Indigenous people.5 Mandatory fortification provides a more equitable, consistent and cheaper source of folic acid to the population than voluntary fortification. Let’s leave mandatory folic acid fortification preventing neural tube defects in our population.

Carol Bower · Fiona J Stanley · Mike Daube

Delayed sleep phase disorder (DSPD) — a circadian rhythm sleep disorder — is most commonly seen in adolescents. The differential diagnosis between DSPD and conventional psychophysiological insomnia is important for correct therapeutic intervention. Adolescent DSPD sleep duration is commonly 9 hours or more. Depression may be comorbid with DSPD. DSPD has a negative impact on adolescent academic performance. DSPD treatments include ...

Delwyn J Bartlett PhD, MAPS · Sarah N Biggs PhD · Stuart M Armstrong BSc, PhD, MAPS