S. Wahie

An open‐label, dose‐ranging study of methotrexate for moderate‐to‐severe adult atopic eczema

Background  Treatment options for moderate‐to‐severe atopic eczema are limited. Although methotrexate (MTX) is a widely used and effective treatment for psoriasis, there have been no previous prospective trials of its use in refractory atopic eczema, despite a few small, retrospective reports suggesting that it is a well‐tolerated and effective treatment.

Pityriasis lichenoides: the differences between children and adults

Background  Pityriasis lichenoides (PL) is a skin disease that affects both children and adults. Anecdotally, it is said to run a more benign course in children, with a frequent tendency to self‐resolution. However, to our knowledge, there have been no published studies comparing PL in both age groups.

Hepatitis: a rare, but important, complication of infliximab therapy for psoriasis

healthy subjects (control) observed by Hamurku et al. are 2.2% and 0.77%, respectively, and these numbers are 7.9and 9.6-fold higher than those reported earlier in subjects of Turkish ethnicity. Very high levels of MN in exfoliated cells of studied subjects (both healthy controls and patients) could be due to the small number of cells studied (500); Hamurçu et al. used a DNA-specific stain, thus this could not be a source of bias. Recently I discussed the necessity of studying at least 2000 exfoliated cells to avoid errors. I completely agree with the authors that the number of samples may be too few for meaningful statistical analyses , but a high number of MN in the lymphocytes of healthy subjects of Turkish ethnicity in this study should be explained by the authors. It is questionable that MN levels in both types of cell are several-fold higher in this study than in the study by Karakaya et al. In addition, P 1⁄4 0.000 is given in the summary, the text on page 567, and Table 3, which is meaningless. In conclusion, Hamurçu et al. presented very interesting data about chronic multisystem disease occurences worldwide, especially in Turkey and Japan. The most intriguing circumstance is that this disease affected the skin. Hence, it is possible that increased MN frequency can be found in exfoliated epithelial cells, but the data presented by Hamurçu et al. are not convincing. Further investigations are certainly warranted to evaluate the level of cytogenetic disorders in exfoliated epithelial cells (at least 2000) and lymphocytes on a larger number of patients.

Psoriasis occurring after myeloablative therapy and autologous stem cell transplantation

1 Kirtschig G, Chow ET, Venning VA et al. Acquired subepidermal bullous diseases associated with psoriasis: a clinical, immunopathological and immunogenetic study. Br J Dermatol 1996; 135:738–45. 2 Brun P, Baran R. Pemphigoide bulleuse induite par photochimiothérapie du psoriasis. Ann Dermatol Venereol 1982; 109:461–8. 3 Hashimoto T, Ogawa MM, Konohana A et al. Detection of pemphigus vulgaris and pemphigus foliaceus antigens by immunoblot analysis using different antigen sources. J Invest Dermatol 1990; 94:327–31. 4 Fujimoto W, Ohtsu T, Toi Y et al. Linear IgA disease with IgA antibodies directed against 200and 280-kDa epidermal antigens. Br J Dermatol 2000; 142:1213–18. 5 Chorzelski TP, Jablonska S, Bean SF et al. Linear IgA bullous dermatosis. In: Immunopathology of the Skin (Beutner EH, Chorzelski TP, Bean SF, eds), 2nd edn. New York: Wiley Medical, 1979; 315–19. 6 Chan LS, Traczyk T, Taylor TB et al. Linear IgA bullous dermatosis. Characterization of a subset of patients with concurrent IgA and IgG anti-basement membrane autoantibodies. Arch Dermatol 1995; 131:1432–7. 7 Takagi Y, Sawada S, Yamauchi M et al. Coexistence of psoriasis and linear IgA bullous dermatosis. Br J Dermatol 2000; 142:513–16. 8 Cox AJ. The dermal-epidermal junction in psoriasis. J Invest Dermatol 1969; 53:428–35.

Cutaneous features of intravascular lymphoma

Intravascular lymphoma (IVL) is a subset of extranodal non‐Hodgkin lymphoma, with an estimated incidence of < 1 case per million people. It is characterised by extensive proliferation of lymphoma cells within small to medium‐sized blood vessels. Most IVLs are B‐cell tumours. IVL can present primarily in any organ system, including the skin. The disease is often disseminated at diagnosis. The overall mortality rate is thought to be > 80%, and > 50% of patients are diagnosed at postmortem examination. There is wide variability in the clinical appearance of cutaneous lesions, which may simulate inflammatory skin disease. Therefore, awareness by dermatologists is important to enable early diagnosis when cutaneous signs are present. We report two patients with unexplained systemic disease and a skin eruption, leading to the diagnosis of IVL, and outline the range of cutaneous features reported.

Cutaneous signs as a presenting manifestation of alcohol excess

We describe three patients who presented with a total of four episodes of an inflammatory dermatosis associated with alcohol abuse. In each case, the rash had similar characteristic features. The patients responded promptly to emollients and topical steroids but not to zinc replacement therapy. Other nutrient deficiencies were not identified. In addition, long‐term remission seemed to be dependent on a reduction in alcohol consumption. We postulate that this is a separate cutaneous manifestation of chronic alcohol misuse and that this syndrome may be more common than previously thought.

Myotoxicity occurring with ciclosporin in a patient with atopic dermatitis

SIR, A 37-year-old Anglo-Caribbean male, with a history of severe atopic dermatitis and asthma, was considered for ciclosporin therapy. Previous treatments such as phototherapy, topical tacrolimus and azathioprine (up to 3 mg kg daily) had failed to control his disease. He was taking sertraline (50 mg daily) for depression. He was on no other medications and had no other medical problems. He did not drink alcohol. His baseline glomerular filtration rate was 114 mL min and full blood count, serum electrolytes, liver function tests, urate and lipid profile were all normal. Ciclosporin was commenced at a dose of 3 mg kg daily. His disease activity quickly responded with a Six Area Six Sign Atopic Dermatitis score reduction from 30 to 12 within 4 weeks of treatment. However, 2 weeks after starting therapy, he began to describe intermittent muscular cramps in his upper limbs and around his paravertebral regions. Unfortunately, the improvement in his atopic dermatitis was not sustained and his ciclosporin dose was increased to 4 mg kg daily. A week later, he complained of more generalized muscle pains, tremor, poor sleep and appetite. Physical examination showed normal muscle strength and reflexes. His creatine kinase (CK) was elevated at 637 (normal 0–160) IU L. Serum electrolytes, erythrocyte sedimentation rate, liver and thyroid function, viral serology, autoantibody screen and electrocardiography were all unremarkable. Urinary myoglobin was not detected. A trough ciclosporin concentration was not raised. Electromyography showed motor unit potentials of short duration and reduced amplitude, in keeping with myopathy, but no necrotizing process. Ciclosporin was discontinued; muscle pain disappeared within 4 days and CK returned to normal levels within 2 weeks. A muscle biopsy was not deemed necessary on an otherwise well patient whose symptoms were improving spontaneously. The temporal relationship between onset and improvement of symptoms and the period of drug administration strongly suggests that myotoxicity was induced by ciclosporin. The only publication suggesting a possible interaction between ciclosporin and sertraline occurred in a post-transplant patient, who was also on four other drugs at the time, including a statin. The concomitant use of statins and ciclosporin is a well-recognized cause of muscle toxicity. On this basis, an interaction between ciclosporin and sertraline resulting in myotoxicity would seem unlikely. There have been no other published reports of sertraline alone, or in combination with ciclosporin, causing myopathy. In contrast, there have been reports of ciclosporin-induced myotoxicity in patients with Behçet’s disease, Graves malignant ophthalmopathy and organ transplants. In the majority, CK levels were elevated and electromyography showed motor unit potentials of short duration and ⁄or amplitude, as in our patient. When muscle biopsies were performed, fibre atrophy consistent with toxic myopathy was observed. Symptoms occurred within 3 weeks to 24 months of introduction of ciclosporin (at doses of 6–12 mg kg daily). All patients responded to a reduction in dosing or cessation of therapy. Myositis recurred in those who were rechallenged with ciclosporin. The pathogenesis of ciclosporin-induced myopathy is probably due to a direct toxic effect on muscle cells. Calcineurin is thought to have an important role in muscle regeneration and, in animal studies, ciclosporin, a potent inhibitor of calcineurin, induced extensive muscle inflammation and marked fibre atrophy. This is the first published report of ciclosporin-induced myotoxicity in the setting of atopic eczema. This case is also unusual in that muscle damage initially developed at a much lower dose (3 mg kg daily) than has been seen in previous reports, which were predominantly of ciclosporin use following organ transplantation. In our patient, muscle damage was dose-dependent and reversible on cessation of therapy. With the increasing use of ciclosporin for the treatment of skin disease, we feel that dermatologists should be alerted to the potential for myotoxicity with this drug.

Oropharyngeal mycosis fungoides.

incidentally, within a tattoo. Doumat et al. most recently reported a 35-year-old man with a 7-mm BCC in a tattoo performed 1 year earlier in the scapular region. In 1987, Weiner and Scher reviewed all BCCs reported to have arisen in a tattoo. These patients (four men, one women, age range 52–76 years) tended to have their BCCs in sun-exposed areas within the dark pigment of tattoos; the authors wondered whether this altered the absorption of ultraviolet rays. Our case is by far the youngest patient to be reported as having a primary BCC arising in a tattoo. This observation, and the fact that it occurred in a site receiving less sun exposure provides a much stronger argument for the trauma of the act of tattooing being a causative factor in the aetiology. In a study by Noodleman and Pollack, BCCs treated with Mohs surgery between 1979 and 1986 were evaluated for previous trauma histories. Of 1774 BCCs, 129 (7.3%) had a positive history of previous trauma at the site. However, trauma has not yet been proven to be an aetiological factor in the development of BCCs, and further study is required on this subject. It is certainly unusual for a 28-year-old to develop a BCC, but not unheard of; indeed, Christenson et al. reported that there has been a significant increase in incidence of BCC in women aged < 40 years between 1976 and 2003 in their Minnesota county, mirroring other reports of a rise in nonmelanoma skin cancer in the younger population. In conclusion, we present, to our knowledge, the youngest reported case of a BCC arising in a tattoo, which may be further evidence in favour of trauma as an aetiological factor in the development of BCC.