BACKGROUND:Wells syndrome is an uncommon inflammatory dermatosis first described in 1971 by Wells. The clinical eruption is characterized by varying morphology and severity and usually follows a relapsing remitting course. The majority of the reported cases are of unknown etiology, drug induced Wells syndrome has rarely been reported. A literature search using MEDLINE was performed. We recorded the features of our case and of the additional cases of drug induced Wells syndrome in the literature.MAIN OBSERVATIONS:Including our case there are 25 cases of drug-induced Wells syndrome reported. Causative drugs include antibiotics, anticholinergic agents, anaesthetics, non-steroidal anti-inflammatory agents, thyroid medications, chemotherapeutic agents, thiomersal containing vaccinations, anti-tumor necrosis factor agents and thiazide diuretics.CONCLUSIONS:To the authors knowledge this is the first reported case of drug-induced Wells syndrome from thiazide diuretics. The diagnosis of Wells syndrome is often controversial and we propose a set of diagnostic criteria.

Sir, Molluscum contagiosum is a common disease in young children and is caused by a member of the poxvirus family. Molluscum is a common dermatological problem in the paediatric population with epidemiological studies showing a cumulative incidence of 17% in healthy children (1). In the majority of patients the disease is self-limiting, but because of the predisposition to unsightly lesions in exposed areas such as the face, there is often considerable social stigma associated with the infection. The course of the disease may be further complicated by recurrent secondary bacterial infections of the skin affected by molluscum lesions. Parents often seek the help of general practitioners, paediatricians and dermatologists in treating their child’s condition. Therapeutic options are based upon physical ablation of the papules using destructive modalities such as cryotherapy, diathermy, or curettage. In addition, chemical destruction is an effective means of treatment and includes the use of salicylic acid, silver nitrate paste and potassium hydroxide. In adults, treatment is usually uneventful, but in young children both the pain and trauma limit the usefulness of these treatments. The challenge therefore lies in finding more comfortable and efficacious ways of treating molluscum in young children. Imiquimod 5% cream (Aldara ) is an immune response modifier that was originally marketed as treatment for genital warts. Since its release, the use of imiquimod has been extended for the treatment of recalcitrant warts (2) and skin cancers (3). Although imiquimod has no direct antiviral properties, the mode of action is thought to be due to the stimulation of the cellular immune system via the induction of interferon, tumour necrosis factor, and interlukins 6 and 8 (4). These cytokines act as chemotactants for T cells, enhance natural killer cell activity and stimulate proliferation of B cells, which in turn potentiates cellmediated immunity against virally infected cells (5). The aim of this small-scale study was to determine the effectiveness of topical imiquimod as a treatment for molluscum in a paediatric population. In this trial we used imiquimod 5% cream (Aldara) for the treatment of molluscum contagiosum in four children between the ages of 6 and 8 y. The parents were instructed to apply the preparation on a nightly basis for a total of 6 wk. The patients were not given any other treatments during this trial period. The objective of this trial was to determine the clearance rate of lesions. This was determined by comparing the number of lesions pretreatment with the number post-treatment, which was in turn expressed as a percentage improvement. The results are summarized in Table 1. We received clearance rates between 60% and 80% after 6 wk of therapy. Moderately severe localized erythema was experienced in 2 patients, but the irritation was not perceived by the parents as severe enough to stop the treatment. Parental ratings, defined as subjective views of effectiveness of treatment, ease of application and patient tolerability at the end of the 6wk period, ranged from “good” in two cases to “excellent” in the remainder. Our experience of imiquimod used in a limited number of children with molluscum and the experience from other small studies (6, 7) show promising results. Drawbacks to its use include the cost of imiquimod (approximately 80 Euro for 12 sachets) and the duration of treatment, which may limit the practicality of this modality. The promising efficacy rate and low irritant potential of imiquimod may make this an effective and pain-free treatment modality for a commonly encountered problem. Large-scale studies have not identified any long-term adverse effects of imiquimod (3, 5, 8), but in order to ascertain the true effectiveness and safety of this treatment in a paediatric population, larger placebo-controlled trials are needed.

A 27-year-old woman presented with linear, flesh-colored papules along her vermillion borders, 4 years after a cosmetic lip tattoo was applied. A biopsy of the lesion was performed and histology showed it to be a granulomatous reaction surrounding the tattoo pigment. Following the biopsy, the lesions began to resolve spontaneously within 4 weeks and were not noticeable at a follow-up review. Granulomatous reactions are rare after cosmetic facial tattoos and may respond to topical corticosteroids or laser ablation. We present a unique report of a delayed granulomatous reaction to a cosmetic tattoo completely resolving without any specific treatment.

A 59-year-old woman undergoing narrowband UVB phototherapy for treatment of psoriasis presented suddenly with tense blisters on both hips. The blisters were asymptomatic and disappeared within 24 hours. Histopathology together with a negative porphyrin screen made the diagnosis of pseudoporphyria. Blood tests including a full blood count, urea and electrolytes, liver function tests and antinuclear autoantibodies were normal. The patient was otherwise healthy; there was no history of extensive sun exposure, sunbeds or medication with non-steroidal anti-inflammatory drugs. This presentation of pseudoporphyria secondary to narrowband UVB radiation is unusual, as UVB radiation is not known to be associated with pseudoporphyria.

A 65-year-old man presented with a history of multiple skin coloured papules on his face that were asymptomatic. He had an adenocarcinoma resected from his proximal colon 12 years prior to presentation as well as a family history of colon cancer on the maternal side. Diagnostic biopsies showed the lesions to be sebaceous adenomas and epitheliomas and the diagnosis of Muir-Torre syndrome was made. The sebaceous tumour tissue showed microsatellite instability and immunohistochemical staining indicated diminished expression in the DNA mismatch-repair protein complex MSH2/MSH6. Genetic analysis showed a germline mutation in the MSH2 gene confirming the diagnosis of Muir-Torre syndrome. The patient and his first-degree relatives have been referred for genetic counselling and screening. We review the diagnostic criteria in this syndrome and review the recommended screening guidelines.

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SUMMARYA 67‐year‐old man presented with a history of lymphadenopathy, fevers and separate skin eruptions of erythrodermic spongiotic dermatitis initially and subsequent toxic epidermal necrolysis. Initial lymph node biopsies showed non‐specific granulomatous changes, and skin biopsies and bone marrow aspirate were not diagnostic. His toxic epidermal necrolysis responded well to 3 days of intravenous immunoglobulin. The patient was discharged from hospital and reviewed regularly as an outpatient. Due to persisting lymphadenopathy, further lymph node biopsy led to the diagnosis of angioimmunoblastic T‐cell lymphoma, a rare form of peripheral T‐cell lymphoma with a poor prognosis. At the time of diagnosis his condition deteriorated rapidly and he died soon after.

It is not known whether patients with anti-epiligrin cicatricial pemphigoid (AECP) have an increased risk of malignancy. We calculated the expected numbers of cancers in a c hort of 35 such patients based on respective incidence rates for all cancers in the National Cancer Institute's Surveillance, Epidemiology, and End Results (NCI SEER) Registry. Ten patients in this cohort had solitary solid cancers; eight patients developed cancer after onset of AECP (seven within 14 months). The relative risk (RR) for cancer in this cohort was 6·8 (95% confidence intervals [CI]: 3·3-12·5). AECP seems to be associated with an increased relative risk for cancer.

Background: Eosinophilic fasciitis is a rare, scleroderma-like disease that usually affects the extremities of young to middle-aged males. The disease may cause flexion contractures and limit joint mobility and is associated with peripheral eosinophilia. The fascia, by definition, is infiltrated with mononuclear cells and typically with eosinophils. Eosinophilic fasciitis may be separated from another sclerodermatous disorder, linear scleroderma, by its response to systemic corticosteroids. The etiology is unclear but eosinophilic fasciitis has numerous disease associations. However, it has not previously been associated with renal failure and hemodialysis. Objective: This article reports a case of eosinophilic fasciitis occurring four weeks following the onset of hemodialysis. Methods: The clinical and histologic features confirmed the diagnosis of eosinophilic fasciitis. He was treated with systemic corticosteroids with good response. Conclusion: This is the first reported patient who developed eosinophilic fasciitis in close temporal relationship with the start of hemodialysis. While eosinophilic fasciitis may be coincidental with a common disorder, namely, renal failure, it is interesting to note that hemodialysis patients often have immune-regulation abnormalities and peripheral eosinophilia.

International Journal of DermatologyVolume 38, Issue 11 p. 818-827 Linear IgA bullous dermatosis Conleth A. Egan, Conleth A. Egan Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this author. Mb, . Mb Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this author. Mrcpi, . Mrcpi Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this authorJohn J. Zone MD, John J. Zone MD Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this author Conleth A. Egan, Conleth A. Egan Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this author. Mb, . Mb Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this author. Mrcpi, . Mrcpi Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this authorJohn J. Zone MD, John J. Zone MD Medicine Service, Section of Dermatology, Salt Lake City Veterans Affairs Medical Center and Department of Dermatology, University of Utah School of Medicine, Salt Lake City, UtahSearch for more papers by this author First published: 25 December 2001 https://doi.org/10.1046/j.1365-4362.1999.00813.xCitations: 81 Conleth A. Egan, mb, mrcpi, Dermatology Branch, National Cancer Institute, Building 10, Room 12N238, NIH, 10 Center Drive MSC 1908, Bethesda, MD 20892–1908 Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Chorzelski, TP, Jablonska, S, Beutner, EH. Linear IgA bullous dermatosis. Adult form of linear IgA bullous dermatosis. In: EH Beutner TP Chorzelski SF. Bean eds. Immunopathology of the Skin. New York: Wiley.,, 1979: 315 319. 2 Zillikens, D, Wever, S, Roth, A et al. Incidence of autoimmune subepidermal blistering dermatoses in a region of central Germany. Arch Dermatol 1995; 131, 957 958. 3 Bernard, P, Vaillant, L, Labeille, B et al. Incidence and distribution of subepidermal autoimmune bullous skin diseases in three French regions. Bullous Diseases French Study Group. Arch Dermatol 1995; 131, 48 52. 4 Bean, SF, Furey, NL, Chorzelski, TP, Jablonska, S. Childhood form of linear IgA bullous dermatosis. (Benign chronic bullous disease of childhood.). In: EH Beutner TP Chorzelski SF. Bean eds. Immunopathology of the Skin. 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Citing Literature Volume38, Issue11November 1999Pages 818-827 ReferencesRelatedInformation