C.B. Archer

The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. I. Derivation of a minimum set of discriminators for atopic dermatitis.

A working party of 13 dermatologists, two family practitioners and a paediatrician was assembled, with the aim of developing a minimum list of reliable discriminators for atopic dermatitis. Each physician was asked to select 10 consecutive new cases of unequivocal mild to moderate atopic dermatitis and 10 controls with other inflammatory dermatoses. Each subject was examined by two independent observers, who were blind to the clinical diagnosis and study aim, with regard to 31 clinically useful diagnostic features for atopic dermatitis. Two hundred and twenty‐four patients were studied (120 cases and 102 controls). Using the key physicians clinical diagnosis as a gold standard, the sensitivity and specificity of each of the 31 diagnostic criteria were tested. Using multiple logistic regression techniques, a minimum set of diagnostic criteria for atopic dermatitis was derived. These were: history of flexural involvement, history of a dry skin, onset under the age of 2, personal history of asthma, history of a pruritic skin condition, and visible flexural dermatitis. Adjustment for age, sex, region, social class and ethnic group did not alter the choice of final criteria. The discriminatory value of these criteria was also satisfactory when tested against a further sample of 150 patients drawn from the community, who did not have skin disease.

Long-term efficacy and safety of cyclosporin in severe adult atopic dermatitis.

A prospective, open, multicentre study was performed to investigate the efficacy and safety of longterm treatment with cyclosporin in adults with severe atopic dermatitis. Subjects were treated for a maximum of 48 weeks. For the first 8 weeks, cyclosporin was administered at 2.5 mg/kg per day. The dose was then adjusted according to response. Disease activity was monitored using the six‐area. six‐sign score and the proportion of skin involved. Pruritus and sleep disturbance were assessed using four‐point scales. Response was further evaluated on a five‐point scale. Adverse events. blood pressure and serum biochemistry were monitored. Tolerability was assessed on a five‐point scale.

A prospective study of the prevalence and incidence of atopic dermatitis in children aged 0–42 months

Backgroundu2003 There is strong evidence that the incidence and prevalence of atopic diseases is increasing. However, estimates of the prevalence of atopic dermatitis (AD) have varied greatly in the U.K. and most parts of the developed world.

Association of parental eczema, hayfever, and asthma with atopic dermatitis in infancy: birth cohort study

Objective: To evaluate the association of parental history of atopic disease with childhood atopic dermatitis, and to examine the relative strength of associations with maternal and paternal disease. Design: Mothers were recruited to the Avon longitudinal study of parents and children (ALSPAC) from the eighth week of pregnancy. Before parturition, both parents were asked, separately, to report their lifetime history of eczema, asthma, and hayfever. Parents reported symptoms of atopic dermatitis in their children at ages 6, 18, 30, and 42 months. Results: Of 8530 children with complete information on rash at ages 6, 18, 30, and 42 months, 7969 had complete information on maternal atopic disease and 5658 on maternal and paternal atopic disease. There was a strong association between parental eczema and childhood atopic dermatitis: odds ratio 1.69 (95% confidence interval, 1.47 to 1.95) for maternal eczema only, 1.74 (1.44 to 2.09) for paternal eczema only, and 2.72 (2.09 to 3.53) for eczema in both parents. Associations with parental asthma or hayfever were attenuated after controlling for parental eczema. There was no evidence that associations with maternal atopy were stronger than with paternal. Conclusions: Associations between parents’ atopic disease and the risk of atopic dermatitis in offspring vary according to the type of atopic disease in the parents, but not according to parental sex. These results are at variance with previous studies reporting stronger associations with maternal than paternal atopy, and suggest that there is no “parent-of-origin” effect in atopic dermatitis. Parental eczema may be a better marker than parental asthma/hayfever in predisposing to childhood eczema.

Minocycline-induced discolouration of the sclerae

Summary We report two patients with minocycline‐induced pigmentation of the sclerae. Cutaneous pigtnentution is a well‐recognized complication of minocycline therapy, but only live cases of pigimentation of the sclerae have been described previously. These five patients have a number of features in common with the two reported here. We propose that these patients represent the most severe end of the spectrum of minocycline‐induced cutaneous changes. Patients should be warned about the possibility of the occurrence of pigmentary changes before starting therapy.

TERBINAFINE-INDUCED ACUTE GENERALIZED EXANTHEMATOUS PUSTULOSIS

with a speckled pattern; double-stranded antibodies were negative as were rheumatoid factor, antismooth muscle, antiRNP and anti-Ro antibodies. The anti-La antibody was positive at 1 : 5. Full blood count, platelets, white cell count, renal and liver profiles as well as urine microscopy were all normal. A skin biopsy confirmed a diagnosis of chronic cutaneous lupus erythematosus with a hyperkeratotic, focally atrophic epidermis, basal vacuolation and follicular plugging. There was a patchy peri-appendageal lymphocytic infiltrate in the dermis. Immunofluorescence was not performed. Terbinafine was discontinued and the patient was commenced on betamethasone valerate 0·1% ointment twice daily and hydroxychloroquine sulphate 200 mg daily. Because of the severity of the rash she was also initially given prednisolone, 20 mg daily, which was reduced over a 4-week period. Over the subsequent 2 months her rash resolved completely with no evidence of scarring. All medications, both topical and oral, were discontinued. Terbinafine is an orally active antifungal drug belonging to the allylamine class of antifungal agents. There exists a large potential population for treatment with terbinafine. It has been estimated that 2·7% of the U.K. population has a fungal nail infection but this is likely to be a conservative estimate as a Finnish study found a prevalence rate of 8·4% for onychomycosis. The incidence rates of systemic lupus erythematosus (SLE) were recently calculated at 3·7 per 100,000 per year for men and 45·5 per 100,000 per year for women. Cutaneous lupus erythematosus is estimated to occur two to three times more frequently than SLE, but population-based epidemiological data are not yet available. Drug-induced lupus erythematosus was first described in 1953 with hydrazaline. Numerous medications since then have been shown to induce lupus erythematosus including the azole antifungal griseofulvin. Terbinafine is known to be associated rarely with severe skin eruptions, such as erythema multiforme and toxic epidermal necrolysis. This report is the first published association of terbinafine with lupus erythematosus. Our patient was known to be ANA-negative in the past; the rash occurred shortly after commencement of terbinafine and resolved soon after treatment. There is a strong possibility therefore that cutaneous lupus erythematosus in our patient was induced by the medication.

The effects of topical doxepin on responses to histamine, substance P and prostaglandin E2 in human skin

The tricyclic antidepressant, doxepin, is known to have H1 and H2 antihistaminic effects. Recently, 5% doxepin cream has been marketed in the U.S.A. for treatment of eczematous dermatoses. We investigated the effects of topical doxepin treatment on histamine‐, substance P‐and prostaglandin E2‐(PGE2) induced responses in the skin of normal and atopic subjects. We compared the effects of topical doxepin with those of the oral antihistamine terfenadine. The weal volume and flare area responses to histamine were significantly reduced by treatment with topical doxepin or oral terfenadine in both normal and atopic subjects (P<0·05). The mean ±SEM percentage reduction in flare area for 10μ/site of histamine in non‐atopics and atopics was 48±8% and 60±17% with terfenadine, and 54 ± 12% and 81 ± 4% with topical doxepin, respectively. The mean percentage reduction in weal volume for the same dose of histamine in non‐atopics and atopics was 70 ± 9% and 63 ± 16% with terfenadine, and 96 ± 2% and 89 ± 6% with topical doxepin, respectively. The flare but not the weal response to substance P was inhibited by both treatments in all subjects (P<0·05). The mean ±SEM percentage reduction in flare area for 200 pmol/site of substance P in non‐atopics and atopics was 53 ± 10% and 73 ±4% with terfenadine, and 74 ± 7% and 75 ± 4% with topical doxepin, respectively. The cutaneous responses to PGE2 were not affected by either drug. The inhibitory effects of doxepin were as great as those of terfenadine, and doxepin had a significantly greater effect than terfenadine in inhibiting the weal response to histamine and flare response to substance P in normal volunteers (P<0·05). There was no significant difference between atopics and non‐atopics in the percentage reduction of cutaneous responses by oral terfenadine or topical doxepin. Marked sedation occurred in three of the first 10 subjects treated with topical doxepin, necessitating a reduction in dosage for the remaining six subjects. In summary, topical doxepin was as effective as, and sometimes more effective than, a standard dose of oral terfenadine in the inhibition of histamine‐induced and axon‐reflex‐mediated cutaneous responses. The marked sedative effect may limit its clinical use in some patients.

Misdiagnosis of hereditary angio-oedema type 1 and type 2

Summary Backgroundu2003Hereditary angio‐oedema is a rare, life‐threatening, autosomal dominant condition caused by deficiency (type 1) or dysfunction (type 2) of complement C1 inhibitor. Serological assays to measure C1 inhibitor concentration and function are widely available. However, expert interpretation may not be.

Urinary leukotriene E4 levels in patients with atopic dermatitis

Leukotriene synthesis may be increased in a variety of inflammatory diseases. Urinary leukotriene E4 is a stable metabolite of leukotrienes C4 and D4 which has previously been found to be increased in exacerbations of severe asthma and after antigen inhalation. Levels of urinary LTE4 in seven patients during and after a severe flare of atopic dermatitis were measured by high‐performance liquid chromatography (HPLC) and radioimmunoassay (RIA). Mean urinary LTE4 levels (± SEM) were not increased during (16·7 ± 3·7pg/μmol) or after (16·9 ± 4·8 pg/μxmol) the acute exacerbation of atopic dermatitis when compared with the normal range (mean = 23·8 [95% confidence interval 19·9–28·2] pg/μmol creatinine). These findings do not provide evidence of cysteinyl leukotriene involvement in the pathogenesis of atopic dermatitis.

11) Lymphangiomata following surgery and radiotherapy for breast carcinoma

93 Examination. There was lymphoedema of the vulva with small, tense, clear, fiuid-filled vesicles. Histology. A skin biopsy showed dilated thin-walled vessels in the superficial dermis. Comment. Dilatation of cutaneous lymphatics producing an appearance that resembles lymphangioma circumscriptum has been described after resection of regional lymph nodes/ after radiography,^-^ and after both forms of treatment for carcinoma ofthe cervix.*