No abstract

Summary There is increasing evidence that neuropeptides may be involved in the pathogenesis of atopic dermatitis (AD). This study examines whether neuropeptide distribution in the skin of patients with AD differs from normal controls. The distribution and density of several neuro‐peptides were examined in lesional and non‐lesional skin of AD patients (n= 5) and in normal controls (n= 4) using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Staining with the general neuronal marker protein gene product 9·5 showed a subepidermal network of nerves with fibres penetrating the epidermis, and nerves around blood vessels, sweat glands and hair follicles. Image analysis of nerves around sweat glands showed a significantly higher nerve density in non‐lesional compared with both normal controls and lesional skin (P < 0·05); lesional compared with control skin showed no significant difference. In the epidermis the density of nerves was not significantly greater in non‐lesional compared with lesional skin and controls. Calcitonin gene‐related peptide immunoreactivity was similar in all subjects except in three of the AD patients, where more nerves appeared to penetrate the epidermis. Substance P immunoreactivity in the papillary dermis was seen in all AD patients hut no controls. Vasoactive intestinal polypeptide and neuropeptide Y staining were similar in all groups. Acetyleholinesterase‐positive nerves were found around sweat glands in all subjects, the staining being greatest in non‐lesional and least in lesional skin. Occasional nerves were seen in the papillary dermis in lesional skin of two out of the four patients. We have demonstrated quantitative differences in nerve growth in clinically normal skin of AD patients, and altered cutaneous neuropeptide expression in these patients which may contribute to the pathogenesis of AD.

Adult patients with severe atopic eczema who had completed a double-blind placebo-controlled crossover trial of a specific formulation of Chinese herbal therapy were offered continued therapy for 1 year. Of 31 patients who completed the original placebo-controlled study and after a washout period and 2 months of further treatment, 17 continued treatment (group 1), 11 chose not to continue treatment (group 2), one was lost to follow-up and two patients originally in group 1 decided to stop treatment and became pregnant. At the end of the year, 12 of the patients in group 1 had greater than 90% reduction and the remaining five had greater than 60% reduction in clinical scores compared with baseline values. Clinical scores of patients in group 2 gradually deteriorated so that by the end of the year the difference between groups 1 and 2 was highly significant (P = 0.005 and P = 0.002 for erythema and surface damage, respectively). At the end of the year no patient in group 1 felt able to discontinue treatment permanently, but eight patients were on an alternate-day regimen by 6 months and remained on this regimen until the end of the year, and seven were able to control their eczema with a 1 in every 3 day treatment by the end of the year. The remaining two patients continued on daily treatments. Toxicology screening revealed no abnormalities in either full blood counts or biochemical parameters in any patient on continued treatment. Improvement in disease was not associated with any significant change in serum IgE level or peripheral blood lymphocyte subsets.(ABSTRACT TRUNCATED AT 250 WORDS)

Although alterations of the CYP21 gene were more common in acne than in controls there is a poor correlation between these events and raised steroids and acne. Factors other than mild impairment of CYP21 contribute to the variability of the clinical phenotype in hyperandrogenic states including acne.

We report a large kindred in which a punctate palmoplantar keratoderma (PPK) is associated with malignancy, including Hodgkin's disease, renal, breast, pancreatic and colonic adenocarcinomas. The family was traced through four generations, and over 320 individuals were identified, of whom 49 had punctate PPK. The punctate PPK appeared to be inherited as an autosomal dominant trait with variable penetrance. Ten of the 43 adults (23%) with punctate PPK developed malignancies, and five of these developed before the age of 50. Of the 271 unaffected individuals, six (2%) have developed malignancies, one prior to the age of 50. The association of keratoderma and malignancy is discussed.