This suggests that weaker corticosteroid dilutions had comparable high efficacy, but lower risk of HPA axis suppression.

Background: ‘Wet-wrap’ dressings with diluted corticosteroids form an alternative treatment in patients with refractory atopic dermatitis (AD). Objective: To evaluate a standardized treatment, using wet-wrap dressings with diluted corticosteroids, in patients with refractory AD. Methods: Results of treatment, complications and possible side effects were retrospectively evaluated in 14 children and 12 adults. Results: Skin lesions improved dramatically during 1 week of inpatient treatment. A significant decrease in early-morning serum cortisol levels was measured. Levels below the normal range were only observed after 1 week in 2 adults and on day 4 in 3 children. Suppression of the hypothalamus-pituitary-adrenal-cortex axis in 1 adult and a new exacerbation of AD in 2 children and 3 adults complicated long-term treatment at home. Additional complications included folliculitis, a Pseudomonas aeruginosa infection, a secondary bacterial infection and refractory skin lesions between bandages. Conclusion: Wet-wrap dressings and diluted corticosteroids form an effective treatment in patients with refractory AD.

IN this issue of the Archives, Baden and Byers1 describe 21 cases of keratosis pilaris atrophicans (KPA). He considers KPA as one disease entity.1 However, our opinion differs in view of the arguments presented here. Keratosis pilaris (KP) is a skin symptom associated with different diseases, mostly of ectodermal origin. By definition, keratinous plugs are observed in the follicular orifices surrounded by a variable degree of erythema. When the keratotic papules are followed by atrophy, one speaks of KPA. Atrophy is preceded with or without inflammation. There is much confusion on KP and KPA entities, especially because different overlapping syndromes have been described and many synonyms are used in both dermatologic and genetic literature.2-4 In this editorial, we present our opinion and arguments on diseases with KPA. KERATOSIS PILARIS ATROPHICANS We distinguish four distinct clinical entities that show KPA. These are keratosis pilaris atrophicans faciei (KPAF), atrophoderma vermiculata, keratosis follicularis spinulosa decalvans (KFSD), and, as proposed, folliculitis spinulosa decalvans.3 Rand and Arndt3 believe that these forms are different stages of a single process of KPA. Baden and Byers1 also propose that KPAF, atrophoderma vermicu¬ lata, and KFSD should be headed under KPA. Baden and

No abstract

A 12 y old girl with the albopapuloid variant (Pasini) of dominant dystrophic epidermolysis bullosa is studied. The albopapuloid lesions developed within the first year of life, contained milia and were associated with pruritus. Mutation detection of the COL7A1 gene revealed a G-->A transition at nucleotide position 6110 in the mutant allele converting a glycine to glutamic acid (G2037E). This report adds to the expanding database on COL7A1 mutations in dystrophic epidermolysis bullosa.