This study was designed to investigate a long-term therapeutic strategy for the management of recurring atopic dermatitis (AD) in adults using fluticasone propionate (FP) ointment (CutivateTM) whereby FP could help to prevent a relapse of AD once symptoms were under control. Adult patients with chronic, moderate to severe AD entered this multicentre study. All patients were initially treated with FP 0.005% (g/g) ointment in two different regimens. Patients whose AD had been completely healed by these treatments then entered a long-term treatment phase applying FP or placebo ointment once daily, two times per week for 16 weeks to 'known' healed lesions. By the end of the initial treatment period, mean SCORAD values had significantly (P < 0.0005) improved from baseline. Patients who entered the maintenance phase and were treated with intermittent FP for up to 16 weeks, demonstrated its superior efficacy (P = 0.018) over placebo, maintaining the improvements achieved after the initial treatment phase, reducing risk of relapse and delaying time to relapse (P = 0.013). No significant changes were detected in either treatment group in serum cortisol levels or in skin thickness measurements. Intermittent FP applied two times per week maintained a significant level of control, and delayed relapse of AD by comparison with placebo.

Circulating IgG from a large subset of bullous pemphigoid (BP) patients reacted on immunoblot with a 120-kDa protein in conditioned keratinocyte culture medium and in keratinocyte cell extracts. A protein with a similar molecular weight was recognized by circulating IgA from a subset of patients with linear IgA dermatosis (LAD). Both affinity-purified 120-kDa-specific BP IgG and 120-kDa-specific LAD IgA bound to the roof of salt-split skin. Both proteins recognized are collagenous glycoproteins. Deglycosylation with N-glycosidase F resulted in an identical reduction in molecular weight for both the BP-IgG-recognized protein and the LAD-IgA-recognized protein. Both proteins were equally susceptible to digestion with type VII collagenase. Furthermore, both proteins were absent from conditioned culture medium of keratinocytes from patients with BP180-deficient general atrophic benign epidermolysis bullosa (GABEB). Immunodepletion studies showed that the 120-kDa LAD antigen could be removed from conditioned culture medium by anti-120-kDa BP IgG. Thus these results indicate that these proteins are either highly related or, most probably, identical. A strong antigenic relationship between the 120-kDa protein and the 180-kDa bullous pemphigoid antigen (BP180) was detected by cross-reaction of affinity-purified anti-120-kDa BP patient antibodies to BP180 and cross-reaction of monoclonal anti-180-kDa antibodies to the 120-kDa protein. Notwithstanding this cross-reactivity, the 120-kDa protein also exhibits unique epitopes demonstrated by the nonreactivity of individual anti-120-kDa BP and LAD patient serum with the 180-kDa antigen.

IntroductionGeneralized atrophic benign epidermolysis bullosa (GA-BEB) is a form of nonlethal junctional epidermolysis bullosa characterized by universal alopecia and atrophy of the skin. We report a deficiency of the 180-kD bullous pemphigoid antigen in three patients with GABEB from unrelated families. We screened specimens of clinically normal skin from nine junctional epidermolysis bullosa patients (3 GABEB, 4 lethal, 1 cicatricial, 1 pretibial) by immunofluorescence using monoclonal antibodies to the 180-kD and 230-kD bullous pemphigoid antigens (BP180 and BP230). In the skin of the three GABEB patients there was no reactivity with antibodies to BP180, whereas staining for BP230 was normal. In the skin of the other six, non-GABEB patients, included in this study the expression of BP180 and BP230 was normal. Immunoblot analysis of cultured keratinocytes from one of the GABEB patients also failed to detect BP180 antigen, whereas BP230 was present in normal amounts. In previous studies on the expression of the bullous pemphigoid antigen in JEB, sera from bullous pemphigoid (BP) patients were used, the specificity of which had not been analyzed by immunoblotting (6-9). The expression was found to be normal or variable. Later it became apparent that BP-serum is a mixture of polyclonal antibodies, which are very difficult to characterize, even after affinity-purification (10). Fortunately, reliable monospecific antibodies for each of the two major bullous pemphigoid antigens have now become available (1 1, 12).In this study we used monoclonal antibodies specific for BPI 80 and BP230 (11,12). In addition we studied the expression of the newly described 500-kD hemidesmosomal plaque protein HD1 (13)

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‐An animal experiment is presented which involved a total of 223 albino hairless mice (Skh hr 1). These mice, excluding 24 of them which served as controls, were divided over 6 groups, each of which received a different but constant daily dose of UV radiation from fluorescent sunlamps (Westinghouse FS40TL12). The range of daily doses encompassed a factor of 33. Data on the response of each group as a whole are presented. The group responses are measured in two ways: (1) the proportion of tumor bearing mice (prevalence), and (2) the average number of tumors per survivor (yield). The data provide information on the variation of the group response with time, daily dose and tumor size. The relationship between the daily dose and the duration of the treatment till 50% of the mice have tumors is given for several sizes of tumors. From these results, and from direct measurements of tumor growth, it appears that the growth of tumors is virtually dose‐independent and, in consequence, only the initiation of tumors is dose‐dependent. This implies that the theoretical model of UV‐tumorigenesis presented by Blum (1959). based on UV‐accelerated growth, is incorrect. It is pointed out that, in similarity to chemo‐ and radiotumorigenesis, the total dose delivered to a mouse for the induction of tumors has to be higher if a high daily dose is used than if a low daily dose is used. It seems as though an animal becomes more resistant to the UV‐stimuius as the rate at which the stimulus is presented is increased: an adaptive phenomenon.