Background: Allergen-reactive Th2-like cells expressing membrane CD30 are present in the circulation of atopic dermatitis (AD) patients during seasonal allergen exposure. Moreover, CD30+ T cells are present in the lesional skin of AD patients and high levels of soluble CD30 (sCD30) are found in the serum of the same atopic patients. To investigate the immunosuppressive capacity of cyclosporin A (CsA) in AD patients, the sCD30 serum level was determined before and after CsA treatment (5 mg/kg/day) in 10 patients with severe, refractory AD. The sCD30 serum levels before and after CsA therapy together with other serum parameters were correlated with disease activity. Methods: sCD30 serum levels were detected using a commercial sandwich ELISA; serum eosinophil cationic protein (ECP) levels were determined using a radioimmunoassay (RIA). Results: In all AD patients sCD30 serum levels were increased ranging from 36 to 300 U/ml, with a mean value equal to 135.7 U/ml. After 6 weeks of CsA treatment, not only was there a significant difference between serum sCD30 levels before (mean 135.7) and after (mean 96.2) treatment but even the serum ECP levels before (mean 57.78) and after (mean 18.69) therapy showed an important reduction. Moreover, no significant difference was found between the mean of serum IgE levels before and after treatment, although the values showed a correlation (p = 0.0003). No significant correlations could be demonstrated between sCD30 levels and serum IgE or between sCD30 and ECP serum levels nor between sCD30 levels and blood eosinophil count after CsA treatment. Moreover, a positive correlation (p = 0.001) was instead documented between sCD30 and the severity of the disease. Conclusions: In this study, CsA therapy results in clinical improvement together with a statistically significant reduction in sCD30 and ECP serum levels in AD patients.

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Our results highlight the presence of a mixed cytokine pattern in the cellular infiltrate of both blistering diseases, with a corresponding increase of Th2-like activity in fully developed lesions, irrespective of the different sites involved. In addition, the constant presence of TGF-beta1 mRNA in the different lesional phases of CP, and its overlapping expression in BP suggest that the involvement of additional factors is responsible for the scarring course typical of CP.

A 57‐year‐old woman was seen in our department in September 1999. At the time of our observation, she complained of fever and malaise and presented many erythematous and squamous lesions on sun‐exposed areas. On the upper third of the back ( Figs 1, 2), she presented a wide patch with irregular borders, due to many coalescing small purplish‐red lesions. Each lesion was covered with branny scales and, on palpation, revealed a variable degree of infiltration. Few areas of uninvolved skin could be seen inside the main patch. Beyond this main patch, small individual scattered lesions with a net‐like distribution were detected. 1 Wide purplish‐red patch and individual scattered lesions of the upper back covered with branny scales 2 Net‐like arrangement of the lesions. Evident pityriasiform scales Similar lesions were present on the neck, chest, and arms. Her face showed diffuse erythema with fine scaling, except for the nasolabial folds which were unaffected. Telangiectasias were present on her face, trunk, limbs, and periungual areas. The patient stated that such lesions had developed after sun exposure. In 1990, a diagnosis of systemic lupus erythematosus (SLE) was made according to the presence of five American Rheumatism Association (ARA) criteria: photosensitivity, malar eruption, diffuse arthralgias (associated with swelling of the finger joints), mild renal involvement with proteinuria, and leukopenia. Since then she has also presented anti‐Ro/SSA antibodies, hypertension, and Raynaud's phenomenon. A histologic study performed on the skin of the back showed a moderate epidermal atrophy with a slight hyperorthokeratosis, a pronounced hydropic degeneration of the basal cell layer, an intense band‐like and perivascular lymphocytic infiltrate, and a moderate diffuse edema of the upper dermis ( Fig. 3). 3 Histopathologic features of the epidermis and superficial dermis in the pityriasiform variety of subacute cutaneous lupus erythematosus (SCLE). Note the epidermal atrophy with slight hyperorthokeratosis, moderate band‐like and perivascular infiltrate, and diffuse edema of the upper dermis (hematoxylin and eosin] original magnification, × 200) Laboratory analysis revealed positive anti‐dsDNA (titer 1 : 160) and anti‐Ro/SSA antibodies, iron‐deficiency anemia, leukopenia (3000/mm3 ), microhematuria, and persistent proteinuria (0.7 g/day). Hypocomplementemia (C3, 47 mg/dL] C4, 10.4 mg/dL) and increased immunoglobulin G (IgG) serum levels were found, while circulating immune complexes could not be demonstrated. The creatinine clearance was found to be decreased (53 mL/min). Chest X‐ray and echocardiography were negative, but a holter examination revealed an abnormal ventricular rhythm. Direct immunofluorescence performed on lesional skin of the back revealed a granular deposition of IgM, C3 at the dermal‐epidermal junction (DEJ), a perivascular deposition of C3, and dust‐like particles of IgG in the epidermis. We confirmed the previous diagnosis of SLE and classified the unusual clinical manifestations as pityr...

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