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Biomedical subjects

K Wolff

Publications and source records attributed to K Wolff.

At least 289 records · Page 16Linked to original sources
PubMed1981

Oral 8-methoxypsoralen photochemotherapy of psoriasis. The European PUVA study: a cooperative study among 18 European centres.

In a multicentre study in eighteen European cities 3175 patients were treated with photochemotherapy (PUVA) for severe psoriasis and data obtained during a period of 39 months were analysed. A response better than marked improvement was obtained in 88.8% of patients; twenty exposures and a total cumulative UVA dose of 96 J/cm2 were required for clearing, the duration of the clearing phase being 5.3 weeks. A comparison of the results of this study with those of a similar multicentre study in the United States on 1300 patients and using a different treatment protocol, revealed that while treatment results and the number of individual treatment sessions were similar the European protocol requires only half the time and less than half the total cumulative UVA dose for clearing of psoriasis. When patients in the European study who received continuous maintenance treatment were compared with patients who received no maintenance treatment the probability that a patient would remain in remission for a period of 80 weeks was the same, irrespective of whether patients received maintenance treatment or not. This study confirms the dramatic efficacy of PUVA in clearing psoriasis and contains two important messages for the reduction of possible long-term hazards of this treatment. Firstly, the total UVA energy requirements for clearing psoriasis strongly depend on the treatment schedule and can be kept low if an individual approach aimed at rapid clearing of psoriasis is used. Secondly, maintenance therapy may not significantly prevent recurrences for prolonged periods of time and may thus not be necessary in most patients.

Administration, Oral↗
PubMed1981

Immunofluorescence mapping of antigenic determinants within the dermal-epidermal junction in the mechanobullous diseases.

The classification of mechanobullous diseases often depends on the electron microscopic distinction of intradermal (dermolytic), junctional and intraepidermal sites of cleavage. Electron microscopy is tedious and time consuming. In this report we describe a different approach to the determination of the cleavage plane by using a method which recognizes subtle differences in the localization of antigenic structures relative to the cleavage plane. Cryostat sections of lesional and extralesional skin of 3 patients with dermolytic epidermolysis bullosa, 3 with epidermolytic epidermolysis bullosa and 8 with junctional epidermolysis bullosa were examined by immunofluorescence, with specific antisera against type IV collagen (localized within the basal lamina); against laminin (noncollagenous protein, localized in the lamina lucida); and with bullous pemphigoid antibodies (directed against the bullous pemphigoid antigen localized in the lamina lucida). All specimens were also examined by electron microscopy. In dermolytic epidermolysis bullosa (where cleft formation occurs intradermally) type IV collagen, laminin and the bullous pemphigoid antigen were consistently found in the roof of the blister, whereas in junctional epidermolysis bullosa (where the cleft occurs in the lamina lucida) type IV collagen and laminin were found on the floor of the blister whereas bullous pemphigoid antigen was present mainly on the roof, but focally also on the floor, of the blister. In epidermolytic epidermolysis bullosa (where the cleft is intraepidermal) all antigens were localized below the cleavage plane. In all cases electron microscopy confirmed the level of cleft formation predicted from the immunofluorescence mapping of the antigenic sites. The described method equals electron microscopy in accuracy but it is more rapid and simpler to perform.

Collagen↗
PubMed1981

Ultraviolet light depletes surface markers of Langerhans cells.

This report defines the influence of ultraviolet light (UV) on Langerhans cells (LC). Human volunteers and hairless mice (Swiss ha/ha) were exposed to various single and/or cumulative doses of either UV-A, UV-B, or UV-A plus small amounts of UV-B (UV-A (+B)). 24 hr after the last irradiation, morphology of the entire epidermis was evaluated by both light and electron microscopy while LC, in addition, were tested for expression of specific histochemical (ATPase) and functional immunological markers (Ia antigens). In both men and mice, cumulative doses of either 80-120 J/cm2 UV-A (+B) or 1-2 X 100 J/cm2 UV-A resulted in a dramatic reduction of cells exhibiting ATPase and Ia-reactivity. In the UV-B spectrum, single doses of 60-80 mJ/cm2 produced a virtually complete elimination of LC membrane markers. By contrast, pemphigus antigens of keratinocytes were unaffected by these energy doses. Electron microscopy revealed cellular damage of some LC after UV-doses which produce a virtually complete abolition of LC membrane markers. At certain dose ranges (15-30 mJ/cm2 UV-B and 1 x 40 to 2 x 100 J/cm2 UV-A) LC were the only epidermal cells to display morphological damage at the ultrastructural level whereas higher doses affected all epidermal cells. The finding that LC surface markers and to a lesser extent the cells themselves are particularly susceptible to UV irradiation has important implications in view of previous findings that LC are potent stimulators of antigen-specific and allogeneic T cell activation. UV-induced alteration of LC plasma membrane integrity may represent a tool to manipulate adverse immune reactions involving the epidermis.

Adenosine Triphosphatases↗
PubMed1981

Dermatitis herpetiformis: immune complex detection with C1q and monoclonal rheumatoid factor.

To determine the significance of circulating immune complexes in dermatitis herpetiformis, serum samples from thirty patients with active disease were tested by a C1q binding radioassay, while serum samples from twenty-one of these patients were tested by a monoclonal rheumatoid factor (mRF) inhibition radioassay. By direct immunofluorescence, all patients demonstrated typical IgA deposition in dermal papillae. Using the C1q binding assay, only seven of forty-two serum samples had elevated C1q binding activity, while by the mRF inhibition assay, thirteen of twenty-five samples had elevated immune complex levels. Nine of these latter thirteen positive serum samples, however, were minimally elevated. Thus, IgG and/or IgM containing immune complexes are infrequently present, or at very low levels, in sera of patients with active dermatitis herpetiformis.

Antigen-Antibody Complex↗
PubMed1981

[Pyoderma gangraenosum].

Pyoderma gangrenosum is a relatively rare, destructive, inflammatory disease of unknown cause which may present as a purely cutaneous disorder or may be associated with an underlying internal disease (ulcerative colitis, Crohn's disease, rheumatoid arthritis, multiple myeloma, lymphoma and others). Four selected patients are described which reflect the clinical spectrum of this condition; these cases and a review of the literature serve as a background for analysis of pyoderma gangraenosum as an entity and a discussion of its pathogenesis.

Aged↗
PubMed1981

[Fasciitis with eosinophilia - Shulman syndrome].

Fasciitis with eosinophilia (also Shulman's disease or eosinophilic fasciitis) is characterized by an inflammatory thickening of the fascia, eosinophilia and hypergammaglobulinemia. It has clinical and histopathological similarities with scleroderma, though evidence for systemic involvement is rarely found. In this report, we describe the clinical and laboratory features of two patients with this disease and their response to treatment and we discuss its relationship to scleroderma and the pseudosclerodermatous syndromes and its prognosis.

Adult↗
PubMed1980

Long-term photochemotherapy: histopathological and immunofluorescence observations in 243 patients.

Skin biopsies of 243 patients treated with photochemotherapy (PUVA) for 1--4 years were examined histologically. Two hundred and six patients were examined retrospectively after total cumulative UV-A doses of 579 . 6 +/- 598 . 0 J/cm2 (mean +/- s.d.). An eosinophilic homogenization and a reduction of elastic fibres at the dermo--epidermal junction, and an increase of dermal macrophages were found as possible abnormalities. However, except for the increase of melanophages there was no statistically significant correlation between the incidence of these changes, the total UV-A dose applied and the skin type of the patients. Neither were such correlations found in thirty-seven patients biopsies twice after 394 . 8 +/- 267 . 6 J/cm2 and 808 . 5 +/- 458 . 9 J/cm2 (mean +/- s.d.), respectively. Studies with direct immunofluorescence techniques revealed no immunoglobulin deposits in PUVA treated skin in fifty-six patients after 469 . 2 +/- 370 . 2 J/cm2; antinuclear antibodies were observed in 4 . 6% of 129 patients after 169 J/cm2 (mean); in 11% of fifty-three patients reexamined after 381 J/cm2 (mean) and in 13 . 6% of twenty-two patients reexamined a second time after 643 J/cm2 (mean). Thirteen out of a total of 572 patients developed a peculiar mottling of skin in areas previously overdosed by PUVA. Subepidermal homogenization and reduction of elastic fibres were found in 45% of the patients, indicating that these changes indeed are a consequence of PUVA. Nuclear and cellular irregularities were found in 45% of the biopsies and 63% showed a disturbed epidermal architecture, but no carcinomas were observed. PUVA-induced mottling was reversible in 31%, partially reversible in 15%, but continued to be present in 54%.

Adult↗
PubMed1980

Diffuse melanosis in metastatic melanoma. Further evidence for disseminated single cell metastases in the skin.

Electron microscopy (EM) and electron microscopic cytochemistry have shown that diffuse melanosis in advanced metastatic melanoma is the result of an unlimited spread of single melanoma cells throughout the dermis; these cells retain their melanogenic capacity and continue to produce melanized melanosomes which eventually are deposited within dermal macrophages and thus impart to the skin a diffuse slate-blue color. These findings are in accordance with previous observations in a similar patient and thus support the concept that single cell metastasis represents a common pathogenic event in these patients.

Adult↗
PubMed1979

[Photoprotection by psoralen-UVA therapy: experimental and clinical results (author's transl)].

Studies on minimum erythema doses, histological investigations and quantitative determination of DNA repair synthesis of epidermal cells revealed that a tan induced by the oral administration of 8-methoxy-psoralen (8-MOP) and subsequent UVA irradiation gives protection from the erythemogenic effects of sunlight, diminishes UVA-induced cellular injury in the epidermis and, possibly, also shields DNA from incident UV radiation. In a study of 14 patients with severe polymorphous light dermatosis the 8-MOP-UVA induced tan proved to be a clinically effective sunscreen. The uncontrolled use of this method for UV protection of normal individual is, however, not recommended.

DNA Repair↗
PubMed1979

[Lupus erythematosus panniculitis (author's transl)].

Lupus erythematosus panniculitis is a rare clinical variant of lupus erythematosus. In this report we described a 38 year-old female patient who had suffered from chronic discoid lupus erythematosus for several years before developing widespread inflammatory, sclerotic and ulcerative lesions, which were first diagnosed as Weber-Christian panniculitis. It was only when the patient developed other signs and symptoms of systemic lupus erythematosus that the subcutaneous lesions were recognized as lupus panniculitis. A combined regimen of tetracyclines and chloroquine resulted in a remission, both with regard to regression of the lesions and suppression of the serological parameters of disease activity. The findings in this particular patient and similar reports in the literature form the basis for a discussion of the entity of lupus panniculitis.

Chloroquine↗