A case of plaque stage mycosis fungoides and one of parapsoriasis en plaque were treated with topical PUVA therapy using a monofunctional furocoumarin derivative, 4,6,4'-trimethylangelicin (TMA). Both patients showed complete clearance of eruptions within 16 treatments. The therapeutic effectiveness of TMA was confirmed by the fact that those eruptions exposed to UVA alone, without TMA application, showed slower and less significant improvement. Histologically, dermal infiltrates of mycosis cells and associated epidermotrophism disappeared almost completely in response to TMA PUVA. No side effects or changes in values in laboratory examinations were observed during treatment.
We herein report a case of a rare variety of the acute eruptive form of lichen planus. The patient was a 51-year-old male who developed an intensely pruritic eruption on the lower legs which spread rapidly to all four extremities and trunk within a few months. The papulosquamous lesions were more than ten thousand in number. Topical steroid, cyclosporine, and systemic griseofulvin treatments were ineffective. However, there was a dramatic response to oral etretinate.
Activities of piasminogen activators (PA) and their inhibitors were studied in the bullous lesions of 2 siblings with recessive dystrophic epidermolysis bullosa (RDEB). The hematological findings of the patients revealed hyperfibrinogenemia, hyper-γ-globulinemia and marked thrombocytosis. The immunofluorescent studies showed strong deposits of piasminogen, fibrin-degenerative products and α1-antitrypsin around the blister lesions. On the other hand, α1-macroglobulin (α2-M) was sparsely deposited.The levels of α2-M in the blister fluid of the patients were also decreased in comparison with those from patients with other bullous dermatoses.The topical application of antibiotic ointment with strong PA inhibitor was clinically effective when applied to the blister and eroded lesions of the patients. These findings suggest that the increased activity of PA may play an important role in the development of blister formation in patients with RDEB.
Weber‐Christian disease in a 25‐year‐old female was reported. She had recurrent erythematous nodules on the trunk and extremities, with fever, and microscopic examination of the nodules showed panniculitis due to lymphocytic and histiocytic infiltration and necrotizing angiitis.
Studies of the peripheral blood showed marked anemia, leucopenia, and especially lymphocytopenia. There was a marked susceptibility to bacterial and viral infections. An increase of serum immunoglobulin level, a marked lymphocytopenia, a rather low percentage of lymphocytes transformed by PHA, and a reversion of the tuberculin reaction from positive to negative were found. She could not be sensitized by DNCB. These findings suggest a deficiency of cellular immunity and it is believed that these immunological abnormalities might be related to the etiology and pathogenesis of Weber‐Christian disease.
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