An unusual vesiculobullous disease and myasthenia gravis occurred concurrently with a malignant thymoma in a Japanese male. The bullous dermatosis had combined clinical and histological features of both dermatitis herpetiformis and pemphigus. Serum showed striated muscle antibodies and intercellular epithelial autoantibodies; the latter had been demonstrated even prior to the development of the skin lesions. Thus, immunologically, this dermatosis was confirmed to be a variety of pemphigus.
A case of myasthenia gravis was associated with thymoma and pemphigus vulgaris. The bullous lesions developed after partial thymomectomy, cobalt (60Co) irradiation, and 3 days' extensive sunbathing, although a retrospective study of the patient's sera by quantitative indirect immunofluorescence method indicated that antiepithelial antibody already was positive before the clinical appearance of pemphigus vulgaris. Serial observation of the patient's clinical course and titrations of antiepithelial, antimuscle, and antithymus antibodies suggested a reverse relationship between the severity of myasthenia gravis and titers of antimuscle and anitithymus antibodies, and a parallel relationship between pemphigus vulgaris and antiepithelial antibody. Review of the literature suggests a close relationship between pemphigus vulgaris and myasthenia gravis and thymoma, particularly thymoma injured by medical procedures.
We examined the time course of lymphocyte responsiveness to acetylcholine receptor (AChR) in rats with experimental autoimmune myasthenia gravis (EAMG). Rats were immunized with purified torpedo AChR. At intervals of one to eight weeks later, lymphocytes from the lymph nodes and spleen were cultured with purified torpedo AChR and rat muscle extract containing AChR. Lymphocyte responsiveness (stimulation index) was determined from uptake of 3H-labeled thymidine by the cultured cells. The response of lymphocytes to torpedo antigen began earlier and rose more rapidly than that to the homologous (rat) antigen. Lymph node cells responded more promptly than spleen lymphocytes. The stimulation indexes peaked at four to six weeks while antibodies to both antigen continued to rise. Delineation of this pattern of lymphocyte responsiveness sheds further light on the pathogenesis of the autoimmune response in EAMG and will be useful in the future design of immunotherapeutic strategies.
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