Letter: Decreased serum-IgA in myasthenia gravis.
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Biomedical subjects
Publications and source records attributed to J A Simpson.
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Clinical and laboratory data continue to support the concept of a genetically determined breakdown of immunological tolerance in myasthenia gravis with immunological damage to the motor end plates. The demonstration of impaired function of thymus-derived lymphocytes and of IgA deficiency correlate well with the clinical data in which there is an increase incidence of autoimmune diseases associated with anergy. Whilst the exact pathogenesis of myasthenia gravis is unknown, the available data support the concept of an immune deficiency disorder.
Torulosis is an uncommon, but potentially lethal disease. The aim of this report is to indicate that resection of isolated pulmonary lesions due to torulosis is a safe procedure. Resection has proved useful in the definitive diagnosis and treatment of eight cases seen in this thoracic surgical unit.
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Humoral antibodies to skeletal muscle and its components and to thymus have been demonstrated in the sera of patients with myasthenia gravis. A role for cellular hypersensitivity to similar antigens in the pathogenesis of the disease has been suggested by some reports of the presence of cellular immunity. A detailed immunological study using muscle and thymic antigens, including those prepared from the patients' own tissues, failed to confirm these findings. It is suggested that previous reports of cellular hypersensitivity represent the demonstration of an epiphenomenon.
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Fifty-four thymus glands removed surgically from patients with myasthenia gravis were examined using an accurate morphometric technique and the data compared with the response to thymectomy. There is a tendency for patients with relatively unreactive thymus glands to obtain a better result from thymectomy but this is not statistically significant.
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