DAVID H. SOLOMON, M.D., F.A.C.P.; L. ROBERT BENNETT, M.D.; JOSIAH BROWN, M.D.; J. B. PETER, M.D., PH.D.; WILLIAM F. POLLOCK, M.D.; JOHN B. RICHARDS, M.D.
The hypothesis that uncoupled or loosely coupled oxidative phosphorylation is a fundamental abnormality in hyperthyroidism is no longer tenable. Rather, mitochondria from hyperthyroid muscle are increased in number but normal in phosphorylative behavior. Sarcotubular vesicles are also increased in amount and appear normal in biochemical function. The cause of muscle weakness remains unknown.
The clinical features of hyperthyroidism are reviewed, with personal observations on their usefulness in diagnosis. The syndrome of Graves' disease is defined as a tri-system disease (thyroid, eye, and skin), and the autoimmune hypothesis of its origin is discussed in the light of the properties of the long-acting thyroid stimulator (LATS), an immunoglobulin unique to Graves' disease.
The choice of treatment of hyperthyroidism is still a matter for controversy. It is agreed that subtotal thyroidectomy, radioiodine, and antithyroid drugs, all have a role in treatment, but opinions differ on their comparative usefulness in various types of patients.
SOLOMON DH, BENNETT LR, BROWN J, PETER JB, POLLOCK WF, RICHARDS JB. Hyperthyroidism. Ann Intern Med. 1968;69:1015–1035. doi: 10.7326/0003-4819-69-5-1015
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Published: Ann Intern Med. 1968;69(5):1015-1035.
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