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GEORGE S. KURLAND, MILTON W. HAMOLSKY, A. STONE FREEDBERG, STUDIES IN NON-MYXEDEMATOUS HYPOMETABOLISM: I. THE CLINICAL SYNDROME AND THE EFFECTS OF TRIIODOTHYRONINE, ALONE OR COMBINED WITH THYROXINE, The Journal of Clinical Endocrinology & Metabolism, Volume 15, Issue 11, 1 November 1955, Pages 1354–1366, https://doi.org/10.1210/jcem-15-11-1354
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Abstract
THE diagnosis of classic primary myxedema usually offers little difficulty and the results of therapy with desiccated thyroid or thyroxine are striking and gratifying. Such patients, however, constitute only a small fraction of all individuals who demonstrate significant depression of the basal metabolic rate. Hypometabolism also accompanies hypopituitarism, hypogonadism, Addison's disease, nephrosis, markedly reduced activity, and malnutrition. When all such causes of hypometabolism have been excluded, however, there remain a large number of individuals with basal metabolic rates of –20 to –30 per cent who do not appear to be myxedematous and who are not improved by the administration of desiccated thyroid. The cause of the low basal metabolism in them is obscure.
The existence of this group of patients was recognized by Plummer as early as 1917 (1) and attention has been called to their clinical characteristics by many subsequent authors under the title “low basal metabolism without myxedema” (2, 3) or “euthyroid hypometabolism.” There has been a remarkable similarity in all clinical descriptions of these patients. The most frequent complaints have been lethargy, easy fatigability, nervousness, irritability, emotional instability, sensitivity to cold, headache, ill defined skeletal plain, diminished sexual potency in the male and menstrual irregularity in the female. The lack of specificity of the complaints has often led to a diagnosis of neurosis. In contrast to true hypothyroidism, such cases demonstrate one or more of the following (4): (i) in the vast majority, a failure of the basal metabolic rate to rise to normal levels after desiccated thyroid, even when administered to the point of toxicity; (ii) in the few instances in which the metabolic rate becomes elevated toward normal, absence of clinical improvement in signs and symptoms; (iii) lack of ultimate beneficial effects in such patients, with progressively increased thyroid dosage (5); and (iv) in all cases, the necessity for a large dose of thyroid to raise the metabolic level, compared to that required to restore a truly myxedematous patient to a euthyroid state.
