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Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man

Leonard Wartofsky, Daniel Martin and Jerry M. Earll

Department of Endocrinology and Metabolism, Walter Reed Army Institute of Research, Washington, D. C. 20012

Harry S. Truman Research Laboratory, Kansas City, Missouri 64108

Published September 1972

Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (T4) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral T4 disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-125I, followed in 5-7 days by 131I-T4 intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound 125I and protein-bound 131I, and urinary 125I and 131I, together with frequent estimates of serum 127I-T4 (Murphy-Pattee) and free T4 (FT4), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of 131I-T4 during infection included significant decreases in the fractional disappearance rate for T4 [(k)], and in the clearance and daily disposal of T4, all of which returned to control values during convalescence. Total serum 127I-T4 increased late in the infected period to become greater during convalescence than either before or during infection, while FT4 did not increase significantly until convalescence. An analysis of serum 131I-T4/127I-T4 and 131I-T4/PB125I ratios confirmed these observations. The slope with time of ratios for urinary 125I/131I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum 127I-T4 concentration in the convalescent phase may reflect in part the slowing of (k), but together with the rising ratios of urine 125I/131I suggests enhanced thyroidal T4 secretion immediately after the acute illness. Thus, with malarial infection, there appears to be an initial depression followed by a rebound in rates of thyroidal iodine release. In contradistinction to other infections, fractional turnover and daily disposal of hormone is decreased in malaria, perhaps due to hepatic dysfunction and the consequent impairment in cellular deiodinative processes.


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