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

Leonard Wartofsky; Daniel Martin; Jerry M. Earll

doi:10.1172/JCI107030

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

Published September 1, 1972 - More info

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Abstract

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.