Accelerated Cellular Uptake and Metabolism of L-Thyroxine during Acute <i>Salmonella typhimurium</i> Sepsis

Frederick R. DeRubertis; Kenneth A. Woeber

doi:10.1172/JCI107176

Accelerated Cellular Uptake and Metabolism of L-Thyroxine during Acute Salmonella typhimurium Sepsis

Published January 1, 1973 - More info

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Abstract

The effects of acute Salmonella typhimurium sepsis on the kinetics of peripheral L-thyroxine (T₄) distribution and metabolism and on serum total and free T₄ concentrations were studied in rhesus monkeys inoculated i.v. with either heat-killed or viable organisms. The rate of disappearance of labeled T₄ from serum was increased within 8 h after inoculation of monkeys with either heat-killed or viable Salmonella. The effects of the heat-killed organisms were transient and no longer evident by 16 h postinoculation. The monkeys inoculated with the viable Salmonella experienced a 2-3 day febrile, septic illness that was accompanied by an increase in the absolute rate of T₄ disposal. In the infected monkeys, serum total T₄ and endogenously labeled protein-bound iodine concentrations fell significantly during the period of acute sepsis and then rose during convalescence to values that exceeded the preinoculation values, suggesting that thyroidal secretion of hormone had increased in response to a primary depletion of the peripheral hormonal pool. Total cellular and hepatic uptakes of T₄ were enhanced by 4 h after inoculation of monkeys with either heat-killed or viable Salmonella, but the increase in total cellular uptake persisted for 24 h only in the monkeys inoculated with the viable organisms. These alterations in T₄ kinetics could neither be correlated with changes in the binding of T₄ in plasma nor attributed to an increase in vascular permeability. Moreover, they could not be ascribed to an in vitro product of bacterial growth, suggesting that the presence of the organisms themselves was required. An acceleration of T₄ disappearance was also observed during Escherichia coli and Diplococcus pucumoniae bacteremias. Our findings are consistent with a primary increase in the cellular uptake and metabolism of T₄ during bacterial sepsis, possibly related to phagocytic cell function in the host.