I J Chopra1. 1. Department of Medicine, UCLA Center for Health Sciences, Los Angeles, CA 90024, USA.
Abstract
OBJECTIVE: To characterize the nonthyroidal illness syndrome (NTIS) and to discuss various underlying potential biochemical mechanisms for this condition. METHODS: The pertinent medical literature was reviewed, and studies of thyroid function in systemic non-thyroidal illnesses were summarized. RESULTS: Abnormalities of thyroid function in the NTIS have been classified into four major categories: (1) low triiodothyronine (T3) syndrome, (2) a combination of low T3 and low thyroxine (T4), (3) high T4 syndrome, and (4) other abnormalities. The NTIS has been noted in essentially all severe systemic illnesses and after caloric deprivation, major operations, and administration of some drugs. Some mechanisms that may contribute to low serum T3 in the NTIS are decreased type I 5 -monodeiodinase in tissues, decreased uptake of T4 by tissues, decreased serum binding, increased reverse T3, alterations in selenium status, cytokines, and a decrease in thyrotropin. Decreased thyrotropin may also contribute to low T4 levels in NTIS, as may decreased serum T4-binding proteins, abnormalities in T4-binding globulin, and circulating inhibitors of binding of T4 to serum proteins. Although T4 treatment of patients with NTIS has yielded little improvement, administration of T3 has produced some beneficial effects. CONCLUSION: Further studies should be conducted to determine appropriate patient populations, dose-response ratios, and possible adverse effects of treatment of the NTIS with T3.
OBJECTIVE: To characterize the nonthyroidal illness syndrome (NTIS) and to discuss various underlying potential biochemical mechanisms for this condition. METHODS: The pertinent medical literature was reviewed, and studies of thyroid function in systemic non-thyroidal illnesses were summarized. RESULTS:Abnormalities of thyroid function in the NTIS have been classified into four major categories: (1) low triiodothyronine (T3) syndrome, (2) a combination of low T3 and low thyroxine (T4), (3) high T4 syndrome, and (4) other abnormalities. The NTIS has been noted in essentially all severe systemic illnesses and after caloric deprivation, major operations, and administration of some drugs. Some mechanisms that may contribute to low serum T3 in the NTIS are decreased type I 5 -monodeiodinase in tissues, decreased uptake of T4 by tissues, decreased serum binding, increased reverse T3, alterations in selenium status, cytokines, and a decrease in thyrotropin. Decreased thyrotropin may also contribute to low T4 levels in NTIS, as may decreased serum T4-binding proteins, abnormalities in T4-binding globulin, and circulating inhibitors of binding of T4 to serum proteins. Although T4 treatment of patients with NTIS has yielded little improvement, administration of T3 has produced some beneficial effects. CONCLUSION: Further studies should be conducted to determine appropriate patient populations, dose-response ratios, and possible adverse effects of treatment of the NTIS with T3.
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