Circulating 3-T1AM and 3,5-T2 in critically ill patients: a cross-sectional observational study.

Circulating 3-T1AM and 3,5-T2 in critically ill patients: a cross-sectional observational study.

Thyroid. 2016 Sep 27;

Authors: Langouche L, Lehmphul I, Vander Perre S, Koehrle J, Van den Berghe G

Abstract
BACKGROUND: Critical illness is hallmarked by low circulating T4 and T3 concentrations, in the presence of elevated rT3 and low-normal TSH, referred to as non-thyroidal illness (NTI). Thyroid hormone (TH) metabolism is substantially increased during NTI, in part explained by enhanced deiodinase 3 (D3) activity. T4- and T3-sulfate concentrations are elevated, due to suppressed D1 activity in the presence of unaltered sulfotransferase activity, and 3,3'-diiodothyronine (3,3'-T2) concentrations are normal. To further elucidate the driving forces behind increased TH metabolism during NTI, two other potential T4 metabolites, 3,5-diiodothyronine (3,5-T2) and 3-iodothyronamine (3-T1AM), were measured and related to their potential TH precursors.
METHODS: Morning blood samples were collected cross-sectionally from 83 critically ill patients on a University Hospital ICU and from 38 demographically matched healthy volunteers. Serum TH and binding proteins were quantified with commercial assays, 3,5-T2 and 3-T1AM with in-house developed immunoassays.
RESULTS: Critically ill patients revealed, besides the NTI, a median 44% lower serum 3-T1AM concentration (p<0.0001) and a 30% higher serum 3,5-T2 concentrations (p=0.01) than healthy volunteers. Non-survivors and patients diagnosed with sepsis upon ICU admission had significantly higher 3,5-T2 (p≤0.01) but comparable 3-T1AM (p>0.2) concentrations than other patients. Multivariable linear regression analysis adjusted for potential precursors revealed that the reduced serum 3-T1AM was positively correlated with the low serum T3 (p<0.001) but unrelated to serum T4 or rT3. The elevated 3,5-T2 concentration did not independently correlate with TH.
CONCLUSIONS: Increased TH metabolism during NTI could not be explained by increased conversion to 3-T1AM, as circulating 3-T1AM was suppressed in proportion to the concomitantly low T3 concentrations. Increased conversion of T4 and/or T3 to 3,5-T2 could be possible, as serum 3,5-T2 concentrations were elevated. Whether 3-T1AM or 3,5-T2 play a functional role during critical illness needs further investigation.

PMID: 27676423 [PubMed - as supplied by publisher]

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