Serum CD5L as potential biomarker of thyroid hormone status during pregnancy.

Jens Mittag, Jens U Marquardt, Britta Wilms, Henrik Oster, Dorota Filipowicz, Ewelina Szczepanek-Parulska, Sabrina Asaad, Waldemar B Minich, Thilo Samson Chillon, Sebastian M Meyhöfer, Lutz Schomburg, Marek Ruchala, Frank Strenge

Journal: BioFactors (Oxford, England) 2024;51(1):e2123

PMID: 39345206

Abstract

The thyroid hormone (TH) status is routinely assessed by thyrotropin (TSH) and thyroxine (T4). Both biomarkers are mainly regulated by TH receptor beta, whereas many peripheral organs employ the alpha receptor. Serum cluster of differentiation 5-like molecule (CD5L) is a liver-derived protein under control of both TH receptor isoforms. However, clinical data on its relation to TH status are sparse. An additional biomarker of TH status is needed in particular during pregnancy, where the routine biomarkers become dynamically disturbed. This study aimed to determine possible covariates regulating serum CD5L and to test its potential suitability as additional TH biomarker during pregnancy. A sandwich ELISA for serum CD5L was established using newly raised antibodies. Circadian effects and the impact of liver disease on serum CD5L concentrations were assessed. Serum samples from pregnant women with well-characterized TH and trace element status were analyzed, and CD5L concentrations were correlated with other indicators of TH status including TSH, fT4, fT3, copper, and selenium concentrations. The new quantitative assay for CD5L showed high accuracy. Serum CD5L was stable in dilution and refreezing experiments and did not show strong circadian variance or dependency on liver disease. In serum of pregnant women, CD5L correlated positively to fT3, but not to fT4 or TSH. Significant positive correlations of CD5L were observed with serum levels of the TH-responsive trace elements selenium and copper. The data support the potential suitability of serum CD5L as an additional marker of TH status, with potential value for pregnancy and thyroid disease.

© 2024 The Author(s). BioFactors published by Wiley Periodicals LLC on behalf of International Union of Biochemistry and Molecular Biology.

Address: The Institute for Experimental Endocrinology, Charité Medical School, Berlin, Germany.; Department of Endocrinology, Metabolism and Internal Medicine, Poznan University of Medical Sciences, Poznan, Poland.; Institute for Endocrinology and Diabetes, Center of Brain Behavior & Metabolism, University of Lübeck/Universitätsklinikum Schleswig-Holstein, Lübeck, Germany.; Institute for Endocrinology and Diabetes, Center of Brain Behavior & Metabolism, University of Lübeck/Universitätsklinikum Schleswig-Holstein, Lübeck, Germany.; Department of Medicine I, University of Lübeck, Lübeck, Germany.; Institute for Endocrinology and Diabetes, Center of Brain Behavior & Metabolism, University of Lübeck/Universitätsklinikum Schleswig-Holstein, Lübeck, Germany.; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.; Department of Medicine I, University of Lübeck, Lübeck, Germany.; Lübeck Institute of Neurobiology, University of Lübeck, Lübeck, Germany.
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