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Gene polymorphisms and thyroid function in patients with heart failure.

TitleGene polymorphisms and thyroid function in patients with heart failure.
Publication TypeJournal Article
Year of Publication2014
AuthorsVasiliadis, I., Kolovou G., Kolovou V., Giannakopoulou V., Boutsikou M., Katsiki N., Papadopoulou E., Mavrogeni S., Sorontila K., Pantos C., & Cokkinos D. V.
JournalEndocrine
Volume45
Issue1
Pagination46-54
Date Published2014 Feb
ISSN1559-0100
KeywordsAged, Cohort Studies, Female, Genotype, Heart Failure, Humans, Male, Middle Aged, NF-kappa B p50 Subunit, Peptidyl-Dipeptidase A, Polymorphism, Genetic, Thyroid Function Tests, Thyroid Gland, Thyrotropin, Thyroxine, Triiodothyronine
Abstract

We evaluated nuclear factor kappa B {NFkB, rs28362491 [-94ins/delATTG (W/D)]} and angiotensin converting enzyme {ACE; rs1799752 [Ins(I)/Del(D)]} gene polymorphisms and their correlation with thyroid function in patients with heart failure (HF). Peak oxygen uptake (VO(2)) was evaluated (by Weber classification) during a symptom-limited cardiopulmonary exercise test in 194 patients. Thyroid-stimulating hormone, triiodothyronine (T3), thyroxine (T4), and free (F) T3 and FT4 were also measured. According to their cardiovascular (CV) capacity, patients were subdivided into four groups: group A included patients with peak VO(2) >20 ml/kg/min, group B 16-20 ml/kg/min, group C 10-16 ml/kg/min, and group D 6-10 ml/kg/min. Patients were also genotyped for NFkB and ACE genetic variants. T3 was increased and FT3 was decreased for every raise in Weber's classification (p = 0.007 and p = 0.012, respectively). Del carriers had elevated FT3 levels compared with Ins carriers (p = 0.021). Patients with II genotype had elevated T4 levels compared with ID genotype (p = 0.044). Both T4 and FT4 were decreased in D allele carriers (p = 0.007 and p = 0.045, respectively). Thyroid hormones correlated with CV capacity. Associations between the NFkB and ACE gene polymorphisms and thyroid hormones levels were also observed. Further larger studies are required to clarify genes contribution in HF.

DOI10.1007/s12020-013-9926-x
Alternate JournalEndocrine
PubMed ID23543433

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