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(Hypertension. 2008;51:e22.)
© 2008 American Heart Association, Inc.

Letters to the Editor

Lack of Association Between the Type 2 Deiodinase A/G Polymorphism and Hypertensive Traits: The Framingham Heart Study

Thyroid Section, Endocrine Division, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil

Shih-Jen Hwang; Daniel Levy

National Heart, Lung, and Blood Institute Framingham Heart Study, Framingham, Mass, and the National Heart, Lung, and Blood Institute Center for Population Studies, Bethesda, Md

Martin G. Larson

Boston University School of Medicine, Boston, Mass

P. Reed Larsen

Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass

Caroline S. Fox

National Heart, Lung, and Blood Institute Framingham Heart Study, Framingham, Mass, and the National Heart, Lung, and Blood Institute Center for Population Studies, Bethesda, Md, and the Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Thyroxine (T4) activation to T3 via the iodothyronine deiodinase type 2 allows for changes in intracellular thyroid status in a tissue-specific manner independent of serum T3. A single nucleotide polymorphism in type 2 deodinase (DIO2) gene (A/G) in humans, in which a threonine changes to alanine at codon 92, has been associated with decreased enzyme activity and higher insulin resistance in type 2 diabetes patients.¹ Nevertheless, these findings were not replicated in larger studies.² Recently, Gumieniak et al³ reported that the alanine allele doubles the risk for development of hypertension in euthyroid subjects. Pituitary and hypothalamic type 2 deiodinase play a critical role in feedback regulation of thyroid-stimulating hormone (TSH) secretion, and higher serum TSH concentrations have been demonstrated in euthyroid hypertensive compared with normotensive control subjects.⁴ In this context, we thought it would be of interest to evaluate whether the previous reported association of Thr92Ala polymorphism and hypertension is also present in a large unselected, community-based population.

The present sample size consists of 1557 individuals who had complete phenotype and genotype information available drawn from a subset of unrelated individuals from the Framingham Heart Study offspring cohort, who had DNA collected between 1995 and 1998 (n=2933). This study was approved by the institutional review boards of Boston University and Brigham & Women’s Hospital, and written informed consent was obtained from each subject. At each examination, blood pressure was measured twice in the left arm by an examining physician using a mercury column sphygmomanometer (Korotkoff phases I . . . [Full Text of this Article]