Abstract

Hypertension frequently occurs in subclinical hypothyroidism (SCH). By bolstering thyroid inflammation, anti-peroxidase antibody (TPO-Ab) causes autoimmune thyroiditis, which is one of the most common causes of SCH. Since the absence of thyroid cysts is associated with TPO-Ab (+) based on the indication of latent thyroid damage, we explored the potential mechanism underlying the association among TPO-Ab, SCH, hypertension, and thyroid cysts. A cross-sectional study of 1,483 Japanese aged 40–74 years was conducted. Thyroid cysts were defined as those having a maximum diameter of ≥ 2.0 mm, containing no solid component. TPO-Ab (+) was positively associated with SCH with hypertension (adjusted odds ratio [OR] and 95% confidence interval [CI], 2.62 [1.40, 4.89]) but not with SCH without hypertension (0.84 [0.37, 1.89]), respectively. Moreover, among participants without thyroid cysts, SCH was positively associated with hypertension (2.15 [1.23, 3.76]) but not among participants with thyroid cysts (0.58 [0.16, 2.16]), respectively. TPO-Ab was positively associated with SCH with hypertension, but not with SCH without hypertension. In addition, status of thyroid cysts might act as a determinant factor on the association between SCH and hypertension. These findings are efficient tools to clarify the background mechanism that underlies SCH.

Highlights

  • Anti-thyroid peroxidase antibody (TPO-Ab) causes autoimmune thyroid disease [1] by bolstering thyroid inflammation [2]

  • High prevalence of TPO-Ab (+) is reported in subclinical hypothyroidism (SCH) [3,4]. Since both low-grade inflammations and hypothyroidism are known factors that are associated with hypertension [5,6], status of hypertension among SCH could act as a determinant factor of the association between TPO-Ab and SCH

  • While similar values of free T3 and T4 were found in SCH with and without hypertension, Table 2

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Summary

Introduction

Anti-thyroid peroxidase antibody (TPO-Ab) causes autoimmune thyroid disease [1] by bolstering thyroid inflammation [2]. High prevalence of TPO-Ab (+) is reported in subclinical hypothyroidism (SCH) [3,4]. Since both low-grade inflammations and hypothyroidism are known factors that are associated with hypertension [5,6], status of hypertension among SCH could act as a determinant factor of the association between TPO-Ab and SCH.

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