High First Trimester Levels of TSH as an Independent Risk Factor for Gestational Diabetes Mellitus: A Retrospective Cohort Study

Abstract

Although numerous articles have found an association between alterations in thyroid function and the risk of gestational diabetes mellitus (GDM), other studies have failed to demonstrate this association. This may be due to the different cut-off points used to define subclinical hypothyroidism. We aim to clarify the role of thyroid stimulating hormone (TSH) level in GDM within pregnant women with normal free thyroxine (fT4) levels. This retrospective cohort study was performed in 6775 pregnant women. The association between TSH and GDM was assessed by bivariate and multivariate logistic regression. Pregnant women with subclinical hypothyroidism are at significantly greater risk for GDM when compared with euthyroid pregnant women (OR = 1.85; 95% CI = 1.36–2.52). We have also observed that TSH levels increase the risk of GDM within euthyroid pregnant women, since the TSH levels between 2.5 and 4.71 showed a higher risk of GDM than those whose TSH levels are between 0.31 and 2.49 (OR = 1.54; 95% CI = 1.28–1.84). In addition, pregnant women with positive thyroid antibodies have almost 2.5 times the risk of developing GDM (OR = 2.47; 95% CI = 1.57–3.89). Our results support that in pregnant women with normal fT4 levels, higher first trimester TSH level implies a higher risk of GDM.

Thyroid dysfunction during gestation and gestational diabetes mellitus: a complex relationship

“…Several studies evaluated whether the presence of SCH during pregnancy was predictive of development of GDM, as summarized in Table 1. Some studies showed a higher prevalence of SCH among women with GDM when compared with controls [139][140][141][142][143], while other studies [144][145][146][147][148] did not find this association. The varying results of these studies should be interpreted in light of differences in study design, different criteria for diagnosing SCH and GDM during pregnancy and timing of evaluation.…”

“…The majority of data come from retrospective cohort studies [139,[142][143][144][145]149], while other studies [140,147,150,151] were designed as case controls (comparing a group of women with GDM and a control of healthy pregnant women). Some authors used a TSH cutoff lower than nonpregnant normal value [143,147,150], while other used trimester-specific ranges [139,142,144,149,151].…”

“…The majority of data come from retrospective cohort studies [139,[142][143][144][145]149], while other studies [140,147,150,151] were designed as case controls (comparing a group of women with GDM and a control of healthy pregnant women). Some authors used a TSH cutoff lower than nonpregnant normal value [143,147,150], while other used trimester-specific ranges [139,142,144,149,151]. In addition, timing of evaluation was not uniform among studies: some studies evaluated thyroid function parameters during the first trimester [139,142], others during second trimester (usually at the same time of OGTT) [140,150], or during the third trimester [144,151].…”

Maternal pre-pregnancy obesity modifies the association between first-trimester thyroid hormone sensitivity and gestational Diabetes Mellitus: a retrospective study from Northern China

“…As a common obstetric metabolic disorder, GDM poses both short- and long-term threats to maternal and child health [ 11 , 24 ]. So far, contradictory conclusions have been drawn to illustrate the causality between thyroid function and the occurrence of GDM [ 11 , 25 , 26 ]. For example, both hypothyroidism (overt/subclinical/isolated) and hyperthyroidism have been reported to be associated with GDM [ 9 , 10 , 27 ].…”

“…For example, both hypothyroidism (overt/subclinical/isolated) and hyperthyroidism have been reported to be associated with GDM [ 9 , 10 , 27 ]. Some studies have indicated adverse relationships of FT4, TSH or both with GDM under euthyroid status [ 4 , 11 , 25 ], whereas other studies indicated contrary relationships [ 7 , 11 , 25 ]. These inconsistencies indicated complex relationships between the thyroid system and glucose homeostasis, which could hardly be explained by a single parameter.…”