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J.M.J.H.: methodology, data curation, software, reviewing and editing. 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% Mianserin hydrochloride CI = 1.28C1.84). In addition, pregnant women with positive thyroid antibodies have almost 2.5 times the risk of developing GDM (OR = 2.47; 95% CI = 1.57C3.89). Our results support that in pregnant women with normal fT4 levels, higher first trimester TSH level implies a higher risk of GDM. 0.001). In addition, the BMI at the beginning of pregnancy was higher in pregnant women with GDM (26.15 kg/m2 vs. 24.10 kg/m2, 0.001). In the group of women with GDM, the prevalence of overweight and obesity were much higher than in the group of pregnant women without GDM (33.5% vs. 26.3% and 27% vs. 15.8% respectively, 0.001). The prevalence of chronic hypertension was significantly higher in the group of women with GDM (3.5% vs. 0.7%). TSH levels were higher in women with GDM than in women without GDM (2.13 vs. 1.86). Moreover, the proportion of pregnant women with subclinical hyperthyroidism was slightly higher in the group of women with GDM (1.74 vs. 1.59). However, the proportion of pregnant women with subclinical hypothyroidism was significantly higher in the group of women with GDM (8.7% vs. 5.31%). 3.2. Bivariate Analysis After bivariate analysis (simple logistic regression), all Mianserin hydrochloride the variables included in the study showed significant association with GDM except parity (OR: 1.12; 95% CI 0.96C1.32) (Table 2). Table 2 Risk of gestational diabetes mellitus (bivariate analysis). Value= 0.422). To illustrate the values predicted by model 1, we determine the risk of GDM based on the first trimester TSH level of a medium pregnant women, 31 years old, with no family history of type 2 DM, normal BMI at the beginning of gestation, singleton pregnancy and without chronic hypertension. Physique 2 shows the result of applying Model 1 to this common patient, both with positive and negative anti-TPO antibodies. In this graph, we can see how the higher the TSH level, the greater the risk of GDM, and how women with positive antithyroid antibodies experienced a 2.47 times higher risk of developing gestational diabetes than women with negative antithyroid antibodies (adjusted OR = 2.38; 95% CI = 1.56C3.89). Open in a separate window Physique 2 Risk of gestational diabetes mellitus predicted by model 1 for any representative 31-year-old patient, with no family history of type 2 diabetes mellitus, BMI between 18.5 and 24.99 kg/m2, and without chronic hypertension. 3.3.2. Model 2 To clarify the risk associated with different first trimester TSH cut-off points, we repeated the multivariate logistic regression analysis but including TSH levels segmented into four groups described above. Table 4 shows a summary of this model (Model 2). Again, gravidity and recurrent abortion were removed from the model due to lack of statistical significance, and again there was no indication of a lack of fit for this second model as indicated by the Hosmer-Lemeshow test (= 0.111). Table 4 Multivariate logistic regression analysis including first trimester TSH as a categoric variable (Model 2). thead th rowspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” colspan=”1″ /th th rowspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” colspan=”1″ B /th th rowspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” colspan=”1″ Mianserin hydrochloride SE /th th rowspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” colspan=”1″ Wald /th th rowspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” colspan=”1″ df /th th rowspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” colspan=”1″ Sig. /th th rowspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” colspan=”1″ Adjusted OR /th th colspan=”2″ align=”center” valign=”middle” style=”border-top:solid thin;border-bottom:solid thin” rowspan=”1″ 95% CI by Adjusted OR /th th align=”center” valign=”middle” style=”border-bottom:solid thin” rowspan=”1″ colspan=”1″ Lower /th th align=”center” valign=”middle” style=”border-bottom:solid thin” rowspan=”1″ colspan=”1″ Upper /th /thead Age (years) 0.0790.00891.6061 0.0011.0821.0651.101 Family history of type 2 DM 0.9320.091105.6461 0.0012.5412.1273.035 Normal BMI (18.5C24.9 kg/m2) 66.0873 0.001 Underweight (BMI 18.5 kg/m2) 0.6270.2655.57810.0181.8721.1133.150 Overweight (BMI 25C29.9 kg/m2) 0.5970.09837.2171 0.0011.8171.5002.202 Obesity (BMI 30 kg/m2) 0.8030.10954.5601 0.0012.2331.8042.763 Chronic hypertension 1.2100.27719.0241 0.0013.3541.9475.779 Fetus number (multiple) 0.6580.17314.5441 0.0011.9311.3772.709 TSH between 0.13C2.49 mIU/L 30.3543 0.001 TSH 0.13 mIU/L (Subclinical hyperthyroidism) 0.1900.3030.39210.5311.2090.6672.191 TSH between 2.5 mIU/LC4.70 mIU/L 0.4290.09321.4221 0.0011.5361.2811.842 TSH 4.7 mIU/L (Subclinical hypothyroidism) 0.6150.15815.1721 0.0011.8491.3572.519 Thyroid-antibody positive 0.8970.23115.0581 0.0012.4531.5593.859 Constant ?5.6380.294368.3821 0.0010.004 Open in FLJ32792 a separate window B = coefficient; SE = standard error; df = degrees of freedom; Sig = significance; OR.