Ming-Jun Hu1, Chi Zhang1, Ling Liang1, Sheng-Ying Wang2, Xu-Cai Zheng2, Qian Zhang1, Chun-Xiao Jiang1, Qi Zhong1, Fen Huang1. 1. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China. 2. Department of Head and Neck, Breast Surgery, Anhui Provincial Cancer Hospital, West Branch of Anhui Provincial Hospital, First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, China.
Abstract
BACKGROUND: This study was to investigate the association of fasting serum glucose (FSG), thyroid-stimulating hormone (TSH), and thyroid hormones with papillary thyroid cancer (PTC). METHODS: A total of 649 participants were included in this case-control study. The associations of FSG, TSH, free triiodothyronine (FT3) and free thyroxine (FT4) with PTC were estimated using an unconditional logistic regression. RESULTS: Compared with the lowest quintile of TSH levels, odds ratios (ORs) and 95% confidence intervals (CIs) for association between PTC risk and highest quintile of TSH levels were 1.67 (95% CI, 0.99-2.83). However, this risk correlation was more significant in PTC cases with ≤1.0 cm tumor size (adjusted OR, 1.95; 95% CI, 1.08-3.54; adjusted P-trend, 0.05). The PTC risk was also inversely associated with the serum FT3 level in all participants (adjusted P-trend, 0.001), but positively associated with the serum FT4 (adjusted P-trend, 0.001) and FSG (adjusted P-trend, 0.01) levels. Among the participants without diabetes, the individuals with high FSG levels and abnormal TSH concentration had an increased PTC risk (adjusted OR, 3.38; 95% CI, 1.78-6.42). CONCLUSION: The current study provides evidence for the association of FSG, TSH, and thyroid hormones (FT3 and FT4) with PTC risk. However, larger relative studies are needed.
BACKGROUND: This study was to investigate the association of fasting serum glucose (FSG), thyroid-stimulating hormone (TSH), and thyroid hormones with papillary thyroid cancer (PTC). METHODS: A total of 649 participants were included in this case-control study. The associations of FSG, TSH, free triiodothyronine (FT3) and free thyroxine (FT4) with PTC were estimated using an unconditional logistic regression. RESULTS: Compared with the lowest quintile of TSH levels, odds ratios (ORs) and 95% confidence intervals (CIs) for association between PTC risk and highest quintile of TSH levels were 1.67 (95% CI, 0.99-2.83). However, this risk correlation was more significant in PTC cases with ≤1.0 cm tumor size (adjusted OR, 1.95; 95% CI, 1.08-3.54; adjusted P-trend, 0.05). The PTC risk was also inversely associated with the serum FT3 level in all participants (adjusted P-trend, 0.001), but positively associated with the serum FT4 (adjusted P-trend, 0.001) and FSG (adjusted P-trend, 0.01) levels. Among the participants without diabetes, the individuals with high FSG levels and abnormal TSH concentration had an increased PTC risk (adjusted OR, 3.38; 95% CI, 1.78-6.42). CONCLUSION: The current study provides evidence for the association of FSG, TSH, and thyroid hormones (FT3 and FT4) with PTC risk. However, larger relative studies are needed.