Frontiers in endocrinology · 2026
Association of 25(OH)D status with calcium metabolism, inflammation, and thyroid autoimmunity in patients with type 2 diabetes mellitus.
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Lv Nannan, Xiang Jianjian, Kuang Jinsong, Liu Fei, Cheng Lan, Yin Shanyu
Аннотация
INTRODUCTION: 25-hydroxyvitamin D [25(OH)D] deficiency is highly prevalent in type 2 diabetes mellitus (T2DM) and may contribute to immune and metabolic dysfunction. This study aimed to investigate the clinical associations of serum 25(OH)D levels with calcium metabolism, inflammation, thyroid function, and autoimmunity in patients with T2DM.
METHODS: This cross-sectional study enrolled 503 patients with T2DM, stratified into four groups based on 25(OH)D levels: severe deficiency (<10 ng/mL), moderate deficiency (10-20 ng/mL), insufficiency (20-30 ng/mL), and sufficiency (>30 ng/mL). Clinical and biochemical parameters were compared across groups and between thyroid autoantibody (TPOAb/TGAb) positive and negative subgroups. A multiple linear regression model identified independent predictors of 25(OH)D levels.
RESULTS: 25(OH)D deficiency (<20 ng/mL) was present in 83.7% of patients. Higher 25(OH)D levels correlated with lower PTH (P = 0.010) and higher calcium (P<0.001). hsCRP peaked in the moderate deficiency group (2.66 mg/L, P<0.001). T3 and fT3 peaked in the insufficiency group and were lowest in severe deficiency (P<0.05). TGAb positivity was associated with higher 25(OH)D levels (13.45 vs. 12.00 ng/mL, P = 0.008), whereas TPOAb positivity was associated with lower levels (11.90 vs. 12.85 ng/mL, P<0.001). No significant associations were found with HbA1c, BMI, TSH, or bone markers.
CONCLUSION: In patients with T2DM, 25(OH)D deficiency is highly prevalent and independently associated with altered calcium-PTH homeostasis, elevated inflammation, and suppressed T3 levels. The opposing relationships with TGAb and TPOAb suggest complex interactions between vitamin D and thyroid autoimmunity in this population.
METHODS: This cross-sectional study enrolled 503 patients with T2DM, stratified into four groups based on 25(OH)D levels: severe deficiency (<10 ng/mL), moderate deficiency (10-20 ng/mL), insufficiency (20-30 ng/mL), and sufficiency (>30 ng/mL). Clinical and biochemical parameters were compared across groups and between thyroid autoantibody (TPOAb/TGAb) positive and negative subgroups. A multiple linear regression model identified independent predictors of 25(OH)D levels.
RESULTS: 25(OH)D deficiency (<20 ng/mL) was present in 83.7% of patients. Higher 25(OH)D levels correlated with lower PTH (P = 0.010) and higher calcium (P<0.001). hsCRP peaked in the moderate deficiency group (2.66 mg/L, P<0.001). T3 and fT3 peaked in the insufficiency group and were lowest in severe deficiency (P<0.05). TGAb positivity was associated with higher 25(OH)D levels (13.45 vs. 12.00 ng/mL, P = 0.008), whereas TPOAb positivity was associated with lower levels (11.90 vs. 12.85 ng/mL, P<0.001). No significant associations were found with HbA1c, BMI, TSH, or bone markers.
CONCLUSION: In patients with T2DM, 25(OH)D deficiency is highly prevalent and independently associated with altered calcium-PTH homeostasis, elevated inflammation, and suppressed T3 levels. The opposing relationships with TGAb and TPOAb suggest complex interactions between vitamin D and thyroid autoimmunity in this population.