Anaraki Parichehr Vahabi, Aminorroaya Ashraf, Amini Massoud, Feizi Awat, Iraj Bijan, Tabatabaei Azamosadat
Isfahan Endocrine and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Department of Biostatistics and Epidemiology, School of Public Health, Isfahan University of Medical Sciences, Isfahan, Iran.
J Res Med Sci. 2017 Jan 27;22:5. doi: 10.4103/1735-1995.199090. eCollection 2017.
The aim of the current trial was to investigate the effect of Vitamin D treatment on metabolic markers in people with Vitamin D deficiency and thyroid autoimmunity.
In this double-blind, randomized, placebo-controlled clinical trial, 65 Vitamin D deficient euthyroid or hypothyroid patients with positive TPO-Ab were enrolled. They randomly allocated into two groups to receive oral Vitamin D50000 IU weekly) and placebo for 12 weeks. Serum concentration of calcium, phosphorus, albumin, C-reactive protein, blood urea nitrogen, creatinine, glycated hemoglobin (HbA1c), insulin, fasting plasma glucose (FPG), triglyceride (TG), total cholesterol, and high-density lipoprotein were measured in both groups before and after the trial. Homeostasis model assessment estimates of beta cell function (HOMA-B) and HOMA-insulin resistance (HOMA-IR) were calculated before and after trial in both groups.
Thirty-three and thirty-two participants were allocated to Vitamin D-treated and placebo-treated groups, respectively. Mean (standard error) level of Vitamin D increased significantly in Vitamin D-treated group (45.53 [1.84] ng/mL vs. 12.76 [0.74] ng/mL, = 0.001). The mean of HbA1c and insulin was increased significantly both in Vitamin D-treated and placebo-treated groups ( < 0.05). Other variables did not meet a significant change after trial ( = NS). In between-group comparison, there was not any significant difference between Vitamin D-treated and placebo-treated groups regarding measures of HOMA-B, HOMA-IR, FPG, HbA1c, and TG ( = NS).
Our findings showed that weekly 50000 IU oral Vitamin D3 for 12 weeks did not improve metabolic markers, IR, or insulin secretion in Vitamin D deficient patients with Hashimoto thyroiditis.
本试验旨在研究维生素D治疗对维生素D缺乏和甲状腺自身免疫患者代谢指标的影响。
在这项双盲、随机、安慰剂对照临床试验中,纳入了65例维生素D缺乏的甲状腺功能正常或减退且TPO-Ab阳性的患者。他们被随机分为两组,分别接受每周口服50000 IU维生素D和安慰剂,为期12周。在试验前后,两组均测量血清钙、磷、白蛋白、C反应蛋白、血尿素氮、肌酐、糖化血红蛋白(HbA1c)、胰岛素、空腹血糖(FPG)、甘油三酯(TG)、总胆固醇和高密度脂蛋白。在试验前后,两组均计算β细胞功能的稳态模型评估估计值(HOMA-B)和HOMA胰岛素抵抗(HOMA-IR)。
分别有33名和32名参与者被分配到维生素D治疗组和安慰剂治疗组。维生素D治疗组的维生素D平均(标准误)水平显著升高(45.53 [1.84] ng/mL对12.76 [0.74] ng/mL,P = 0.001)。维生素D治疗组和安慰剂治疗组的HbA1c和胰岛素平均值均显著升高(P < 0.05)。试验后其他变量未出现显著变化(P = 无显著性差异)。在组间比较中,维生素D治疗组和安慰剂治疗组在HOMA-B、HOMA-IR、FPG、HbA1c和TG测量方面没有任何显著差异(P = 无显著性差异)。
我们的研究结果表明,对于患有桥本甲状腺炎的维生素D缺乏患者,每周口服50000 IU维生素D3,持续12周,并未改善代谢指标、胰岛素抵抗或胰岛素分泌。