| ORIGINAL ARTICLE |
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| Year : 2016 | Volume
: 21
| Issue : 1 | Page : 85 |
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Effects of Vitamin D treatment on thyroid autoimmunity
Yasin Simsek1, Ilkay Cakir2, Mikail Yetmis2, Oguzhan Sitki Dizdar3, Osman Baspinar3, Ferhat Gokay1
1 Department of Endocrinology and Metabolism, Kayseri Training and Research Hospital, Kayseri, Turkey
2 Department of Internal Medicine, Bagcilar Training and Research Hospital, Istanbul, Turkey
3 Department of Internal Medicine, Kayseri Training and Research Hospital, Kayseri, Turkey
Correspondence Address:
Oguzhan Sitki Dizdar
Department of Internal Medicine, Kayseri Training and Research Hospital, Ataturk Avenue, Hastane Street, No: 78, Kocasinan, Kayseri
Turkey
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1735-1995.192501
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Background: Vitamin D was shown to be related to autoimmune thyroid diseases (AITDs) in the previous studies. We aimed to investigate the relationship between Vitamin D and thyroid autoimmunity. Materials and Methods: Eighty-two patients, diagnosed with AITD by the endocrinology outpatient clinic, were included in this prospective study. All of the patients had both AITD and Vitamin D deficiency, defined as serum values <20 ng/mL. They were randomly assigned into two groups. The first group included 46 patients and the second one included 36 patients. The first group was treated with Vitamin D for 1 month at 1000 IU/day. The second group served as the control group and was not treated with Vitamin D replacement. Serum thyroid-stimulating hormone, free T4 (fT4), thyroid peroxidase antibody (TPO-Ab), thyroglobulin antibody (TgAb), and Vitamin D levels were measured at the initiation of the study and again at 1 month in all patients. Results: Two groups were similar with regard to age, sex, and type of thyroid disease. Whereas TPO-Ab (before; 278.3 ± 218.4 IU/ml and after; 267.9 ± 200.7 IU/ml) and TgAb (before; 331.9 ± 268.1 IU/ml and after; 275.4 ± 187.3 IU/ml) levels were significantly decreased by the Vitamin D replacement therapy in group 1 (P = 0.02, P = 0.03, respectively), the evaluated parameters in the control group did not significantly change (P = 0.869, P = 0.530, respectively). In addition, thyroid function tests did not significantly change with Vitamin D replacement in two groups. Conclusion: Vitamin D deficiency may contribute to the pathogenesis of AITDs. Since supplementation of the Vitamin D decreased thyroid antibody titers in this study in Vitamin D deficient subjects, in the future Vitamin D may become a part of AITDs' treatment, especially in those with Vitamin D insufficiency. Further clinical and experimental studies are required to understand the effect of Vitamin D on AITD. |
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