Vitamin D supplementation does not prevent the recurrence of Graves’ disease

Abstract

Recent literature has reported a higher prevalence of vitamin D deficiency among people with Graves' disease. No study has examined the effect of vitamin D supplementation on the clinical outcomes of Graves' disease. We aimed to evaluate whether daily vitamin D supplementation reduces Graves' disease recurrence. We enrolled 210 subjects with Graves' disease and vitamin D deficiency and followed them for at least one year after anti-thyroid drug (ATD) discontinuation. Among 210 individuals, 60 (29%) were amenable to taking vitamin D supplements, resulting in sufficient vitamin D levels (from 10.6 to 25.7 ng/mL), whereas the mean vitamin D level was 11.6 ng/mL in the 150 patients who did not take vitamin D supplements. The recurrence rate was similar in both groups (38% vs. 49%, P = 0.086). However, recurrence occurred earlier in the latter group (7 months vs. 5 months, P = 0.016). In the multivariate analysis, vitamin D levels and TSH-binding inhibitory immunoglobulin (TBII) titers at ATD discontinuation remained significant factors for recurrence. Vitamin D levels and TBII titers at ATD discontinuation exhibited a weak negative correlation (R = −0.143, P = 0.041). Vitamin D supplementation might have a protective effect against Graves' disease recurrence with a borderline significant recurrence rate reduction. Autoimmune thyroid diseases (AITDs), including Graves' disease and Hashimoto's thyroiditis, are the most common organ-specific autoimmune disorders 1. AITDs are caused by various environmental triggers, such as iodine, drugs, radiation, and infection in genetically predisposed individuals 2. AITDs are characterized by T-cell-mediated autoimmune diseases, and Graves' disease is primarily related to hyperactive humoural responses that lead to the production of stimulatory autoantibodies for the thyroid stimulating hormone (TSH) receptor 1. Vitamin D regulates bone metabolism and the homeostasis of calcium and phosphorus. The active form of vitamin D binds to the nuclear vitamin D receptor (VDR) and controls the expression of over 200 genes responsible for the regulation of cell proliferation, differentiation, and apoptosis in most tissues and cells, including immune cells 3. Non-skeletal actions of vitamin D have been studied over the past few decades, and evidence suggests that there is a relationship between vitamin D deficiency and various diseases, such as autoimmune diseases 4 , cardiovascular disease 5,6 , and cancer 5,7. Recent studies have reported that low vitamin D levels are prevalent in patients with Graves' disease. Kivity et al. observed a higher prevalence of vitamin D deficiency (defined as 25-hydroxyvitamin(OH)D < 10 ng/mL) in 22 Graves' disease patients compared with 98 healthy controls (64% vs. 30%, P < 0.01) 8. Yasuda et al. reported reduced levels of vitamin D in 26 Graves' disease patients compared to the levels in 46 controls (25(OH)D 3 levels of 14.4 ng/mL vs. 17.1 ng/mL, P < 0.05) 9. Two meta-analyses implicated vitamin D deficiency as a risk factor for Graves' disease 4,10 , although...

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