# Effects of vitamin D replacement combined with Graves’ disease therapy: a retrospective cohort study

## TL;DR

This study examined whether adding vitamin D to standard treatment for Graves’ disease improves thyroid hormone levels, but found no significant effect from vitamin D supplementation.

## Contribution

The study is one of the first to investigate vitamin D replacement therapy in Graves’ disease patients alongside standard treatment.

## Key findings

- GD patients had significantly lower baseline vitamin D levels compared to healthy controls.
- Vitamin D replacement significantly increased serum VitD levels after three months, but had no significant effect on thyroid hormone levels.
- No significant difference in thyroid receptor antibodies was observed between groups.

## Abstract

In Graves’ disease (GD), an autoimmune disease, antibodies targeting the thyroid stimulating hormone (TSH) receptor cause the production of excessive amounts of thyroid hormone. A significant association was reported between low 25-hydroxy [25(OH)] vitamin D3 (VitD) levels and various autoimmune disorders. Therefore, this study aimed to investigate the effects of VitD deficiency and replacement therapy on laboratory and clinical parameters in GD patients.

Forty GD patients and 37 healthy controls were included in this study. The GD patients were divided into two groups: the nonreplacement group was administered antithyroid treatment only (n = 18), and the replacement group was administered antithyroid treatment + VitD replacement (n = 22). Clinical and laboratory data of all the participants were compared at the time of diagnosis and 3 months after treatment.

Baseline serum VitD levels in the GD patients were significantly lower than the baseline serum VitD levels in the control group (16.1 ± 9.9 vs. 22.2 ± 8.5 ng/mL, p < 0.005). A significant improvement was observed in the serum VitD levels in the replacement group after three months (14.6 ± 8.3 vs. 40.4 ± 17.2 ng/mL, p < 0.001). A significant increase in the serum TSH levels and a significant decrease in the serum free triiodothyronine (fT3) and free thyroxine (fT4) levels were observed in the replacement and nonreplacement groups at the end of three months. However, there was no significant effect of VitD replacement on the serum TSH, fT3, and fT4 levels. There was no difference in the serum thyroid receptor antibodies levels between the replacement and nonreplacement groups.

Although VitD deficiency was detected in the GD patients, there was no significant accelerating effect of VitD replacement on the thyroid hormone levels. These results need to be confirmed with studies that have larger patient numbers and longer follow-up periods.