Objective To investigate whether vitamin D deficiency is involved in Graves disease (GD) occurrence and development and whether vitamin D supplementation can improve the efficacy of ¹³¹I in GD treatment.

Methods A retrospective analysis was conducted on 200 GD patients in the nuclear medicine department of Qingdao Municipal Hospital from January 2017 to June 2018. The study included 60 males and 140 females aged 13–78 (42.1±12.1) years old. Two hundred patients with GD were divided into two groups, namely, GD1 group (100 cases) and GD2 group (100 cases) by random remainder grouping method, and 200 normal healthy people were selected to serve as the control. The levels of thyroid stimulating hormone (TSH), free triiodothyronine (FT₃), free thyroxine (FT₄), thyrotrophin receptor antibody (TRAb), thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb), and 25-(OH)D₃ in GD group and control group were detected before treatment. After 12 months, the levels of TRAb, TgAb, TPOAb and 25-(OH)D₃ were reexamined. Two independent samples were compared by t-test. Paired samples were compared by t-test. Spearman rank correlation analysis was used. The effective rates of GD1 and GD2 groups were compared by χ² test.

Results Before treatment, the level of 25-(OH)D₃ in GD group was (29.32±12.43) nmol/L, and that of normal control group was (51.46±25.92) nmol/L. The vitamin D level of GD group was lower than that of normal control group, and the difference was statistically significant (t=−18.106, P<0.01). Serum 25-(OH)D₃ level was negatively correlated with TRAb, FT₃, FT₄, TgAb, and TPOAb levels (r=−0.688~−0.219, all P<0.05), and positively correlated with TSH level (r=0.259, P<0.05). Twelve months after treatment, the serum 25-(OH)D₃ level in GD2 group (44.68±17.45) nmol/L was higher than that in GD1 group (29.86±12.78) nmol/L, and the difference between the two groups before and after treatment was statistically significant (t=−7.920, P<0.01). The levels of TRAb, TgAb, and TPOAb in GD2 group were (1.96±1.52) IU/L, (106.78±76.37) IU/mL, and (59.74±37.26) IU/mL, while in GD1 group were (3.12±1.80) IU/L, (146.33±103.81) IU/mL, and (100.41±63.11) IU/mL, respectively. The difference between the two groups before and after treatment was statistically significant (t=−8.767, −4.106, −7.259, all P<0.01). Twelve months after treatment, the effective rate of GD1 group was 63% (63/100), whereas that of GD2 group was 78% (78/100). The difference between the two groups was statistically significant (χ²=5.409, P=0.020).

Conclusion Vitamin D deficiency may be involved in GD development. Vitamin D supplementation may improve the efficacy of ¹³¹I in GD treatment.