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Objective  While vitamin D regulates immune cells, little is known about it in autoimmune Addison’s disease (AAD). We investigated the vitamin D status in AAD patients from five European populations to assess its deficiency. In addition, we studied two case-control cohorts for vitamin D metabolism and pathway genes.    Design  Cross-sectional study.    Methods  A total of 1028 patients with AAD from Germany ( n  = 239), Italy ( n  = 328), Norway ( n  = 378), UK ( n  = 44) and Poland ( n  = 39) and 679 controls from Germany ( n  = 301) and Norway ( n  = 378) were studied for 25(OH)D 3  (primary objective).  Secondary objectives (1,25(OH) 2 D 3  and pathway genes) were examined in case-controls from Germany and Norway correlating 25(OH)D 3  and single nucleotide polymorphisms within genes encoding the vitamin D receptor (VDR), 1-α-hydroxylase (CYP27B1), 25-hydroxylase (CYP2R1), 24-hydroxylase (CYP24A1) and vitamin D binding protein (GC/DBP).    Results  Vitamin D deficiency (25(OH)D 3  10–20 ng/mL) was highly prevalent in AAD patients (34–57%), 5–22% were severely deficient ( 30 ng/mL). Lower 25(OH)D 3  and 1,25(OH) 2 D 3  levels were observed both in Norwegian and German AAD ( P  = 0.03/0.003 and  P  = 1 × 10 -5 /&lt; 1 × 10 -7  ,  respectively) the former was associated with  CYP2R1  (rs1553006) genotype G. Whereas controls achieved sufficient median 25(OH)D 3  in summers (21.4 to 21.9 ng/mL), AAD patients remained largely deficient (18.0 to 21.2 ng/mL) and synthesize less 1,25(OH) 2 D 3 .    Conclusion  Vitamin D deficiency and insufficiency are highly prevalent in AAD patients. The vitamin D status of AAD may be influenced by genetic factors and suggests individual vitamin D requirements throughout the year.

Vitamin D status and pathway genes in five European autoimmune Addison’s disease cohorts