Background/Purpose:

Unlike other autoimmune diseases in which an association with vitamin D deficiency has been established, the role of vitamin D in Sjogren’s syndrome has been much less studied and data are conflicting. Vitamin D deficiency may contribute to B cell hyperactivity and autoantibody production in SLE. Given some autoantibody, genetic, and clinical similarities between Sjogren’s syndrome and SLE, we hypothesized that vitamin D levels would be lower in patients with primary Sjogren’s syndrome (SS) compared to patients with sicca symptoms who do not meet SS criteria and healthy controls. We studied a well characterized cohort of primary SS patients for prevalence of vitamin D deficiency as well as for the relationship between vitamin D levels and autoantibody positivity. 

Methods:

Samples from 70 patients who met the 2002 American-European Consensus Group classification criteria for primary SS, 78 patients with sicca symptoms who did not meet SS criteria, and 148 healthy controls matched for age, gender and race were studied. Participants were enrolled and evaluated as part of the multidisciplinary Oklahoma Sjogren’s Syndrome Cohort. Clinical and laboratory data, including 25(OH)D levels, presence of sicca symptoms, anti-nuclear antibody (ANA) status, anti-SSA/Ro status, and anti-SSB/La status were utilized in the study.

Results:

Mean age for primary SS patients and patients with sicca symptoms who did not meet SS criteria was 51.8 years and mean age for controls was 51.9 years. Eighty-nine percent of the population studied was Caucasian. The prevalence of Vitamin D deficiency (as defined by recommendations put forth by the Institute of Medicine) in patients with primary SS and patients with sicca symptoms who did not meet SS criteria was 16.9% whereas prevalence of Vitamin D deficiency in matched healthy controls was 52.7%.  Patients with primary SS had higher 25(OH)D levels when compared to matched healthy controls (28.1 ng/mL vs. 19.1 ng/mL; p <0.0001). Patient with sicca symptoms who did not meet SS criteria also had higher vitamin D levels when compared to matched healthy controls (30.1 ng/mL vs. 22.5 ng/mL; p <0.0001). No difference in 25(OH)D levels between patients with primary SS and patients with sicca symptoms who did not meet SS criteria (p=0.78) was detected. No difference in the 25(OH)D levels of anti-SSA/Ro positive vs. anti-SSA/Ro negative patients (p=0.22) nor in the 25(OH)D levels of anti-SSB/La positive vs. anti-SSB/La negative patients (p=0.42) were detected. We also detected no difference in the 25(OH)D levels of ANA positive vs. ANA negative patients (p=0.96).

Conclusion:

In our well characterized cohort, patients with either primary SS or sicca symptoms who did not meet SS criteria had significantly higher vitamin D levels than matched healthy controls. These findings are similar to those of the few studies conducted in the past, which did not show a lower vitamin D level in patients with primary SS as compared to controls, and suggest that vitamin D deficiency does not contribute to the pathogenesis of Sjogren’s syndrome. Furthermore, these results also suggest that vitamin D deficiency does not contribute to autoantibody production as it may in SLE.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/vitamin-d-in-sjogrens-syndrome/