Vitamin D status in a population of scleroderma patients

Background: Epidemiological evidence indicates a significant association between vitamin D deficiency and an increased incidence of several autoimmune diseases. Low vitamin D levels have also been reported in patients with systemic sclerosis (SSc), but the number of studies is limited with conflicting data. Objective: To investigate vitamin D status in a group of systemic sclerosis (SSc) patients and establish connections with markers of SSc disease activity and severity score, clinical and imunologic features. Method: 50 scleroderma patients were evaluated during June 2010–June 2012 in Internal Medicine and Rheumatology Department of Sf. Maria Hospital, Bucharest, Romania. All patients gave their informed consent for all procedures, which were carried out with the local ethics committee's approval. We performed a complete evaluation of all patients following: MEDS evaluation sheets (cutaneous, musculoarticular, gastrointestinal, cardiac, pulmonary or renal involvement, inflammatory markers, autoantibodies, complement, capilaroscopy), DXA evaluation of osteoporosis, disease activity was evaluated with the Disease Activity Score (DAS) according to the European Scleroderma Study Group guidelines, HAQ (Health assessment questionnaires) have been also completed. Vitamin D was measured with the RIA Diasorin kit or expressed as“RIA Diasorin equivalent”. According to current recommendations, vitamin D concentrations <30 ng/ml were considered as indicating insufficiency, while values <10 ng/ml were classified as deficiency. Results: 86.8% of all patients were women, 52.9% had diffuse skin involvement, mean age 55.65 (SD 12.45) years, medium disease duration 11.7 years (SD 6.9), mean Rodnan 9.59 (SD 5.9), mean activity score = 3.43 (2.14), mean Medsger 6.8 (SD 3.15), mean HAQ 0.8 (SD 0.6); mean sPAP was 33.4 (SD 13.94), mean DLCO 62.19 (SD 19.15); 40% had osteoporosis. Most frequent gastrointestinal involvement was esophageal 84.3%, most frequent joint involvement was joint contractures (45.1%), 64.7% had muscle weakness. Mean vitamin D was 17.06 ng/ml (SD9.13). Only 3 patients had optimal levels of 25(OH)2 D; most of the patients had an insufficient (70%) or deficient (24%) level. Although levels below normal were found in most of the patients significant correlations of vitamin D status were found only in muscle weakness (p = 0.000), muscle atrophy (p = 0.02), gastrointestinal involvement (p = 0.005) and the use of immunosuppressive drugs (p = 0.02). Conclusions: Vitamin D deficiency and insufficiency were no mather of subtype, disease duration, visceral involvement and vitamin D supplementation. This suggests that common vitamin D supplementation does not correct the deficiency in SSc patients, and that a higher dose is probably needed. We are aware of the limitations of the study that are: small group, lack of control group and the fact that measurements of vitamin D were not done in the same period of the year. Given the most recent findings, we consider further research would be clinically important to elucidate the causes of hypovitaminosis D in SSc, its relevance to disease progression, its influence on immune functions and the potential effects of supplementation.