Background Vitamin D (vit D) is an immunoregulatory hormone which seems to mediate immune tolerance. Several studies have suggested that vit D deficiency may be related to increased disease activity in patients with systemic lupus erythematosus (SLE).
Objectives To analyze 25-hydroxyvitamin D (25-OHD) levels in a cohort of patients with SLE and to investigate their relationship with clinical, analytical, immunological and densitometric parameters.
Methods Prospective study including patients with SLE (according to SLICC criteria 2013) performed in an Academic Hospital with a referral area of 800.000 inhabitants. 152 patients with SLE were included (138 women [46 postmenopausal]/14 men) with a mean age of 46±12 years (range: 20–75). Clinical parameters (including risk factors for osteoporosis, presence of skeletal fractures, treatment with glucocorticoids (GCC) as well as SLE involvement including haematologic, renal, neurological and skin), biochemical determinations (including 25-OHD, parathormone (PTH)), immunological (ANA, DNA and complement) and SLE activity and severity (assessed by SLEDAI and SLICC index) were assessed in all patients. Bone mineral density was performed by DXA (at lumbar spine and proximal femur). Vit D deficiency was defined as 25-OHD values under 20 ng/mL. Low bone mass was considered as T or Z scale <-1 SD; and osteoporosis as T <-2.5 SD [age>50 years] or Z <-2 SD [age <50 years]. The study was approved by the Clinical Research Ethics Committee and all patients provided informed consent to participate. Statistical analysis was performed by SPSS.20.
Results The mean values of 25-OHD were 19.8±11.4 (range, 4.2–66.6). 87.5% of patients had 25-OHD levels below 30 ng/mL, 61.2% below 20 ng/mL and 15.1% below 10 ng/mL. The lowest values were in winter (80%) and spring (64.3%). 42.8% of patients received vitamin D supplements. 56.5% of patients had low bone mass (T or Z scale < -1 SD), and 15.8% had osteoporosis. Levels of 25-OHD showed no correlation with SLE disease activity (complement, Ac antiDNAds, SLICC/SLEDAI) neither with bone mass by DXA. Patients with low bone mass (T or Z <-1 SD scale) were older (at the time of inclusion and age of SLE diagnosis), had higher SLICC and lower complement levels whereas no differences were observed in SLEDAI and 25-OHD values. 37.5% of the patients were treated with GCC. Patients without GCC treatment had higher prevalence of vit D deficiency (73.9% vs. 55.6%, p=0.034) compared to patients with GCC treatment.
Conclusions 61.2% of patients with SLE have 25-OHD deficiency, which is more frequent in winter and spring, and mostly in those patients without GCC treatment. 25-OHD values showed no correlation with the disease activity and damage. However, patients with low bone mass had higher SLICC and hypocomplementemia. Thus, our results suggest the need to perform clinical guidelines to assess bone mass and bone metabolism in this clinical condition. Additionally, we recommend quantifying vit D levels in winter/spring and don't forget to assess those patients without GCC treatment.
Disclosure of Interest None declared
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