Objectives: A role for vitamin D in the pathogenesis of autoimmune and inflammatory diseases is emerging. We undertook an audit of 25-hydroxyvitamin D (25OHD) investigation and treatment in rheumatology outpatients.
Methods: Serum 25OHD requests were matched to electronic medical records from rheumatology and metabolic bone clinics (April 2006-March 2007). Data were analysed separately for two groups, 'Documented osteoporosis/osteopaenia' (Group 1) and 'General rheumatology outpatients' (Group 2, sub-divided by diagnosis). Hypovitaminosis D was defined by 25OHD levels <50 nmol/l. Values were compared with healthy adults to calculate geometric z-scores.
Results: A total of 263 patients were included (Group 1, n =122; Group 2, n = 141) with an overall median 25OHD of 44 nmol/l. The 25OHD level among general rheumatology patients (median 39 nmol/l, mean z score -1.2, was statistically significantly lower than among osteoporotic/osteopaenic patients (median 49 nmol/l, mean z score of -0.9, p < 0.05 for the difference). 25OHD was lower in inflammatory arthritis and chronic pain/fibromyalgiathan in other groups. Prescribing was recorded in 100 in Group 1 (of whom 95% were prescribed calcium/800 IU cholecalciferol) and 83 in Group 2 (91% calcium/800 IU). Only 31% of the patients with 25OHD <50 nmol/l would have been identified using general guidelines for screening patients at 'high risk' of hypovitaminosis D.
Conclusions: Improved guidelines for managing hypovitaminosis D in rheumatology patients are needed. We found a high prevalence of hypovitaminosis D among secondary care patients in rheumatology and widespread supplementation with 800 IU cholecalciferol. Substantially reduced levels of serum 25OHD were identified among patients with inflammatory arthritis and chronic pain.
Inadequate levels of serum 25-hydroxyvitamin D (25OHD) are not only detrimental to musculoskeletal health and calcium homeostasis but may also have a role in immunopathology. Understanding of the role of the active vitamin D hormone (1, 25-hydroxyvitamin D) in immunodysregulation via down-regulation of Th1 immunity is increasing. Indeed, it is even hypothesized that the latitude-related prevalence of autoimmune diseases is at least in part due to regional differences in the prevalence of hypovitaminosis D. Recently, 25OHD levels were found to inversely correlate with disease activity scores in RA, inflammatory arthritis and SLE but little has been published regarding the assessment and management of 25OHD (the stored and readily assayed metabolite) in routine clinical practice. Just as understanding of cardiovascular risk and its profiling in rheumatological practice has increased, so rheumatologists are ideally placed to assess and manage hypovitaminosis D in the outpatient clinic setting. We wished to audit patterns of investigation and treatment of hypovitaminosis D (by serum 25OHD assay) in general rheumatology patients and osteoporotic patients among local physicians.
For rheumatology patients, there is a dearth of formal guidance on investigation for hypovitaminosis D levels in high-risk individuals (with no specific recommendations to guide routine rheumatological practice). However, from a general medical perspective, a recent consensus position statement (CSP; from Australia) identified high-risk groups in whom a serum 25OHD assay should be performed. Here we assess whether these guidelines would adequately identify hypovitaminosis D in rheumatology patients.
For patients with low bone mass, we audited our vitamin D treatment against existing UK clinical guidelines. However, it is increasingly clear that there is no 'One size fits all' approach to supplementing or treating osteoporotic patients, and we sought to investigate whether new guidelines are needed.