Autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematous, occur when the body attacks its own tissue because it cannot differentiate between self and non-self. This is mainly through deregulation of the immune system. Vitamin D has been known to play a critical role in bone mineralization and bone health. Activated vitamin D is a hormone that plays a role in calcium and phosphorus absorption.1 More recently, studies have shown that vitamin D also has receptors in the bone marrow and thymus, where the immune system develops and matures.3,4 T cells in the thymus, once activated, increase vitamin D receptors fivefold.5 Activated vitamin D has been shown to inhibit interleukin 6 (IL-6), an inflammatory cytokine.1 The Iowa Women’s Health Study showed rheumatoid arthritis disease risk and vitamin D intake were inversely related.6 Another study has shown disability and RA to be inversely related to vitamin D intake. Thus, based on the studies reviewed regarding vitamin D and RA, it’s important to keep vitamin D at a sufficient level for RA patients.
In our federally qualified health center (FQHC), most of the patients are underinsured or uninsured; thus, most patients with RA are unable to follow up with private rheumatologists.
The question addressed in this quality-improvement project was to ascertain whether patients with RA at our FQHC are getting their vitamin D checked at least once a year and where their levels fall.
A retrospective chart review was performed. Patients were identified using clinic encounters with an associated ICD-9 code for RA (714.0) in the EMR at our FQHC, from Jan. 1, 2012, through Dec. 31, 2014. Charts were searched for lab work results and/or documentation of a vitamin D order during the past year (2014). The level of vitamin D was identified in one of four categories: deficient (<20 ng/mL), insufficient (20–30 ng/mL), sufficient (30–100 ng/mL) and toxic (>100 ng/mL).
A total of 104 patients with RA were identified, of which 91 were included. The 13 excluded did not have encounters or lab work performed in 2014. Of those included, 28.5% of patients had their vitamin D checked at least once during the year. Two patients had documentations that indicated vitamin D deficiency, but lab work with the exact numbers was not available. Of those who had their vitamin D checked, 30.7% had levels that were deficient, 34.6% had insufficient levels and 26.9% had sufficient levels. No patient had a toxic level of vitamin D.
RA is the most common autoimmune disease, and it is a chronic inflammatory process that affects the joints most often, but RA also has extra-articular manifestations.8 According to the ACR Classification Criteria for Rheumatic Diseases, the criteria for RA diagnosis include morning stiffness of more than one hour on most mornings for at least six weeks; arthritis and soft tissue swelling of more than three of the 14 joints, present for least six weeks; positive rheumatoid factor and/or anti-cyclic citrullinated peptide, elevated C-reactive protein or erythrocyte sedimentation rate.2,10 Core measures in assessing RA are primarily to evaluate joint inflammation and the rheumatologist’s global assessment.
Vitamin D plays an essential role in calcium absorption, but also has an immunomodulatory role through vitamin D receptors. Activated vitamin D inhibits the expression of IL-6, thus decreasing inflammation.
The etiology of RA is still unknown, but progress in the pathophysiology of RA has shown that increased production of tumor necrosis factor (TNF-alpha) is a key protein involved in synovial inflammation and joint destruction. Some studies have shown that increased production of TNF-alpha plays a key role in the synovial inflammation and joint destruction. TNF-alpha activates IL-6, which causes inflammation and joint destruction. Another study shows TNF-alpha, IL-1 and IL-6 through their inflammatory effects cause osteoclast activation in RA patients. IL-6 stimulates Th17 cells and results in inflammation and joint destruction. Interestingly, studies have shown that activated vitamin D inhibits the expression of IL-6.1 Additionally, long-term steroid treatment and disease-modifying anti-rheumatic drugs can cause a decrease in bone formation and weaken bones overall, thus increasing the risk of fracture in RA patients.11