Improve RA Care with Vitamin D

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Background

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.

Dr. Fahima

Objective

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.

Method

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).

Results

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.

Discussion

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