Vitamin D Deficiency Linked With High Inflammation and BMD Decline in Patients With SLE

Hypovitaminosis D, or too little vitamin D, is fairly common in patients with systemic lupus erythematosus (SLE) and is linked with high inflammatory activity and decline in bone mineral density (BMD), according to study findings published in Lupus Science and Medicine.

Status of vitamin D was not linked with patient age or disease course.

Vitamin D deficiency in patients with SLE is known to be linked with decreased BMD, but scientific information on the relationships between vitamin D level and markers of bone turnover, disease duration, and glucocorticoid (GC) therapy is limited.

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Researchers aimed to ascertain vitamin D levels in patients with SLE and analyze their relationship to BMD and the disease course. They hypothesized that vitamin D deficiency and insufficiency is widespread among patients with SLE and might be linked with long-term use of GCs and sunscreens, kidney damage, vitamin D antibody presence, and more.

A total of 101 patients with SLE and 29 people in the control group were included in the study.

Study participants were tested for vitamin D level, erythrocyte sedimentation rate (ESR), C reactive protein (CRP), IL-6, osteocalcin (OC), and collagen type I C-terminal telopeptide (CTX), and dual-energy X-ray absorptiometry was performed to evaluate BMD in the lumbar spine and hip.

The mean (SD) serum vitamin D level was 18.98 (0.88) ng/mL, and women possessed 25.42% lower vitamin D levels than men (P < .05). No correlation was observed between vitamin D levels and cumulative dose of GCs (r = ­­–0.26) and serum inflammatory markers, especially CRP (r =­–0.39). IL-6 (r = –0.37) and ESR (r =–0.15). Vitamin D level was linked with bone turnover markers (BTMs). In women of reproductive age with vitamin D deficiency, BMD of the lumbar spine and the hip was 9.5% to 23.1% greater than in those with no vitamin deficiency, respectively, and the mean lumbar spine Z-score in those with vitamin D insufficiency and deficiency was 2.0 and 2.9 times lower, respectively, than in patients with normal vitamin D level.

“Although the lowest 25(OH)D level was found in the group with the shortest disease duration, in general, the levels of the vitamin tested had no associative relation to disease duration,” explained the researchers.

Additionally, the literature data also presented no correlation between disease duration and vitamin D levels.

The researchers also found a strong associative inverse correlation (r = –0.26) of cumulative dose of GCs with vitamin D levels, so in the group of patients with a cumulative dose of GCs greater than 42.8 g, the average vitamin D level was 31.7% lower than in the patient group with a cumulative dose less than 42.8 g. The proportion of people in the high-dose GC group with vitamin D deficiency was 72.5%, while it was 52% in the low-dose GC group.

“Another pathogenetic factor adversely affecting vitamin D levels in patients with SLE is the systemic inflammatory process,” said the researchers.

Correlation analyses uncovered more evidence that the lowered 25(OH)D level is linked with inflammatory activity.

Since excessive autoantibody synthesis by B lymphocytes is a main element in pathogenesis of multiple autoimmune diseases, especially SLE, it can be determined that vitamin D influence on B cells causes inhibition of autoantibody synthesis.

“Thus, it is obvious that vitamin D can regulate at least some immune reactions, and its role is predominantly anti-inflammatory, which helps to prevent hyperinflammation and autoimmunity,” continued the researchers.

The researchers noted that all mechanisms of a relationship between SLE activity, vitamin D levels, BMD, and bone synthesis markers and resorption are not specifically known and need further investigation.

This study had some limitations. First, it was undertaken with only 1 measurement of serum 25 (OH)D levels, and it included mostly patients with high inflammatory activity.

“Hypovitaminosis D was associated with high inflammatory activity (SLEDAI, ESR, CRP, IL-6), severity of organ damage (DI), cumulative dose of GCs, BTMs (OC, CTX) and BMD. Vitamin D status was not associated with the patient’s age or disease duration,” concluded the researchers.

Reference

Shevchuk S, Marynych L, Malovana T, Denyshchych L. Vitamin d level in patients with systemic lupus erythematosus: its relationship to disease course and bone mineral density. Lupus Sci Med. Published online August 9, 2023. doi:10.1136/lupus-2023-000968