Vitamin D deficiency was highly prevalent in rheumatoid arthritis (RA) patients and was associated with worse mental/physical quality-of-life (QOL) scores, as well as greater disease activity, according to Polish researchers.
Vitamin D deficiency (<20 ng/dL) was detected in 76.3% of RA patients of whom 38.1% were severely deficient (<10 ng/dL). In the comparator osteoarthritis (OA) group, 78.6% were deficient in D and 35.7% had levels of <0 ng/dL, reported Anna Raczkiewicz, PhD, of the Military Institute of Medicine in Warsaw, and colleagues.
Overall, severely deficient patients had slightly longer disease duration (8.8 years versus 5.8 years), more hypertension (60.9% versus 49%), and osteoporosis (20.3% versus 8.7%), they wrote in the Journal of Clinical Rheumatology.
However, regular physical activity correlated with higher vitamin D titers and better QOL, they added.
“Vitamin D deficiency may increase the risk of variousautoimmune diseases, including rheumatoid arthritis (RA), and negatively affect RA activity,” the group wrote. “In addition, many researchers have shown the association between vitamin D deficiency and chronic pain, skeletal muscle weakness, mood disorders, and deterioration of cognitive function in the elderly.”
The authors sought to establish the relationship between serum vitamin D levels, disease activity, physical activity (PA), and QOL in RA patients.
They enrolled 97 consecutive RA patients who were not taking vitamin D supplements. Patients had a mean age of 59.4, and the majority (86) were women. The control group consisted of 28 OA patients with an average age of 56.2.
As in many studies, there was a negative correlation between 25(OH)D serum concentration and DAS28 score, specifically in 28 patients with active arthritis (DAS>2.6). Those with moderate disease activity had lower vitamin D serum concentration than those with mild disease activity; levels were the lowest in those with high disease activity
“It has been suggested that 25(OH)D serum concentrations may decrease in the acute-phase response, thereby explaining the low levels in patients with high disease activity,” the authors wrote, adding that low vitamin D may also be a consequence of disease activity.
No correlation surfaced between vitamin D level and VAS pain or VAS fatigue.
A positive correlation emerged between serum 25(OH)D, physical activity level and most aspects of the SF-36. After factoring in physical activity to the multivariable analysis, however, only the correlations between 25(OH)D and SF-36 mental subscale (MCS) and pain remained significant.
A negative correlation was noted between serum 25(OH)D and the HAQ and BDI in patients with disease duration of at least 1 year.
With regard to RA therapy, the authors noted that glucocorticosteroid monotherapy was associated with a trend to lower vitamin D level versus patients treated with disease-modifying drugs or in patients without RA treatment (P=0.33).
The authors called for further studies to confirm the evidence that lower 25(OH)D3 relates to higher disease activity.
Addressing the study’s limitations, they noted its exclusion of vitamin D-supplemented patients and its consecutive recruitment design, which resulted in a large number of early RA patients with probable higher disease activity and worse outcomes. Also, vitamin D serum levels were only measured once. The authors also did not factor in smoking status, alcohol use, and marital, education, and economic status, which may impact vitamin D levels.
“Despite this, and probably because of the high prevalence of vitamin deficiency in [the] examined group, we managed to find significant associations between vitamin D status and mental and physical aspects of quality of life, as well as with disease activity,” they wrote.
Raczkiewicz and co-authors disclosed no relevant relationships with industry.
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Journal of Clinical Rheumatology