Patients who took supplements had improvements, although they did not become apparent until patients had been taking supplements for a year.
Vitamin D supplementation appears to lead to improvements in disease activity and fatigue in patients with systemic lupus erythematosus (SLE), according to new research.
The study suggests vitamin D may be a low-cost method of improving outcomes for some patients with SLE, although the report was based on a small sample size and requires further study, according to the authors. The report was published in the journal BMC Rheumatology.
Corresponding author Rosalie Magro, MD, of the University of Malta, and colleagues explained that while vitamin D deficiency is common in the general population, the problem is even more pronounced in patients with SLE. The reasons for this are unknown, although Magro and colleagues said it may simply be that patients with SLE spend less time in sunlight compared with the general population.
Recent evidence has identified the presence of vitamin D receptor (VDR) in innate and adaptive immune systems, raising the possibility that vitamin D deficiency may play a bigger role in diseases like SLE than previously thought.
The investigators recruited a cohort of 31 patients with SLE who did not have adequate vitamin D levels. Thirteen of the patients were categorized as being vitamin D-deficient (serum 25-hydroxyvitamin D < 20 ng/mL). The remaining 18 patients were vitamin D-insufficient (serum 25-hydroxyvitamin D 21-29 ng/mL). The patients in the study were 90% female, and their average age was 47.9 years.
Patients were put on a regimen of vitamin D3 supplementation based on their baseline condition. Patients who were deficient in vitamin D received 8000 IU of vitamin D3 daily for 8 weeks. Those in the insufficient category received 4 weeks of therapy at the same dose. Following the initial therapy, patients were given a daily maintenance dose of 2000 IU.
Investigators conducted assessments at baseline, 6 months, and 12 months, using interviews, questionnaires, and blood tests. They also assessed interferon signature genes in patient ribonucleic acid.
Patients in the study taking disease-modifying therapies were not allowed to increase their dosage or start new therapies during the study, to ensure that they did not skew the results.
At 6 months, 83.9% of patients had reached sufficient levels of vitamin D (defined as serum vitamin D ≥ 30 ng/mL. However, by 12 months, the rate of vitamin D sufficiency had dropped to 35.5%. The investigators said this may be due to a lack of adherence to study protocols, based on a count of how many vitamin D pill boxes patients picked up from patients’ pharmacies. The data suggested 64.5% of patients did not pick up enough tablets to meet the recommended dosing.
Still, investigators noted an improvement in overall scores on the SLE disease activity index-2K scale, as well as improvement in fatigue severity scale scores at 12 months. They also found a decrease in anti-double stranded deoxyribonucleic acid, a sign that disease severity may be improving. Mean interferon signature gene expression scores changed at 6 months, but failed to reach statistical significance, the authors said.
Magro and colleagues noted that while there were much higher levels of vitamin D sufficiency at 6 months, the improvements in disease activity and fatigue did not arrive until the 12-month assessment, suggesting that long-term supplementation is necessary to achieve meaningful results.
The authors concluded that their study supports the idea of vitamin D screening for patients with SLE, in order to identify those who might benefit from supplementation.
“The correction of vitamin D deficiency in SLE patients has potential benefits with regards to the suppression in the expression of genes in the interferon pathway, consequently resulting in an improvement in SLE disease activity,” they wrote.
Magro R, Saliba C, Camilleri L, Scerri C, and Borg AA. Vitamin D supplementation in systemic lupus erythematosus: relationship to disease activity, fatigue and the interferon signature gene expression. BMC Rheumatol. Published online December 3, 2021. doi:10.1186/s41927-021-00223-1