Vitamin D Insufficiency May Trigger Inflammation in Lupus

The science supporting vitamin D supplementation in lupus patients is catching up to the recommendation that all patients with the autoimmune disease increase their intake of the fat-soluble secosteroids.

Findings from a new study by Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria (Egypt), and her associates demonstrate that there is a high prevalence of vitamin D deficiency associated with an increased inflammatory burden and thrombophilic state in patients with systemic lupus erythematosus (SLE).

The findings also suggest that oral vitamin D supplementation ameliorates chronic inflammatory and hemostatic markers in this patient group.

The use of supplementary calcium and vitamin D is routinely recommended for SLE patients to help minimize the bone loss and increased risk of developing osteoporosis associated with the disease and its treatment. Beyond supporting bone and mineral hemostasis, “vitamin D is now recognized as having additional pleiotropic roles,” according to Dr. Abou-Raya.

“We've learned that it has potent immunomodulatory properties that have promoted its potential use in the treatment of autoimmune conditions, including lupus,” she said.

The study was designed to evaluate vitamin D status in lupus patients and to assess alterations in disease-related inflammatory and hemostatic markers before and after vitamin D supplementation.

To do this, Dr. Abou-Raya and her fellow researchers conducted a randomized, placebo-controlled trial comprising 148 males and premenopausal females who fulfilled the ACR (American College of Rheumatology) classification criteria for SLE. Also enrolled in the study were 75 lupus-free adults who served as controls and who matched the cases in age, sex, ethnicity, and body mass index. Individuals with other inflammatory disorders and those taking supplemental vitamin D at the time of the study were excluded, she noted.

Study patients were randomized in a 1:1 fashion to receive either 2,000 IU per day of oral cholecalciferol (vitamin D₃) or placebo for 6 months together with standard SLE treatment, Dr. Abou-Raya explained.

Before and after 6 months of vitamin D supplementation, the investigators evaluated disease activity using the SLE disease activity index (SLEDAI), levels of serum 25-hydroxyvitamin D (25[OH]D) via DiaSorin's Liaison immunoassay, levels of proinflammatory cytokines interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor (TNF)–alpha, C-reactive protein (CRP), and the hemostatic markers fibrinogen and von Willebrand factor (vWF). Individuals with 25(OH)D levels of 10-30 ng/mL were classified as having vitamin D insufficiency; those with levels lower than 10 ng/mL were considered vitamin D deficient, she noted.

The mean age of the SLE patients was 38.8 years and the mean disease duration was 5.2 years. The mean baseline vitamin D level in the SLE patients, 19.8 ng/mL, was significantly lower than the mean 28.7 ng/mL in the control group. The baseline levels of the inflammatory and hemostatic markers were significantly higher in the SLE patients. “The overall prevalence of vitamin D insufficiency and deficiency, respectively, was 69% and 39%,” she said.

At 6 months, “there was a significant decrease in levels of inflammatory and hemostatic makers in lupus patients who were supplemented with vitamin D” compared with patients who were given placebo together with ongoing therapy, Dr. Abou-Raya reported at the annual European Congress of Rheumatology in London. After multivariate adjustment, there was a negative correlation between vitamin D levels and IL-1, IL-6, IL-18, TNF-alpha, CRP, fibrinogen, and vWF, “and lower vitamin D levels were associated with significantly higher SLEDAI scores,” she said.

The results suggest that hypovitaminosis D contributes to a chronic inflammatory and thrombophilic state in SLE patients, said Dr. Abou-Raya. “The findings support the routine recommendation for oral vitamin D supplementation,” she said.

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

The science supporting vitamin D supplementation in lupus patients is catching up to the recommendation that all patients with the autoimmune disease increase their intake of the fat-soluble secosteroids.

Findings from a new study by Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria (Egypt), and her associates demonstrate that there is a high prevalence of vitamin D deficiency associated with an increased inflammatory burden and thrombophilic state in patients with systemic lupus erythematosus (SLE).

The findings also suggest that oral vitamin D supplementation ameliorates chronic inflammatory and hemostatic markers in this patient group.

The use of supplementary calcium and vitamin D is routinely recommended for SLE patients to help minimize the bone loss and increased risk of developing osteoporosis associated with the disease and its treatment. Beyond supporting bone and mineral hemostasis, “vitamin D is now recognized as having additional pleiotropic roles,” according to Dr. Abou-Raya.

“We've learned that it has potent immunomodulatory properties that have promoted its potential use in the treatment of autoimmune conditions, including lupus,” she said.

The study was designed to evaluate vitamin D status in lupus patients and to assess alterations in disease-related inflammatory and hemostatic markers before and after vitamin D supplementation.

To do this, Dr. Abou-Raya and her fellow researchers conducted a randomized, placebo-controlled trial comprising 148 males and premenopausal females who fulfilled the ACR (American College of Rheumatology) classification criteria for SLE. Also enrolled in the study were 75 lupus-free adults who served as controls and who matched the cases in age, sex, ethnicity, and body mass index. Individuals with other inflammatory disorders and those taking supplemental vitamin D at the time of the study were excluded, she noted.

Study patients were randomized in a 1:1 fashion to receive either 2,000 IU per day of oral cholecalciferol (vitamin D₃) or placebo for 6 months together with standard SLE treatment, Dr. Abou-Raya explained.

Before and after 6 months of vitamin D supplementation, the investigators evaluated disease activity using the SLE disease activity index (SLEDAI), levels of serum 25-hydroxyvitamin D (25[OH]D) via DiaSorin's Liaison immunoassay, levels of proinflammatory cytokines interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor (TNF)–alpha, C-reactive protein (CRP), and the hemostatic markers fibrinogen and von Willebrand factor (vWF). Individuals with 25(OH)D levels of 10-30 ng/mL were classified as having vitamin D insufficiency; those with levels lower than 10 ng/mL were considered vitamin D deficient, she noted.

The mean age of the SLE patients was 38.8 years and the mean disease duration was 5.2 years. The mean baseline vitamin D level in the SLE patients, 19.8 ng/mL, was significantly lower than the mean 28.7 ng/mL in the control group. The baseline levels of the inflammatory and hemostatic markers were significantly higher in the SLE patients. “The overall prevalence of vitamin D insufficiency and deficiency, respectively, was 69% and 39%,” she said.

At 6 months, “there was a significant decrease in levels of inflammatory and hemostatic makers in lupus patients who were supplemented with vitamin D” compared with patients who were given placebo together with ongoing therapy, Dr. Abou-Raya reported at the annual European Congress of Rheumatology in London. After multivariate adjustment, there was a negative correlation between vitamin D levels and IL-1, IL-6, IL-18, TNF-alpha, CRP, fibrinogen, and vWF, “and lower vitamin D levels were associated with significantly higher SLEDAI scores,” she said.

The results suggest that hypovitaminosis D contributes to a chronic inflammatory and thrombophilic state in SLE patients, said Dr. Abou-Raya. “The findings support the routine recommendation for oral vitamin D supplementation,” she said.

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

The science supporting vitamin D supplementation in lupus patients is catching up to the recommendation that all patients with the autoimmune disease increase their intake of the fat-soluble secosteroids.

Findings from a new study by Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria (Egypt), and her associates demonstrate that there is a high prevalence of vitamin D deficiency associated with an increased inflammatory burden and thrombophilic state in patients with systemic lupus erythematosus (SLE).

The findings also suggest that oral vitamin D supplementation ameliorates chronic inflammatory and hemostatic markers in this patient group.

The use of supplementary calcium and vitamin D is routinely recommended for SLE patients to help minimize the bone loss and increased risk of developing osteoporosis associated with the disease and its treatment. Beyond supporting bone and mineral hemostasis, “vitamin D is now recognized as having additional pleiotropic roles,” according to Dr. Abou-Raya.

“We've learned that it has potent immunomodulatory properties that have promoted its potential use in the treatment of autoimmune conditions, including lupus,” she said.

The study was designed to evaluate vitamin D status in lupus patients and to assess alterations in disease-related inflammatory and hemostatic markers before and after vitamin D supplementation.

To do this, Dr. Abou-Raya and her fellow researchers conducted a randomized, placebo-controlled trial comprising 148 males and premenopausal females who fulfilled the ACR (American College of Rheumatology) classification criteria for SLE. Also enrolled in the study were 75 lupus-free adults who served as controls and who matched the cases in age, sex, ethnicity, and body mass index. Individuals with other inflammatory disorders and those taking supplemental vitamin D at the time of the study were excluded, she noted.

Study patients were randomized in a 1:1 fashion to receive either 2,000 IU per day of oral cholecalciferol (vitamin D₃) or placebo for 6 months together with standard SLE treatment, Dr. Abou-Raya explained.

Before and after 6 months of vitamin D supplementation, the investigators evaluated disease activity using the SLE disease activity index (SLEDAI), levels of serum 25-hydroxyvitamin D (25[OH]D) via DiaSorin's Liaison immunoassay, levels of proinflammatory cytokines interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor (TNF)–alpha, C-reactive protein (CRP), and the hemostatic markers fibrinogen and von Willebrand factor (vWF). Individuals with 25(OH)D levels of 10-30 ng/mL were classified as having vitamin D insufficiency; those with levels lower than 10 ng/mL were considered vitamin D deficient, she noted.

The mean age of the SLE patients was 38.8 years and the mean disease duration was 5.2 years. The mean baseline vitamin D level in the SLE patients, 19.8 ng/mL, was significantly lower than the mean 28.7 ng/mL in the control group. The baseline levels of the inflammatory and hemostatic markers were significantly higher in the SLE patients. “The overall prevalence of vitamin D insufficiency and deficiency, respectively, was 69% and 39%,” she said.

At 6 months, “there was a significant decrease in levels of inflammatory and hemostatic makers in lupus patients who were supplemented with vitamin D” compared with patients who were given placebo together with ongoing therapy, Dr. Abou-Raya reported at the annual European Congress of Rheumatology in London. After multivariate adjustment, there was a negative correlation between vitamin D levels and IL-1, IL-6, IL-18, TNF-alpha, CRP, fibrinogen, and vWF, “and lower vitamin D levels were associated with significantly higher SLEDAI scores,” she said.

The results suggest that hypovitaminosis D contributes to a chronic inflammatory and thrombophilic state in SLE patients, said Dr. Abou-Raya. “The findings support the routine recommendation for oral vitamin D supplementation,” she said.

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.