Vitamin D Status Unaffected by Anti-Inflammatory Treatment

Major Finding: Treatment with adalimumab lowered the disease activity score among a group of rheumatoid arthritis patients, but did not affect serum vitamin D levels.

Data Source: A prospective study of 170 consecutive patients with rheumatoid arthritis seen at an outpatient facility in Amsterdam.

Disclosures: The authors stated that they had no competing interests. The study was supported by the European League Against Rheumatism and the Jan van Breemen Institute, in Amsterdam.

Four months of treatment with the anti–tumor necrosis factor drug adalimumab did not affect serum vitamin D levels in rheumatoid arthritis patients, though it did ease symptoms.

The finding refutes the theory that systemic inflammation may negatively affect circulating serum 25-hydroxyvitamin D (25[OH]D) levels, wrote Dr. Paul Welsh and his colleagues.

Moreover, the data confirm a high prevalence of vitamin D insufficiency and frank deficiency among RA patients, they added.

According to Dr. Welsh of the British Heart Foundation Glasgow Cardiovascular Research Center at the University of Glasgow and his associates, there are several reasons why treatment with a potent anti-inflammatory medication, such as the tumor necrosis factor–alpha blocker adalimumab, might be hypothesized to increase vitamin D levels.

Data from a 2006 study showed an inverse relationship between serum vitamin D and DAS-28 scores (Clin. Exp. Rheumatol. 2006;24:702–4). “Furthermore, data for an apparent beneficial effect of statins on circulating 25[OH]D concentrations have been speculated to be attributable to statin 'pleiotropic' anti-inflammatory effects,” the researchers said. They also noted that serum vitamin D levels are known to drop in the acute phase following surgery, when inflammation is likely to be elevated.

To test the hypothesis that lowering inflammation would result in an increase of vitamin D, the researchers looked at 170 consecutive patients with RA seen at an outpatient clinic in Amsterdam (Ann. Rheum. Dis. 2010 [doi:10.1136/ard.2010.137265]).

Patients were treated either with adalimumab alone, at a dose of 40 mg administered every 2 weeks, or with adalimumab plus other disease-modifying antirheumatic drugs (DMARDs).

At baseline, 66 patients (39%) were vitamin D deficient, with a serum concentration of less than 15 ng/mL. Sixty-three patients (39%) had vitamin D insufficiency, with levels between 15 and 25 ng/mL. The remaining patients had adequate vitamin D levels.

After 16 weeks of treatment with adalimumab, patients' mean disease activity score-28 (DAS-28) had dropped significantly, from 5.1 to 3.2 (P less than .001). However, median circulating levels of vitamin D were not significantly altered, moving from 18.5 ng/mL at baseline to 19.0 ng/mL at the study's completion (P = .67). Nor did the prevalence of patients with vitamin D deficiency and insufficiency change after treatment, wrote the authors.

“Whether longer-term biological therapy has any beneficial effect on circulating 25[OH]D concentrations requires further study, although any such effect may be attributable to increased sunlight exposure rather than decreasing inflammation,” concluded the authors.

“Our observations also weaken the possibility that TNF-alpha blockers, which improve bone mineral density and potentially lower cardiovascular risk, do so via changes in 25[OH]D levels.”

They added: “Further research is needed to address determinants of poor 25[OH]D status in RA.”

Major Finding: Treatment with adalimumab lowered the disease activity score among a group of rheumatoid arthritis patients, but did not affect serum vitamin D levels.

Data Source: A prospective study of 170 consecutive patients with rheumatoid arthritis seen at an outpatient facility in Amsterdam.

Disclosures: The authors stated that they had no competing interests. The study was supported by the European League Against Rheumatism and the Jan van Breemen Institute, in Amsterdam.

Four months of treatment with the anti–tumor necrosis factor drug adalimumab did not affect serum vitamin D levels in rheumatoid arthritis patients, though it did ease symptoms.

The finding refutes the theory that systemic inflammation may negatively affect circulating serum 25-hydroxyvitamin D (25[OH]D) levels, wrote Dr. Paul Welsh and his colleagues.

Moreover, the data confirm a high prevalence of vitamin D insufficiency and frank deficiency among RA patients, they added.

According to Dr. Welsh of the British Heart Foundation Glasgow Cardiovascular Research Center at the University of Glasgow and his associates, there are several reasons why treatment with a potent anti-inflammatory medication, such as the tumor necrosis factor–alpha blocker adalimumab, might be hypothesized to increase vitamin D levels.

Data from a 2006 study showed an inverse relationship between serum vitamin D and DAS-28 scores (Clin. Exp. Rheumatol. 2006;24:702–4). “Furthermore, data for an apparent beneficial effect of statins on circulating 25[OH]D concentrations have been speculated to be attributable to statin 'pleiotropic' anti-inflammatory effects,” the researchers said. They also noted that serum vitamin D levels are known to drop in the acute phase following surgery, when inflammation is likely to be elevated.

To test the hypothesis that lowering inflammation would result in an increase of vitamin D, the researchers looked at 170 consecutive patients with RA seen at an outpatient clinic in Amsterdam (Ann. Rheum. Dis. 2010 [doi:10.1136/ard.2010.137265]).

Patients were treated either with adalimumab alone, at a dose of 40 mg administered every 2 weeks, or with adalimumab plus other disease-modifying antirheumatic drugs (DMARDs).

At baseline, 66 patients (39%) were vitamin D deficient, with a serum concentration of less than 15 ng/mL. Sixty-three patients (39%) had vitamin D insufficiency, with levels between 15 and 25 ng/mL. The remaining patients had adequate vitamin D levels.

After 16 weeks of treatment with adalimumab, patients' mean disease activity score-28 (DAS-28) had dropped significantly, from 5.1 to 3.2 (P less than .001). However, median circulating levels of vitamin D were not significantly altered, moving from 18.5 ng/mL at baseline to 19.0 ng/mL at the study's completion (P = .67). Nor did the prevalence of patients with vitamin D deficiency and insufficiency change after treatment, wrote the authors.

“Whether longer-term biological therapy has any beneficial effect on circulating 25[OH]D concentrations requires further study, although any such effect may be attributable to increased sunlight exposure rather than decreasing inflammation,” concluded the authors.

“Our observations also weaken the possibility that TNF-alpha blockers, which improve bone mineral density and potentially lower cardiovascular risk, do so via changes in 25[OH]D levels.”

They added: “Further research is needed to address determinants of poor 25[OH]D status in RA.”

Major Finding: Treatment with adalimumab lowered the disease activity score among a group of rheumatoid arthritis patients, but did not affect serum vitamin D levels.

Data Source: A prospective study of 170 consecutive patients with rheumatoid arthritis seen at an outpatient facility in Amsterdam.

Disclosures: The authors stated that they had no competing interests. The study was supported by the European League Against Rheumatism and the Jan van Breemen Institute, in Amsterdam.

Four months of treatment with the anti–tumor necrosis factor drug adalimumab did not affect serum vitamin D levels in rheumatoid arthritis patients, though it did ease symptoms.

The finding refutes the theory that systemic inflammation may negatively affect circulating serum 25-hydroxyvitamin D (25[OH]D) levels, wrote Dr. Paul Welsh and his colleagues.

Moreover, the data confirm a high prevalence of vitamin D insufficiency and frank deficiency among RA patients, they added.

According to Dr. Welsh of the British Heart Foundation Glasgow Cardiovascular Research Center at the University of Glasgow and his associates, there are several reasons why treatment with a potent anti-inflammatory medication, such as the tumor necrosis factor–alpha blocker adalimumab, might be hypothesized to increase vitamin D levels.

Data from a 2006 study showed an inverse relationship between serum vitamin D and DAS-28 scores (Clin. Exp. Rheumatol. 2006;24:702–4). “Furthermore, data for an apparent beneficial effect of statins on circulating 25[OH]D concentrations have been speculated to be attributable to statin 'pleiotropic' anti-inflammatory effects,” the researchers said. They also noted that serum vitamin D levels are known to drop in the acute phase following surgery, when inflammation is likely to be elevated.

To test the hypothesis that lowering inflammation would result in an increase of vitamin D, the researchers looked at 170 consecutive patients with RA seen at an outpatient clinic in Amsterdam (Ann. Rheum. Dis. 2010 [doi:10.1136/ard.2010.137265]).

Patients were treated either with adalimumab alone, at a dose of 40 mg administered every 2 weeks, or with adalimumab plus other disease-modifying antirheumatic drugs (DMARDs).

At baseline, 66 patients (39%) were vitamin D deficient, with a serum concentration of less than 15 ng/mL. Sixty-three patients (39%) had vitamin D insufficiency, with levels between 15 and 25 ng/mL. The remaining patients had adequate vitamin D levels.

After 16 weeks of treatment with adalimumab, patients' mean disease activity score-28 (DAS-28) had dropped significantly, from 5.1 to 3.2 (P less than .001). However, median circulating levels of vitamin D were not significantly altered, moving from 18.5 ng/mL at baseline to 19.0 ng/mL at the study's completion (P = .67). Nor did the prevalence of patients with vitamin D deficiency and insufficiency change after treatment, wrote the authors.

“Whether longer-term biological therapy has any beneficial effect on circulating 25[OH]D concentrations requires further study, although any such effect may be attributable to increased sunlight exposure rather than decreasing inflammation,” concluded the authors.

“Our observations also weaken the possibility that TNF-alpha blockers, which improve bone mineral density and potentially lower cardiovascular risk, do so via changes in 25[OH]D levels.”

They added: “Further research is needed to address determinants of poor 25[OH]D status in RA.”