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Weight affected insulin sensitivity in rheumatoid arthritis patients assigned anti-TNF-a
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Anti-tumor necrosis factor-alpha therapy improved insulin sensitivity in patients of normal weight with rheumatoid arthritis but not in obese patients with the disease, a study has discovered.
Researchers evaluated 32 patients with rheumatoid arthritis (RA) assigned anti-tumor necrosis factor-alpha (anti-TNF-a) treatment. The cohort was divided into four groups (n=8): normal weight with insulin resistance (N+IR), obese with IR (O+IR), normal weight without IR (N−IR) and obese without IR (O−IR). Patients with diabetes mellitus or on anti-diabetic medication were excluded from the study. Patients with and without IR were compared by age, gender, body mass index (BMI), disease duration and smoking status. BMI, homeostasis model assessment of insulin resistance (HOMA), quantitative insulin sensitivity check index (QUICKI) and RA disease characteristics before and after 6 months of anti-TNF-a treatment were assessed.
Disease activity and inflammation for all patients were reduced (P<.05) after 6 months of treatment. While a trend toward improvement was seen in HOMA (mean reduction= −0.2 ± 0.1) and QUICKI (mean increase=0.03 ± 0.022) without statistical significance, the N+IR group showed a decrease in HOMA (mean reduction= −0.54 ± 0.2; P=.002) and an increase in QUICKI (mean increase=0.046 ± 0.02; P=.011). The changes were significantly different compared with other cohorts (P<.05). Multivariate analysis for the N+IR group showed that the change in erythrocyte sedimentation rate (ESR) and in C-reactive protein (CRP) were related to improvement in HOMA (ESR: F1-7=5.143, P=.019; CRP: F1-7=3.122, P=.022) and QUICKI (ESR: F1-7=3.814, P=.021; CRP: F1-7=2.67; P=.041) in that group only.
Sample size was the main study limitation, the researchers said, and “a larger sample size might have been able to identify improvements in IR in the O+IR group.”
“[Anti-TNF-a] seems to improve IR in normal-weight but not in the obese RA patients,” the researchers concluded. “In the latter group, obesity-related processes seem to counteract the potential benefits of anti-TNF-a. It is possible that the mechanisms leading to insulin resistance are partly different in normal-weight and obese patients with RA.”
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