Anti-TNF therapy did not produce statistically significant changes in LDL-C, HDL-C, triglycerides, total cholesterol, or blood pressure compared to controls in adults with rheumatoid arthritis (e.g., LDL-C MD 0.35, p=0.20).
Meta-Analysis (n=295)
Does anti-TNF therapy improve conventional cardiovascular risk markers (lipid parameters and blood pressure) in adults with rheumatoid arthritis?
Anti-TNF therapy does not significantly alter conventional lipid profiles or blood pressure in patients with rheumatoid arthritis, highlighting the need for larger trials to assess its true cardiovascular impact.
Effect estimate: No statistically significant differences for LDL-C (MD 0.35, 95% CI [-0.19, 0.88], p=0.20), HDL-C (MD -0.85, 95% CI [-3.15, 1.46], p=0.47), triglycerides (MD 11.67, 95% CI [-4.00, 27.34], p=0.14), total cholesterol (MD 1.05, 95% CI [-0.86, 2.96], p=0.28), systolic BP (MD -0.24, 95% CI [-5.17, 4.69], p=0.92), diastolic BP (MD 0.98, 95% CI [-2.17, 4.14], p=0.54)
Rheumatoid arthritis (RA) is linked with a high risk of cardiovascular disease (CVD), which is mainly triggered by chronic systemic inflammation. Tumour necrosis factor (TNF) inhibitors are effective in managing RA disease activity; however, their impact on cardiovascular risk markers is also unclear. The systematic review and meta-analysis aimed to assess the effects of anti-TNF therapy on conventional cardiovascular risk markers, specifically lipid parameters and blood pressure, in patients with rheumatoid arthritis. We searched PubMed, Embase, Google Scholar, and the Cochrane Library for randomised controlled trials published after 2010 that compared anti-TNF therapy with control treatments in adults with RA; 4 trials met the inclusion criteria. The lipid parameters (low-density lipoprotein cholesterol LDL-C, high-density lipoprotein HDL-C, triglycerides, and total cholesterol) and blood pressure were the outcomes. The Cochrane RoB 2.0 tool was used to measure risk of bias. Mean differences and 95% confidence intervals were used to produce random-effects meta-analyses. There were four randomised controlled trials with 295 participants. No statistically significant differences were found between the anti-TNF therapy and control groups for LDL-C, HDL-C, triglycerides, total cholesterol, systolic blood pressure, or diastolic blood pressure. The sensitivity analysis revealed that triglyceride results were unstable due to a single study, whereas the remaining results were very stable. In available RCTs, no statistically significant differences were observed between anti-TNF therapy and control treatments for conventional cardiovascular risk markers in patients with RA. More extensive and prolonged studies that include standardised cardiovascular outcomes should be undertaken to elucidate the cardiovascular effects of anti-TNF therapy.
Shah et al. (Fri,) conducted a meta-analysis in Adults aged ≥18 years with rheumatoid arthritis receiving anti-TNF therapy versus controls (n=295). Anti-TNF therapy (infliximab, adalimumab, etanercept) vs. Placebo, conventional synthetic DMARDs, or non-TNF biologics was evaluated on Changes in conventional cardiovascular risk markers including lipid profile (LDL-C, HDL-C, triglycerides, total cholesterol) and blood pressure (systolic and diastolic) (No statistically significant differences for LDL-C (MD 0.35, 95% CI [-0.19, 0.88], p=0.20), HDL-C (MD -0.85, 95% CI [-3.15, 1.46], p=0.47), triglycerides (MD 11.67, 95% CI [-4.00, 27.34], p=0.14), total cholesterol (MD 1.05, 95% CI [-0.86, 2.96], p=0.28), systolic BP (MD -0.24, 95% CI [-5.17, 4.69], p=0.92), diastolic BP (MD 0.98, 95% CI [-2.17, 4.14], p=0.54)). Anti-TNF therapy did not produce statistically significant changes in LDL-C, HDL-C, triglycerides, total cholesterol, or blood pressure compared to controls in adults with rheumatoid arthritis (e.g., LDL-C MD 0.35, p=0.20).