The effect of anti-TNF treatment on body composition and insulin resistance in patients with rheumatoid arthritis

Abstract

Given the link between systemic inflammation, body composition and insulin resistance (IR), anti-inflammatory therapy may improve IR and body composition in inflammatory joint diseases. This study assesses the IR and beta cell function in rheumatoid arthritis (RA) patients with active disease compared to osteoarthritis (OA) patients and investigates the effect of anti-TNF treatment on IR, beta cell function and body composition in RA. 28 Consecutive RA patients starting anti-TNF treatment (adalimumab), and 28 age, and sex-matched patients with OA were followed for 6 months. Exclusion criteria were use of statins, corticosteroids, and cardiovascular or endocrine co-morbidity. Pancreatic beta cell function and IR, using the homeostasis model assessment (HOMA2), and body composition, using dual-energy X-ray absorptiometry (DXA) were measured at baseline and 6 months. At baseline, IR [1.5 (1.1–1.8) vs. 0.7 (0.6–0.9), 100/%S] and beta cell function (133% vs. 102%) were significantly ( p < 0.05) higher in RA patients with active disease as compared to OA patients. After 6 months of anti-TNF treatment, IR [1.5 (1.1–1.8) to 1.4 (1.1–1.7), p = 0.17] slightly improved and beta cell function [133% (115–151) to 118% (109–130), p <0.05] significantly improved. Improvement in IR and beta cell function was most pronounced in RA patients with highest decrease in CRP and ESR. Our observations indicate that IR and increased beta cell function are more common in RA patients with active disease. Anti-TNF reduced IR and beta cell function especially in RA patients with highest decrease in systemic inflammation and this effect was not explained by changes in body composition.

Causal Biological Network Model for Inflammasome Signaling Applied for Interpreting Transcriptomic Changes in Various Inflammatory States

“…All these entities were inferred to be upregulated in the synovial tissues of RA patients (the TNF, TLR4, and BCL2 scores did not reach statistically significant values for RA) and downregulated in OA patients' synovial tissues (the TLR2 and STAT1 scores did not reach statistically significant values for OA). Consistent with this finding, anti-TNF treatment has been reported to show beneficial outcomes in RA patients when compared with OA patients [ 56 , 57 ].…”

Cumulative Inflammation and HbA1c Levels Correlate with Increased Intima-Media Thickness in Patients with Severe Hidradenitis Suppurativa

“…This relationship seems to be clear for anti-TNF and anti-IL6 agents, and it remains still uncertain for other biologic drugs [67]. In addition, recent reports include the improvement of insulin resistance and that pancreatic beta cells have beneficial effects on the anti-TNF therapy in rheumatoid arthritis [68], which supports its potential for improvement cardiovascular risk.…”

<p>Characterization and Treatment of Inflammation and Insulin Resistance in Obese Adipose Tissue</p>

“…87 After 3-6 months of anti-TNF treatment in patients with rheumatoid arthritis and insulin resistance, insulin sensitivity and β-cell function were significantly improved. 88 Additionally, the non-steroidal anti-inflammatory drug Figure 2 Intracellular signal transduction of adipokines and insulin resistance. In obese adipose tissue, inflammatory factors IL-1 and TNF-α can enter cells through the JNK/ AP-1 and IKK/NF-κB signaling pathways, which increases the transcription of adipokines MCP-1, recruits more pro-inflammatory immune cells, and produces more inflammatory factors IL-1 and TNF-α; they can also directly inhibit the phosphorylation of IRS-1, leading to insulin resistance.…”