Anti-tumour necrosis factor agents reduce non-steroidal anti-inflammatory drug-induced small bowel injury in rheumatoid arthritis patients.
retrospective_cohort · Level III
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- Record sourced from PubMed, PMID 23697473.
- Also identified by DOI 10.1136/gutjnl-2013-304713.
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Abstract
The role of tumour necrosis factor α (TNFα) in the pathogenesis of non-steroidal anti-inflammatory drug (NSAID)-induced small intestinal damage remains unclear. We evaluated the preventive effect of anti-TNF therapy against NSAID-induced enteropathy in rheumatoid arthritis (RA) patients. Capsule endoscopy was performed in 95 consecutive RA patients who received NSAID for more than 3 months, with or without anti-TNF therapy over a period of 3 months. The findings were scored from 0 to 4: 0, normal; 1, red spots; 2, one to four erosions; 3, more than four erosions; and 4, large erosions/ulcers. The relationship between the use of anti-TNF therapy and the risk of severe damage (scores 3 or 4) or the most severe damage (score 4) was assessed using multiple logistic regression analysis. Furthermore, a propensity score matching analysis was performed to reduce the effects of TNF selection bias. By stratifying the patients on the basis of anti-TNF therapy, we obtained crude OR of 0.23 for severe damage (95% CI 0.09 to 0.65) and 0.37 for the most severe damage (95% CI 0.16 to 0.86). This protective effect of anti-TNF therapy remained robust to adjustments for baseline characteristics, with the adjusted OR for severe damage and the most severe damage ranging from 0.23 to 0.26 and 0.06 to 0.41, respectively. Propensity score matching yielded similar results and showed the protective effects of anti-TNF therapy against severe and most severe damage. Anti-TNF therapy may protect against NSAID-induced small intestinal damage in RA patients.
Medical subject headings
- Anti-Inflammatory Agents, Non-Steroidal
- Antibodies, Monoclonal
- Antibodies, Monoclonal, Humanized
- Arthritis, Rheumatoid
- Immunoglobulin G
- Intestinal Diseases
- Intestine, Small
- Receptors, Tumor Necrosis Factor