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Ischaemic colitis in rheumatoid arthritis patients receiving tumour necrosis factor-α inhibitors: an analysis of reports to the US FDA Adverse Event Reporting System.
BACKGROUND: Tumour necrosis factor-α (TNF-α) inhibitors are immunosuppressants, approved for the treatment and maintenance of rheumatoid arthritis (RA). Immunosuppression has been shown to induce ischaemic colitis (IC) in an animal model; however, a relationship between TNF inhibitors and IC has rarely been reported in the published literature.
OBJECTIVE: The aim of this study was to better characterize the association between TNF-α inhibitors with IC in RA patients, by analysing adverse event reports submitted to the US FDA Adverse Event Reporting System (AERS) and the published literature.
METHODS: The FDA AERS database was searched and we identified all reports between January 2003 and June 2011. The search was limited to an indication of RA, a 'primary suspect' drug of TNF-α inhibitors and a reaction of IC. Full-length reports were obtained and analysed utilizing the Freedom of Information Act. The cases were organized by age, sex, type of TNF-α inhibitor, concomitant drugs and medical co-morbidities. Cases were labelled as definite, probable, possible or doubtful drug-induced adverse events based on the Naranjo Scale. A PubMed search was performed to obtain published literature documenting events of anti-TNF-associated IC.
RESULTS: Twelve cases were eliminated because of more likely causes for IC. Thirty-five primary suspect reports of TNF-α inhibitors associated with IC in RA patients were identified in the FDA AERS. Thirteen cases were reported with infliximab, 12 with adalimumab, 7 with etanercept and 3 with certolizumab. The majority of the cases were in females (29/35) and those between the ages of 50 and 65 years (18/35). Use of the Naranjo Scale revealed 17 probable and 18 possible cases of anti-TNF-induced IC. In the literature, one report of IC associated with adalimumab was identified.
CONCLUSION: TNF-α inhibitors may be initiating factors or co-factors in the development of IC in RA patients, and further research to determine the mechanism of this association is warranted.
OBJECTIVE: The aim of this study was to better characterize the association between TNF-α inhibitors with IC in RA patients, by analysing adverse event reports submitted to the US FDA Adverse Event Reporting System (AERS) and the published literature.
METHODS: The FDA AERS database was searched and we identified all reports between January 2003 and June 2011. The search was limited to an indication of RA, a 'primary suspect' drug of TNF-α inhibitors and a reaction of IC. Full-length reports were obtained and analysed utilizing the Freedom of Information Act. The cases were organized by age, sex, type of TNF-α inhibitor, concomitant drugs and medical co-morbidities. Cases were labelled as definite, probable, possible or doubtful drug-induced adverse events based on the Naranjo Scale. A PubMed search was performed to obtain published literature documenting events of anti-TNF-associated IC.
RESULTS: Twelve cases were eliminated because of more likely causes for IC. Thirty-five primary suspect reports of TNF-α inhibitors associated with IC in RA patients were identified in the FDA AERS. Thirteen cases were reported with infliximab, 12 with adalimumab, 7 with etanercept and 3 with certolizumab. The majority of the cases were in females (29/35) and those between the ages of 50 and 65 years (18/35). Use of the Naranjo Scale revealed 17 probable and 18 possible cases of anti-TNF-induced IC. In the literature, one report of IC associated with adalimumab was identified.
CONCLUSION: TNF-α inhibitors may be initiating factors or co-factors in the development of IC in RA patients, and further research to determine the mechanism of this association is warranted.
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