Premium
Neurological events with tumour necrosis factor alpha inhibitors reported to the Food and Drug Administration Adverse Event Reporting System
Author(s) -
Deepak P.,
Stobaugh D. J.,
Sherid M.,
Sifuentes H.,
Ehrenpreis E. D.
Publication year - 2013
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/apt.12385
Subject(s) - medicine , infliximab , adverse event reporting system , etanercept , adalimumab , adverse effect , inflammatory bowel disease , peripheral neuropathy , concomitant , rheumatoid arthritis , gastroenterology , disease , diabetes mellitus , endocrinology
Summary Background The association between inhibition of tumour necrosis factor alpha ( TNF ‐α) and new onset of neurological adverse events ( AE s) is unclear. Aims To evaluate neurological AE s with TNF ‐α inhibitors reported to the Food and Drug Administration Adverse Event Reporting System ( FAERS ) utilising a standardised scoring tool for drug‐induced AE s. Methods A search of FAERS for neurological AE s (January 1, 2000 to December 31, 2009) reported with infliximab, adalimumab, certolizumab and etanercept was performed. Full‐text reports were accessed using the Freedom of Information Act and scored using Naranjo score, while accounting for temporal association, previous conclusive reports of the neurological AE with any TNF ‐α inhibitor, and alternate explanations including underlying disease, concomitant medications and comorbidities, such as diabetes mellitus. Results There were 772 reports. Most were in patients who had rheumatoid arthritis (393, 50.9%) followed by inflammatory bowel disease (140, 18.1%). No significant differences in age or gender were seen between IBD patients compared with rheumatological diseases ( P = 0.584 and P = 0.055 respectively). Etanercept was reported most (327, 42.4%) followed by infliximab (276, 35.8%) ( P = 0.008). Peripheral neuropathy was the most common neurological AE (296 reports, 38.3%) followed by central nervous system and/or spinal cord demyelination (153 reports, 19.8%). Majority (551, 71.4%) of the reports were of ‘possible’ AE with the remaining ‘probable’ AE and none identified as ‘definite’ AE . Conclusion While several neurological AE s have been described, definite association between de novo development of these AE s and exposure to TNF ‐α inhibitors was not established using the Naranjo score.