New Onset Autoimmune Hepatitis during Anti-Tumor Necrosis Factor-Alpha Treatment in Children - 23/02/18
Abstract |
Objectives |
To evaluate a large anti-tumor necrosis factor (TNF)-treated pediatric inflammatory bowel disease cohort for drug-induced liver injury (DILI) following presentation of an index case with suspected DILI with autoimmune features after infliximab exposure. To characterize the incidence, natural history, and risk factors for liver enzyme elevation with anti-TNF use.
Study design |
We reviewed the index case and performed a retrospective cohort study of 659 children receiving anti-TNF therapy between 2000 and 2015 at a tertiary pediatric inflammatory bowel disease center. Patients with alanine aminotransferase (ALT) ≥×2 the upper limit of normal were included. The incidence, evolution, and risk factors for liver injury were examined with univariate and multivariable proportional hazards regression. Causality was assessed using the Roussel-Uclaf Causality Assessment Method.
Results |
The index case, a teenage girl with Crohn's disease, developed elevated liver enzymes and features of autoimmune hepatitis on liver biopsy 23 weeks after starting infliximab. The injury resolved entirely within 4 months of withdrawing infliximab without additional therapy. Overall, 7.7% of our cohort developed new ALT elevations while on anti-TNF. Most ALT elevations were mild and transient and attributable to alternate etiologies. No additional clear cases of autoimmune hepatitis were identified.
Conclusions |
Transient liver enzyme abnormalities are relatively common among anti-TNF-treated children. Anti-TNF-related DILI with autoimmune features is rare but must be recognized so that therapy can be stopped.
Le texte complet de cet article est disponible en PDF.Keywords : anti-tumor necrosis factor, drug-induced liver injury, hepatitis, inflammatory bowel disease, infliximab
Abbreviations : ADA, aHR, AIH, ALP, ALT, ANA, AST, CD, DILI, GGT, HR, IBD, IBD-U, IFX, MRCP, NAFLD, RUCAM, TNF, UC, ULN
Plan
A.R. has received speaker fees and receives consulting fees from AbbVie and receives research fellowship funding from Janssen. T.W. received speaker and consulting fees from AbbVie and Janssen. K.F. received consulting fees from AbbVie and Janssen. N.C. received speaker fees from AbbVie. P.C. received consulting fees from AbbVie and Janssen. A.G. received consulting and speaker fees and research support from AbbVie (10282 IIS) and Janssen. The other authors declare no conflicts of interest. |
Vol 194
P. 128 - mars 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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