Background: Increase in lipid levels associated with the treatment of inflammatory bowel disease (IBD) has previously been reported. However, it is unknown if this effect is similar for all IBD drug classes. Aim: To precisely assess the effect of different IBD drug classes on lipid profiles. Methods: We performed a systematic literature search of randomised controlled trials and observational cohort studies that assessed lipid levels before and after induction (≤10 weeks) and maintenance (>10 weeks) of IBD treatment. Data of 11 studies (1663 patients) were pooled using random effects models. The influence of patient and disease characteristics on treatment effects on total cholesterol levels was analysed in 6 studies (1211 patients) for which individual data were available, using linear mixed models. Results: A statistically significant increase in total cholesterol was observed after induction treatment with corticosteroids (+1.19 mmol/L, 95% confidence interval [CI95] +0.52 to +2.59), and tofacitinib (+0.66 mmol/L, CI95 +0.42 to +0.79), but not after anti−TNFα treatment (−0.11 mmol/L, CI95 −0.26 to +0.36 mmol/L). Similar differences were observed after maintenance treatment. Treatment effects were significantly related to age, but not with other factors. Lipid changes were inversely correlated with but not modified by CRP changes. Conclusions: Increase in total cholesterol levels was strongest for corticosteroids followed by tofacitinib but was not observed for anti-TNFα agents. Whether total cholesterol change associated with IBD treatment has an effect on cardiovascular risk requires further study.
Bibliographical noteFunding Information:
There has been no financial support for this work. We would like to thank the following contributors: biomedical information specialist W.M. Bramer for literature search; R.W.M. Pauwels for title/abstract screening and quality scoring; A. Balint, M. Motobayashi and Galapagos NV, Belgium (NCT02048618) for sharing aggregated data. This publication is based on research using data from Pfizer (NCT00787202, NCT01465763, NCT01458951, NCT01458574) that has been made available through Vivli, Inc Vivli has not contributed to or approved, and is not in any way responsible for, the contents of this publication. Declaration of personal interests: J.A.M. Sleutjes: nothing to declare. J.E. Roeters van Lennep: nothing to declare. E. Boersma: nothing to declare. L.A. Menchen: received unrestricted grants from MSD and Abbvie, and served as an advisory board member and/or speaker for MSD, Abbvie, Pfizer, Janssen, Takeda, Biogen, Sandoz, Dr Falk-Pharma, FAES, Ferring, General Electric and Medtronic. M. Laudes: nothing to declare. K. Farkas: received speaker's honoraria from AbbVie, Janssen, Ferring, Takeda and Goodwill Pharma, and served as an advisory board member of Takeda. T. Moln?r: received speaker's honoraria from AbbVie, Egis, Goodwill Pharma, Takeda, Pfizer and Teva, and served as an advisory board member of Takeda. N.A. Kennedy: has received honoraria from Janssen, Falk, Allergan, Pharmacosmos and Takeda for unrelated topics and is an associate editor of Alimentary Pharmacology & Therapeutics. M.J. Pierik: has served on an advisory boards, or as speaker or consultant for Abbvie, Janssen-Cilag, MSD, Takeda, Ferring, Dr Falk and Sandoz and has received unrestricted grants from Janssen-Cilag, Abbvie and Takeda outside the submitted work. C.J. van der Woude: served as an advisory board member of Celltrion, Takeda and Abbvie. A.C. de Vries: served as an advisory board member of Jansen, Abbvie and Takeda. Declaration of funding interests: This study was not funded by any party.
© 2021 The Authors. Alimentary Pharmacology & Therapeutics published by John Wiley & Sons Ltd.