P586 Drug-induced lipid changes in patients with Inflammatory Bowel Disease: a single center, prospective study

SleutjesAM, J.(1);de Vries, A.C.(1);Roeters van Lennep, J.E.(2);van der Woude, C.J.(1);

(1)Erasmus Medical Center, Gastroenterology & Hepatology, Rotterdam, The Netherlands;(2)Erasmus Medical Center, Internal Medicine, Rotterdam, The Netherlands


Drug use in the treatment of inflammatory bowel disease (IBD) might negatively impact lipid levels. In this study, we assessed drug-induced changes in the lipid profile after IBD induction therapy.


In this single center, prospective study IBD patients aged ≥17 years who started systemic drug therapy (corticosteroids, thiopurines, methotrexate, infliximab, adalimumab, vedolizumab, ustekinumab and tofacitinib) for IBD were included. Exclusion criteria were pregnancy, history of liver transplantation and use of lipid lowering drugs. Data on cardiovascular risk profile, disease activity (HBI, SCCAI, CRP, FCP) and concomitant medication use were collected. To calculate mean lipid changes after induction therapy, nonfasting lipid levels (total cholesterol (TC), HDL-c, LDL-c, triglycerides (TG)) were measured before and 8-10 weeks after start of therapy. Pearson correlation test was performed to assess the association between lipid changes and CRP.


A total of 183 patients (87 males (48%), median age 36 years (IQR 28-48), 128 Crohn’s disease (70%), 46 CU (3%), 9 IBD-U (7%)) were included. (Table 1) Fourty-nine patients were on concomitant steroids at baseline (31%). Relative increases in TC, HDL-c and LDL-c were significant after treatment with corticosteroids and tofacitinib (+9%, +17%, +8% and +19%, +29%, +24%, respectively) and decrease in TG after treatment with corticosteroids, thiopurines, infliximab, adalimumab, ustekinumab and tofacitinib (-9%, -14%, -10%, -8%, -11%, -8%, respectively). (Table 2, Figure 1) A significant inverse relationship was found between CRP and TC (R -.171), HDL-c (R -.202), LDL-c (R -.153) but not with TG.


Serum lipid levels increased most after start of corticosteroids and tofacitinib as compared to other drug therapies. Whether these changes are explained by the control of inflammation or by the mechanism of action of these agents remains undetermined.