www.uptodate.com/contents/hepatobiliary-manifestations-of-inflammatory-bowel-disease I posted this in the fatty liver discussion previously but it is pertinent here too.
Most of the drugs used in the medical management of inflammatory bowel disease (IBD) have been associated with liver toxicity, although the overall incidence of serious complications is low [6,7]. The following are among the reactions that can be seen:
Sulfasalazine can cause both hepatocellular and cholestatic enzyme abnormalities, often related to a hypersensitivity reaction. Newer sulfa-free aminosalicylate preparations deliver increased amounts of the pharmacologically active ingredient of sulfasalazine (5-ASA, mesalamine) to the site of active bowel disease and are associated with a lower systemic toxicity. 5-ASA can rarely cause pancreatitis. (See "Sulfasalazine and 5-aminosalicylates in the treatment of inflammatory bowel disease".)
Azathioprine can cause a spectrum of hepatic injury, ranging from asymptomatic aminotransferase elevations (in approximately 5 percent of patients) to cholestasis, veno-occlusive disease, and peliosis hepatis. Mercaptopurine (6-MP), a metabolite of azathioprine, can also cause hepatocellular and cholestatic hepatitis. Thus, patients treated with azathioprine or 6-MP should have their liver biochemistries monitored regularly. Liver abnormalities usually resolve after discontinuation of therapy. (See "Immunomodulator therapy in Crohn's disease", section on 'Toxicity'.)
A metabolite of azathioprine, 6-thioguanine (6-TG), has been evaluated as an alternative immunosuppressant in inflammatory bowel disease. Unfortunately, in one study, elevated liver enzymes were noted in 26 percent of patients on 6-TG [8]. Nodular regenerative hyperplasia was found in 76 percent of liver biopsies of patients with liver enzyme abnormalities. In another study, nodular regenerative hyperplasia resulted in higher hepatic venous pressure gradients, causing clinically significant portal hypertension in some patients [9]. Because of these findings the authors recommended that this agent should not be used as therapy for patients with IBD. (See "Nodular regenerative hyperplasia of the liver".)
Methotrexate has been associated with macrovesicular steatosis, hepatic fibrosis, and cirrhosis in a cumulative dose response fashion. Routine liver biopsy has been advocated as a baseline and then after a cumulative dose of 1.5 to 2.0 gm. However, this recommendation has been challenged in light of the very low incidence of liver disease in patients with rheumatoid arthritis who, despite long-term use of methotrexate, are managed according to guidelines issued by the American College of Rheumatology [10]. Alcohol is a risk factor for methotrexate-induced liver disease and patients should be counseled about
strict avoidance of alcohol. (See "Hepatotoxicity associated with chronic oral methotrexate for nonmalignant disease".)
Infliximab has been associated with an increase in aminotransferases in patients with Crohn's disease. The increased ALT was usually less than twice the upper limit of normal and there is usually no clinical sequelae [11]. (See "Infliximab in Crohn's disease".) However, there have been case reports of severe cholestatic liver disease related to infliximab. Two patients recovered upon cessation of infliximab while one patient required liver transplantation [12-14]. (See "Tumor necrosis factor-alpha inhibitors: An overview of adverse effects".) Similarly, with adalimumab, mild elevations in liver enzymes have been reported [15]. In general, patients were asymptomatic; however, there are case reports of adalimumab-induced subacute liver failure and autoimmune hepatitis [16].
there is a great list of studies at that link.