Send to

Choose Destination
Am J Gastroenterol. 2007 Feb;102(2):344-50. Epub 2006 Nov 13.

Abnormal hepatic biochemistries in patients with inflammatory bowel disease.

Author information

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota 55905, USA.



The relationship between abnormal hepatic biochemistries and inflammatory bowel disease (IBD) is unclear. We determined the prevalence of abnormal hepatic biochemistries and chronic liver disease in a cohort of IBD patients, and we compared patients with normal and abnormal liver biochemistries.


Patients with IBD evaluated at our institution between January 1, 2000 and December 31, 2000 were identified. Data on gender, age, IBD subtype, extent and activity, medications, liver disease history, liver biochemistries, and vital status were collected. The chi(2) test, Student's t-test, and Cox proportional regression were used.


We identified 544 patients with available hepatic biochemistries. Abnormal hepatic biochemistries were found in 159 (29%). Defined chronic liver disease was present in 5.8% of patients (primary sclerosing cholangitis in 4.6%). The prevalence of abnormal hepatic biochemistries was 27% for those with active IBD and 36% for those in remission (P= 0.06). Patients with abnormal hepatic biochemistries were less frequently on 5-aminosalicylates (35%vs 51%, P < 0.001), and a smaller proportion was alive at last follow-up (90.4%vs 98.5%, P < 0.0001). The age-adjusted risk of death was 4.8 times higher in patients with abnormal hepatic biochemistries, after excluding patients with any diagnosis of liver disease.


Abnormal hepatic biochemistries were present in nearly one-third of our patients, and surprisingly, they were not associated with IBD activity. Abnormal hepatic biochemistries and chronic liver disease appeared to have a negative impact on vital status. Persistently abnormal hepatic biochemistries should be evaluated, and not attributed to IBD activity.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center