BACKGROUND/AIMS: An ability to measure inflammatory activity in alcoholic hepatitis is desirable for assessing its natural history and therapeutic responses, but convenient and simple parameters are lacking. To determine whether acute phase proteins could be useful for this purpose, we studied serum CRP and several other acute phase proteins in a series of patients with alcoholic hepatitis. MATERIALS AND METHODS: We examined sequential sera from 72 patients with serum bilirubin greater than 5 mg/dl. RESULTS: The short-term mortality during the approximately 30 day study period was 18%. There was moderate to marked elevation of serum c-reactive protein at initial testing in all patients with alcoholic hepatitis. In consecutive sera within the first week of testing, a further rise in c-reactive protein was noted significantly more frequently among patients that did not survive subsequently. Serum c-reactive protein levels gradually declined in recovering patients but were still abnormal at the end of the study period. In contrast, serum haptoglobin levels were subnormal initially, as well as throughout the subsequent short-term course. Among other acute phase proteins, serum ceruloplasmin, transferrin, a-1 acid glycoprotein and a-2 macroglobulin remained in the normal range. CONCLUSIONS: These results suggest that the expression of c-reactive protein but not haptoglobin is upregulated in alcohol-induced acute liver injury. Serial measurements of serum c-reactive protein should be useful in assessing the clinical activity of alcoholic hepatitis.
BACKGROUND/AIMS: An ability to measure inflammatory activity in alcoholic hepatitis is desirable for assessing its natural history and therapeutic responses, but convenient and simple parameters are lacking. To determine whether acute phase proteins could be useful for this purpose, we studied serum CRP and several other acute phase proteins in a series of patients with alcoholic hepatitis. MATERIALS AND METHODS: We examined sequential sera from 72 patients with serum bilirubin greater than 5 mg/dl. RESULTS: The short-term mortality during the approximately 30 day study period was 18%. There was moderate to marked elevation of serum c-reactive protein at initial testing in all patients with alcoholic hepatitis. In consecutive sera within the first week of testing, a further rise in c-reactive protein was noted significantly more frequently among patients that did not survive subsequently. Serum c-reactive protein levels gradually declined in recovering patients but were still abnormal at the end of the study period. In contrast, serum haptoglobin levels were subnormal initially, as well as throughout the subsequent short-term course. Among other acute phase proteins, serum ceruloplasmin, transferrin, a-1 acid glycoprotein and a-2 macroglobulin remained in the normal range. CONCLUSIONS: These results suggest that the expression of c-reactive protein but not haptoglobin is upregulated in alcohol-induced acute liver injury. Serial measurements of serum c-reactive protein should be useful in assessing the clinical activity of alcoholic hepatitis.