V Simko1, S Michael, V Prego. 1. Section of Gastroenterology, Brooklyn Veterans Administration Medical Center.
Abstract
OBJECTIVES: to determine whether ursodeoxycholic acid (UDCA) is effective in improving primary biliary cirrhosis (PBC) or chronic hepatitis (CH). METHODS: Meta-analysis (MA) was performed on nine papers and three abstracts describing PBC and on nine papers and two abstracts with CH that were published between 1985 and 1992 and were identified through MEDLINE. Studies were included if they fulfilled established quality criteria and the patients had at least liver histology at the start and two to three relevant laboratory tests repeated after UDCA. A total of 800 patients with PBC were treated for 6-48 months. In CH, 285 patients were treated for 1-21 months. RESULTS: In PBC, an average daily UDCA of 13 mg/kg.day improved the liver tests AST, ALT, ALP, and GGT (all p < 0.001). The effect on serum bilirubin was too heterogeneous to evaluate. When evaluated individually, the studies showed an indeterminate effect on histologic progression and treatment failure. When pooled in MA, UDCA improved the liver histology (p < 0.001) and prevented treatment failure (p < 0.04). In CH, UDCA at an average of 11 mg/kg.day improved AST, ALT, GGT, and total bilirubin (all p < 0.001) and also ALP (p = 0.014). There was no effect on histology of CH and no data on treatment failure. CONCLUSIONS: MA confirmed a beneficial effect of UDCA in PBC on liver tests, histology, and treatment failure. In CH, there was an improvement in liver tests, but the evidence for histologic effect was sparse and insignificant. Future studies in PBC must explore the disease after UDCA is discontinued. Trials in CH should distinguish between the diagnostic subgroups, document patient compliance with UDCA, and include histology and treatment failure as end points.
OBJECTIVES: to determine whether ursodeoxycholic acid (UDCA) is effective in improving primary biliary cirrhosis (PBC) or chronic hepatitis (CH). METHODS: Meta-analysis (MA) was performed on nine papers and three abstracts describing PBC and on nine papers and two abstracts with CH that were published between 1985 and 1992 and were identified through MEDLINE. Studies were included if they fulfilled established quality criteria and the patients had at least liver histology at the start and two to three relevant laboratory tests repeated after UDCA. A total of 800 patients with PBC were treated for 6-48 months. In CH, 285 patients were treated for 1-21 months. RESULTS: In PBC, an average daily UDCA of 13 mg/kg.day improved the liver tests AST, ALT, ALP, and GGT (all p < 0.001). The effect on serum bilirubin was too heterogeneous to evaluate. When evaluated individually, the studies showed an indeterminate effect on histologic progression and treatment failure. When pooled in MA, UDCA improved the liver histology (p < 0.001) and prevented treatment failure (p < 0.04). In CH, UDCA at an average of 11 mg/kg.day improved AST, ALT, GGT, and total bilirubin (all p < 0.001) and also ALP (p = 0.014). There was no effect on histology of CH and no data on treatment failure. CONCLUSIONS: MA confirmed a beneficial effect of UDCA in PBC on liver tests, histology, and treatment failure. In CH, there was an improvement in liver tests, but the evidence for histologic effect was sparse and insignificant. Future studies in PBC must explore the disease after UDCA is discontinued. Trials in CH should distinguish between the diagnostic subgroups, document patient compliance with UDCA, and include histology and treatment failure as end points.