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PubMed1992

Changes of the fibrinolytic system in liver dysfunction: role of portal hypertension.

The contribution of hemodynamic changes to the pathogenesis of accelerated fibrinolysis in liver disease was investigated in rats. In animals with hepatic lesions induced by a 7-week inhalation of carbon tetrachloride there was a significant increase in blood t-PA activity and PAI activity, with no significant change in portal pressure. Following a 10-min portal vein occlusion there was a marked increase in portal pressure and t-PA activity and a significant decrease in PAI activity. Following ligation of both portal vein and hepatic artery, t-PA activity increased to a higher extent and PAI activity was reduced to a lesser extent than changes found in portal-stenosed rats. Our data suggest that high t-PA circulating levels in liver disease could be related not only to the reduced t-PA clearance as a consequence of liver injury but also to hemodynamic changes.

Amino Acid Sequence↗
PubMed2003

Role of liver biopsy in the management of liver dysfunction after hematopoietic stem-cell transplantation in a hepatitis B virus-prevalent patient population.

BACKGROUND: Derangement of liver function tests (LFT) is common after hematopoietic stem-cell transplantation (HSCT). The role of liver biopsy in such cases has not been defined in hepatitis B virus (HBV)-prevalent patients. The impact of liver biopsy in the management of LFT derangement after HSCT in an HBV-prevalent population was examined. METHODS: Seventy-five liver biopsies, performed for 323 patients with LFT derangement post-HSCT (263 allogeneic, 60 autologous), were analyzed. The HBV carrier rate was 13.6%. RESULTS: Significantly more LFT derangements and therefore liver biopsies occurred in allogeneic versus autologous HSCT. Before biopsy, graft-versus-host disease (GVHD) and HBV reactivation were clinically diagnosed in 70.6% and 25.3% of cases, respectively. A definite histopathologic diagnosis was obtained after biopsy in 53 cases, with GVHD, HBV hepatitis, and concomitant GVHD-HBV hepatitis found in 33%, 21%, and 8% of cases, respectively. The clinical and histopathologic diagnoses were concordant in 43 cases and discordant in 9 cases. Clinical management was altered in six of nine discordant cases, five of which were caused by HBV or hepatitis C virus (HCV) reactivation. Twenty-two biopsy specimens showed nondiagnostic histopathologic features. Twenty of these cases were successfully managed on the basis of clinical diagnoses. The clinical-biochemical features of patients clinically diagnosed to have GVHD did not differ significantly whether or not they were HBV-HCV carriers. However, liver biopsies in HBV-HCV carriers resulted in significantly more treatment alterations as compared with noncarriers. CONCLUSIONS: Clinical diagnoses of LFT derangements post-HSCT might be adequate for initiation of treatment, but liver biopsies in HBV-HCV carriers were needed, as this might impact on management.

Adolescent↗