L. Santos

Liver transplantation for fulminant and subfulminant hepatic failure.

AIMS The aim of this study was to assess the long-term course and outcome after liver transplantation (LTX) for fulminant/subfulminant hepatic failure (FSHF) to determine which factors relate to outcome. PATIENTS AND METHODS Between April 1990 and October 2002, 30 adult patients with FSHF underwent LTX. Kings College criteria were used to decide which patients needed LTX. Pretransplantation parameters (age, sex, degree of hepatic encephalopathy, etiology, and time between onset of symptoms and LTX) were examined as risk factors for LTX outcome. RESULTS Mean age at LTX was 40.4+/-13.9 years and 46.7% were men. The most frequent causes of FSHF were virus B in 23.3%, autoimmune hepatitis in 23.3%, and cryptogenic in 20%. Fifty percent of the patients with a survival longer than 15 days suffered episodes of acute rejection; chronic rejection occurred in 25%. One- and five-year patient and allograft survival rates for FSHF were 56.3% and 54.7%, respectively. Autoimmune hepatitis was the only factor associated with better posttransplantation outcome, although there were no differences in posttransplant course. Patient survival rates increased during the study period. During the first 5 years (1990-1995) the survival rates were 53.3% (1-year and 5-year), whereas they were 60% at 1 and 5 years in the second interval (1996-2002). CONCLUSIONS The mortality rate of FSHF is high during the first year post-LTX. LTX for FSHF of autoimmune etiology showed better outcomes with increasing patient survival rates during the study period.

Modulation of ICAM‐1 tissue expression in patients with liver transplantation (LT) and acute rejection (AR) after glucocorticoid treatment

Abstract Acute rejection (AR) is a frequent complication following liver transplantation (LT). ICAM‐1 may be involved in its pathogenesis. High doses of glucocorticoids are the standard treatment in these patients. The aim of this study was to describe corticoid effects on ICAM‐1 tissue expression in liver biopsies of patients with LT and AR. The study included liver biopsies performed before and after treatment in 12 patients with LT and proven AR. In 10 patients AR was reversible and in 2, was steroid resistant. For immunohistochemistry, an indirect immunoperoxidase technique was used. Each histology section was semiquantitatively evaluated as follows: 0: <10% staining, 1: 10‐25%, 2: 25‐50%, 3: >50%. The control group comprised nine patients with LT and normal liver biopsies. In pre‐treatment liver biopsy samples, ICAM‐1 was markedly expressed on sinusoidal cells (2.41 ± 0.66), and there was also expression on periportal (0.66 ± 0.65) and perivenular hepatocytes (0.83 ± 0.57). By contrast, in the liver tissue from the control group, sinusoidal ICAM‐1 reactivity was significantly lower (0.88 ± 0.33; P < 0.05), and hepatocytes showed no reliable ICAM‐1 expression. After steroid treatment the intensity of ICAM‐1 decreased significantly in sinusoids (1.5 ± 0.67; P < 0.05) and in perivenular hepatocytes (0.25 ± 0.86; P < 0.05). Additionally, we also observed a decreased ICAM‐1 reactivity in portal hepatocytes (0.25 ± 0.62), but these differences did not reach statistical significance. Remarkably, after treatment, hepatocytes did not show ICAM‐1 reactivity in resolved AR, but in corticoid‐resistant patients AR did not change or increase. In conclusion, in patients with LT and AR, ICAM‐1 was expressed in hepatocytes and with more intensity in sinusoid cells. Additionally, a down‐regulation of the ICAM‐1 tissue expression after corticoid treatment may exist, although in corticoid‐resistant AR no modulation on ICAM‐1 tissue expression was observed.