Search

Liver disease due to hepatitis C virus (HCV) is an increasingly frequent indication for liver transplantation. We performed a clinical and virological study of 20 HCV-infected liver transplant recipients to correlate virological markers with histological recurrence of disease.In ninety-four patients who were given transplants for end-stage cirrhosis, IgG and IgM antibodies to HCV and IgM to HCV tested by ELISA; all samples were further examined in a four-antigen recombinant immunoblot assay (2-RIBA). HCV viremia was measured by the conventional nested PCR, HCV genotype was determined by PCR amplification using type-specific primers. We have analyzed de novo infection by HCV, HCV recurrence and the influence of genotype in these recurrence.Nineteen of 20 antibody-positive patients (95%) had HCV RNA before transplantation. All 19 patients who were viremic before transplantation had persistent infection after LT. HCV genotype 1b was the predominant type before and after LT (75%). Ten of the 20 (50%) patients developed histological findings of chronic hepatitis (CH) in liver allografts. HCV recurrent liver disease after LT was not related with HCV genotype. Of 4 deaths after transplant in hepatitis C group, only one was related to recurrent disease. We have not found de novo hepatitis C.Our results indicate the general persistence of hepatitis C virus infection and the excellent short-term prognosis after liver transplantation. Chronic hepatitis by HCV in liver transplant was not related with HCV genotype.

The prevalence of HBV and HCV infections in patients with hepatocellular carcinoma may be related to variations in the geographic area of study. For this reason, we have analized the relative prevalence of HBV and HCV infections in 94 patients with hepatocellular carcinoma from Cantabria (North of Spain).We have studied 94 patients with hepatocellular carcinoma from January 1988 to December 1993. Commercially available radioimmunoassay or ELISA were used for detection of HBsAg, anti-HBs and anti-HBc. The HBV DNA was analized by PCR. The HCV infection was assayed by ELISA-2 and RT-PCR.The HBV infection was detected in 27 patients: 19 patients were HBsAg positive and 8 patients HBsAg negative, anti-HBc positive, DNA HBV positive by PCR. The HCV infection was found in 57 patients. Forty patients were infected with both viruses. Of the remain twenty-four, forty were alcoholics. We found in 61 patients more than one etiological factor. Hepatoma was the first manifestation of liver disease in 24 cases and these were more frequently in HCV than in those with HBV infection. Moreover, the first group were older and have lower alcohol intake.1) In Cantabria, Spain, the majority of cases of hepatocellular carcinoma are related to HBV, HCV and alcohol. 2) Analysis of DNA HBV and RNA HCV by PCR allows the diagnosis of cryptic infections by both viruses, especially in the cases of HBV and HCV coinfection. 3) Hepatoma is the first manifestation of liver disease in a high percentage of cases.

Chylous ascites is an accumulation of lymph in the abdominal cavity. The diagnosis is established when the concentration of triglycerides in plasma is greater than in ascitic fluid over a level of 200 mg/dl. The clinical and biochemical characteristics of 22 patients with chylous ascites (11 cirrhotics and 11 non cirrhotics) were studied in order to assess differences between patients with and without hepatic cirrhosis. The cirrhotic patients with chylous ascites showed lower protein (1.3 +/- 0.74 mg/dl, p = 0.002) and cholesterol concentration (46.0 +/- 45.2 mg/dl, p = 0.02) in ascitic fluid than non cirrhotic patients (3.1 +/- 1.09 mg/dl, and 100.85 +/- 41.7 mg/dl, respectively). In addition, the cellularity in the ascitic fluid was also lower in cirrhotic patients (209.09 +/- 113.96 cel/mm3) versus (831.8 +/- 945.08 cel/mm3; p0.05). Four patients (18.18%) presented high adenosine deaminase levels (ADA) in the ascitic fluid in the absence of tuberculous peritonitis. The authors conclude that the biochemical differences observed in the ascitic fluid of the cirrhotic patients with chylous ascites may be explained by a dilutional mechanism due to the combination of "clear" ascites secondary to portal hypertension and chylous ascites. Furthermore, chylous ascites could be the cause of an elevation in ADA in the absence of tuberculous peritonitis.