Carbohydrate-deficient transferrin in alcoholics with liver disease.

To assess the relationship between carbohydrate-deficient transferrin (CDT) and alcoholic liver disease, we measured the ratio of carbohydrate-deficient transferrin to total transferrin (rCDT) in 32 male alcoholics with liver disease (Child-Pugh class A, 8; B, 11; C, 13) and 14 male alcoholics without clinically evident liver disease. Twenty of 32 with liver disease and six of 14 without clinically apparent liver disease had recent abstinence. The 32 patients with liver disease were assessed, in addition to the Child-Pugh class, using a linear prognostic score, the Combined Clinical and Laboratory Index (CCLI). Transferrin and CDT were measured by isocratic anion exchange chromatography and a radio-immunoassay. When the total group (n = 46) was divided into those with recent abstinence (n = 26) and those without (n = 20), the rCDT was lower in the abstainers than non-abstainers (0.7 +/- 0.6 vs 2.9 +/- 2.4, P < 0.005). Similarly, abstainers with liver disease (n = 20) had a significantly lower rCDT than non-abstainers (n = 12) with liver disease (0.7 +/- 0.7 vs 3.5 +/- 2.8, P < 0.005). The rCDT in the 20 abstaining patients with liver disease did not differ significantly between Child-Pugh classes. Furthermore, there was no correlation between the CCLI and rCDT (r = 0.05). We conclude that the relationship between rCDT and alcohol abuse is not appreciably altered by the presence of clinically severe liver disease in male alcoholics.

Diagnosis and treatment of the major hepatotropic viruses.

The hepatotropic viruses currently include hepatitis A, B, C, D, and E, and are associated with a spectrum of acute and chronic liver disease syndromes. The epidemiology and natural history of each are discussed, with emphasis on uncommon or newly recognized clinical presentations. The serodiagnosis of hepatitis A, B, and D is well established; the serodiagnosis of hepatitis C and E continues to evolve as serologic and virologic assays become refined. Hepatitis A and E only cause acute liver injury; current medical approaches therefore focus on vaccination strategies. Hepatitis B, C, and D can cause both acute and chronic liver injury. Sequelae of chronic liver disease, including portal hypertension and hepatocellular carcinoma, are not uncommon. Medical therapy of resulting chronic liver disease currently consists of interferon, though other anti-viral strategies are being explored. Advanced chronic liver disease due to hepatitis B, C, or D can be treated by orthotopic liver transplantation, but viral recurrence is near uniform and can be problematic. Further study of the hepatotropic viruses at the molecular biologic, epidemiologic, and clinical levels will continue to provide greater insight into the diagnosis and management of their associated clinical syndromes.