The aim of this study was to assess the prognostic value of total serum bilirubin (TSB), gamma-glutamyl transpeptidase (GGT) and the TSB/GGT ratio in 129 consecutive cirrhotic patients, and to determine how seven other clinical and biochemical variables affect the prognostic value of these measurements. The Cox model and log rank test were used to compare survival rates at 1 year. Considered alone, encephalopathy, ascites, TSB, prothrombin time, serum albumin, GGT and the TSB/GGT ratio (TSB expressed in mumoles per liter and GGT in IU per liter were associated to the 1-year survival (p less than 0.10). The estimated per cent surviving at the end of 1 year was 20% for those with encephalopathy and 59% for those without, 46% and 62% for those with and without ascites, 28% for those with TSB greater than 3.0 mg per dl, 68% for those with TSB less than or equal to 3.0 mg per dl, 44% for those with GGT less than or equal to 100 IU per liter, 60% for those with GGT greater than 100 IU per liter, and 12% for those with TSB/GGT greater than 1, 66% for those with TSB/GGT less than or equal to 1. With the Cox model, which was used to assess the combined effect of several prognostic variables, GGT was the only biochemical variable which added significant prognostic value to TSB. The combination of TSB and GGT added significant prognostic value to encephalopathy and ascites.
Between March 1982 and September 1983, 40 inpatients (25 men and 15 women, mean age 53 years) with alcoholic cirrhosis and total serum bilirubin greater than or equal to 5 mg per dl were studied. Those with hepatocellular carcinoma, renal failure, hyponatremia, septicemia, spontaneous bacterial peritonitis, gastrointestinal bleeding, and hepatic coma were excluded. Patients were studied for 28 days. The two groups were offered an oral diet containing 40 kcal per kg per day. Patients in the supplementary parenteral nutrition group received 40 kcal per kg per day and 200 mg nitrogen per kg per day using a central catheter. The major endpoint was total serum bilirubin on Day 28. On admission, serum bilirubin was not significantly different in the two groups: oral group, 12.5 +/- 6.6 mg per dl; supplementary parenteral nutrition group, 12.3 +/- 8.5 mg per dl. On Day 28, serum bilirubin was lower in the supplementary parenteral nutrition group (2.5 +/- 1.4 mg per dl) than in the oral group (4.1 +/- 2.2 mg per dl) (p less than 0.02). Serum bilirubin was also lower in the supplementary parenteral nutrition group than in the oral group on Days 7, 14 and 21 (p less than 0.05). Analysis of covariance, considering serum bilirubin on admission and at randomization and time between admission and randomization, confirmed these results. On Day 28, anthropometric parameters, serum transferrin, prealbumin and retinol-binding protein were higher in the supplementary parenteral nutrition group, but the differences were not significant. Serum albumin was significantly lower in the supplementary parenteral nutrition group. The incidence of encephalopathy and sepsis was not significantly different between the two groups.
The in vivo activation state of the interferon system was biochemically evaluated in patients with HBsAg-positive liver disease by assaying the interferon-induced enzyme, 2'5'-oligoadenylate synthetase, in peripheral blood mononuclear cells. All patients with chronic active hepatitis had normal levels of enzyme activity. Increased values were found in 77% of patients with acute hepatitis, 50% of those with chronic persistent hepatitis and 54% chronic healthy carriers. These results provide evidence for lack of activation of the interferon system in HBsAg-positive chronic active hepatitis and support the hypothesis that an in vivo defective interferon response may aid in development of chronic active hepatitis.
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