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Background: Serum carbohydrate deficient transferrin is a marker of chronic alcohol consumption; it increases above normal in healthy individuals after a daily alcohol intake of more than 60 g/d for more than 2 weeks. The influence of liver disease itself on carbohydrates deficient transferrin levels has not been sufficiently established. Methods: We investigated serum levels of carbohydrate deficient transferrin in 196 consecutive patients admitted to our Gastroenterology and Hepatology Unit and correlated this parameter with the patients' statements about alcohol intake during the previous 2 weeks and with other markers of chronic alcohol consumption. Results: In our patient population, carbohydrate deficient transferrin had the best overall performance with respect to sensitivity (88%), specificity (82%), and negative predictive value (98%), as compared to other markers, although specificity was much lower than previously reported in patients without liver disease. In the group of patients with liver disease, sensitivity and specificity were 90% and 73%, respectively, and in patients without liver disease, 80% and 88%. The negative predictive value was excellent (96% for patients with liver disease and 99% for patients without liver disease). Conclusions: Thus, in a patient with a negative interview for chronic alcohol abuse and normal carbohydrate deficient transferrin level, alcohol is unlikely to be the cause of liver disease, and further investigations to establish the etiology of liver disease are warranted. An increased carbohydrate deficient transferrin level, however, cannot be regarded as reliable evidence for chronic alcohol abuse in patients with liver disease.

Elevated concentrations of lipopolysaccharide have been found in serum of patients with severe parenchymal liver disease and its toxic effect is thought to involved in hemodynamic disturbances seen in cirrhosis. A soluble form of the receptor (sCD14) for lipopolysaccharide is present in serum and is released by stimulated macrophages, indicating macrophage activation. We investigated sCD14 serum levels and in vitro production by lipopolysaccharide stimulated peripheral blood monocytes in patients with various liver diseases. In acute viral hepatitis serum sCD14 levels were significantly higher during the first 2 weeks after onset of jaundice (n=11; 3.6 +/- 0.9 microg /ml (mean +/- SD)) than in healthy control individuals (n=52; 2.5 +/- 0.7 microg/ml; p

Serum levels and production of soluble CD8 and soluble CD4 antigens by peripheral blood mononuclear cells were determined in patients with alcoholic cirrhosis and acute or chronic viral hepatitis. Patients with chronic viral hepatitis had significantly increased soluble CD8 serum levels (n = 18; 734 +/- 143 U/ml) (mean +/- SD) compared to healthy controls (n = 80; 312 +/- 141 U/ml; p0.001) and patients with alcoholic cirrhosis (n = 12; 505 +/- 256 U/ml; p = 0.006), whose soluble CD8 concentrations were also higher than controls (p0.001). In contrast, soluble CD4 antigen serum levels were similar in all groups. In addition, patients with chronic hepatitis showed an increased production of soluble CD8, but not soluble CD4, after mitogenic stimulation of their peripheral blood mononuclear cells compared to controls or patients with alcoholic cirrhosis. Patients with acute viral hepatitis, studied within the first 2 weeks after onset of jaundice, showed markedly elevated serum concentrations of soluble CD8 (n = 4; 807 +/- 379 U/ml; p0.001 vs. controls), but not soluble CD4. In addition, nine patients with chronic hepatitis C were studied during and after treatment with alpha interferon. Soluble CD8 serum concentrations of six treatment responders were not found to be different from the low levels seen in controls, whereas three non-responders had increased soluble CD8 levels which were similar to levels in untreated patients with chronic hepatitis C. After interferon-alpha therapy ended, a significant elevation of soluble CD8 serum concentrations was observed in four relapsing patients, which paralleled the serum ALT increase.(ABSTRACT TRUNCATED AT 250 WORDS)