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Relative Versus Absolute Carbohydrate‐Deficient Transferrin as a Marker of Alcohol Consumption in Patients With Acute Alcoholic Hepatitis
Author(s) -
Halm Ulrich,
Tannapfel Andrea,
Mössner Joachim,
Berr Frieder
Publication year - 1999
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1999.tb04051.x
Subject(s) - carbohydrate deficient transferrin , alcoholic liver disease , alcoholic hepatitis , transferrin , cirrhosis , medicine , gastroenterology , hepatitis , liver disease , alcohol , alcohol consumption , chemistry , biochemistry
Background : Carbohydrate‐deficient transferrin has been described as a sensitive and specific marker for alcohol consumption. This study investigated the usefulness of carbohydrate‐deficient transferrin as a marker of alcohol consumption in acute alcoholic hepatitis. Methods : Absolute concentrations (U/l) and relative values (%) of carbohydrate‐deficient transferrin dctermined in serum with commercial assays, as well as conventional markers for alcohol consumption, were compared with the alcohol consumption (as estimated by a questionaire) in patients with acute alcoholic hepatitis ( n = 19), alcoholic liver cirrhosis ( n = 37), and nonalcoholic liver diseases ( n = 16). Results : The concentration of carbohydrate‐deficient transferrin was increased ( p < 0.001) in nonabstaining paticnts (median intake 80 g alcohol/day) with alcoholic liver cirrhosis (45.7 ± 30 U/l), but not in patients with acute alcoholic hepatitis (20.0 ± 7.8 U/l) despite higher alcohol consumption (median 130 gid), nor in abstaincrs with alcoholic livcr cirrhosis (19.4 ± 6.0 U/l) or nonalcoholic liver disease (18.5 ± 6.7 U/l). However, the relative values of carbohydrate‐deficient transferrin were increased both in acute alcoholic hepatitis (7.9 ± 2.1%) and nonabstainers with alcoholic liver cirrhosis (7.4 ± 2.8%), but not in abstaincrs with alcoholic liver cirrhosis (4.6 ± 3.5%) or nonalcoholic liver disease (3.8 ± 0.9%) ( p < 0.001). In acute alcoholic hepatitis, the sensitivity and specificity were only 32% and 87% for absolute concentrations, rcspcctively, but 79% and 97% for relative values of carbohydrate‐deficient transferrin. The concentrations of carhohydrate‐deficient and total transferrin in serum were strongly correlated ( r = 0.60; p = 0.008). Conclusions : The relative value (% of total), but not the absolute concentration, of carbohydrate‐deficient transferrin in serum is a useful marker of alcohol consumption in acute alcoholic hepatitis.