title: Relationship of Abnormal Chromatographic Pattern for Carbohydrate-Deficient Transferrin with Severe Liver Disease.
abstract: OBJECTIVE
  Serum carbohydrate-deficient transferrin (CDT) is a validated test for chronic heavy alcohol drinking, but CDT abnormalities have been associated with liver disease, limiting its use in these patients. We report here on the association between poor chromatographic resolution of disialotransferrin from trisialotransferrin (the so-called 'di-tri bridging') and liver disease severity and etiology.
  
  
  METHODS
  Subjects were patients in whom detailed clinical data, including histology results, were available on their existing liver diseases (n=139). Percent disialo-CDT (%dCDT) was measured by high-performance liquid chromatography, and the risks for di-tri bridging associated with cirrhosis, with and without adjustment for alcohol use and alcohol-related liver disease, were estimated.
  
  
  RESULTS
  Di-tri bridging was present in 22/73 (30%) cirrhotic subjects and 7/66 (11%) non-cirrhotic subjects. The unadjusted risk for di-tri bridging in cirrhotics relative to non-cirrhotics was 3.6 (95% confidence interval 1.4-9.2). Adjustment for alcohol-related liver disease and current drinking had little effect on this estimate (adjusted odds ratio 3.4), and neither alcohol-related liver disease nor current drinking were independently associated with di-tri bridging after accounting for the effect of cirrhosis.
  
  
  CONCLUSIONS
  The presence of di-tri bridging was associated with cirrhosis in individuals with both alcohol-related and non-alcoholic liver disease, although most cirrhotic subjects did not exhibit di-tri bridging. When di-tri bridging is seen in individuals being tested for chronic heavy drinking, investigation for cirrhosis should be considered.
  
  
  OBJECTIVE
  There are known liver-disease-associated abnormalities in CDT. In this study, we found that such abnormalities were strongly associated with cirrhosis rather than less-advanced disease, but were only clinically evident in 30% of cirrhotics. Abnormalities also occurred in severe hepatitis without cirrhosis and were not specific for liver disease etiology.
authors.affiliation: Division of General Internal Medicine, University at Buffalo , 462 Grider Street, Buffalo, NY 14215, USA ss243@buffalo.edu.
authors.forename: Scott H
authors.initials: SH
authors.lastname: Stewart
authors.affiliation: Division of Gastroenterology and Hepatology, Medical University of South Carolina, 96 Jonathan Lucas Street, Charleston, SC 29425, USA.
authors.forename: Adrian
authors.initials: A
authors.lastname: Reuben
authors.affiliation: Addiction Sciences Division, Medical University of South Carolina, 96 Jonathan Lucas Street, Charleston, SC 29425, USA.
authors.forename: Raymond F
authors.initials: RF
authors.lastname: Anton
mesh_terms: D000328:Adult; D000437:Alcoholism / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology; D015415:Biomarkers / Q000097:blood; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D005260:Female; D006801:Humans; D008104:Liver Cirrhosis, Alcoholic / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology; D008875:Middle Aged; D012720:Severity of Illness Index; D014168:Transferrin / Q000031:analogs & derivatives* / Q000378:metabolism
chemical_list: D015415:Biomarkers; D014168:Transferrin; C056759:carbohydrate-deficient transferrin