title: Increased plasma tumor necrosis factor in severe alcoholic hepatitis.
abstract: OBJECTIVE
  To determine whether elevated tumor necrosis factor levels contribute to the clinical manifestations and complications of severe acute alcoholic hepatitis and to evaluate the relation between tumor necrosis factor and plasma levels of endotoxin and interleukin-1 beta.
  
  
  METHODS
  Prospective, controlled study.
  
  
  METHODS
  The liver unit of a university teaching hospital.
  
  
  METHODS
  We studied 21 patients with acute severe alcoholic hepatitis. There were four control groups: patients with inactive alcoholic cirrhosis, alcoholic persons without liver disease, patients with impaired renal function, and normal subjects.
  
  
  RESULTS
  With one exception, patients with alcoholic hepatitis had higher tumor necrosis factor levels (mean, 26.3 ng/L; 95% CI, 21.7 to 30.9) than normal subjects (6.4 ng/L; CI, 5.4 to 7.4). Patients who subsequently died had a higher tumor necrosis factor level (34.7 ng/L; CI, 27.8 to 41.6) than survivors (16.6 ng/L; CI, 14.0 to 19.2). In patients with alcoholic hepatitis, tumor necrosis factor levels correlated positively with serum bilirubin (r = 0.74; P = 0.0009) and serum creatinine (r = 0.81; P = 0.0003). Patients with alcoholic hepatitis had higher tumor necrosis factor levels than patients with inactive alcoholic cirrhosis (11.1 ng/L; CI, 8.9 to 13.3) and severely alcoholic persons without liver disease (6.4 ng/L; CI, 5.0 to 7.8). Patients with abnormal renal function had lower tumor necrosis factor levels (14.1 ng/L; CI, 5.4 to 22.8) than patients with alcoholic hepatitis. Serial samples obtained during a 1-week period from patients with alcoholic hepatitis showed no significant change in tumor necrosis factor when patients who died were compared with survivors. No correlation was found between tumor necrosis factor and plasma endotoxin. Levels of interleukin-1 beta did not exceed 20 ng/L.
  
  
  CONCLUSIONS
  Elevations in tumor necrosis factor in alcoholic hepatitis are most marked in severe cases, suggesting that tumor necrosis factor plays a role in the pathogenesis.
authors.affiliation: King's College Hospital, Denmark Hill, London, United Kingdom.
authors.forename: G L
authors.initials: GL
authors.lastname: Bird
authors.forename: N
authors.initials: N
authors.lastname: Sheron
authors.forename: A K
authors.initials: AK
authors.lastname: Goka
authors.forename: G J
authors.initials: GJ
authors.lastname: Alexander
authors.forename: R S
authors.initials: RS
authors.lastname: Williams
mesh_terms: D000437:Alcoholism / Q000097:blood; D001663:Bilirubin / Q000097:blood; D003627:Data Interpretation, Statistical; D004731:Endotoxins / Q000097:blood; D005260:Female; D006519:Hepatitis, Alcoholic / Q000097:blood* / Q000401:mortality; D006801:Humans; D007375:Interleukin-1 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood; D008104:Liver Cirrhosis, Alcoholic / Q000097:blood; D008297:Male; D011446:Prospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D004731:Endotoxins; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D001663:Bilirubin