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Increased Plasma Tumor Necrosis Factor in Severe Alcoholic Hepatitis

George L.A. Bird, MB; Nick Sheron, MB; A.K. John Goka, MB; Graeme J. Alexander, MB; and Roger S. Williams, MD
[+] Article and Author Information

Grant Support: Dr. Sheron is supported by the Wellcome Trust.

Requests for Reprints: Roger Williams, MD, Liver Unit, King's College Hospital, Denmark Hill, London SE5 9RS, United Kingdom.

Current Author Addresses: Drs. Bird, Sheron, Goka, Alexander, and Williams: Liver Unit, King's College Hospital, Bessemer Road, London SE5 9RS, United Kingdom.


© 1990 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1990;112(12):917-920. doi:10.7326/0003-4819-112-12-917
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Study 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-1ß

Design: Prospective, controlled study.

Setting: The liver unit of a university teaching hospital.

Patients: 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.

Measurements and Main 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-1ß 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.

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