Current issues of ACP Journal Club are published in Annals of Internal Medicine


Long-term course of non-A, non-B post-transfusion hepatitis

ACP J Club. 1993 Nov-Dec;119:85. doi:10.7326/ACPJC-1993-119-3-085

Source Citation

Koretz RL, Abbey H, Coleman E, Gitnick G. Non-A, non-B post-transfusion hepatitis. Looking back in the second decade. Ann Intern Med. 1993 Jul 15;119:110-5.



To determine the long-term course of non-A, non-B post-transfusion hepatitis.


Inception cohort followed for 12 to 20 years.


A university hospital.


90 patients (mean age 53 y, 59 men) with normal serum alanine aminotransferase (ALT) levels before transfusion in whom non-A, non-B post-transfusion hepatitis developed. Successful follow-up was achieved in 80 patients (89%).

Assessment of prognostic factors

At least a telephone interview and laboratory tests were obtained to assess current and past health status.

Main outcome measures

Presence or absence of symptoms or signs of hepatitis and evidence of clinical hepatic failure. Symptomatic hepatitis was defined as the presence of one or more of jaundice, loss of appetite, weight loss, or fatigue. Clinical hepatic failure was defined as the presence of one or more of gastrointestinal bleeding of variceal origin, ascites, hepatic encephalopathy, hepatic coagulopathy, hypersplenism, or hypoalbuminemia.

Main results

40% of the patients had symptoms in the early phase of the illness; approximately 15% had jaundice. None of those in whom chronic hepatitis developed continued to have important symptoms. Evidence of clinical hepatic disease developed in 8 patients, 7 of whom had chronic hepatitis. It took ≥ 6 years for liver failure to become clinically apparent and, in 6 of the 8 patients, this event was observed in the second decade. After 16 years, the probability of demonstrable liver failure was 18% in the entire cohort, 21% in the subgroup in whom chronic hepatitis developed, 17% in the patients who had hepatitis C, and 20% in those with chronic hepatitis C. At least 33 of the original 90 patients who died had no evidence of liver failure. {The probability of death from nonhepatic causes was 41%.} (Information supplied by author.)


Non-A, non-B post-transfusion hepatitis was not a symptomatic disease for most patients. Clinical hepatic failure developed in few patients. If hepatic failure did occur, it was usually seen only after 10 years of disease.

Source of funding: Not stated.

For article reprint: Dr. R.L. Koretz, Department of Medicine, Olive View Medical Center, 14445 Olive View Drive, Sylmar, CA 91342, USA. FAX 818-364-4206.


Koretz and colleagues, in agreement with another recent study (1), report that only a few patients with post-transfusion hepatitis die from hepatic causes. In agreement with the literature, most cases (81.9%) were caused by hepatitis C. The authors conclude that chronic non-A, non-B hepatitis is purely a biochemical and histologic disease, and they hope to decrease the current therapeutic enthusiasm about using interferon for hepatitis C.

Strictly speaking, this conclusion applies only to patients with post-transfusion hepatitis who had decreased life-expectancy because of the disease that necessitated transfusions. Although hepatitis C is a major cause of liver transplantation and has been implicated in hepatocarcinogenesis, its natural history remains ill defined. Although most authors agree that the chronicity rate is about 50%, few survival curves have been published. Lashner and colleagues (2) reported a mortality rate of 5% for non-A, non-B hepatitis with histologic and liver function results being major predictors of death.

Although I agree with a conservative therapeutic approach for middle-aged patients with post-transfusion hepatitis, a more aggressive stance for younger patients with histologically active disease seems justified, because they may die from chronic hepatitis C. However, we clearly need better predictors of the natural evolution of the disease. In particular, a need exists for early identification of those patients likely to progress to liver cirrhosis and failure who may benefit from treatment. Viral load and genetic heterogeneity of the virus (3) and, perhaps, of the host are emerging as such predictors.

Jürg Reichen, MD
University of Berne Berne, Switzerland