The clinical problem of hepatitis transmission;

Although blood banks in this country have been testing every unit of blood for hepatitis B surface antigen (HBSAg) by one of the highly sensitive "third generation" methods (radioimmunoassay or reversed passive hemagglutination) since September, 1975, post-transfusion hepatitis (PTH) still remains the major hazard to patients who require transfusion with blood and blood products. Since there may be an interval of many months between transfusion and onset of PTH and many cases are subclinical, the best data on the incidence of PTH have come from prospective studies with careful follow-up of transfused patients. Such studies first established the validity of HBSAg as a marker for the presence of hepatitis B virus (HBV), and they have shown a dramatic reduction in the incidence of post-transfusion type B hepatitis following the elemination of HBSAg positive blood from transfusion. Nevertheless, PTH cases not associated with HBV or HAV, which are termed non-A, non-B hepatitis, continue to occur commonly among transfused patients. Non-A, non-B hepatitis appears to be subclinical in many instances, but it can produce prolonged persistence of abnormal liver function tests, which may be associated with chronic liver disease. The outstanding risk factor responsible for the development of PTH has been shown to be blood from paid donors in every study which has evaluated this factor. HBSAg and anti-HBS prevalences were found to be much higher in paid donor groups than in voluntary donors. Accordingly, the Food and Drug Administration has proposed that all units of blood be labeled to indicate whether they were collected from voluntary or paid donors in order to inform consumers of the relative hepatitis risks of blood units from these different donor populations. In addition to HBSAg testing and reduced use of blood from paid donors, measures which may provide future reduction of the hepatitis hazard associated with blood transfusion include avoidance of unnecessary transfusions, identification of the agent(s) responsible for non-A non-B hepatitis and development of tests for these agents, idenfification and avoidance of blood from donors implicated in PTH cases, development of methods for immunizing transfused patients against the various agents responsible for PTH, and use of frozen-washed red blood cells for transfusion. Efforts to develop and/or evaluate these various approaches are currently being actively pursued in many laboratories.