The Declining Risk of Post-Transfusion Hepatitis C Virus Infection

The most common serious complication of blood transfusion is post-transfusion hepatitis from the hepatitis C virus (HCV). Blood banks now screen blood donors for surrogate markers of non-A, non-B hepatitis and antibodies to HCV, but the current risk of post-transfusion hepatitis C is unknown. From 1985 through 1991, blood samples and medical information were obtained prospectively from patients before and at least six months after cardiac surgery. The stored serum samples were tested for antibodies to HCV by enzyme immunoassay, and by recombinant immunoblotting if positive. Of the 912 patients who received transfusions before donors were screened for surrogate markers, 35 seroconverted to HCV, for a risk of 3.84 percent per patient (0.45 percent per unit transfused). For the 976 patients who received transfusions after October 1986 with blood screened for surrogate markers, the risk of seroconversion was 1.54 percent per patient (0.19 percent per unit). For the 522 patients receiving transfusions since the addition in May 1990 of screening for antibodies to HCV, the risk was 0.57 percent per patient (0.03 percent per unit). The trend toward decreasing risk with increasingly stringent screening of donors was statistically significant (P<0.001). After we controlled for the method of donor screening, the risk of seroconversion was strongly associated (P<0.001) with the volume of blood transfused, but not with the use of particular blood components. The incidence of post-transfusion hepatitis C has decreased markedly since the implementation of donor screening for surrogate markers and antibodies to HCV. The current risk of post-transfusion hepatitis is about 3 per 10,000 units transfused. (N Engl J Med 1992; 327:369–73.), THE current risk of transfusion-associated non-A, non-B hepatitis is unknown, but it is undoubtedly lower than the estimates of 5 to 18 percent that were given in prospective studies conducted in the 1970s and early 1980s.^{1 2 3} Research conducted during that period to identify the etiologic agent or agents of non-A, non-B hepatitis was unsuccessful, as were attempts to develop an assay to screen blood obtained from potentially infectious donors.⁴ In the absence of a specific test, in late 1986 blood-collection agencies began screening donated blood for surrogate markers of non-A, non-B hepatitis — namely, elevated levels of alanine aminotransferase and…