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Risk of hepatitis A in Dutch hemophilia patients
E P Mauser-Bunschoten1, H L Zaaijer, A A van Drimmelen
1Van Creveld Clinic, University Hospital Utrecht, The Netherlands.
Recently, clotting factor preparations transmitted hepatitis A virus (HAV) to hemophilia patients. To study the risk of HAV infection in Dutch hemophilia patients, serum samples of 341 patients with hemophilia were tested for HAV antibodies (anti-HAV). 197/341 patients (group 1) were treated with clotting factor concentrates produced from large plasma pools, 144/341 patients (group 2) were treated with small pool cryoprecipitate. The test results were compared to those of healthy blood donors (n = 19,746) of the same age. In addition stored serum samples (1983-1994) from hemophilia patients were tested for HAV antibodies. No increased risk of HAV infection was found in Dutch hemophilia patients. The anti-HAV prevalence in group 1 was 20%, in group 2 13% and in blood donors 41%. A significantly (p < 0.002) lower percentage of HAV antibodies was found in hemophilia patients born in the 1950s using cryoprecipitate (11%) as compared to blood donors of the same age (40%), probably caused by passive administration of anti-HAV through clotting product. Passive immunization in the past was significantly (p < 0.02) more often found in group 2 (41.7%) than in group 1 (28%). In the period 1983 till 1988 five seroconversions were seen in group 1 (2%) and one in group 2 (0.7%). Anti-HAV seroconversions were not observed after 1988. In a risk analysis we estimated that 2 plasma pools of 10,000 Dutch blood donors per year may contain HAV. The absence of HAV among Dutch hemophilia patients suggests that this contamination is successfully inactivated.
Recently, clotting factor preparations transmitted hepatitis A virus (HAV) to hemophilia patients. To study the risk of HAV infection in Dutch hemophilia patients, serum samples of 341 patients with hemophilia were tested for HAV antibodies (anti-HAV). 197/341 patients (group 1) were treated with clotting factor concentrates produced from large plasma pools, 144/341 patients (group 2) were treated with small pool cryoprecipitate. The test results were compared to those of healthy blood donors (n = 19,746) of the same age. In addition stored serum samples (1983-1994) from hemophilia patients were tested for HAV antibodies. No increased risk of HAV infection was found in Dutch hemophilia patients. The anti-HAV prevalence in group 1 was 20%, in group 2 13% and in blood donors 41%. A significantly (p < 0.002) lower percentage of HAV antibodies was found in hemophilia patients born in the 1950s using cryoprecipitate (11%) as compared to blood donors of the same age (40%), probably caused by passive administration of anti-HAV through clotting product. Passive immunization in the past was significantly (p < 0.02) more often found in group 2 (41.7%) than in group 1 (28%). In the period 1983 till 1988 five seroconversions were seen in group 1 (2%) and one in group 2 (0.7%). Anti-HAV seroconversions were not observed after 1988. In a risk analysis we estimated that 2 plasma pools of 10,000 Dutch blood donors per year may contain HAV. The absence of HAV among Dutch hemophilia patients suggests that this contamination is successfully inactivated.