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Thromb Haemost 1995; 74(02): 616-618
DOI: 10.1055/s-0038-1649785
Original Article
Clinical Studies
Schattauer GmbH Stuttgart

Risk of Hepatitis A in Dutch Hemophilia Patients

E P Mauser-Bunschoten
1   The Van Creveld Clinic, University Hospital Utrecht, The Netherlands
,
H L Zaaijer
2   The Department of Viral Serology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands
,
A A J van Drimmelen
3   The Wilhelmina Childrens Hospital, Utrecht, The Netherlands
,
H M van den Berg
1   The Van Creveld Clinic, University Hospital Utrecht, The Netherlands
3   The Wilhelmina Childrens Hospital, Utrecht, The Netherlands
,
G Roosendaal
1   The Van Creveld Clinic, University Hospital Utrecht, The Netherlands
,
P N Lelie
2   The Department of Viral Serology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands
› Author Affiliations
Further Information

Publication History

Received 09 January 1995

Accepted after revision 29 March 1995

Publication Date:
04 July 2018 (online)

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Summary

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 213% 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.

 

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