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Interferon-α Treatment and Formation of Factor VIII Antibodies
- Eveline P. Mauser-Bunschoten, MD, PhD;
- Marjolein Damen, MD; and
- H. Marijke van den Berg, MD, PhD
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IN RESPONSE:
Dr. Stricker states that if no patients with mild hemophilia were included in our study, the conclusion should be that interferon-α therapy for chronic hepatitis C is not associated with alloantibody formation in patients with severe hemophilia. Indeed, we agree with this conclusion because the interferon-α group included only one patient with mild hemophilia. Most patients with severe hemophilia who received clotting factor concentrate before 1991 are infected with hepatitis C virus and need antiviral treatment (including interferon-α); thus, the conclusion of our study is of importance for such patients. The patient in our study who had clinical evidence of a factor VIII inhibitor during interferon-α therapy also had severe hemophilia.
We believe that the extent to which the reported cases of formation of factor VIII autoantibody in interferon-α recipients [1, 2] were related to the use of interferon-α remains unclear. The risk formation of factor VIII autoantibody associated with interferon-α therapy in patients with mild hemophilia and persons without hemophilia is unknown and must be studied.
Makris and Preston state that the incidence of new factor VIII inhibitors was 20 times greater than that reported in the Netherlands. The reported incidence of type A (persistent) inhibitors in the Netherlands is indeed 4.4 cases per 1000 patient-years [3]. However, the overall incidence of type A and B (transient) inhibitors is 29 per 1000 patient-years. Therefore, the incidence in our control group was three times greater (92 per 1000 patient-years) and the incidence in the interferon-α group was two times greater (69 per 1000 patient-years). This difference is not significant. The study by Rosendaal and colleagues on inhibitor incidence [3] was retrospective and was conducted after inhibitor levels suddenly increased as a result of a pasteurized intermediate product. In the interferon-α group, 13 of 21 patients received this product during treatment and 5 of 21 patients received this product before treatment began. In the control group, 10 of 14 patients were treated with this product. We found no correlation between the incidence of inhibitors in our study group and the pasteurized product. The higher incidence of inhibitors may be explained by the fact that inhibitor levels were measured more frequently during the study. Transient inhibitors will be detected more often.
Only through controlled studies can we estimate the risk for inhibitor development during interferon-α treatment. We found no increased risk in our study.
Eveline P. Mauser-Bunschoten, MD, PhD
Marjolein Damen, MD
H. Marijke van den Berg, MD, PhD
University Hospital Utrecht; 3508 AG Utrecht, the Netherlands
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
