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Interferon-α Treatment and Formation of Factor VIII Antibodies
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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 Unpublished letters cannot be returned.
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TO THE EDITOR:
Mauser-Bunschoten and colleagues [1] describe an apparent lack of association between formation of factor VIII inhibitors and long-term interferon-α therapy in patients with hemophilia A and chronic hepatitis C. The study addresses two reports of acquired factor VIII inhibitors in “dissimilar” patients with and without hemophilia who received long-term interferon-α treatment [2, 3]. Although the current findings are reassuring, they also raise intriguing questions about the pathogenesis of factor VIII antibodies and interferon-α-induced autoimmunity.
Factor VIII inhibitors may arise as alloantibodies in patients with severe hemophilia A (factor VIII level < 1%) or as autoantibodies in persons without hemophilia [2]. Immunosuppressive therapy is generally ineffective against alloantibody inhibitors but may work against autoantibody inhibitors [4]. This observation suggests that different immunologic mechanisms may be involved in the pathogenesis of the two inhibitor subtypes [5]. Furthermore, alloantibodies and autoantibodies against factor VIII are associated with different patterns of bleeding [3]. In this regard, the previous “dissimilar” cases of interferon-α-associated factor VIII inhibitors have a strong common feature: Both cases involved bleeding patterns typical of autoantibody inhibitors. In particular, one of the patients had mild hemophilia [3], with a baseline factor VIII level of 8%; this patient seems to have developed an autoantibody rather than an alloantibody inhibitor against factor VIII after long-term interferon-α therapy.
In light of these facts, it would be important to know the number (if any) of patients with mild hemophilia in Mauser-Bunschoten and colleagues' study. If there were few or none, then the conclusion of the study should be that long-term interferon-α therapy is not associated with formation of alloantibody inhibitors in patients with severe hemophilia A. A plausible explanation is that the immunopathogenesis of alloantibodies is not influenced by interferon-α [5]. In contrast, the risk for development of autoantibody inhibitors in patients with mild hemophilia and persons without hemophilia who receive interferon-α remains poorly defined and potentially fatal [2].
Raphael B. Stricker, MD
California Pacific Medical Center; San Francisco, CA 94120
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
