Abstract
A deficiency of ADAMTS13 leads to platelet clumping and/or thrombi formation, finally resulting in thrombotic thrombocytopenic purpura (TTP). In this study, a 62-year-old male with chronic hepatitis C developed TTP a month after long-term pegylated-interferon (PEG-IFN) treatment. The observed low level of activity of plasma ADAMTS13 following PEG-IFN treatment was shown to gradually increase with the improvement of TTP, while the titer of an inhibitory anti- ADAMTS13 IgG antibody decreased concomitant with the increase in ADAMTS13 activity. Serial determination of ADAMTS13 activity and its inhibitor may provide useful information for the diagnosis and treatment of IFN-associated TTP, as well as its pathogenesis.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
MeSH terms
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ADAM Proteins / deficiency*
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ADAM Proteins / immunology
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ADAMTS13 Protein
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Female
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Hepatitis C, Chronic / drug therapy
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Hepatitis C, Chronic / immunology
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Hepatitis C, Chronic / metabolism*
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Humans
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Interferon alpha-2
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Interferon-alpha / adverse effects*
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Interferon-alpha / therapeutic use
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Male
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Middle Aged
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Polyethylene Glycols / adverse effects*
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Polyethylene Glycols / therapeutic use
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Purpura, Thrombotic Thrombocytopenic / chemically induced*
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Purpura, Thrombotic Thrombocytopenic / diagnosis
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Purpura, Thrombotic Thrombocytopenic / immunology
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Recombinant Proteins
Substances
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Interferon alpha-2
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Interferon-alpha
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Recombinant Proteins
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Polyethylene Glycols
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ADAM Proteins
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ADAMTS13 Protein
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ADAMTS13 protein, human
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peginterferon alfa-2a