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Platelet lipoxygenase defect (wien‐penzing defect) in two patients with myocardial infarction
Author(s) -
Sinzinger Helmut,
Kaliman Josef,
O'Grady John
Publication year - 1991
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830360308
Subject(s) - platelet , medicine , myocardial infarction , arachidonic acid , in vivo , bone marrow , thromboxane , lipoxygenase , pathological , cardiology , enzyme , chemistry , biochemistry , biology , microbiology and biotechnology
Abstract In 2 male patients (35 and 38 years) presenting with myocardial infarction an abnormal conversion of exogenous 14C‐arachidonic acid by the patients' platelets, incubated in vitro, was observed. Neither patient's platelets showed evidence of a lipoxygenase pathway. Platelet thromboxane formation from exogenous and endogenous substrate was high, while the platelet aggregation responses were normal. A myeloproliferative syndrome was excluded by bone marrow puncture. Similar defects have only been described so far in patients with myeloproliferative syndrome. This defect may be causative for the onset of clinical thrombotic events. It is speculative whether in vivo therapy with r‐IFNα1c might be able to eradicate the pathological platelet clone.