title: Platelet lipoxygenase defect (Wien-Penzing defect) in two patients with myocardial infarction.
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-IFN alpha 1c might be able to eradicate the pathological platelet clone.
authors.affiliation: Atherosclerosis Research Group, University of Vienna, Austria.
authors.forename: H
authors.initials: H
authors.lastname: Sinzinger
authors.forename: J
authors.initials: J
authors.lastname: Kaliman
authors.forename: J
authors.initials: J
authors.lastname: O'Grady
mesh_terms: D000328:Adult; D001095:Arachidonic Acids / Q000378:metabolism; D001791:Blood Platelet Disorders / Q000150:complications / Q000201:enzymology* / Q000503:physiopathology; D001792:Blood Platelets / Q000201:enzymology* / Q000502:physiology; D002855:Chromatography, Thin Layer / Q000379:methods; D015232:Dinoprostone / Q000378:metabolism; D006801:Humans; D008084:Lipoxygenase / Q000097:blood*; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000201:enzymology* / Q000473:pathology; D010974:Platelet Aggregation / Q000502:physiology; D015230:Prostaglandin D2 / Q000378:metabolism; D013931:Thromboxanes / Q000378:metabolism
chemical_list: D001095:Arachidonic Acids; D013931:Thromboxanes; D008084:Lipoxygenase; D015232:Dinoprostone; D015230:Prostaglandin D2