Elikowski Waldemar, Hanszke Ewelina, Biczysko Wiesława, Rzeźniczak Janusz, Kruk-Zagajewska Aleksandra, Zawilska Krystyna
Oddział Chorób Wewnetrznych Szpitala Miejskiego ZOZ Poznań-Nowe Miasto, ul. Szwajcarska 3, 61-285 Poznań, Poland.
Kardiol Pol. 2007 Aug;65(8):985-91; discussion 992-3.
Some inherited platelet disorders may be revealed late, as in the presented case of a 68-year-old-man. Recurrent epistaxis following peri-interventional antiplatelet therapy (after three elective percutaneous coronary interventions) and an episode of upper gastrointestinal haemorrhage required aspirin withdrawal and less frequent clopidogrel use. Platelet studies showed an aspirin-like defect resulting in a lack of arachidonate-induced platelet aggregation. During dose-reduced (2-3 times a week) clopidogrel administration ADP-induced platelet aggregation was effectively inhibited and neither important bleeding nor stent thrombosis occurred. The inherited defect of cyclooxygenase-1, responsible for platelet thromboxane synthesis, did not protect the patient against coronary and extra-cardiac atherosclerosis.