[Antiplatelet therapy can unmask an inherited bleeding disorder. Aspirin-like defect of platelets does not protect against atherosclerosis].
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.
Elikowski
Waldemar
W
Oddział Chorób Wewnetrznych Szpitala Miejskiego ZOZ Poznań-Nowe Miasto, ul. Szwajcarska 3, 61-285 Poznań, Poland. welikowski@wp.pl
Hanszke
Ewelina
E
Biczysko
Wiesława
W
Rzeźniczak
Janusz
J
Kruk-Zagajewska
Aleksandra
A
Zawilska
Krystyna
K
D000368:Aged; D001241:Aspirin / Q000009:adverse effects*; D001791:Blood Platelet Disorders / Q000175:diagnosis* / Q000201:enzymology*; D003324:Coronary Artery Disease / Q000517:prevention & control; D051545:Cyclooxygenase 1 / Q000187:drug effects; D006801:Humans; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects*; D013931:Thromboxanes / Q000096:biosynthesis
D010975:Platelet Aggregation Inhibitors; D013931:Thromboxanes; D051545:Cyclooxygenase 1; D001241:Aspirin