ABSTRACT
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.
Subject(s)
Aspirin/adverse effects , Blood Platelet Disorders/diagnosis , Blood Platelet Disorders/enzymology , Platelet Aggregation Inhibitors/adverse effects , Aged , Coronary Artery Disease/prevention & control , Cyclooxygenase 1/drug effects , Humans , Male , Platelet Aggregation/drug effects , Thromboxanes/biosynthesisABSTRACT
Antiphospholipid syndrome (APS) is a systemic autoimmune disorder, where the essence of the matter is the existence of antiphospholipid antibodies. The typical symptoms of APS are: venous thrombo-embolic disease and artery thrombosis in a brain. The authors present 5 patients (2 females and 3 males) at the age of 36-54 with ischemic stroke and one 26-year-old women with thrombosis of central retinal vein caused by APS. In 4 cases in secondary prevention anticoagulant (acenocumarol) was used and in 2--antiplatelet drug (aspirin). In 2 cases congenital disturbances of coagulation were also discovered. We suggest that in ischemic stroke and visual disturbances of not-well-known origin it is useful to make examinations concerning APS, as well as congenital thrombophilias.
