PLATELETS, ALCOHOL-CONSUMPTION, AND ONSET OF BRAIN INFARCTION

Objectives-Previous investigations have suggested that recurrent rebou nd thrombocytosis after alcohol misuse may be a factor in the pathogen esis of thromboembolic disease. Alcohol consumption, platelet count, a nd platelet function were examined among patients of working age with brain infarction. Methods-Platelet count and risk factors for stroke w ere studied in 426 stroke patients and 157 control patients in hospita l. The measures were platelet count obtained within four days after th e stroke onset, in vitro adenosine diphosphate induced platelet aggreg ation, associated thromboxane B2 formation, and urinary excretion of 1 1-dehydrothromboxane B2. Results-After adjustment for sex, age, cardia c disease, diabetes, and alcohol intake, hypertension (OR 3.4, 95% con fidence interval (95% CI) 2.0-6.0) and current smoking (OR 2.1, 95% CI 1.4-3.3) were associated with an increased risk for brain infarction. Platelet count shortly after the onset of disease was higher in the s troke patients than in the controls (OR 1.05/10(10)/1 platelets; 95% C I 1.02-1.09). The patients with brain infarction who were heavy alcoho l drinkers (n = 144) showed both thrombocytosis (OR 2.30, 95% CI 0.82- 6.44) and thrombocytopenia (OR 3.20, 95% CI 1.19 to 8.59) more often a t the onset of the stroke than the other patients with brain infarctio n. The thromboxane variables showed inconsistent associations with the onset of stroke. There was no consistent platelet abnormality among a lcohol misusers at the onset of ischaemic brain infarction. Conclusion s-Alcohol induced thrombocytopenia and rebound thrombocytosis were bot h often seen at the onset of brain infarction in patients who were hea vy alcohol drinkers. Therefore, other mechanisms which could contribut e to the high frequency of recurrences of ischaemic stroke among heavy drinkers should be investigated.