Platelet prostaglandin production in alcoholic liver disease.
Impaired platelet aggregation is a common finding in patients with alcoholic liver disease. This may be due to impairment of prostaglandin synthesis and alterations in the proportions of platelet membrane lipids secondary to changes in circulating lipids. Platelet prostaglandin synthesis was measured by the production of malonaldehyde (MDA), and was increased in patients with alcoholic cirrhosis compared with normal controls. Mean MDA production in cirrhotics was 3.37 nmoles MDA/10(9) platelets, and in controls 1.01 nmoles MDA/10(9) platelets (p less than 0.01). Platelet prostaglandin synthesis was significantly related to the serum cholesterol:triglyceride ratio (r = 0.73, p less than 0.005). Platelet aggregation was impaired in 12/14 cirrhotics. Five of the cirrhotics had a factor in their plasma which appeared to enhance the aggregation of normal platelets. Impaired platelet aggregation in patients with alcoholic liver disease appears to be due to a defect in intraplatelet metabolism.
D000328:Adult; D001792:Blood Platelets / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D005260:Female; D006801:Humans; D008104:Liver Cirrhosis, Alcoholic / Q000097:blood; D008108:Liver Diseases, Alcoholic / Q000097:blood*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010974:Platelet Aggregation; D011453:Prostaglandins / Q000096:biosynthesis*; D014280:Triglycerides / Q000097:blood
D011453:Prostaglandins; D014280:Triglycerides; D008315:Malondialdehyde; D002784:Cholesterol