Platelet secretion defect in patients with the attention deficit disorder and easy bruising.
Platelet function was evaluated in 12 patients with the attention deficit disorder and lifelong history of easy bruising. Aggregation and 14C-serotonin secretion studies in platelet-rich plasma in response to adenosine diphosphate (ADP), epinephrine, and arachidonic acid did not reveal striking abnormalities. Secretion of adenosine triphosphate (ATP), ADP, beta-hexosaminidase, and beta-glucuronidase by gel-filtered platelets in response to the divalent cation ionophore A23187 and low concentrations of thrombin (less than or equal to 0.1 U/ml) was impaired in patients as compared to normals. The aggregation response to A23187 (4 microM) was absent in 8 of the 12 patients. The total stores of the secretable constituents, the retention of incorporated 14C-serotonin, and the arachidonate metabolism of the platelets were normal. Our findings suggest a new platelet disorder with impaired secretion mechanism, without storage pool deficiency or impaired arachidonate metabolism. The secretion defect in platelets represents a tissue disorder in a functional psychiatric disease. We refocus attention on the role of platelets as a model for neurons in functional disorders, with emphasis on secretion mechanisms rather than amine uptake, storage, and metabolism.
D000293:Adolescent; D000328:Adult; D001095:Arachidonic Acids / Q000378:metabolism; D001289:Attention Deficit Disorder with Hyperactivity / Q000097:blood* / Q000150:complications; D001791:Blood Platelet Disorders / Q000150:complications*; D001792:Blood Platelets / Q000378:metabolism*; D002648:Child; D002850:Chromatography, Gel; D005260:Female; D006487:Hemostasis; D006801:Humans; D008297:Male; D010974:Platelet Aggregation; D012701:Serotonin / Q000378:metabolism; D013929:Thromboxane B2 / Q000096:biosynthesis
D001095:Arachidonic Acids; D012701:Serotonin; D013929:Thromboxane B2