Showing papers on "Blood Platelet Disorders published in 1988"

"Sticky platelet syndrome": a congenital platelet abnormality predisposing to thrombosis?

Abstract: We have identified a number of patients with coronary artery disease, TIAs and/or strokes and idiopathic ischemic optic neuropathy who have a platelet population which is in vitro hyperaggregable with epinephrine and ADP and hyperresponsive to surface contact. These patients have no identifiable risk factors. Several families have been identified in which multiple members had these findings. Many, but not all have had clinical symptoms. An autosomal (dominant) pattern of heredity seems to evolve. We refer to this as "sticky platelet syndrome" and hypothesize that it may represent a congenital platelet abnormality which potentially predisposes to thromboembolisms. The precise nature of the defect is not known at this time.

A Rapid Assay for Platelet Thromboxane Production and Its Use in Assessing Prior Aspirin Ingestion

Abstract: In the laboratory evaluation of platelet disorders, there are a number of situations in which determining the capacity of platelets to synthesize thromboxane is of diagnostic value. An assay for thromboxane production is required for the diagnosis of cyclooxygenase and thromboxane synthetase defects and is useful in detecting prior aspirin ingestion. The authors describe an assay for platelet thromboxane production that is simple, rapid, inexpensive, and suitable for routine use in the clinical coagulation laboratory. It is based on platelet synthesis of 14C-thromboxane from 14C-arachidonate. 14C-thromboxane is isolated by thin-layer chromatography and its radioactivity quantitated by scintillation counting. The results are expressed as the thromboxane index: 14C-arachidonate converted to thromboxane/platelet count. The assay is linear with respect to platelet concentration and substrate concentration and is independent of recovery. Using this assay, the authors demonstrated that platelet thromboxane production, expressed as thromboxane index (mean +/- standard deviation) was completely inhibited 12-16 hours after ingestion of a single aspirin dose of 650 mg (0.27 +/- 0.14), 325 mg (0.29 +/- 0.18), or 163 mg (0.13 +/- 0.13), with partial inhibition by 81 mg (0.41 +/- 0.46) or 41 mg (1.41 +/- 0.75) (n = 3 for each dose). Thromboxane index for normal controls was 2.41 +/- 0.77 (n = 25). The authors also determined the time for recovery of thromboxane synthetic capacity to normal levels in four subjects followed longitudinally after ingesting a single 650-mg dose of aspirin. Platelets from three of the four subjects recovered normal thromboxane synthetic capacity by the fifth day after aspirin ingestion, consistent with platelet half-life in the circulation. Thus, the authors have developed a rapid, inexpensive assay for assessing the function of cyclooxygenase and thromboxane synthetase in platelets, which can be especially useful as a screening test to detect ingestion of aspirin before performance of expensive and labor-intensive platelet function studies.