Sticky Platelet Syndrome (SPS) as a Cause of Unexplained Thrombosis.

Abstract

Background: Sticky platelet syndrome (SPS) was first described in 1983 by Holliday. The results of recent studies suggest SPS to be a common cause of arterial and venous thrombosis. With respect to otherwise unexplained venous thrombosis, the prevalence of SPS approximates that of activated protein C resistance (APC-R). It has been found that SPS accounted for about 21% of otherwise unexplained arterial events (acute myocardial infarction, cerebrovascular thrombosis, transient cerebral ischemic attacks, retinal thrombosis, and peripheral arterial thrombosis) and accounted for about 13,2% of otherwise unexplained venous events (deep vein thrombosis, with or without pulmonary embolus).SPS is an autosomal dominant platelet disorder associated with arterial and venous thromboembolic events, frequently recurrent under oral anticoagulant therapy. It is characterized by hyperaggregability of platelets in platelet-rich plasma with adenosine diphosphate (ADP) and epinephrine (type I), epinephrine alone (type II), or ADP alone (type III). Combination of SPS with other congenital thrombophilic defects have been described. Low-dose aspirin treatment (80–100 mg) ameliorates the clinical symptoms and normalizes hyperaggregability. The precise etiology of this defect is at present not known, but receptors on the platelet surface may be involved.Patients and methods: We examined fifty patients with otherwise unexplained arterial or venous thrombosis. SPS evaluations were performed according to the method of Mammen. The equipment used was PACKS-4 aggregometer.Results: SPS was detected in eight patients. Clinically SPS resulted as an arterial thrombosis in five patients (2 coronary thrombosis, 2 cerebral ischemic attacks, 1 peripheral arterial thrombosis), two individuals showed deep venous thrombosis (DVT) and one patient passed recurrent abortions. SPS was classified as type I in 2 cases, 5 patients had type II and only 1 patient was diagnosed as type III, respectively (4 of them showed a glycoprotein IIIa abnormality).Conclusion: Because treatment with heparin or warfarin will not alleviate the thrombotic tendency of SPS, but simple aspirin therapy almost always will correct the defect and protect the individual from second event, it is particularly important to define the presence of this defect.