ristocetin and Cerebrovascular-Disorders

We report an unusual case of severe abdominal arterial thrombosis in a young woman using oral desmopressin. Only a few cases with cerebrovascular accidents and coronary syndromes have been described so far, which could be attributed to intravenous administration of desmopressin. Because extensive diagnostic and laboratory investigations for (un)common coagulation disorders could not identify an alternative explanation associated with arterial thrombosis, we hypothesise that desmopressin in an oral dose of at least 200 ug once daily must have been sufficient to cause this dramatic vascular complication. Supportive of our hypothesis, we found remarkably high levels of factor VIII activity, Von Willebrand factor (vWF) antigen and vWF ristocetin cofactor activity (268%, 740%, 590% respectively). To the best of the authors' knowledge, this is the first report suggesting a relationship between oral desmopressin use and life-threatening abdominal arterial thrombosis.

Topics: Abdominal Pain; Adult; Blood Coagulation Disorders; Cerebrovascular Disorders; Deamino Arginine Vasopressin; Echocardiography; Factor VIII; Female; Hemostatics; Humans; Ristocetin; Thrombosis; Tomography, X-Ray Computed; von Willebrand Factor

Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable.. An 86-year-old male patient was among the 23 AMI patients enrolled in the platelet study for the GUSTO-III trial. He received 325 mg of aspirin daily for at least 6 years, suffered an AMI, and was successfully reperfused with alteplase, but after 44 hours developed a large hemorrhagic stroke resulting in paraplegia. Platelet aggregation and receptor expression were measured by flow cytometry and ELISA before thrombolysis and at 3, 6, 12, and 24 hours thereafter. The percentage of platelet aggregation was lower in the stroke patient at every time point when induced by 5 micromol/L of ADP, by 10 micromol/L of ADP, and by thrombin than in the rest of the AMI group. Ristocetin and collagen-induced aggregability were within the group range. Decreased platelet glycoprotein Ib, IIb, IIIa, and IIb/IIIa and vitronectin receptor expression were observed in the stroke patient. No other differences in p24 (CD9), very late antigen-2, P-selectin, and platelet/endothelial cell adhesion molecule-1 expression were determined.. Profound depression of platelet status preceded the occurrence of hemorrhagic stroke in an elderly long-term aspirin user treated with thrombolytic therapy. Initial "exhausted" platelets may be responsible for the increased risk for hemorrhagic stroke after coronary thrombolysis.

Topics: Adenosine Diphosphate; Aged; Aged, 80 and over; Antigens, CD; Aspirin; Blood Platelets; Cerebral Hemorrhage; Cerebrovascular Disorders; Collagen; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Follow-Up Studies; Humans; Male; Membrane Glycoproteins; Myocardial Infarction; P-Selectin; Paraplegia; Plasminogen Activators; Platelet Aggregation; Platelet Aggregation Inhibitors; Platelet Endothelial Cell Adhesion Molecule-1; Platelet Membrane Glycoproteins; Prospective Studies; Receptors, Very Late Antigen; Ristocetin; Tetraspanin 29; Thrombin; Thrombolytic Therapy; Tissue Plasminogen Activator; Vitronectin