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Results for “THROMBOCYTOPATHY”

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At least 109 records · Page 6Linked to original sources
PubMed1989

[Epistaxis caused by an acquired thrombocytopathy].

Epistaxis may be the sole manifestation of a platelet aggregation dysfunction. Bleeding time according to Ivy within normal ranges does not exclude a severe disturbance of primary haemostasis. In two women (aged 53 and 76 yr, respectively) persistent epistaxis could not be stopped by local therapy. The bleeding time according to Ivy was within normal ranges in both cases. In one patient a bleeding disorder was not recognized as laboratory screening tests were normal and her situation became life-threatening. Anamnesis, clinical history and platelet aggregation tests led to the correct diagnosis; in one patient the relation with acetylsalicylic acid treatment was clear. After administration of platelet concentrate the bleeding stopped within a few hours in both cases and did not recur.

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PubMed1987

Hemorrhagic thrombocytopathy with platelet thromboxane A2 receptor abnormality: defective signal transduction with normal binding activity.

Subnormal platelet responses to thromboxane A2 (TXA2) were found in a patient with polycythemia vera, and the mechanism of this dysfunction was analyzed. The patient's platelets showed defective aggregation and release reaction to arachidonic acid, enzymatically generated TXA2 and synthetic TXA2 mimetics (STA2, U-46619). In contrast, they showed normal responses to thrombin. When the platelet TXA2 receptor was examined with both a 125I-labelled derivative of a TXA2 receptor antagonist ([125I]-PTA-OH) and a 3H-labelled TXA2 agonist ([3H]U-46619), the equilibrium dissociation rate constants (Kd) and the maximal concentrations of binding sites (Bmax) of the patient's platelets to both ligands were within normal ranges, suggesting that the binding capacity of their TXA2 receptor was normal. STA2 failed to induce normal elevation in the cytoplasmic free calcium ion concentration, phosphatidic acid formation and 40 kD protein phosphorylation in the patient's platelets, whereas these responses to thrombin were within normal ranges. 12-O-Tetradecanoyl-phorbol-13-acetate (TPA) also evoked normal response in the 40 kD protein phosphorylation in the patient's platelets. These results suggested that the patient's platelets had TXA2 receptor abnormalities which were characterized by defective transduction of the binding signal to postreceptor reactions after normal TXA2 binding.

Adenine Nucleotides↗