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Results for “THROMBOCYTOPATHY”

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At least 55 records · Page 3Linked to original sources
PubMed1979

Thrombocytopathy in preleukaemia: association with a defect of thromboxane A2 activity.

Platelet aggregation and the platelet prostaglandin pathway have been investigated in two patients with preleukaemic states who had a haemorrhagic tendency but a normal platelet count. In both patients platelet aggregation induced by collagen adenosine diphosphate (ADP) and arachidonic acid (AA) were abnormal. Malonyldiadehyde (MDA) production from exogenous AA was normal in both patients thus excluding cyclo-oxygenase deficiency. The platelet aggregating and rabbit aorta contracting activities of thromboxane A2 (TxA2) were very low in both patients. Production of thromboxane B2 (TxB2) assessed by thin layer chromatographic separation of the metabolites of [1(-14)C]AA and by radioimmunoassay, was normal. These abnormalities of platelet function appear to be due to the production of TxA2 with a low biological activity.

Adenine Nucleotides↗
PubMed1981

Haemorrhagic thrombocytopathy associated with dilatation of the platelet--membrane complex.

We evaluated eight patients from four families because of a history of excessive bleeding. Most patients had prolonged bleeding times, absent secondary wave of platelet aggregation in response to epinephrine, collagen and adenosine diphosphate (ADP), and defective 14C-serotonin release and platelet factor 3 availability. These findings are characteristic of a platelet release defect. Electron-microscopy examination of the platelets of seven patients revealed a common abnormality. From 30% to 70% of the platelets in any given sample exhibited a prominent membrane complex and dilated, tortuous surface-connected canalicular system ('swiss-cheese' platelet). In two patients there was coincident storage-pool disease, but the remainder had adequate dense bodies and a normal ratio of ATP to ADP. SDS-polyacrylamide gel electrophoresis of platelet proteins and glycoproteins showed no abnormalities. The patency of the canalicular system was demonstrated in one patient by the observation that dense bodies appeared in the cannaliculi and outside the platelets following collagen-induced aggregation of polylysine-treated platelets. Since platelet-aggregation responses to the calcium ionophore A23187 were normal, we conclude that the defective platelet function in these patients may be due to impaired calcium mobilization from the morphologically abnormal membrane complex.

Bleeding Time↗
PubMed1983

Familial exudative vitreoretinopathy associated with familial thrombocytopathy.

Two families with familial exudative vitreoretinopathy were studied in which platelet aggregation defects were found in all the affected members. The major defect observed was absent platelet aggregation with arachidonic acid. In addition platelet aggregation with collagen and adrenaline was reduced in one severely affected member. The implication of the platelet aggregation defect in the pathogenesis of this retinal vascular disorder is discussed.

Blood Platelet Disorders↗
PubMed1986

Lack of evidence for the role of secondary hyperparathyroidism in the pathogenesis of uremic thrombocytopathy.

The possible relationship between platelet dysfunction and secondary hyperparathyroidism (HPT) in chronic renal failure was examined in 23 uremic patients on conservative therapy (group I) and in 27 patients on maintenance hemodialysis (group II). Platelet function was assessed by measuring the degree of aggregation in response to various concentrations of adenosine diphosphate. Secondary HPT was evaluated by means of serum biochemistry (parathyroid hormone, calcium, phosphorus, and alkaline phosphatase) and radiographic examinations (x-ray films of the hand skeleton). This study showed impaired platelet aggregation in group I patients, compared to either group II patients or controls. There were no significant differences when group II patients were compared to controls. No significant correlations between platelet aggregation and the hematochemical changes associated with secondary HPT were found. No differences in platelet aggregation were found with regard to the activity (alkaline phosphatase) and the severity (x-ray findings) of secondary HPT. Effective treatment of secondary HPT with 1,25-dihydroxycholecalciferol in both group I and group II patients was not associated with consequent changes in platelet aggregation. It is concluded that secondary HPT is probably not a major factor in the pathogenesis of platelet dysfunction in chronic renal failure.

Adenosine Diphosphate↗