Accelerated Prostacyclin Degradation in Thrombotic Thrombocytopenic Purpura

Chen, Yao‐Chang; Hall, Elizabeth R.; McLeod, Bruce C.; Ke-gui, WU

doi:10.1016/s0140-6736(81)90522-5

Cited by 107 publications

(25 citation statements)

References 21 publications

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“…Earlier, some authors have reported that thromboem bolic events might be induced by increased PGH degrada tion due to the disturbance of plasma protein ability to stabilize PGH [5,12,13], However, a study of PGH deg radation in plasma may not express the process of its deg radation entirely. It is known that the velocity of PGI2 degradation depends on the ability of erythrocytes to destroy PGH [13,14], Our results show that in blood the velocity of PGH degradation is more marked than in plas ma, especially in patients with cerebrovascular disorders.…”

Section: Discussionmentioning

confidence: 99%

Elevated Velocity of Prostacyclin Degradation in Blood as a Possible Risk Factor in Patients with Cerebrovascular Disorders

Akopov

Дарбинян²,

Grigorian³

et al. 1993

Eur Neurol

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Blood and plasma from 193 patients at risk of cerebrovascular disorders and 87 patients with brain infarction were tested to study prostacyclin (PGI2) degradation. It has been reported that patients at risk for cerebrovascular disorders and especially with brain infarction have an enhanced velocity of PGI2 degradation. The increase in velocity was more marked in blood than in plasma. A direct relation between this enhancement and the manifestation of intravascular platelet activation was observed. These data suggest that elevated PGI2 degradation might be a risk factor for thromboembolic events in patients with cerebrovascular disorders.

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Section: Discussionmentioning

confidence: 99%

Elevated Velocity of Prostacyclin Degradation in Blood as a Possible Risk Factor in Patients with Cerebrovascular Disorders

Akopov

Дарбинян²,

Grigorian³

et al. 1993

Eur Neurol

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“…It has been reported that biologically active PGI2 shows an extremely enhanced degradation in human plasma in thrombotic thrombocytopenic purpura [5]. In these patients the normal in vitro half-life of around 10 min [39] was shortened to less than 1 min.…”

Section: Degradation Of Pgi2 In Plasmamentioning

confidence: 92%

Eicosanoids of Platelets and Vascular Wall in Chronic Renal Insufficiency

Sinzinger

Leithner²

1987

Am J Nephrol

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There is good evidence that retention products accumulating in chronic renal insufficiency influence prostaglandin (PG) synthesis, thus affecting platelet-vascular wall interaction. The vascular PGI2 synthesis is increased and prolonged in vitro, the plasma factor activity enhanced. A defective platelet function is frequently observed; it is completely restored by peritoneal dialysis, but only partially by hemodialysis. The sensitivity of platelets to PGI2 and its plasmatic degradation are unchanged. There is evidence of a shift of arachidonic acid metabolism from cyclooxygenase to lipoxygenase. These changes may be attributed to undialyzable plasma constituents, the ‘middle molecules’.

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“…This work was supported in part by a program project grant from the National Institutes of Health (POI-NS-18494) and a grant from the Chicago Heart Association (8 [1][2][3][4][5][6][7][8][9][10].…”

Section: Acknowledgmentsmentioning

confidence: 99%

“…aggregate formation by platelet aggregating factor (2) and the presence of abnormal Factor VIII:von Willebrand Factor multimers (3). We have recently detected accelerated serum prostacyclin (PG12) degradation (nonenzymatic hydrolysis) in a patient with chronic TTP (4). Detailed clinical and laboratory correlates suggest that reduced PG12 bioavailability may play an important role in the pathogenesis of TTP.…”

Section: Introductionmentioning

confidence: 99%