12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Myeloproliferative-Disorders
12-hydroxy-5-8-10-14-eicosatetraenoic-acid has been researched along with Myeloproliferative-Disorders* in 3 studies
Other Studies
3 other study(ies) available for 12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Myeloproliferative-Disorders
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Deficient lipoxin synthesis: a novel platelet dysfunction in myeloproliferative disorders with special reference to blastic crisis of chronic myelogenous leukemia.
The capacity to convert exogenous leukotriene A4 to lipoxins (LXs) was investigated in platelet suspensions from patients with myeloproliferative disorders (MPD) (n = 22) and healthy control subjects (n = 14). Platelets isolated from the controls produced mainly LXA4, but also 6(S)-LXA4 and the all-trans isomers of lipoxins A4 and B4, as determined by high-performance liquid chromatography and computerized UV spectroscopy. In comparison to control levels, the mean LX synthesis was significantly lower in platelets from the MPD patients (438.7 +/- 62.8 and 157.4 +/- 31.2 pmol LXA4 per 10(9) platelets, respectively; mean +/- SEM; P = .0001). Platelets from six of the patients showed a particularly low capacity to produce LXs, resulting in LX levels below the detection limit or less than 7% of mean control levels. Notably, all these patients were in blastic crisis of chronic myelogenous leukemia (CML). This severely deficient LX production was paralleled by a dramatically attenuated conversion of arachidonic acid to 12-HETE (12-hydroxyheptadecatrienoic acid), a product formed via the prostaglandin endoperoxide synthase pathway, was normal. In addition, longitudinal studies of CML patients showed that blastic metamorphosis was associated with a markedly reduced capability to synthesize LXs, while this capacity improved after retransformation into a second chronic phase. The results reveal deficient LX synthesis as a novel platelet dysfunction in MPD, particularly in blastic crisis of CML in which an essentially abolished 12-lipoxygenase activity may be a general phenomenon. Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Blast Crisis; Blood Platelets; Fatty Acids, Unsaturated; Humans; Hydroxyeicosatetraenoic Acids; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukotriene A4; Leukotrienes; Lipoxins; Myeloproliferative Disorders; SRS-A | 1991 |
Impaired conversion of exogenous arachidonic acid by platelets to thromboxane B2 and correction of that deficiency by interferon-alpha.
In the course of an investigation of cyclooxygenase and 12-lipoxygenase activity in platelets of patients with myeloproliferative syndrome receiving treatment with interferon-alpha 2 patients showed unusual results which have not been reported so far. Both patients had thrombocytosis, in one case associated with polycythaemia. In platelets of both patients, a reduced conversion of exogenous 14C arachidonic acid to TXB2 was observed accompanied by a shift in conversion to PGE2 and 12-HETE in one patient and to 12-HETE alone in the other before therapy. These findings were paradoxically associated with evidence of enhanced platelet activation in vivo. Treatment of both patients with interferon-alpha resulted in reversal of the biochemical abnormalities and in clinical remission. Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Aged; Arachidonate 12-Lipoxygenase; Arachidonic Acid; Arachidonic Acids; Blood Platelets; Dinoprostone; Humans; Hydroxyeicosatetraenoic Acids; Interferon Type I; Male; Myeloproliferative Disorders; Platelet Activation; Polycythemia Vera; Prostaglandin-Endoperoxide Synthases; Thrombocythemia, Essential; Thromboxane B2 | 1990 |
Aspirin and risk of bleeding in patients with thrombocythemia.
Thirty-two patients with thrombocythemia associated with myeloproliferative syndromes were selected on the basis of normal bleeding time and absence of hemorrhagic or thrombotic history. Twenty-five control subjects were studied simultaneously. They were all given a single intravenous infusion of 500 mg of aspirin (lysine acetylsalicylate), and bleeding time was measured two hours later. Both in the control group and in the patient group, aspirin significantly prolonged the bleeding time, but the average prolongation was significantly more pronounced in the patients. In comparison with the control subjects, the patients had a statistically significant reduction of platelet serotonin content and no difference in the production of platelet lipoxygenase derivative 12-HETE or plasma von Willebrand factor properties. Fourteen patients had abnormal platelet aggregation in response to adenosine diphosphate, adrenaline (epinephrine), or collagen. In six of them, all with very low serotonin content, the bleeding time was prolonged above the upper limit of the post-aspirin values in the control group. Thus, cyclooxygenase inhibition by aspirin unmasked a bleeding tendency in patients with a severe reduction in platelet dense bodies content. These findings might be relevant in relation to the use of antiplatelet drugs. Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Adolescent; Adult; Aged; Aspirin; Bleeding Time; Blood Platelets; Female; Humans; Hydroxyeicosatetraenoic Acids; Male; Middle Aged; Myeloproliferative Disorders; Polycythemia Vera; Risk; Serotonin; Thrombocythemia, Essential; Thromboxane B2; Time Factors; von Willebrand Factor | 1987 |