Platelets
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Essential thrombocythaemia (ET) is associated with a broad spectrum of microvascular circulation disturbances including erythromelalgia and its ischaemic complications, episodic neurological symptoms of atypical and typical transient ischaemic attacks (TIAs), transient ocular ischaemic attacks, acute coronary syndromes, and superficial 'thrombophlebitis'. The microvascular circulation disturbances are caused by spontaneous activation and aggregation of hypersensitive thrombocythaemic platelets at high shear stress in the endarterial microcirculation involving the peripheral, cerebral and coronary circulation. As this microvascular syndrome is a pathognomonic feature of essential thrombocythaemia and of thrombocythaemia associated with polycythaemia vera (PV) in complete remission with normal haematocrit, we have labelled these two variants of thrombocythaemia as thrombocythaemia vera. ⋯ On top of this, major arterial and venous thrombotic events and haemorrhages are related to increased haematocrit, red cell mass and its concomitant increased blood viscosity. Correction of increased blood viscosity and haematocrit to normal values (0.40-0.44) by bloodletting alone will significantly reduce the risk of major thrombotic complications, but does not prevent the microvascular circulation disturbances because thrombocythaemia persists. The microvascular syndrome associated with thrombocythaemia in PV patients in remission after bloodletting is best controlled by low-dose aspirin (50-100 mg/day) or by reduction of platelet count to normal (< 350 x 10(9)/l).
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Randomized Controlled Trial Comparative Study Clinical Trial
Effects of preemptive therapy with milrinone or amrinone on perioperative platelet function and haemostasis in patients undergoing coronary bypass grafting.
Preemptive therapy with a phosphodiesterase III inhibitor preserves cardiac function and oxygen transport after cardiac surgery, and its safety on platelet function and haemostasis must be verified. We examined the effects of preemptively administered milrinone or amrinone on platelet function and haemostasis. In 45 cardiac surgery patients, we randomly administered milrinone 50 microg/kg plus 0.5 microg/kg/min for 10 hours, amrinone 1.5 mg/kg plus 10 microg/kg/min infusion for 10 hours, or placebo at release of aortic cross-clamp. ⋯ The mean platelet counts 3 days postoperative in the milrinone and amrinone groups did not significantly differ from the placebo group (10.9 +/- 3.3 and 12.1 +/- 3.8, vs. 12.1 +/- 3.4x10(4) per cubic millimeter, respectively), and chest-tube drainage in the first 24 hours did not significantly differ (450 +/- 156 and 391 +/- 184, vs. 448 +/- 140 ml, respectively). Although there were changes in platelet aggregation consequent to surgery there was no significant differences in platelet aggregation or other haematological values among the three groups. Preemptive therapy of milrinone or amrinone does not deteriorate perioperative platelet function and haemostasis beyond surgical interventions.
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Whether the simultaneous administration of ciprofloxacin or tazobactam/piperacillin increases the risk of thrombocytosis is unknown. Broncho-pulmonary infection in a 50-year-old male with acute, hypertensive, intracerebral bleeding, necessitated therapy with cefpirome (2 g/day, 6 days), ciprofloxacin (800 mg/d, 11 days) and tazobactam/piperacillin (9 g/day, 11 days). Starting with the 8th hospital day, the thrombocyte count steadily increased from 410000/microl to a maximum of 1132000/microl on hospital day 16. ⋯ Since the thrombocyte count started to increase immediately after initiation and dropped immediately after discontinuation of ciprofloxacin and tazobactam/piperacillin and all other drugs were discontinued already before or were started after the nadir of the thrombocyte count, these two antibiotics were regarded causative. It is concluded that simultaneous administration of ciprofloxacin and tazobactam/piperacillin may cause marked thrombocytosis. Discontinuation of these two antibiotics results in an immediate decline of the thrombocyte count to normal values within three weeks.
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It has been suggested that thromboelastography TEG) can help in limiting or directing the appropriate use of blood products during surgery. However, the contribution of platelets to the TEG profile has not been studied in detail. Blood was taken from eight healthy subjects and eight patients with peripheral arterial disease (PAD). ⋯ In both controls and PAD patients there was a strong linear correlation between Log10 [platelet count] and MA (r = 0.97 for controls, r = 0.89 for PAD) and K time (r = -0.86 for controls, r = -0.68 for PAD). Correlation between Log10 [platelet count] and R time was poor in both groups. The MA and K TEG parameters may be most useful for assessing platelet transfusion requirements.
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It is important to distinguish between decreased platelet/megakaryocyte production or increased peripheral platelet destruction as causes of thrombocytopenia. The measurement of reticulated platelets, plasma glycocalicin and thrombopoietin (TPO) levels are potentially of use as discriminators. Thrombocytopenia occurs in many HIV+ patients, and plasma glycocalicin has previously been shown to be elevated in this patient group. ⋯ Thrombocytopenic HIV+ subjects had significantly elevated mean GCI (2.8 and 1.4, p < 0.0001), TPO (85.2 and 27.2 pg/ml, p = 0.002), percentage of reticulated platelets (15.3 and 10.8%, p = 0.01), and significantly reduced absolute numbers of reticulated platelets (16.2 and 24.5 x 10(9)/l, p = 0.0004) when compared to non-thrombocytopenic HIV+ subjects. GCI and percentage of reticulated platelets exhibited a significant positive correlation (r = 0.4, p = 0.002) in HIV+ subjects. The reticulated platelet, TPO and GCI data suggests that thrombocytopenic HIV+ subjects have normal platelet production, and increased peripheral platelet destruction.