Prostacyclin and iloprost do not affect action of standard dose heparin on haemostatic function during haemodialysis

1988 ◽  
Vol 49 (4) ◽  
pp. 385-392 ◽  
Author(s):  
J.B Dibble ◽  
P.A Kalra ◽  
M.A Orchard ◽  
J.H Turney ◽  
J.A Davies
Keyword(s):  
2015 ◽  
Vol 187 ◽  
pp. 389-392 ◽  
Author(s):  
Ahmet Çağrı Aykan ◽  
Tayyar Gökdeniz ◽  
Ilker Gül ◽  
Ezgi Kalaycıoğlu ◽  
Mustafa Çetin ◽  
...  

Cureus ◽  
2020 ◽  
Author(s):  
Forat Lutfi ◽  
Rohit Bishnoi ◽  
Vikas Patel ◽  
Aisha Elfasi ◽  
Michael Setteducato ◽  
...  

Author(s):  
Matthew Moll ◽  
Rebecca L. Zon ◽  
Katelyn W. Sylvester ◽  
Evan C. Chen ◽  
Auyon J. Ghosh ◽  
...  

1976 ◽  
Vol 36 (01) ◽  
pp. 157-164 ◽  
Author(s):  
P. M Mannucci ◽  
Luisa E. Citterio ◽  
N Panajotopoulos

SummaryThe effect of subcutaneous low-dose heparin on postoperative deep-vein thrombosis (D. V. T.) (diagnosed by the 125I-labelled fibrinogen test) has been investigated in a trial of 143 patients undergoing the operation of total hip replacement. Two randomized studies were carried out: in one the scanning for D.V.T. was carried out daily for 7 days post operatively and in the other for 15 days. In both, the incidence of D.V.T. was significantly lower in the heparin-treated patients (P<0.005). Bilateral D.V.T. was also prevented (P<0.05), through the extension of D.V.T. to the distal veins of the thigh was not significantly reduced. Heparin treatment was, however, followed by a higher incidence of severe postoperative bleeding (P< 0.02) and wound haematoma formation (P< 0.005), and the postoperative haemoglobin was significantly lower than in the control group (P<0.005). A higher number of transfused blood units was also needed by the heparin treated patients (P<0.001).


1999 ◽  
Vol 19 (03) ◽  
pp. 128-133 ◽  
Author(s):  
B.E. Lewis ◽  
W. P. Jeske ◽  
F. Leya ◽  
Diane Wallis ◽  
M. Bakhos ◽  
...  

SummaryDespite the use of potent anticoagulants such as r-hirudin and argatroban, the morbidity and mortality in heparin-induced thrombocytopenia (HIT) patients remains unacceptable. Data from our in vitro investigations show that thrombin inhibitors do not block platelet activation induced by heparin antibodies and heparin but that GPIIb/IIIa receptor inhibitors do block this process. We have treated four HIT positive patients with a combined therapy of thrombin inhibitor and GPIIb/IIIa receptor inhibitor when treatment with thrombin inhibitor alone failed to alleviate acute thrombosis. Combination therapies included r-hirudin (Refludan®) with tirofiban (Aggrastat®) and argatroban (Novastan®) with abciximab (ReoPro®). A reduced dose of the thrombin inhibitor was used with the standard dose of the anti-platelet drug. In all cases, there was no overt bleeding which required intervention, and all patients exhibited clinical improvement or full recovery. These case studies suggest that treatment of active thrombosis in HIT patients with adjunct GPIIb/IIIa receptor inhibitor therapy may be more effective than thrombin inhibitor treatment alone.


1982 ◽  
Vol 47 (03) ◽  
pp. 296-296
Author(s):  
Gordon Lowe ◽  
Jill Belch ◽  
Karen Regan ◽  
Charles Forbes ◽  
Colin Prentice

1972 ◽  
Vol 70 (1) ◽  
pp. 196-208 ◽  
Author(s):  
Bengt Karlberg ◽  
Sven Almqvist

ABSTRACT The effects of the administration of normal saline in four normal subjects and the single iv injections of synthetic pyroglutamyl-histidyl-proline amide (TRH) in doses of 6.25, 12.5, 25, 50, 100, 200 and 400 μg in 12 healthy subjects were evaluated by clinical observations and serial measurements from −10 to + 360 minutes of serum TSH, PBI, STH, cholesterol, glucose and insulin. Normal saline and TRH 6.25 μg iv did not change the serum TSH level. The minimum iv dose of TRH increasing serum TSH within 10 minutes was 12.5 μg. Nine of 12 subjects gave maximal increases of serum TSH after TRH 100 μg and all after 200 and 400 μg. The time for the peak response varied with the dose from 15 to 60 minutes. The dose-response curves, average and individual, were complex and not linear. This was interpreted as a varying degree of stimulation of both pituitary synthesis and release of TSH by TRH. PBI changes were measured at 2 h and 6 h. Minimum dose for a significant increase of PBI was 12.5 μg and 6.25 μg of TRH for the respective times. No change in basal STH-levels occurred in 53 of 65 TRH-stimulation tests. Nine of the 12 changes in serum STH occurred in four subjects with varying basal STH-levels. No changes were found in serum cholesterol, glucose or insulin. Our results show that 50 μg of TRH can be used as a standard dose for the single iv stimulation of pituitary release of TSH. TRH stimulated both TSH and STH release in 18% of our tests.


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