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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double blind study of 134 patients was undertaken to compare the effectiveness of hydroxychloroquine sulfate, Plaquenil, and heparin in the prophylaxis of deep venous thrombosis. By the 125I fibrinogen scanning technique, deep venous thrombosis was detected in six patients in the placebo group, in one patient in the Plaquenil group and none in the heparin group. These results indicate that both heparin and Plaquenil do diminish the incidence of thrombosis.
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PMID:Prophylaxis of deep venous thrombosis by hydroxychloroquine sulfate and heparin. 33 43

Eighty-five patients suspected of having lower-extremity deep venous thrombosis (DVT) participated in a prospective study to test the diagnostic accuracy of four noninvasive techniques: Doppler ultrasonic flow study, electrical impedance plethysmography, the serial dilution protamine sulfate test, and an extensive physical examination. Ascending radiocontrast phlebography was the diagnostic standard of reference. We found that (1) when both Doppler and impedance examinations were positive, the diagnosis of DVT could be considered virtually certain; (2) impedance and Doppler examinations, when used in combination, were reliable screening tests capable of establishing or excluding the presence of thigh DVT; (3) physical examination and the serial dilution protamine sulfate test were unreliable screening techniques for DVT; (4) techniques other than the noninvasive methods investigated were needed to reliably detect or to exclude popliteal and call DVT.
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PMID:Noninvasive diagnosis of deep venous thrombosis. 78 65

The D-Dimer (D-D) assay for measuring cross-linked fibrin degradation products is now available for the clinical laboratory. We combined this assay with other tests to assess patients with diagnosed or suspected DIC. Also, a small group of patients (20) with deep venous thrombosis (DVT) were studied. The D-D test, antithrombin-III assay, FDP titer, fibrinopeptide-A level, protamine sulfate test, fibrinogen, prothrombin time, and activated partial thromboplastin time were used. The D-D test was abnormal in 93.7%, the AT-III level was abnormal in 87.5%, the fibrinopeptide-A level was abnormal in 89.5%, and the FDP titer was elevated in 83.7% of patients with DIC. When assessing patients found not to have confirmed DIC the D-D assay was abnormal in 20%, the AT-III level was abnormal in 6%, and the fibrinopeptide-A level was elevated in 13%. We conclude the D-Dimer assay to be a useful molecular marker of hemostasis in diagnosing DIC and this test will often discriminate between those patients with or without DIC, especially when used with the AT-III and fibrinopeptide-A assays. Of the battery of tests used in this study, the most useful, in descending order of efficacy, appear to be the D-dimer assay (93.7% abnormal), the fibrinopeptide-A titer (89.5% abnormal), the AT-III level (87.5% abnormal), and the FDP titer (83.7% abnormal). Of the global tests, the diagnostic efficacy of the prothrombin time activated partial thromboplastin time, and protamine sulfate test were no greater than chance and appear to be of little use in aiding in a diagnosis of DIC. Also, the D-Dimer assay is similar in cost to the FDP titer and is cost effective for the routine clinical laboratory.
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PMID:Diagnostic efficacy of the D-dimer assay in disseminated intravascular coagulation (DIC). 163 67

Anticoagulation is being used increasingly in the critical care areas. Thrombolytic therapy is now commonly used in emergency departments and coronary care units for treatment of AMI. Heparin therapy for unstable angina and for a 48 to 72 hour period following thrombolytic therapy for AMI is becoming commonplace. Beginning warfarin therapy concomitantly with heparin to decrease the total duration of heparin and the duration of hospital stay for DVT therapy is encouraged. The use of low-dose warfarin to prevent DVT in hip surgery, improve catheter patency, and prevent catheter-related subclavian thrombosis is increasing. Along with the increased use of anticoagulation must come a greater appreciation of the complications associated with the agents used, and of how to prevent or treat the hemorrhagic or thrombotic morbidity that may arise. Acute hemorrhage with thrombolytic agents must be recognized and the immediate implementation of conservative and aggressive measures begun. Heparin-induced thrombocytopenia with thrombosis is an often-unrecognized problem that may occur in 1% to 2% of heparin recipients and result in limb amputations. A delayed onset (6-10 days) requires frequent platelet counts for early diagnosis and treatment. The resurgence of warfarin use for prevention of cardiovascular and cerebrovascular disorders demands observation for skin necrosis from protein C and S inhibition. Early recognition of symptoms and syndromes associated with organ system hemorrhage in patients receiving chronic anticoagulation is imperative. The use of antagonists, such as protamine sulfate for heparin, vitamin K1 for warfarin, and antifibrinolytic drugs for thrombolytic agents, may be necessary in treating hemorrhagic events. However, their use may worsen the thromboembolic event initially treated.
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PMID:Toxic effects of drugs used in the ICU. Anticoagulants and thrombolytics. Risks and benefits. 186 82

Using affinity chromatography on lysine Sepharose 4B, a fast-acting tissue plasminogen activator inhibitor (t-PAI) was partially purified from t-PAI-rich plasma from patients with recurrent DVT. Its inhibition of tissue plasminogen activator (t-PA) was demonstrated in functional assays and its reaction with 125I-t-PA was analyzed by autoradiography following SDS-PAGE (sodium dodecyl sulfate polyacrylamide gel electrophoresis). When the t-PAI was mixed with an equimolar concentration of t-PA at 37 degrees C, the half-life of free one-chain and two-chain 125I-t-PA was 1.8 and 0.8 min, respectively. The rate of complex formation between 125I-t-PA and t-PAI was similar both in patient plasma, pregnancy plasma and platelet lysates made from platelet-rich normal, patient and pregnancy plasma. The molecular weights of the complexes between t-PA and the inhibitors in patient plasma and in the different platelet lysates were identical, while that of the inhibitor complex formed in pregnancy plasma was found slightly higher by SDS-PAGE indicating that the pregnancy plasma t-PAI differs from the fast-acting t-PAI found in plasma from thrombotic patients and in platelet lysates.
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PMID:Plasminogen activator inhibitors in plasma and platelets from patients with recurrent venous thrombosis and pregnant women. 308 15

An assay system for determination of the "fast"-acting inhibitor (antiactivator, AA) of tissue-type plasminogen activator (tPA) in human plasma was developed. The system is based on incubation of plasma samples with various amounts of vessel wall-derived tPA for 8 minutes at 25 degrees C, followed by acidification and determination of the residual tPA activity by an indirect spectrophotometric assay. One unit of AA was defined as the amount inhibiting 1 U of tPA. AA levels in normal controls (n = 26) were 1.4 to 17.4 U/ml (median 3.0 U/ml) and 0.9 to 17.5 U/ml (median 3.0 U/ml) in patients with a history of deep venous thrombosis (n = 26). When plasma was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by reverse fibrin autography, AA activity appeared as an inhibitory band corresponding to a relative molecular mass of 50,000. In six samples the inhibitory activity of this band was directly correlated to the functional AA activity of the plasma samples.
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PMID:Tissue plasminogen activator inhibitor in human plasma: development of a functional assay system and demonstration of a correlating Mr = 50,000 antiactivator. 392 46

Impedance plethysmography (IPG) and the Doppler ultrasonographic probe were used to assess whether thrombophlebitis, initiated by injection of a sclerosant into superficial varicose veins, extended to involve the deep veins of the leg. Sixty-seven legs were treated with compression sclerotherapy in 50 patients (26 men, 24 women) whose mean age was 53 years. Indications for this therapy were unacceptable appearance (n = 37), pain (n = 13), cramps (n = 11), and stasis ulcer (n = 6). Each leg received an average of six injections (range, three to 11) of 0.5 mL of sodium tetradecyl sulfate. Blood flow in the deep veins was studied immediately before injection of the sclerosant and one week and two weeks afterward. In each leg, no change in either of these studies was found at one and two weeks following injection treatment. In nine extremities, delayed venous emptying was found on IPG. This persisted after sclerosis and was interpreted as evidence of a previous deep vein thrombosis.
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PMID:Sclerosant treatment of varicose veins and deep vein thrombosis. 649 33

An assay measuring the thrombin inactivating effect of human plasma in the presence of dermatan sulfate (DS) is described. Test plasma, diluted 1/50, is incubated with human thrombin in the presence of DS. Remaining thrombin is determined with chromogenic substrate 2AcOH . H-D-CHG-Ala-Arg-pNA. Three dilutions of reference plasma suffice and the standard curve is linear. Antithrombin III (AT) exerts a small (3-8%) effect in the assay. When test plasma contains heparin above 0.05 U/ml, this unspecific effect of AT increases, but it may be abolished by antibodies against AT. In a normal material (n = 50), the SD of DS cofactor activity was greater (15%) than that of AT (8.7%). DS cofactor was normal in hereditary AT deficiency and in 15 patients with deep venous thrombosis. In liver cirrhosis and in DIC, both inhibitors were markedly depressed, to similar degrees (r = 0.84).
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PMID:Assay of dermatan sulfate cofactor (heparin cofactor II) activity in human plasma. 654 86

The rate of postoperative deep vein thrombosis was studied by the 125I-fibrinogen method in 35 patients after total hip replacement. 12 out of 18 patients treated prophylactically with hydroxychloroquine sulfate developed deep vein thrombosis compared with 11 out of 17 patients in the control group. Platelet aggregability was inhibited in vitro by high concentrations of hydroxychloroquine sulfate, but these concentrations were not obtained in vivo and platelet aggregation was not limited in patients treated with hydroxychloroquine sulfate (Plaquenil).
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PMID:Clinical and experimental evaluation of the thromboprophylactic effect of hydroxychloroquine sulfate after total hip replacement. 700 79

The goal of heparin therapy in deep vein thrombosis is to prevent thrombus extension. The relationship between thrombus extension and the results of coagulation tests used to monitor heparin therapy is unclear. To explore this relationship, we studied the effect of several heparin regimens on the accretion of indium-111-labeled platelets on fresh venous thrombi, as detected by gamma imaging, and monitored the activated partial thromboplastin time (APTT). Six dogs were treated with a 300-U/kg bolus of heparin followed by a 90-U/kg/hour heparin infusion, a dose of heparin sufficient to increase the APTT to levels greater than eight times baseline (APTT ratio); platelet accretion (thrombus imaging) occurred only after the heparin effect was reversed with protamine sulfate. Nineteen dogs were treated with a 150-U/kg bolus of heparin followed by a 4-hour, 45-U/kg/hour heparin infusion; a thrombus was demonstrated only after protamine injection in 12 (mean APTT ratio 1.3 +/- 0.19) and before protamine injection in seven. In thirteen of these 19 dogs, 30 minutes separated the platelet injection from heparin therapy, while in six this duration was less than 30 minutes. In four of these six dogs, thrombi were demonstrated before protamine therapy and at APTT ratios greater than 3.0. Finally, 10 dogs were treated with a 100-U/kg bolus followed by a 3-hour, 50-U/kg/hour heparin infusion, after which the APTT was allowed to return to baseline values spontaneously. In all 10 dogs, a thrombus was demonstrated only after cessation of the heparin infusion, and at a mean APTT ratio of 1.4 +/- 0.15 times baseline. These results suggest that, except with very early platelet injection, platelet accretion by thrombi is consistently inhibited by heparin at APTT ratios greater than 2.5. Platelet accretion by venous thrombi occurs within narrow limits of heparin effect as reflected by the APTT.
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PMID:Indium-111-labeled platelets: effects of heparin on uptake by venous thrombi and relationship to the activated partial thromboplastin time. 709 73


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