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Biomedical subjects

A Perkash

Publications and source records attributed to A Perkash.

At least 19 recordsLinked to original sources

Functional magnetic stimulation: a new modality for enhancing systemic fibrinolysis.

OBJECTIVE: To investigate whether functional magnetic stimulation (FMS) of the leg muscles could enhance systemic fibrinolysis. DESIGN: A within-subject analysis of systemic fibrinolysis before and after 60 minutes of FMS. SETTING: The Functional Magnetic Stimulation and Special Coagulation Laboratories in the Spinal Cord Injury Service at a Veterans Administration health care facility. PARTICIPANTS: Twenty healthy volunteers were recruited. The exclusion criteria were: (1) personal or family history of venous or arterial thrombosis, (2) personal or family history of cardiac arrythmias, (3) current use of medication, and (4) the presence of a cardiac pacemaker or other metallic implants. MAIN OUTCOME MEASURES: Whole blood clot lysis time (WBCLT) and tissue plasminogen activator (t-PA) antigen determined at baseline and 10 and 60 minutes after FMS. RESULTS: A significant decrease was observed in the mean WBCLT after FMS. The WBCLT decreased from 17+/-1.3 h before FMS to 12+/-1.0 h and 11+/-0.8 h at 10 and 60 minutes post-FMS, respectively. The mean t-PA antigen levels did not show a significant change (p = .6701) from pre-FMS (6.7+/-0.91 ng/mL) to 10 min post-FMS (6.8+/-0.91 ng/mL) and 60 min post-FMS (7.0+/-1.02 ng/mL). Several patterns of fibrinolytic response to FMS were observed. They differed in relation to the degree of enhancement, the period at which maximum enhancement occurred, and the corresponding t-PA antigen levels observed. CONCLUSIONS: The FMS-induced contractions of the leg muscles enhanced systemic fibrinolysis ex vivo. The improvement in fibrinolysis occurred immediately after FMS and was also observed at 60 minutes post-FMS. FMS appears to produce a sustained enhancement of systemic fibrinolysis that may prove useful in deep-vein thrombosis prophylaxis.

Adult↗

Persistent hypercoagulation associated with heterotopic ossification in patients with spinal cord injury long after injury has occurred.

Three patients are presented with traumatic spinal cord injury (SCI) complicated by acute heterotopic ossification (HO), and concurrent deep vein thrombosis 15 months, 18 months and 22 years after SCI, accompanied by persistent hypercoagulation. The diagnosis of HO preceded deep vein thrombosis in all three patients. All were treated with etidronate disodium and therapeutic heparin followed by oral anticoagulation. As these patients were not acutely injured, the questions arose as to what predisposed them to deep vein thrombosis and when was the appropriate time to discontinue anticoagulation. Over a course of 3 years following deep vein thrombosis, these patients were monitored for evidence of hypercoagulation by D-dimer assay, plasma fibrinogen estimation, and rate of whole blood clotting by Sonoclot coagulation analyzer. The activity of acute HO was assessed by three-phase bone scan. A steady state of hypercoagulation, reflected by an increase in all three parameters, ran parallel to the extent of acute HO for the entire observation period. Moreover, hypercoagulation was persistently greater during increased acute HO activity even when the warfarin-induced prothrombin time ratio was 1.2-1.5. In addition, as acute heterotopic ossification activity decreased, the test values returned to near normal during warfarin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Deep venous thrombosis associated with heterotopic ossification.

The differential diagnosis of the swollen lower extremity in the patient with spinal cord injury includes deep venous thrombosis, fracture, cellulitis, joint sepsis, heterotopic ossification, hematoma formation, and neoplasm. A patient with an asymmetrically swollen limb who was found to have concurrent ipsilateral acute deep venous thrombosis and active heterotopic ossification is described. The diagnostic workup included various laboratory and radiologic studies. Therapy included anticoagulation with heparin and warfarin. To treat the heterotopic ossification, indomethacin, etidronate, and graded range of motion were used. We learned from this patient and several similar cases that acute deep-venous thrombosis and active heterotopic ossification may occur concurrently, and therapeutic anticoagulation did not lead to bleeding within or around the area of active heterotopic ossification. The possibility of a relationship between heterotopic ossification and deep venous thrombosis is presently being studied at our institution.

Diagnosis, Differential↗

Enhanced parasitization of platelets by Plasmodium berghei yoelii.

In previous studies plasmodia have been found by electron microscopy within human platelets naturally infected with Plasmodium vivax and within platelets of mice infected intraperitoneally with P. berghei. In both situations the number of parasitized platelets was low. An enhancement of platelet parasitization was attempted in order to study in greater detail the mechanisms and implications of such a phenomenon. Various in vitro incubation mixtures of normal mouse platelets and free merozoites of the 17X strain of P. berghei yoelii failed to produce any recognizable parasitization of platelets. In vivo, however, large numbers of invaded platelets were obtained by the use of massive intraperitoneal inocula of plasmodia (5 X 10(8) infected erythrocytes). By the 5th day of infection the proportion of parasitized platelets was 13.2 times higher in the animals receiving the large dose than in those receiving the regular passage inoculum (6 X 10(6) infected erythrocytes). Ultrastructural study of 266 intrathrombocytic parasites over eight days of infection failed to show schizogonic maturation beyond the trophozoite state.

Animals↗

Experience with the management of deep vein thrombosis in patients with spinal cord injury. Part II: a critical evaluation of the anticoagulant therapy.

Eight acute spinal injury patients with deep vein thrombosis and/or pulmonary emboli are presented witn an in-depth analysis and management of anticoagulation therapy. Special considerations for acute spinal cord injury patients with regards to prophylactic and therapeutic anticoagulation by heparin and coumadin are discussed. There was a wide variation in the requirement of heparin and/or coumadin to maintain effective coagulability which could only be elicited by frequent laboratory monitoring. Inadequate dose and shorter duration of administration of anticoagulant resulted in recurrence of thromboembolism in three out of eight patients in the present series. Haemorrhagic complications were minor and easily manageable. Co-trimoxazole potentiation of coumadin action occurred in two of our patients and it requires special mention as the drug is used increasingly in the treatment of urinary tract infections.

Administration, Oral↗

A comparison of the quantitative action of protamine and heparin on blood coagulation. Significance in clinical and laboratory usage.

Protamine is a considerably weaker anticoagulant than heparin. At a concentration in plasma of 0.05 mg (5 units/ml), heparin rendered the plasma incoagulable, while protamine produced only a mild-to-moderate lengthening of activated partial thromboplastin time (APTT) and prothrombin time (PT). Protamine concentrations between 0.3 and 1.0 mg/ml of plasma produced marked prolongation of APTT and PT, but the thrombin time (TT) was shortened. Between protamine concentrations of 1 and 2 mg/ml of plasma, the fibrinogen was precipitated to a variable degree, the APTT and PT were more than 200 sec, and the TT was moderately prolonged. High doses of protamine prolonged APTT, simulating heparin effect. Although APTT is prolonged both by heparin and protamine, TT is either normal or shortened in protamine excess and prolonged in heparin excess. To differentiate between the protamine and heparin excess, a combination of APTT and TT, supplemented by an estimation of fibrinogen and fibrin-fibrinogen split products, is recommended. The significance of these observations in the interpretation of the tests on blood coagulation is discussed.

Blood Coagulation Tests↗