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Biomedical subjects

M Aiach

Publications and source records attributed to M Aiach.

234 records · Page 13Linked to original sources
PubMed1975

Discontinued thrombolytic treatment: initial biological results.

Changes in blood coagulation following the action of intermittent treatment with streptokinase are studied : 1) Fibrinogenemia remains at a concentration slightly higher than that obtained after the first 16 hour perfusion. 2) The thrombin time becomes considerably longer on the first day, then becomes shorter and remains slightly long throughout treatment. The theoretical interest of the rise in plasminogen levels during interruption of perfusions of streptokinase is discussed.

Humans↗
PubMed1975

[Intermittent thrombolytic treatment. Results during severe, chronic arterial diseases].

38 patients with severe chronic arteritis of the lower limbs were treated with streptokinase intermittently. All had been refused for surgical operation. One patient died, 4 others had early interruption of treatment. Eleven of the 38 patients had efficient thrombolysis confirmed by arteriography. The facts confirm the possibility of thrombolysis during chronic arterial disease. The fact that the aggravation was recent was favourable factor in prognosis. The eleven patients improved, had severe aggravation of symptomes for less than 2 months. Thus thrombolytic treatment has a place of choice in the treatment of severe arterial disease where surgery is impossible, or dangerous, owing to the uncertain state of the vascular bed below the lesion. Efficacious, it permits reconstructive surgery in cases where it had been at first refused. The use of intermittent treatment, apart from advantages of confort and cost, seems to increase the efficacy of treatment.

Adult↗
PubMedDate not supplied

[Analytical choices for biological tests in thrombotic pathology].

The knowledge of genetic and occurred risk factors allows us to propose laboratory investigations in patients with thromboembolism (TE) to evaluate the risk for recurrence. Beside coagulation inhibitor deficiencies accounting for less than 10% of cases, factor V Leiden and prothrombin G20210A mutations are found in around 30% and 10% respectively. Increased factor VIII and hyperhomocysteinemia resulting from interaction of genetic factors and environmental factor are also risk factors for TE. Finally, antiphospholipid antibodies, a complex family of antibodies recognizing various phospholipid or phospholipid binding proteins, are also associated with TE.

Clinical Laboratory Techniques↗
PubMedDate not supplied

Intermittent treatment with streptokinase in arterial disease of the limbs.

Sixty-two patients with arterial disease of the lower limbs were treated with streptokinase by intermittent administration. All patients had experienced recent aggravation of their arterial disease, and 22 had thrombolysis confirmed by arteriography. In 20 cases clinical study showed repermeation--in 8 cases during the first perfusion and in 8 cases during the third perfusion. During the first perfusion the fall in fibrinogen was significantly greater in the 8 patients with thrombolysis. Further, the third perfusion corresponded to a new phase of fibrinogenolysis. These results support the possibility of the relationship between plasminemia and thrombolysis, and emphasize the limits of the classic theory of Sherry, Fletcher, and Alkjaersig. Permitting phases of repeated but limited plasminemia, the interruption method used here is a compromise between the risk of hemorrhage and the efficacy of treatment at low dosage.

Angiography↗
PubMedDate not supplied

[Interaction of estrogens and genetic risk factors for thrombosis].

Deep venous thrombosis (DVT) is associated with a genetic risk factor in about half of all cases. Antithrombin, protein C or protein S deficiencies account for 5 to 10 per cent of hereditary thrombophilia whereas the Arg 506 Gln factor V mutation is found in 20 to 30 per cent of DVTs and the G20210A factor II gene mutation in 5 to 10 per cent of them. The risk for DVT is increased three- to fourfold in women using oral contraceptives (OC); it is also increased during menopause hormonotherapy. Oestrogens modify the haemostatic balance, inferring a role in the thrombotic risk. The only thrombophilic factor which in association with OC was demonstrated to multiply the risk is the factor V Arg 506 Gln mutation, with a relative risk around 30. This observation reinforces the hypothesis that venous thrombosis is a multifactorial disease.

Amino Acid Substitution↗
PubMedDate not supplied

[Heparin induced autoimmune thrombocytopenia: assessment of a rapid functional assay].

Heparin-induced thrombocytopenia (HIT) diagnosis is often difficult. Depending on the patients, the thrombocytopenia could be due to various causes. Despite their poor sensitivity and specificity, biological tests are necessary to clarify the diagnosis. In 1985, a new heparin-induced platelet aggregation assay was described that consists in determining the percentage of aggregated platelets by using an automated cell counter. Plasma samples from 18 patients with a definite HIT were tested with this quick easy-to-perform HIT diagnosis test. Positive results were obtained with 11 plasma (61%) when the test was performed with platelets from 3 different healthy volunteers (control platelets). As for the other functional tests, results are depending on control platelets and sensitivity seems to be increased when control platelets FcgammaRIIa-131 polymorphism was of His/His (but difference is not significant). In emergency situation, it is difficult to perform a functional test with control platelets from several healthy donors, and it is even more difficult to select volunteers on their FcgammaRIIa-131 polymorphism. In conclusion, in spite of its practicability, the test is not reliable to help in the rapid diagnosis of HIT. Indeed, 7 patients of 18 (39%) with definite HIT have been found negative with this test.

Anticoagulants↗
PubMedDate not supplied

[Validation of a diagnostic kit for factor V Leiden mutation].

The Stagen factor V Leiden mutation is a new kit allowing to perform all steps necessary to identify the Leiden mutation of Factor V, from DNA extraction from patient's blood sample to electrophoresis of amplification products. The method is based on an allele specific amplification, which allows patient's genotype to be established in a single step. Analytical properties of the kit have been tested first, and revealed the robustness of the kit. In a second step, a prospective study of a cohort of 300 thrombophilic patients demonstrated the specificity and the sensitivity of the method. In additions, several controls and methodological ingenious processes allow to minimize the risk of human or method errors, making the reliability of the kit. Finally, the Stagen factor V Leiden mutation is easy and rapid to use in hospital or private laboratories, and is well-suited for small series of patients of the latter.

Factor V↗
PubMedDate not supplied

[Antithrombin III in 86 patients with venous thrombosis (author's transl)].

Antithrombin III concentration was studied in 86 patients with recurrent or extensive venous thrombosis. Two of them were found to have an hereditary antithrombin III deficiency. 25 patients receiving heparin therapy had low antithrombin III concentration. After stopping heparin treatment antithrombin rose to a normal level. Pathological antithrombin III modifications are recalled (synthesis decrease in liver diseases, intra vascular consumption during active venous thrombosis). Antithrombin III decreased activity induced by heparin treatment is pointed out.

Antithrombin III↗
PubMedDate not supplied

[Treatment of deep venous thrombosis. Comparative study of a low molecular weight heparin fragment (Fragmin) by the subcutaneous route and standard heparin by the continuous intravenous route. A multicenter study].

This open, randomised multicenter trial compares the efficacy and safety of Fragmin administered subcutaneously twice daily with standard heparin administered by continuous infusion in the treatment of deep vein thrombosis (DVT). The initial dose of Fragmin is 100 U anti-Xa/kg/12 h and the further doses are adjusted according to the anti-Xa activity between 0.5 and 0.8 U/ml, 3 hours after the morning injection. The initial dose of standard heparin is 240 UI/kg/12 h. The dose adjustments are based on the daily results of APTT (1.5 - 3 times the control). Treatments efficacy are appreciated when comparing the venography performed before and after 10 days of treatment. The safety is evaluated on clinical parameters and iterative biological tests. Sixty-six patients have been included in this study. Efficacy of the two treatments is equivalent with a phlebographic improvement in respectively 79.3 p. 100 (Heparin Group) and 71.0 p. 100 (Fragmin Group) of the cases and an aggravation in 3.4 p. 100 and 6.4 p. 100 (NS) respectively. The frequency of dosage adjustments is lower and the stability of biological tests is better in the Fragmin group. In conclusion, the administration of Fragmin twice daily by subcutaneous route seems to be equivalent at least to standard heparin continuous infusion in the treatment of recent DVT. The better convenience and safety of Fragmin have to be verified on a larger panel of patients.

Adult↗
PubMedDate not supplied

Peripheral artery thrombolysis with urokinase-lys-plasminogen. A disappointing experience.

Thirty-five patients with peripheral arterial occlusion were treated by intra-arterial infusion of low dose urokinase associated with bolus of lys-plasminogen. Systemic fibrinolysis was moderate, thrombolysis was achieved in 26 patients (74%). Only one patient required blood transfusion, five patients (14%) had distal emboli. Infection at the catheter entry site occurred in 2 patients, 3 patients experienced proximal embolism. Six patients required leg amputation, 4 died, in 2 of them deaths were related to arterial catheterization. Local thrombolysis with limited systemic fibrinolysis is associated to a high rate of catheter-related complications.

Adult↗
PubMedDate not supplied

Streptokinase after late failure of reconstructive surgery for peripheral arteriosclerosis.

After the failure of reconstructive surgery for arterial occlusions of the lower limbs, 25 patients with severe ischemia were treated with streptokinase (SK) to avoid amputation of the limbs and sometimes death, in the absence of any other possible treatment. In 16 subjects, thrombolysis, assessed by the Doppler ultrasound technique, occurred rapidly; in 12 cases, SK combined with surgery or with symptomatic medical treatment gave good results saving limbs and improving the quality of life. Three of the 16 patients died from a cerebral vascular accident which occurred before the 10th hour. Whatever the type and the number of surgical operations performed before the use of SK, the indications and the results of the treatment are governed by the condition of the vascular tree below the arterial lesions. SK seems to be justified in endarterectomy or venous grafts with severe ischemia less than two months old. For dacron by-passes, the possibility of prosthesis dissection makes SK debatable in spite of frequent lysis. In axillofemoral by-passes, the risk of embolism of the upper limbs makes the use of SK inadvisable.

Adult↗
PubMedDate not supplied

[Evaluation of hemostasis in venous thromboembolism pathology].

Thromboembolic disease results from an hypercoagulable state and multifactorial causes may lead to hypercoagulability. Thrombogenic risk factors can be acquired and/or inherited. For each thrombophilic patient, the main clinical features retained are: the patient age, the familial history, the recurrence of thromboembolic events, an unusual site of thrombosis. Anti-phospholipid antibodies, which are considered as acquired thrombogenic risk factors, can be detected with coagulation tests and/or Elisa methods. The association of antiphospholipid antibodies with thrombosis is defined as the anti-phospholipid syndrome. Last decades, genetic risk factors were identified. First of all, antithrombin, protein C and protein S deficiencies were described. These deficiencies are involved in about 10% of patients who develop thrombosis before the age of 50. In 1993, a new genetic risk factor was discovered: activated protein C resistance which is due to the Q506 mutation in factor V. This defect represents the most prevalent abnormality of inherited thrombophilia, affecting 20 to 40% of thrombophilic patients. Interestingly, hyperhomocysteinemia, known as potentially predisposing to arterial disease, was also recognized as a risk factor for venous occlusive disease. Several genes encoding homocystein metabolism enzymes, such as cystathionine beta-synthase or methylenetetrahydrofolate reductase are concerned. Establishment of a causal association between the presence of a biological abnormality and the occurrence of thrombosis may lead to an adapted prophylaxis whatever the risk situation.

Antiphospholipid Syndrome↗