Massive rectal bleeding due to colonic tuberculosis.
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Adolescent↗
Biomedical subjects
A Kher
Publications and source records attributed to A Kher.
[Comparison of the efficacy and tolerance of Kabi 2165 and standard heparin in the prevention of deep venous thrombosis in total hip prosthesis].
A series of 80 patients operated for total hip prosthesis under epidural anesthesia was randomly allocated to treatment with Kabi 2165 (n = 40): 2,500 U anti-Xa preoperatively and evening of operation and 2,500 U anti-Xa morning and evening daily up to the 9th or 10th day postoperatively, or standard heparin (n = 40): 3,750 U preoperatively and then 8 hourly, at a dose adjusted with thrombin time and cephalin + activator time, daily up to the 9th or 10th day. Phlebography was performed routinely on the 9th or 10th day. Venous thrombosis occurred in 7 patients (17.5%) in the Kabi 2165 group, including two high, potentially emboligenic, localizations (5%), and in 4 patients (10%) in the standard heparin group, including 2 potentially emboligenic clots (5%). The difference is not statistically significant (total number: p = 0.5; potentially emboligenic: p = 0.33). Pulmonary embolism did not occur. Overall tolerance, evaluated from hemoglobin and hematocrit values, intra- and post-operative bleeding and operation wound hematoma and at injection site was comparable in the two groups.
Aged↗
[Biological criteria for the evaluation of prophylactic treatment with a low molecular weight heparin (Kabi 2165)].
Efficacy of a low molecular weight heparin (Kabi 2165) was compared with that of non-fractionated heparin in the prevention of abdominal surgery postoperative venous thrombosis by means of a double-blind randomized trial in 79 patients. Determination of D. dimers in these patients allowed assessment of specificity of this assay for detection of postoperative venous thrombosis.
Abdomen↗
Sarcocystis infection in man (a case report).
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Aged↗
[Low molecular weight heparins].
Heparin is a heterogeneous component consisting of anionic polysaccharides chains of variable molecular weight ranging from 3 000 to 40 000 daltons. It is by potentiating antithrombin III (AT III) a natural inhibitor of coagulation, that heparin exerts its anticoagulant effect. Actually, it has been demonstrated that only 30% of the molecule in commercial heparin preparations are capable of binding to AT III: moreover, several procedures were used to prepare low molecular weight heparin fractions or fragments. These preparations were lacking in ability to prolong the clotting time (APTT) and to inhibit thrombin, but were capable of potentiating the inhibition of factor Xa. The hypothesis that low molecular weight heparins may exhibit antithrombotic effect by inhibition the coagulation cascade system at the initial stages is very attractive. Moreover, on animal models, heparin fractions with molecular weight less than 3 000 had limited ability to prevent experimental thrombosis despite good anti-Xa activity. Thus, the anti-Xa activity did not alone reflect the antithrombotic effect. Experimental studies have shown less bleeding with low molecular weight heparins compared to standard heparin. Some data have suggested other properties of low molecular weight heparins such as enhancement of fibrinolysis and a slighter effect on platelets. The risk of thrombocytopenia induced heparin could be reduced by the use of low molecular weight heparins. The pharmacokinetics of low molecular weight heparins have been studied in human subjects. A higher bioavailability and a longer duration of action were reported compared to heparin. Preliminary clinical trials have shown that one daily injection is sufficient to protect against post-operative thrombosis.
Animals↗
[Thrombolytic treatment in the acute phase of myocardial infarction. Evaluation in 1986].
Fibrinolytic therapy is effective in reducing the extent of myocardial infarction by lysing intracoronary clots. An overview of twelve trials of prolonged intravenous infusion of SK showed a highly significant reduction in short term mortality. Intra coronary SK infusion achieved reperfusion of the coronary artery in 60 to 90 p. 100 of patients and improvement of left ventricular function was reported. Mortality was also significantly reduced at 6 months. The frequency of bleeding was relatively low and ventricular arrhythmias were not a serious problem. High dose brief duration intravenous SK therapy achieved reperfusion of the occluded coronary artery in 44 to 60 p. 100 of patients. Left ventricular function was also improved. An Italian multicentre trial has shown a significant decrease in the overall hospital mortality of a randomized population. There is no evidence that UK was more effective than SK. New fibrinolytic agents (T-PA, acylated SK-plasminogen activator), with more fibrin specific activity, were successful in inducing coronary thrombolysis in patients with acute myocardial infarction. The rate of reocclusion was about 20 p. 100 and additional stabilising procedure (percutaneous transluminal coronary angioplasty) was necessary in many patients.
Fibrinolytic Agents↗
Comparative pharmacokinetics of a low molecular weight heparin (PK 10 169) and unfractionated heparin after intravenous and subcutaneous administration.
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Factor X↗
Comparative beta-adrenoceptor blocking effect and pharmacokinetics of bucindolol and propranolol in man.
The beta-adrenoceptor blocking properties and pharmacokinetics of bucindolol 150 mg were compared to those of propranolol 80 mg and a placebo in a double-blind trial in 6 healthy volunteers. Heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressures and peak expiratory flow rate (PEFR) at rest and during vigorous exercise, and plasma renin activity (PRA) at rest, were measured before and at intervals up to 24 h after oral administration of the drugs. Bucindolol reduced exercise tachycardia and decreased exercise PEFR, thus behaving as a non-selective beta-adrenoceptor blocking drug. In contrast to propranolol, bucindolol did not reduce resting HR and PRA, probably because of its intrinsic sympathomimetic activity. It decreased resting DBP in relation to its peripheral vasodilator properties. The effects of bucindolol developed as early as 30 min after administration and lasted up to 24 h, whereas its Tmax and T 1/2 were 1.6 and 3.6 h respectively. Comparison of the time courses of plasma bucindolol and the cardiac beta-adrenoceptor blockade strongly suggests that in man bucindolol undergoes an extensive first-pass effect, leading to the formation of one or more active metabolites.
Adrenergic beta-Antagonists↗
Long-term efficacy and safety of oral encainide in the treatment of chronic ventricular ectopic activity: relationship to plasma concentrations--a French multicenter trial.
To establish long-term efficacy and safety of encainide, 48 patients with chronic premature ventricular contractions (PVCs) underwent 6 months of therapy with encainide. Twenty-four-hour ambulatory ECGs were obtained at baseline for each daily dosage of 75 mg, 150 mg, and 225 mg of encainide during the in-hospital titration period and at the end of the first and sixth months during the follow-up period. There was a significant reduction in the median hourly total PVC rates from 480.6 at baseline to 2.0 at the end of the titration period with the highest dosage and to 22.1 at the last visit of the chronic dosing period. Nearly total suppression of PVCs was observed in 56% of patients at the end of the titration period and in 30% at the end of the 6-month follow-up period. The most common side effects were vertigo, vision disturbance, and headache. PR, QRS, and QTc intervals showed consistent significant increases from baseline during the various encainide trial periods. Encainide may have worsened ventricular arrhythmia in four patients who received more than 200 mg of encainide daily. Plasma concentrations of encainide and encainide metabolites showed wide interpatient variation, and no relationship was found between antiarrhythmic efficacy and plasma levels of encainide, O-demethyl-encainide, or 3-methoxy-O-demethyl-encainide.
Adolescent↗
Increased anti-Xa bioavailability for a low molecular weight heparin (PK 10169) compared with unfractionated heparin.
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Adult↗
[Anti-arrhythmia effect of long-term encainide in chronic ventricular extrasystole].
The long term efficacy and tolerance of encainide were studied in 48 patients with chronic/ventricular extrasystoles (VES) treated for 6 months. Holter monitoring was performed before treatment and at each dose increment (75 mg/day; 150 mg/day and 225 mg/day) during the first week of titration, and then after 1 month and 6 months of treatment. The dose administered in the long-term study corresponded to the minimum effective dose during the titration phase (the dose which reduced the number of VES/24 hours by at least 75%). The average number of VES/hour decreased significantly from 480.6 before treatment to 2.0 at the end of the study. The frequency of episodes of ventricular tachycardia decreased significantly during treatment. The commonest side effects were vertigo, visual disturbances and headaches. Treatment was interrupted because of side-effects or inefficacy in 6 patients. The surface ECG showed significant lengthening of the PR, QRS and QTc periods and encainide appeared to have aggravated the ventricular arrhythmias of 4 patients receiving 200 mg/day. The plasma concentrations of encainide and its two principal metabolites were measured during the titration phase, at 1 month and after 6 months of treatment. 15.6 per cent of patients were slow and 84.4% of patients were rapid metabolizers. The wide individual variations of plasma concentrations and the absence of correlation between the plasma concentrations of encainide and its metabolites and the antiarrhythmic effect suggest that the compound and its metabolites play a role in the antiarrhythmic effect of the drug.
Adolescent↗
[Anti-arrhythmia and electrophysiological effects of encainide in supraventricular tachycardias].
In order to assess the electrophysiologic effects and anti-arrhythmia effects of encainide after acute IV injection and chronic oral therapy, a group of 10 patients (mean age 54) with recurrent supraventricular tachycardia was studied. Seven patients had more than 2 attacks per month, and supraventricular tachycardia (SVT) resulted in severe symptoms in the three remaining SVT was due to AV nodal re-entry in 6 patients and to concealed accessory pathway in 4. After a control study, SVT was initiated, and encainide (0.75 mg/kg) was infused intravenously in attempt to stop the tachycardia. A second study was achieved. After 4 days of oral therapy (25 or 50 mg T.I.D.) a third study was performed, including SVT initiation attempts. Encainide depressed conduction in all cardiac tissues, and this effect was more evident after oral administration. Antegrade I:I conduction cycle length increased of 13.9% (p less than 0.05), and the same parameter in retrograde conduction increased of 30.03% (p less than 0.05). IV injection interrupted 2 of 10 SVT only. However, after 30 minutes, 5 re-initiated SVT were nonsustained, and mean cycle length increased from 326 +/- 21 to 397 +/- 51 (p less than 0.01). After oral therapy, SVT was initiated in 4 of 10 patients, nonsustained in 3. During long term follow-up (one year or more), no severe adverse effect has been reported. Three patients are still experiencing short events of well-tolerated SVT. Hence, moderate or low doses or oral encainide may safely control recurrent supraventricular tachycardia.
Administration, Oral↗
Pharmacokinetics of a fixed combination of sotalol and hydrochlorothiazide in hypertensive patients with moderate renal insufficiency.
Decreased elimination of a combined formulation of Sotalol (160 mg) and hydrochlorothiazide (25 mg) was found in patients with moderate renal insufficiency. Very slight accumulation of sotalol and hydrochlorothiazide was observed, so it appears unnecessary to reduce the dosage in patients with a creatinine clearance of 30 ml/min or more.
Drug Combinations↗
Spontaneous platelet aggregation in heparin-treated patients.
To evaluate the influence of heparin on spontaneous platelet aggregation (SPA) two groups of patients, one treated with heparin and the other without heparin, were compared. The frequency of SPA is highly increased in patients with prosthetic heart valves treated with heparin as compared to patients not treated with heparin. Thus, the high frequency of SPA in prosthetic heart valve carriers treated with heparin might be due either to the prosthesis itself or to heparin. In contrast, in patients with thromboembolic disease, SPA does not seem to be more frequent in heparin-treated than in untreated patients.
Adult↗
[Development and dissemination of malignant tumors, and hemostasis].
Strong circumstantial evidence suggests that the activation of the hemostatic system is involved in the growth and spread of malignant tumors. Nevertheless, the considerable experimental and clinical data presently available cannot be interpreted in one specific direction. The presence of a fibrin and/or a platelet thrombus in the environment of tumor cells only represents the visible end product of a complex biochemical and biophysical process during which other phenomena like haemodynamic changes and the generation of many biologically active enzymes occur. In the interpretation of experimental studies and clinical trials of anticoagulants in cancer disease, a wider concept of the hemostatic process and its multiple interactions with other biological systems is needed. The complement system, adhesive glycoproteins of the cell surface, chemotaxis, growth factors and prostaglandins are some examples of factors which interact with the hemostatic system as well as with the pathology of cancer. The definite pathogenic connection between the clinically observed hypercoagulability of patients with malignant disease and the biology of tumor growth and tumor dissemination remains unclear. Agents which modify hemostatic reactions must be evaluated in specific tumor categories using carefully controlled prospective trials. The results of such studies on tumor regression and also on longevity will permit to assess the efficacy of these agents as adjuvant therapy in the treatment of cancer.
Animals↗
[Pharmacology of anti-platelet agents].
A new class of drugs has appeared alongside classical anti-thrombotic agents such as heparin and oral anticoagulants, characterised by their ability to modify the behaviour of platelets: "anti-platelet" agents. This article reviews the platelet actions, pharmacokinetics, conditions of use and side effects of the four chief agents available: acetylsalicylic acid (ASA), sulfinpyrazone, dipyridamole and ticlopidine. The mode of action of the first of them is that best studied. ASA opposes the conversion of arachidonic acid to prostaglandins and thromboxane, by the irreversible acetylation of cyclo-oxygenase. Nevertheless, major therapeutic trials involving ASA have yielded only poor results. There are at least two possible explanations for this state of affairs: --aggregation may occur even when thromboxane is blocked, in particular in response to thrombin; --ASA has been used at doses also capable of inhibiting the formation by the vascular wall of an anti-aggregant prostaglandin, PGI2. Current efforts by pharmacologists which should result in better adapted and hence more effective anti-thrombotic methods, are essentially concerned with the following points: --to understand why sulfinpyrazone, which in principle has the same mode of action as ASA, seems sometimes more active and sometimes less active than the latter according to whether coronary or cerebrovascular accidents are involved; --to propose a rational prescription programme for ASA, in such a way that it inhibits only little, and for as short a time as possible, the production of PGI2 (e.g. 200 mg every three days): --to perfect more active combinations; --synthesis of new substances, e.g. thromboxane synthetase inhibitors, or stable analogues of PGI2. The reasons which suggest that such substances could be used more beneficially in man are expanded.
Animals↗
[Heparin treatment of thromboembolic complications].
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Aged↗
[Development and dissemination of malignant tumors and hemostasis].
Strong circumstantial evidence suggests that the activation of the hemostatic system is involved in the growth and spread of malignant tumors. Nevertheless, the considerable experimental and clinical data presently available cannot be interpreted in one specific direction. The presence of a fibrin and/or a platelet thrombus in the environment of tumor cells only represents the visible end product of a complex biochemical and biophysical process during which other phenomena like haemodynamic changes and the generation of many biologically active enzymes occur. In the interpretation of experimental studies and clinical trials of anticoagulants in cancer disease, a wider concept of the hemostatic process and its multiple interactions with other biological systems is needed. The complement system, adhesive glycoproteins of the cell surface, chemotaxis, growth factors and prostaglandins are some examples of factors which interact with the hemostatic system as well as with the pathology of cancer. The definite pathogenic connection between the clinically observed hypercoagulability of patients with malignant disease and the biology of tumor growth and tumor dissemination remains unclear. Agents which modify hemostatic reactions must be evaluated in specific tumor categories using carefully controlled prospective trials. The results of such studies on tumor regression and also on longevity will permit to assess the efficacy of these agents as adjuvant therapy in the treatment of cancer.
Animals↗