A coumarin that is used as an anticoagulant. Its actions and uses are similar to those of WARFARIN. (From Martindale, The Extra Pharmacopoeia, 30th ed, p233)
Coumarin derivative that acts as a long acting oral anticoagulant.
OXIDOREDUCTASES which mediate vitamin K metabolism by converting inactive vitamin K 2,3-epoxide to active vitamin K.
Agents that prevent clotting.
System established by the World Health Organization and the International Committee on Thrombosis and Hemostasis for monitoring and reporting blood coagulation tests. Under this system, results are standardized using the International Sensitivity Index for the particular test reagent/instrument combination used.
Math calculations done for preparing appropriate doses of medicines, taking into account conversions of WEIGHTS AND MEASURES. Mistakes are one of the sources of MEDICATION ERRORS.
A liver microsomal cytochrome P450 enzyme that catalyzes the 16-alpha-hydroxylation of a broad spectrum of steroids, fatty acids, and xenobiotics in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme is encoded by a number of genes from several CYP2 subfamilies.
A branch of genetics which deals with the genetic variability in individual responses to drugs and drug metabolism (BIOTRANSFORMATION).
A large group of cytochrome P-450 (heme-thiolate) monooxygenases that complex with NAD(P)H-FLAVIN OXIDOREDUCTASE in numerous mixed-function oxidations of aromatic compounds. They catalyze hydroxylation of a broad spectrum of substrates and are important in the metabolism of steroids, drugs, and toxins such as PHENOBARBITAL, carcinogens, and insecticides.
An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.
Clotting time of PLASMA recalcified in the presence of excess TISSUE THROMBOPLASTIN. Factors measured are FIBRINOGEN; PROTHROMBIN; FACTOR V; FACTOR VII; and FACTOR X. It is used for monitoring anticoagulant therapy with COUMARINS.
Bleeding or escape of blood from a vessel.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Synthetic or naturally occurring substances related to coumarin, the delta-lactone of coumarinic acid.
Multinucleated cells (fused macrophages) seen in granulomatous inflammations such as tuberculosis, syphilis, sarcoidosis, and deep fungal infections. They resemble foreign-body giant cells (GIANT CELLS, FOREIGN BODY) but Langhans giant cells contain less chromatin and their nuclei are arranged peripherally in a horseshoe-shaped pattern. Langhans giant cells occur frequently in delayed hypersensitivity.
Liquids that are suitable for drinking. (From Merriam Webster Collegiate Dictionary, 10th ed)
A basis of value established for the measure of quantity, weight, extent or quality, e.g. weight standards, standard solutions, methods, techniques, and procedures used in diagnosis and therapy.
Aching sensation that persists for more than a few months. It may or may not be associated with trauma or disease, and may persist after the initial injury has healed. Its localization, character, and timing are more vague than with acute pain.
Intensely discomforting, distressful, or agonizing sensation associated with trauma or disease, with well-defined location, character, and timing.
An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.
A form of therapy that employs a coordinated and interdisciplinary approach for easing the suffering and improving the quality of life of those experiencing pain.
Scales, questionnaires, tests, and other methods used to assess pain severity and duration in patients or experimental animals to aid in diagnosis, therapy, and physiological studies.
A mass spectrometry technique using two (MS/MS) or more mass analyzers. With two in tandem, the precursor ions are mass-selected by a first mass analyzer, and focused into a collision region where they are then fragmented into product ions which are then characterized by a second mass analyzer. A variety of techniques are used to separate the compounds, ionize them, and introduce them to the first mass analyzer. For example, for in GC-MS/MS, GAS CHROMATOGRAPHY-MASS SPECTROMETRY is involved in separating relatively small compounds by GAS CHROMATOGRAPHY prior to injecting them into an ionization chamber for the mass selection.
Chromatographic techniques in which the mobile phase is a liquid.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
An extraction method that separates analytes using a solid phase and a liquid phase. It is used for preparative sample cleanup before analysis by CHROMATOGRAPHY and other analytical methods.
An analytical method used in determining the identity of a chemical based on its mass using mass analyzers/mass spectrometers.
A mass spectrometry technique used for analysis of nonvolatile compounds such as proteins and macromolecules. The technique involves preparing electrically charged droplets from analyte molecules dissolved in solvent. The electrically charged droplets enter a vacuum chamber where the solvent is evaporated. Evaporation of solvent reduces the droplet size, thereby increasing the coulombic repulsion within the droplet. As the charged droplets get smaller, the excess charge within them causes them to disintegrate and release analyte molecules. The volatilized analyte molecules are then analyzed by mass spectrometry.
Determination, by measurement or comparison with a standard, of the correct value of each scale reading on a meter or other measuring instrument; or determination of the settings of a control device that correspond to particular values of voltage, current, frequency or other output.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
Flaps of tissue that prevent regurgitation of BLOOD from the HEART VENTRICLES to the HEART ATRIA or from the PULMONARY ARTERIES or AORTA to the ventricles.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
Placing of a hydroxyl group on a compound in a position where one did not exist before. (Stedman, 26th ed)
Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.
A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
Widely distributed enzymes that carry out oxidation-reduction reactions in which one atom of the oxygen molecule is incorporated into the organic substrate; the other oxygen atom is reduced and combined with hydrogen ions to form water. They are also known as monooxygenases or hydroxylases. These reactions require two substrates as reductants for each of the two oxygen atoms. There are different classes of monooxygenases depending on the type of hydrogen-providing cosubstrate (COENZYMES) required in the mixed-function oxidation.
A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
7-Hydroxycoumarins. Substances present in many plants, especially umbelliferae. Umbelliferones are used in sunscreen preparations and may be mutagenic. Their derivatives are used in liver therapy, as reagents, plant growth factors, sunscreens, insecticides, parasiticides, choleretics, spasmolytics, etc.
Substances found in many plants, containing the 4-hydroxycoumarin radical. They interfere with vitamin K and the blood clotting mechanism, are tightly protein-bound, inhibit mitochondrial and microsomal enzymes, and are used as oral anticoagulants.
A chemical reagent that reacts with and modifies chemically the tryptophan portion of protein molecules. Used for 'active site' enzyme studies and other protein studies. Sometimes referred to as Koshland's reagent.
Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.
A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.
The interchange of goods or commodities, especially on a large scale, between different countries or between populations within the same country. It includes trade (the buying, selling, or exchanging of commodities, whether wholesale or retail) and business (the purchase and sale of goods to make a profit). (From Random House Unabridged Dictionary, 2d ed, p411, p2005 & p283)
The relative equivalency in the efficacy of different modes of treatment of a disease, most often used to compare the efficacy of different pharmaceuticals to treat a given disease.

A placebo-controlled study of interaction between nabumetone and acenocoumarol. (1/76)

AIMS: The use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients treated with oral anticoagulants is generally discouraged due to the risk of interactions that could increase the risk of bleeding complications. Available data suggest the NSAID, nabumetone, does not produce such an interaction. We investigated whether nabumetone would interact with acenocoumarol, an oral anticoagulant widely used in some European countries. METHODS: A double-blind, randomized, placebo-controlled study was conducted evaluating nabumetone (1-2 g daily for up to 4 weeks) in osteoarthritis patients with thromboembolic risk previously stabilized on acenocoumarol. The primary efficacy end point was the proportion of patients whose International Normalized Ratio (INR) remained within established margins and whose acenocoumarol dose was not changed. Fifty-six patients were randomized to receive nabumetone (n=27) or placebo (n=29). RESULTS: Eighteen patients in each group (67% for nabumetone and 62% for placebo) completed the study without showing INR or acenocoumarol dose changes, and were considered as study successes. Nine patients (33%) with nabumetone and 11 (38%) with placebo were considered study failures in the intention-to-treat analysis (one patient on nabumetone and four on placebo did not complete the study due to reasons not related to INR and acenocoumarol dose changes). No significant differences were found between groups with regard to study successes. There were two minor bleeding complications, one in each group. Six patients per group presented with eight adverse experiences in each group. CONCLUSIONS: Treatment with nabumetone did not alter INR levels compared with placebo in patients stabilized on oral acenocoumarol who require NSAID therapy. These results suggest that nabumetone does not produce a clinically relevant interaction with acenocoumarol. In orally anticoagulated patients without other associated risk factors, treatment with nabumetone for up to 4 weeks does not require increased monitoring of INR levels.  (+info)

Prediction of pharmacokinetic drug/drug interactions from In vitro data: interactions of the nonsteroidal anti-inflammatory drug lornoxicam with oral anticoagulants. (2/76)

CYP2C9 is involved in the metabolism of the oral anticoagulants warfarin, phenprocoumon, and acenocoumarol. It is also responsible for the 5'-hydroxylation of the nonsteroidal anti-inflammatory drug lornoxicam. Therefore, lornoxicam and the oral anticoagulants are potential inhibitors of their metabolism. Their inhibitory potency was investigated in microsomes from six human livers. An approach to predict pharmacokinetic interactions of lornoxicam from in vitro inhibition data was developed. Where possible, the forecasts were verified by comparison with data from clinical interaction studies. The following increases in steady-state plasma concentrations or areas under the plasma concentration-time curve of the oral anticoagulants by concomitant lornoxicam medication were predicted (values in parentheses are for healthy volunteers): (S)-warfarin, 1. 58-fold (1.32-fold for racemate); racemic-acenocoumarol, 1.28-fold (1.09-fold); (R)-acenocoumarol, 1.10-fold (1.0-fold); racemic-phenprocoumon, 1.11-fold (1.18-fold); and (S)-phenprocoumon, 1.13-fold (1.24-fold). Lornoxicam 5'-hydroxylation was competitively inhibited in vitro by both phenprocoumon (K(i) = 1.2 +/- 0.4 microM) and acenocoumarol (K(i) = 5.5 +/- 3.5 microM). The present results indicate that relatively close predictions of the interactions of lornoxicam with oral anticoagulants from in vitro data are possible under the assumption that hepatic lornoxicam concentrations are similar to its total plasma concentrations. The degree of pharmacokinetic interactions exhibited by oral anticoagulants and lornoxicam is dependent on the respective contribution of CYP2C9 to their total clearance.  (+info)

Assessment of patient capability to self-adjust oral anticoagulant dose: a multicenter study on home use of portable prothrombin time monitor (COAGUCHECK). (3/76)

BACKGROUND AND OBJECTIVES: Self-testing and self-monitoring with portable prothrombin time (PT) monitors has been shown to be feasible and safe. However the ability of patients on chronic oral anticoagulant therapy (OAT) to self-adjust their dose without specific training has never been properly evaluated. The aims of this study were to evaluate: 1) the ability of patients on chronic OAT to self-adjust their dose without specific training; 2) the integration of a portable PT monitor (Coagucheck, Roche Diagnostics, Germany) for home use into routine patient care in anticoagulation clinics. DESIGN AND METHODS: A nested case-control study was conducted in four centers of the Italian Federation of Anticoagulation Clinics (FCSA). Patients (n=78) on stable OAT for at least 6 months (cases: 47 men, 31 women, age range: 18-75 years) were enrolled on a volunteer basis after passing an Abbreviated Mental Test and providing informed consent. After three instruction sessions on the use of Coaguchek, subjects performed the PT test at home, communicated the INR results to the Center and suggested the dose adjustment and date for next control as they thought appropriate. However, they were requested to follow the prescription made by the Center. Controls (78 subjects) matched by age (+/- 5 years), sex and therapeutic range with the cases, were selected from among those who attended the anticoagulation clinics and managed by usual care. RESULTS: When compared with the dose prescribed by the Clinic, the dose suggested by warfarin and acenocoumarol users was equal to or within +/- 6% of the mean weekly dose in 80% and 82% of suggestions, respectively. Time spent in the therapeutic range during the study was the same (80%) for cases and controls. INTERPRETATION AND CONCLUSIONS: Selected patients on chronic anticoagulant therapy can acquire a satisfactory ability for self-adjustment of OAT dose without specific training.  (+info)

Cytochrome P4502C9 is the principal catalyst of racemic acenocoumarol hydroxylation reactions in human liver microsomes. (4/76)

The oral anticoagulant acenocoumarol is given as a racemic mixture. The (S)-enantiomer is rapidly cleared and is the reason why only (R)-acenocoumarol contributes to the pharmacological effect. The objective of the study was to establish the cytochrome P450 (CYP) enzymes catalyzing the hydroxylations of the acenocoumarol enantiomers. Of various cDNA-expressed human CYPs, only CYP2C9 hydroxylated (S)-acenocoumarol. Hydroxylation occurred at the 6-, 7-, and 8-position with equal K(m) values and a ratio of 0.9:1:0.1 for V(max). CYP2C9 also mediated the 6-, 7-, and 8-hydroxylations of (R)-acenocoumarol with K(m) values three to four times and V(max) values one-sixth times those of (S)-acenocoumarol. (R)-Acenocoumarol was also metabolized by CYP1A2 (6-hydroxylation) and CYP2C19 (6-, 7-, and 8-hydroxylation). In human liver microsomes one enzyme only catalyzed (S)-acenocoumarol hydroxylations with K(m) values < 1 microM. In most of the samples tested the 7-hydroxylation of (R)-acenocoumarol was also catalyzed by one enzyme only. The 6-hydroxylation was catalyzed by at least two enzymes. Sulfaphenazole could completely inhibit in a competitive way the hydroxylations of (S)-acenocoumarol and the 7-hydroxylation of (R)-acenocoumarol. The 6-hydroxylation of (R)-acenocoumarol could be partially inhibited by sulfaphenazole, 40 to 50%, and by furafylline, 20 to 30%. Significant mutual correlations were obtained between the hydroxylations of (S)-acenocoumarol, the 7-hydroxylation of (R)-acenocoumarol, the 7-hydroxylation of (S)-warfarin, and the methylhydroxylation of tolbutamide. The results demonstrate that (S)-acenocoumarol is hydroxylated by a single enzyme, namely CYP2C9. CYP2C9 is also the main enzyme in the 7-hydroxylation of (R)-acenocoumarol. Other enzymes involved in (R)-acenocoumarol hydroxylation reactions are CYP1A2 and CYP2C19. Drug interactions must be expected, particularly for drugs interfering with CYP2C9. Also, drugs interfering with CYP1A2 and CYP2C19 may potentiate acenocoumarol anticoagulant therapy.  (+info)

Low molecular weight heparin versus oral anticoagulants in the long-term treatment of deep venous thrombosis. (5/76)

PURPOSE: The purpose of this study was to evaluate whether low molecular weight heparin (LMWH) could be equal or more effective than conventional oral anticoagulants (OAs) in the long-term treatment of deep venous thrombosis (DVT). METHODS: One hundred fifty-eight patients with symptomatic DVT of the lower limbs confirmed by means of duplex ultrasound scan were randomized to receive 3 to 6 months' treatment with nadroparine calcium or acenocoumarol. Quantitative and qualitative duplex scan scoring systems were used to study the evolution of thrombosis in both groups at 1, 3, 6, and 12 months. RESULTS: During the 12-month surveillance period, two (2.5%) of the 81 patients who received LMWH and seven (9%) of the 77 patients who received OAs had recurrence of venous thrombosis (not significant). In the LMWH group no cases of major bleeding were found, and four cases (5.2%) occurred in the OA group (not significant). The mortality rate was nine (11.1%) in the LMWH group and 7.8% in the OA group (not significant). The quantitative mean duplex scan score decreased in both groups during the follow-up and had statistical significance after long-term LMWH treatment on iliofemoral DVT (1, 3, 6, and 12 months), femoropopliteal DVT (1-3 months), and infrapopliteal DVT (first month). Duplex scan evaluation showed that the rate of venous recanalization significantly increased in the common femoral vein at 6 and at 12 months and during each point of follow-up in the superficial and popliteal veins in the LMWH group. Reflux was significantly less frequent in communicating veins after LMWH treatment (17.9% vs 32.2% in the OA group). The reflux rates in the superficial (22.4% in the LMWH group, 30.6% in OA group) and deep (13.4% vs 17.7%) venous system showed no significant differences between groups. CONCLUSIONS: The unmonitored subcutaneous administration of nadroparine in fixed daily doses was more effective than oral acenocoumarol with laboratory control adjustment in achieving recanalization of leg thrombi. With nadroparine, there was less late valvular communicating vein insufficiency, and it was at least as efficacious and safe as oral anticoagulants after long-term administration. These results suggest that LMWHs may therefore represent a real therapeutic advance in the long-term management of DVT.  (+info)

Optimal oral anticoagulant intensity to prevent secondary ischemic and hemorrhagic events in patients after infrainguinal bypass graft surgery. Dutch BOA Study Group. (6/76)

OBJECTIVES: The purpose of this study was to determine the optimal intensity of oral anticoagulation in patients who participated in a randomized trial of oral anticoagulants or aspirin after infrainguinal bypass graft surgery. METHODS: The distribution of patient-time spent in international normalized ratio (INR) classes of 0.5 INR unit was calculated assuming a linear change between successive measurements. INR-specific incidence rates of ischemic and hemorrhagic events were calculated as the ratio of the number of events at a certain INR category and the total patient-time spent in that class. The relationship between INR class and event rates was quantified by rate ratios calculated in a Poisson regression model. RESULTS: In 1326 patients (mean age, 69 years) 41,928 INR measurements were recorded in 1698 patient-years. Patients spent 50% of the total time within the target range of 3.0 to 4.5 INR. Most of the patient-time (60%) was spent between 2.5 and 3.5 INR. For each increasing class of 0.5 INR, the incidence of ischemic events (n = 154, INR data on event available in 49%) decreased by a factor of 0.97 (95% CI, 0.87-1.08). The incidence of major bleeding (n = 123, INR data on event available in 65%) increased significantly by a factor of 1.27 (95% CI, 1.19-1.34) for each increasing 0.5 INR category. The optimal target range was 3.0 to 4.0 INR, with an incidence of 3.8 events (0.9 ischemic and 2.9 hemorrhagic) per 100 patient-years. CONCLUSIONS: The target range of 3.0 to 4.0 INR is the optimal range of achieved anticoagulation intensity and is safe for the prevention of ischemic events in patients after infrainguinal bypass graft surgery.  (+info)

Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. Warfarin Optimal Duration Italian Trial Investigators. (7/76)

BACKGROUND: In patients with idiopathic deep venous thrombosis, continuing anticoagulant therapy beyond three months is associated with a reduced incidence of recurrent thrombosis during the period of therapy. Whether this benefit persists after anticoagulant therapy is discontinued is controversial. METHODS: Patients with a first episode of idiopathic proximal deep venous thrombosis who had completed three months of oral anticoagulant therapy (with warfarin, in 97 percent of the cases and acenocoumarol in 3 percent) were randomly assigned to the discontinuation of oral anticoagulants or to their continuation for nine additional months. The primary study outcome was recurrence of symptomatic, objectively confirmed venous thromboembolism during at least two years of follow-up. RESULTS: The primary intention-to-treat analysis showed that of 134 patients assigned to continued oral anticoagulant therapy, 21 had a recurrence of venous thromboembolism (15.7 percent; average follow-up, 37.8 months), as compared with 21 of 133 patients assigned to the discontinuation of oral anticoagulant therapy (15.8 percent; average follow-up, 37.2 months), resulting in a relative risk of 0.99 (95 percent confidence interval, 0.57 to 1.73). During the initial nine months after randomization (after all patients received three months of therapy), 1 patient had a recurrence while receiving oral anticoagulant therapy (0.7 percent), as compared with 11 of the patients assigned to the discontinuation of oral anticoagulant therapy (8.3 percent; P=0.003). The incidence of recurrence after the discontinuation of treatment was 5.1 percent per patient-year in patients in whom oral anticoagulant therapy was discontinued after 3 months (95 percent confidence interval, 3.2 to 7.5 percent; average interval since discontinuation, 37.2 months) and 5.0 percent per patient-year in patients who received an additional 9 months of oral anticoagulant therapy (95 percent confidence interval, 3.1 to 7.8 percent; average interval since discontinuation, 29.4 months). None of the recurrences were fatal. Four patients had non-fatal major bleeding during the extended period of anticoagulant therapy (3.0 percent). CONCLUSIONS: In patients with idiopathic deep venous thrombosis, the clinical benefit associated with extending the duration of anticoagulant therapy to one year is not maintained after the therapy is discontinued.  (+info)

Determination of coumarin-type anticoagulants in human plasma by HPLC-electrospray ionization tandem mass spectrometry with an ion trap detector. (8/76)

BACKGROUND: Coumarin-type anticoagulants are used for the long-term treatment and prevention of thromboembolic disorders. The identification of these drugs is crucial in patients with an increased prothrombin time of unknown origin. The aim of this study was to develop a sensitive and specific method for the simultaneous determination of phenprocoumon, acenocoumarol, and warfarin in human plasma by HPLC-electrospray ionization tandem mass spectrometry. METHODS: After addition of the internal standard, p-chlorowarfarin, plasma samples were extracted using Oasis MCX solid-phase extraction cartridges. The compounds were separated on a Symmetry C18 column (Waters) with a mobile phase of acetonitrile-1 g/L formic acid (75:25 by volume) at a flow rate of 0.5 mL/min. RESULTS: Extraction and separation of the three drugs and the internal standard were accomplished in 9 min. The overall extraction efficiency was >89% for all three compounds. The limits of detection were 1 microg/L for phenprocoumon and warfarin and 10 microg/L for acenocoumarol. Regression analysis of the calibration data revealed good correlation (r(2) >or=0.995) for all compounds. Within-run accuracies for quality-control samples were +/- 1% to 7% of the target concentration, with CVs <9%. CONCLUSIONS: The proposed method enables the unambiguous identification and quantification of phenprocoumon, warfarin, and acenocoumarol in both clinical and forensic specimens. This method combines a new, rapid solid-phase extraction procedure with an extremely fast chromatographic analysis, which is especially advantageous for clinical laboratories.  (+info)

The oral anticoagulant acenocoumarol is given as a racemic mixture. The (S)-enantiomer is rapidly cleared and is the reason why only (R)-acenocoumarol contributes to the pharmacological effect. The objective of the study was to establish the cytochrome P450 (CYP) enzymes catalyzing the hydroxylations of the acenocoumarol enantiomers. Of various cDNA-expressed human CYPs, only CYP2C9 hydroxylated (S)-acenocoumarol. Hydroxylation occurred at the 6-, 7-, and 8-position with equal Km values and a ratio of 0.9:1:0.1 for Vmax. CYP2C9 also mediated the 6-, 7-, and 8-hydroxylations of (R)-acenocoumarol with Km values three to four times and Vmax values one-sixth times those of (S)-acenocoumarol. (R)Acenocoumarol was also metabolized by CYP1A2 (6-hydroxylation) and CYP2C19 (6-, 7-, and 8-hydroxylation). In human liver microsomes one enzyme only catalyzed (S)-acenocoumarol hydroxylations with Km values | 1 mM. In most of the samples tested the 7-hydroxylation of (R)-acenocoumarol was also catalyzed by one enzyme
Reversal of anticoagulation can be needed in patients undergoing heart valve surgery. ROTEM® has been correlated with international normalized ratio (INR) in patients on warfarin but not with patients on acenocoumarol. This study investigates the reliability of ROTEM® for detecting INR values below the 1.5 threshold in patients on acenocoumarol therapy. Patients on oral anticoagulation with acenocoumarol after elective heart valve replacement were prospectively included in the study. INR and the ROTEM® were measured simultaneously. ROTEM® parameters included coagulation time, clot formation time, alpha angle, and maximal clot firmness after tissue factor activation (EXTEM). Concordance between INR and ROTEM® was analyzed by Lins concordance coefficient (LCC) and the correlation with Spearmans rho. Fifty-four consecutive patients (40 female; median age 67years) were included. Clotting time (CT) was the parameter that best correlated with INR (r=0.81, ...
OBJECTIVE: The aim of this study was to investigate the respective contribution of the different cytochrome P450 (CYP) 2C9 genetic polymorphisms to the interindividual variability of acenocoumarol pharmacodynamic response. METHODS: A total of 263 healthy volunteers were genotyped for CYP2C9*2, CYP2C9*3, CYP2C9*4, and CYP2C9*5 alleles, as well as for the nicotinamide adenine dinucleotide phosphate, reduced, quinone oxidoreductase 1 genetic polymorphism (NQO1*2). Moreover, the 5-flanking region of the CYP2C9 gene was investigated for new polymorphisms, and haplotype analysis was then performed. Finally, CYP2C9 phenotype was evaluated after a single oral dose of 4 mg of acenocoumarol. Factor VII coagulant activity was measured before and 24 hours after acenocoumarol intake. RESULTS: The CYP2C9*3 allele was the only nonsynonymous single nucleotide polymorphism (SNP) influencing acenocoumarol pharmacodynamics; the percentages of remaining factor VII were 60% +/- 19%, 39% +/- 17%, and 17% for ...
Acenocoumarol is an oral anticoagulant of the coumarin series, synthesized and developed in the Geigy laboratoires in the late 1960s and sold in the United States under the brand name of Sintrom. It lowers the prothrombin level of the blood. It is a white crystalline powder without taste and odor and has a molecular weight of 353. It is soluble in alkaline solutions but only slightly soluble in water and organic solvents. Chemically, acenocoumarol is 3-(alpha-acetonyl-4-nitrobenzyl)-4-hydroxycoumarin. ...
Montes R, Ruiz de Gaona E, Martínez-González M, Alberca I, Hermida J (2006). The c.-1639G , A polymorphism of the VKORC1 gene is a major determinant of the response to acenocoumarol in anticoagulated patients. Br J Haematol. 133 (2): 183&ndash, 7. doi:10.1111/j.1365-2141.2006.06007.x. PMID 16611310 ...
Acenocoumarol reference standards, CAS number: 152-72-7, for unparalleled analytical testing within the food and beverage sector. Buy online at LGC Standards.
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In a study that our research group published recently in this journal, we demonstrated the relative safety of intra-articular injection in patients anticoagulated with acenocoumarol.1 These results agreed with those that had been previously reported for warfarin users.2,3 In the last few years, other oral anticoagulants have been made available for the secondary prevention of stroke or primary prevention of thrombotic phenomena of any type in patients in whom the anticoagulation achieved with acenocoumarol was difficult to control.4 After the experience in our registry of patients taking acenocoumarol, we reviewed our findings concerning complications following intra-articular injection of the knee and periarticular injection in shoulder in patients receiving dabigatran, a drug from a new generation of oral anticoagulants, with proven efficacy in the prevention of primary and secondary embolic events, which is especially indicated in patients in the geriatric population who have been diagnosed ...
Concomitant use of probenecid is not recommended. Probenecid decreases the renal tubular secretion of amoxicillin. Concomitant use with AUGMENTIN may result in increased and prolonged blood levels of amoxicillin but not of clavulanate. Concomitant use of allopurinol during treatment with amoxicillin can increase the likelihood of allergic skin reactions. There are no data on the concomitant use of AUGMENTIN and allopurinol. In common with other antibiotics, AUGMENTIN may affect the gut flora, leading to lower oestrogen reabsorption and reduced efficacy of combined oral contraceptives. In the literature there are rare cases of increased international normalised ratio in patients maintained on acenocoumarol or warfarin and prescribed a course of amoxicillin. If co-administration is necessary, the prothrombin time or international normalised ratio should be carefully monitored with the addition or withdrawal of AUGMENTIN ...
The small size of the penicillins increases their potency, by allowing them to penetrate the entire depth of the cell wall. [url=http://valleyofshadowsanddreams.com/]viagra coupon[/url] The more you know about your anxiety the more you can avoid anxiety mistakes. List of excipients Citric acid anhydrous E330 Sodium Benzoate E211 Aspartame E951 Talc E553b Sodium citrate, anhydrous E331 Guar E412 Silicon dioxide, precipitated E551 Lemon flavouring, powdered Peach-apricot flavouring, powdered Orange flavouring, powdered 6. [url=http://valleyofshadowsanddreams.com/]viagra online[/url] However, in the literature there are cases of increased international normalised ratio in patients maintained on acenocoumarol or warfarin and prescribed a course of amoxicillin.. ...
A 72-year old man had a collapse, severe hypertension (RR 200/100 mmHg), and malaise. He had a history of nicotine abuse and had been started on acenocoumarol because of pulmonary embolism four months earlier. At the outpatient clinic, his blood pressure was 180/95 mmHg and no oedema or skin lesions were observed. Screening blood tests showed acute renal insufficiency, with an estimated glomerular filtration rate (eGFR) that had decreased from 74 to 41 ml/min/1.73 m2 over the past five months. Urinary sediment microscopy showed 3-10 non-dysmorphic erythrocytes per view. The albumin/creatinine ratio was 44 mg/mmol. Abdominal ultrasonography did not show any postrenal obstruction or renal parenchymal abnormalities; the kidneys were normal in size. It did, however, show aneurysmatic dilatation of the abdominal aorta, maximum diameter 3.6 cm. Doppler ultrasonography did not show renal artery stenosis. Analyses of secondary causes of hypertension were negative. Because of progressive renal failure ...
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Proportions of patients who will achieve Recanalization of thrombus (complete i.e No thrombus is seen or partial i.e up to 50% of the lumen become patent.)on oral anticoagulant acenocoumarol during the study period of 2 year from randomization ...
Coumarins are widely prescribed worldwide, and in Mexico acenocumarol is the preferred form. It is well known that despite its efficacy, coumarins show a high variability for dose requirements. We investigated the pharmacogenetic variation of 110 genes in patients receiving acenocumarol using a targeted NGS approach. We report relevant population differentiation for variants on CYP2C8, CYP2C19, CYP4F11, CYP4F2, PROS, and GGCX, VKORC1, CYP2C18, NQO1. A higher proportion of novel-to-known variants for 10 genes was identified on 41 core pharmacogenomics genes related to the PK (29), PD (3), of coumarins, and coagulation proteins (9) including, CYP1A1, CYP3A4, CYP3A5, and F8, and a low proportion of novel-to-known variants on CYP2E1, VKORC1, and SULT1A1/2 ...
Coumarins are widely prescribed worldwide, and in Mexico acenocumarol is the preferred form. It is well known that despite its efficacy, coumarins show a high variability for dose requirements. We investigated the pharmacogenetic variation of 110 genes in patients receiving acenocumarol using a targeted NGS approach. We report relevant population differentiation for variants on CYP2C8, CYP2C19, CYP4F11, CYP4F2, PROS, and GGCX, VKORC1, CYP2C18, NQO1. A higher proportion of novel-to-known variants for 10 genes was identified on 41 core pharmacogenomics genes related to the PK (29), PD (3), of coumarins, and coagulation proteins (9) including, CYP1A1, CYP3A4, CYP3A5, and F8, and a low proportion of novel-to-known variants on CYP2E1, VKORC1, and SULT1A1/2 ...
Differences in relevance in the obtainable pharmacogenetic data, they also indicate differences inside the assessment of your high-quality of these association
A 62-year-old previously asymptomatic man was attended in the emergency room for anginal chest pain of 6 hours evolution. His medical history was remarkable for a combined aortic and mitral valve replacement 15 years previously for endocarditis (anticoagulation with acenocoumarol) and an aneurysm of the noncoronary sinus and ascending aorta, treated with an end-to-end anastomosis (Dacron graft) 2 months previously.. The patient was hemodynamically stable and had persistent pain. The physical examination was not contributory and the surgical wound appeared to be healing well. The ECG showed a known left bundle branch block without changes. During the initial evaluation, echocardiography showed inferior akinesia that was not present on the postoperative study, and a normally functioning graft, without clear visualization of the ascending aorta. An onset of infarction was suspected and 250 mg of aspirin was administered. Angioplasty was contemplated, and coronary angiography performed 60min after ...
In April 2003, Janet Woodcock, MD, the director of the FDAs Center for Drug Evaluation and Research, told an agency committee that the time had arrived to incorporate pharmacogenetic data in drug labels.
The maximum sample volume was calculated for a range of separation ratio values (a) and capacity ratio values (k) for the first eluted peak. The results are shown in figure 2.. ...
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The aim of the study is to explore the contribution of genetic factors related either to drug metabolism (cytochrome P450 2C9) or to drug target (vitamin K epoxide reductase) to variability in the response to acenocoumarol among 222 healthy volunteers after a single oral dose. Associations between a pharmacodynamic index (reduction in factor VII activity and international normalized ratio [INR] change) and several genetic polymorphisms (VKORC1: -4931T,C, -4451C,A, -2659G,C, -1877A,G, -1639G,A, 497C,G, 1173C,T, and CYP2C9*3) were investigated using haplotype and univariate analyses. VKORC1 haplotypes were associated with the pharmacologic response, and this association can be explained only by the effect of the -1639G,A polymorphism (or alternatively by 1173C,T, which is in complete association with it). Indeed, it explains about one third of the variability of the pharmacologic response (37% of factor VII decrease and 30% of INR change). Moreover, the previously observed effect of the CYP2C9*3 ...
Rationale:. The narrow therapeutic range and wide inter-patient variability in dose requirement make anticoagulation response to coumarin derivatives unpredictable. As a result, patients require frequent monitoring to avert adverse effects and maintain therapeutic efficacy. Polymorphisms in cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) jointly account for about 40% of the inter-individual variability in dose requirements. To date, several pharmacogenetic guided dosing algorithms for coumarin derivatives, predominately for warfarin, have been developed. However, the potential benefit of these dosing algorithms in terms of their safety and clinical utility has not been adequately investigated in randomised settings. Objective: To determine whether a dosing algorithm containing genetic information increases the time within therapeutic INR range during anticoagulation therapy with each of warfarin, acenocoumarol and phenprocoumon compared to a dosing regimen that ...
The Pregnant patients with a prosthetic mechanical valve are at high risk for valve thrombosis and the optimal treatment strategy in the pre-pregnancy period and during pregnancy itself is a matter of debate. Prosthetic heart valve (PHV) thrombosis is a rare condition with serious life-threatening complications diagnosed optimally by TOE followed by a radio-cinema; and which needs to be revaluated frequently by echocardiography transthoracic in case of an increase in trans valvular gradient. We report here a case of a 37-year-old woman, pregnant at 31 weeks of amenorrhea, with a double mitro-aortic mechanical replacement suspected dysfunction in front of an increase of trans-valvular gradient and confirmed on the radio cinema. The patient was treated with a low molecular weight heparin (LMWH); acetylsalicylic acid 160 mg daily; and oral anticoagulation (Acenocoumarol) with great clinical and biological results. In some cases; Pregnant patients with prosthetic valve thrombosis may be treated ...
In successive checkups in our offices, the patient showed improvement in terms of ischemia but polyarthritis persisted. The result for cryoglobulins was positive. Given the persistence of polyarthritis (although she continued to take MTX and leflunomide) and cryoglobulinemia, it was decided that she begin rituximab. Anticoagulation was maintained with acenocoumarol for a year, until the cryoglobulins were negative, when antiplatelet therapy was begun with ASA. During follow-up, the patient was repeatedly positive for ANA at low titers, with a homogeneous pattern, and was negative for anti-dsDNA. The immunological study was extended and we found antinucleosome antibodies and antibodies against the collagen-like region of C1q. The patient has continued to take rituximab, MTX, HCQ and ASA. She has not had any further ischemic episodes and there is no evidence of involvement of kidneys or of any other organ.. Discussion. We report the case of a patient with polyarthritis, a frequent cause for ...
Cytochrome P450 2C9 (abbreviated CYP2C9) is an enzyme that in humans is encoded by the CYP2C9 gene. CYP2C9 is an important cytochrome P450 enzyme with a major role in the oxidation of both xenobiotic and endogenous compounds. CYP2C9 makes up about 18% of the cytochrome P450 protein in liver microsomes (data only for antifungal). Some 100 therapeutic drugs are metabolized by CYP2C9, including drugs with a narrow therapeutic index such as warfarin and phenytoin and other routinely prescribed drugs such as acenocoumarol, tolbutamide, losartan, glipizide, and some nonsteroidal anti-inflammatory drugs. By contrast, the known extrahepatic CYP2C9 often metabolizes important endogenous compound such as serotonin and, owing to its epoxygenase activity, various polyunsaturated fatty acids, converting these fatty acids to a wide range of biological active products. In particular, CYP2C9 metabolizes arachidonic acid to the following eicosatrienoic acid epoxide (termed EETs) stereoisomer sets: ...
Background The indications for continuous oral anticoagulant treatment, the target interval and the procedures for withdrawing treatment have changed in the last 10 years.
[125 Pages Report] Check for Discount on Global Oral Anticoagulants Sales Market Report 2016 report by QYResearch Group. Notes: Sales, means the sales volume of Oral Anticoagulants Revenue,...
SCVS 2021 Abstracts: New Class Of Medication Yields Better Outcomes: Direct Oral Anticoagulants Improve Treatment Success For Lower Extremity Acute DVT
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Miller AL, Loscalzo J. Miller A.L., Loscalzo J Miller, Amy L., and Joseph Loscalzo.. Management of Patients Receiving a Direct Oral Anticoagulant. Harrisons Online Updates Kasper D. Kasper D Kasper, Dennis. New York, NY: McGraw-Hill, 2019, http://accessmedicine.mhmedical.com/updatesContent.aspx?gbosid=497653§ionid=227114133. ...
Direct oral anticoagulants (DOACs) have distinct bleeding profiles and require individualized management approaches, according to a new review.
Despite the emergence of direct oral anticoagulants (DOAC) in recent years, vitamin K antagonists (VKA) remain popular due to clinician familiarity, superior anticoagulation efficacy for mechanical heart valves, ability to easily monitor efficacy, and availability of reversal agents [1-3]. VKA include warfarin, acenocoumarol, phenprocoumon, dicoumarol, tecarfarin, and fluindione [2]. In the United States, warfarin is the most frequently used VKA and is frequently associated with bleeding complications that require treatment in the emergency department (ED) [3]. Warfarin and other VKA work by inhibiting vitamin K-dependent carboxylation of coagulation factors II, VII, IX, and X [2, 4]. This reduces the activity of these clotting factors and reduces clotting ability [2]. Anticoagulant effects can be measured via the international normalized ratio (INR) and higher INR values reflect reduced ability to form blood clots [2, 3]. Risk of hemorrhage also increases with increasing INR, although patients ...
The broader impact/commercial potential of this Small Business Technology Transfer (STTR) project is to establish a bio-based manufacturing process for the production of the commodity chemical 4-hydroxycoumarin (4-HC) in an economical and renewable way. 4-HC is a direct synthetic precursor used to manufacture widely used oral anticoagulants, such as warfarin, acenocoumarol, and phenprocoumon. In a .... ...
Blood thinners basically inhibit the appearance of fibrin; they prevent thrombosis, contribute to stopping the growth of existing blood clots, enhance the effects of blood clots in the endogenous fibrinolytic enzymes.. Anticoagulants are divided into 2 groups: a) direct anticoagulants - quick action (heparin sodium, nadroparin calcium, enoxaparin sodium, etc.), efficient in vitro and in vivo; b) antiakoagulyanty indirect (vitamin K antagonists) - long-acting (warfarin, phenindione, acenocoumarol, etc.), are in vivo only after a latent period ...
https://www.futuremarketinsights.com/reports/sample/REP-GB-10058. Direct Oral Anticoagulants: Market Dynamics. Adoption of direct oral anticoagulants over the exciting alternative to warfarin and is used for the first line choice of treatment for venous thromboembolism and atrial fibrillation which is expected to spur the global direct oral anticoagulants market. Growing approval from the FDA and CE mark for the direct oral anticoagulants will further boost the direct oral anticoagulants market in the near future. Rising cases of thrombosis which is the major cause of morbidity and mortality in various parts of the world is expected to further drive the direct oral anticoagulants market in the forecast period.. However, some factors which might restraint the growth of the direct oral anticoagulants include high cost when compared to warfarin and shorter acting dose which makes it important not to miss any doses. Furthermore, stringent regulations for development of drug is expected to restraint ...
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St. Jude Medical announced the launch of a U.S. IDE clinical trial of its St. Jude Medical Masters HP Series 15 mm mechanical heart valve in pediatric patients.
The study indicated that, after accounting for differences in baseline characteristics, there were no apparent differences in outcomes between patients who were and were not prescribed oral anticoagulants. There was also no relationship between the CHA2DS2-VASc score and the probability that patients had filled a prescription for an oral anticoagulant, and ultimately no evidence that the CHA2DS2-VASc risk score can effectively indicate the potential benefits of systemic oral anticoagulants for patients initiating hemodialysis with preexisting Afib.. Additional research is necessary to further guide using anticoagulants in this population.. For more information, read the research poster (which was presented at ASN) here.. ...
Alexandre da Silveira Gerzson, Lorenzo Grassi, Luis Artur Zenni Lopes e Lucia Hiromi Hiwatashi Gallicchio Dental surgeries performed in patients undergoing antiplatelet drugs and/or oral anticoagulants therapy is a controversial issue. Many professionals unaware of those medications or the proper means to treat those patients recommend, without any scientific basis, suspension or dosage alteration of those medications without consulting the physician assisting the patients. Objective: to perform a literature review on the proper and safer means employed to treat those patients, thus enlightening how to reach diagnosis, determine the previous examination to be requested as well as the risks arising from the maintenance or interruption of therapy with anticoagulants. This article also reviewed the drugs used for those purposes, their mechanism of action and clinical behavior, aiming to elucidate the real risks to which patients are exposed.. Anticoagulants, International normalized ratio, Blood ...
Signa Vitae is a journal designed to publish articles from the neonatal, pediatric, and adult intensive care, along with the emergency medicine.
NARCOTICS ANTITUSSIVES NIKOMETAMIDE NICOGAMOL NICOLAR NICOLET nicomethanol NICOMOL Takign NICOMORPHOLINE NICONACID NICOPHOLINE NICORANDIL NICORETTE NICOTAFURYL NICOTHIAZONE NICOTIANA NICOTIBIN NICOTIBINE Ibuprьfen NICOTINAMIDE nicotinamide-adenine-dinucleotide when taking ibuprofen after drinking phosphate NICOTINAMIDE-ASCORBATE nicotinamide-hypovitaminosis nicotinamide-mononucleotide NICOTINAMIDE-N-OXIDE NICOTINATE NICOTINATE-BENZYL nicotinate-butoxyethyl-ester NICOTINATE-BUTYL-ESTER NICOTINATE-ETHYL NICOTINATE-HEXYL nicotinate-hydrazide NICOTINATE-METHYL NICOTINATE-OCTYL Lortab felony 81 ппNICOTINE NICOTINE-N-OXIDE NICOTINE-POLACRILEX NICOTINIC nicotinic-antagonist nicotinohydroxamate nicotinolytic Ibuproefn NICOTINOYL-PROCAINE NICOTINOYLALANINE NICOTINOYLHYDRAZINE nicotinoylmorphine-3 nicotinoylmorphine-6 NICOTINOYLTRYPTAMINE-N NICOTINURATE NICOTINYL-ALCOHOL NICOTINYL-AMINONICOTINATE-6 nicotinylamidoantipyrine NICOTINYLMETHYLAMIDE nicoumalone NICOVITOL NICOX NICOXAMAT NICRAZIN NICTIAZEM NICTINDOLE
Indications: Used to be a bleeding disorder, whether congenital or acquired, examination serves primarily to monitor patients on oral anticoagulant treatment based on anticoagulants. These drugs ...
A five-year-old KwaZulu-Natal boy made history when he became the youngest person in Africa to receive a mechanical heart implantation.
Mark Crowther, MD discusses the results of various analyzes regarding the reversal of direct oral anticoagulants, including PCCs and Tailored Reversal Agents idarucizumab and andexanet alfa., TV Network
The Hillingdon Method adjusts oral anticoagulant dosing based on the target and observed International Normalized Ratios (INR). Hillingdon Hospital is in Uxbridge, Middlesex in England.
Direct oral anticoagulants offer several advantages over warfarin, but reversal agents for most DOACs are not available, which puts patients at risk if they need emergency surgery or experience breakthrough bleeding. Food and Drug Administration-approved assays that measure DOACs activity also are lacking.
Laura Talamo, MD discusses the results of retrospective analysis of a random sample of patients prescribed direct oral anticoagulants (DOACs) for any indication from May 2011 through April 2016. , TV Network
When and how to use antidotes for the reversal of direct oral anticoagulants: guidance from the SSC of the ISTH Academic Article ...
For 50 years, warfarin was the only choice for people who needed to take an oral anticoagulant (blood thinner). New drugs called direct oral anticoagulants…
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These drugs deplete the active form of the vitamin by inhibiting the enzyme vitamin K epoxide reductase and thus the recycling of the inactive vitamin K epoxide back to the active reduced form of vitamin K. The drugs are structurally similar to vitamin K and act as competitive inhibitors of the enzyme. The term "vitamin K antagonist" is a misnomer, as the drugs do not directly antagonise the action of vitamin K in the pharmacological sense, but rather the recycling of vitamin K. Vitamin K is required for the proper production of certain proteins involved in the blood clotting process. For example, it is needed to carboxylate specific glutamic acid residues on prothrombin. Without these residues carboxylated, the protein will not form the appropriate conformation of thrombin, which is needed to produce the fibrin monomers that are polymerized to form clots.[1] The action of this class of anticoagulants may be reversed by administering vitamin K for the duration of the anticoagulant's residence in ...
B01AA07 Acenocoumarol. B01AA08 Ethyl biscoumacetate. B01AA09 Clorindione. B01AA10 Diphenadione. B01AA11 Tioclomarol. B01AA12 ...
... may increase the anticoagulant activities of acenocoumarol. The risk or severity of adverse effects can be ...
Other examples are acenocoumarol, phenprocoumon, atromentin, and phenindione. The coumarins brodifacoum and difenacoum are used ...
In some European countries, other coumarin derivatives (phenprocoumon and acenocoumarol) are used. These agents known as ...
The fluoroquinolones have been shown to increase the anticoagulant effect of acenocoumarol, anisindione, and dicumarol. ...
In some countries, other coumarins are used instead of warfarin, such as acenocoumarol and phenprocoumon. These have a shorter ... acenocoumarol) or longer (phenprocoumon) half-life, and are not completely interchangeable with warfarin. Several types of ...
Minor neurological dysfunction was found in children exposed to the anticoagulants acenocoumarol or phenprocoumon during ...
For many years, vitamin K antagonists (warfarin or less commonly acenocoumarol or phenprocoumon) have been the cornerstone. As ...
A 1987 report described the use of DCP determination in the detection of intoxication with acenocoumarol, a vitamin K ...
... is pharmacologically important as a target of anticoagulant drugs warfarin and related coumarins such as acenocoumarol, ...
2008). "Improvement in the regulation of the vitamin K antagonist acenocoumarol after a standard initial dose regimen: ...
Pharmaceutical examples of 4-hydroxycoumarin pharmaceuticals include: acenocoumarol dicoumarol ethyl biscoumacetate ...
... coumarin or acenocoumarol. The enzyme also regulates bioactivation of various drugs, e.g. the anti-malarial drug pafuramidine ...
... doses guided by genotype-phenotype and in their standard management in patients who initiate anticoagulation with acenocoumarol ...
... acenocoumarol MeSH D03.438.150.446.520.203 - dicumarol MeSH D03.438.150.446.520.451 - ethyl biscoumacetate MeSH D03.438.150.446 ... acenocoumarol MeSH D03.830.219.446.520.203 - dicumarol MeSH D03.830.219.446.520.451 - ethyl biscoumacetate MeSH D03.830.219.446 ...
... and other routinely prescribed drugs such as acenocoumarol, tolbutamide, losartan, glipizide, and some nonsteroidal anti- ...
... and acenocoumarol are vitamin K antagonists (VKA), decreasing a number of coagulation factors, including Factor X. Rivaroxaban ...
... acenocoumarol (INN) Aceon aceperone (INN) Acephen acepromazine (INN) aceprometazine (INN) acequinoline (INN) acesulfame (INN) ...
... evaluating the use of SR34006 compared to warfarin or acenocoumarol in patients with atrial fibrillation) study". Journal of ...
... is an anticoagulant that functions as a vitamin K antagonist (like warfarin). It is a derivative of coumarin and ... Drugs.com Drugs.com international listings for acenocoumarol Diseases Database (DDB): 29202 Cesar J, García-Avello A, Navarro J ... Lengyel M; SPORTIF-III Altanulmány Vizsgálói (2004). "Warfarin or acenocoumarol is better in the anticoagulant treatment of ... Ufer M (2005). "Comparative pharmacokinetics of vitamin Kd antagonists: warfarin, phenprocoumon and acenocoumarol". Clin ...
... is an anticoagulant that functions as a vitamin K antagonist (like warfarin). It is a derivative of coumarin and ... Cesar J, García-Avello A, Navarro J, Herraez M (2004). "Aging and oral anticoagulant therapy using acenocoumarol". Blood Coagul ... Lengyel M; SPORTIF-III Altanulmány Vizsgálói (2004). "Warfarin or acenocoumarol is better in the anticoagulant treatment of ... Ufer M (2005). "Comparative pharmacokinetics of vitamin Kd antagonists: warfarin, phenprocoumon and acenocoumarol". Clin ...
When plasmin breaks down fibrin, a number of soluble parts are produced. These are called fibrin degradation products (FDPs). FDPs compete with thrombin, and thus slow down clot formation by preventing the conversion of fibrinogen to fibrin. This effect can be seen in the thrombin clotting time (TCT) test, which is prolonged in a person that has active fibrinolysis.. FDPs, and a specific FDP, the D-dimer, can be measured using antibody-antigen technology. This is more specific than the TCT, and confirms that fibrinolysis has occurred. It is therefore used to indicate deep-vein thrombosis, pulmonary embolism, DIC and efficacy of treatment in acute myocardial infarction. Alternatively, a more rapid detection of fibrinolytic activity, especially hyperfibrinolysis, is possible with thromboelastometry (TEM) in whole blood, even in patients on heparin. In this assay, increased fibrinolysis is assessed by comparing the TEM profile in the absence or presence of the fibrinolysis inhibitor aprotinin. ...
... intercalates into the DNA double helix where it is ideally positioned to form one or more adducts with adjacent pyrimidine bases, preferentially thymine, upon excitation by an ultraviolet photon. Several physicochemical methods have been employed to derive binding constants for psoralen-DNA interactions. Classically, two chambers of psoralen and buffered DNA solution are partitioned by a semi-permeable membrane; the affinity of the psoralen for DNA is directly related to the concentration of the psoralen in the DNA chamber after equilibrium. Water solubility is important for two reasons: pharmacokinetics relating to drug solubility in blood and necessitating the use of organic solvents (e.g. DMSO). Psoralens can also be activated by irradiation with long wavelength UV light. While UVA range light is the clinical standard, research that UVB is more efficient at forming photoadducts suggests that its use may lead to higher efficacy and lower treatment times.[15] The photochemically ...
In 2001, Eli Lilly's chairman, president and CEO, Sidney Taurel, told shareholders: "No medicine better symbolizes our mission than Xigris," calling it "one of our industry's genuine breakthroughs."[5]. Xigris was designed to fight sepsis, a condition that kills more than 200,000 Americans annually. It was the only approved drug for sepsis, and it costs $8,000 to treat a single patient. Lilly hoped it would be a blockbuster, with sales of at least a billion dollars a year. But after five years on the market, sales were only $200 million.. Eli Lilly used the Belsito & Company PR firm in a marketing campaign to promote Xigris, its drug for treatment of sepsis. A report in the New England Journal of Medicine (NEJM) accused the company of initiating false reports of a shortage of the drug to boost sales.[6] Belsito and Company spread the word that the drug was being "rationed" and physicians were being 'systematically forced' to decide who would live and who would die. As part of this effort, Lilly ...
Acetylsalicylic acid is a weak acid, and very little of it is ionized in the stomach after oral administration. Acetylsalicylic acid is quickly absorbed through the cell membrane in the acidic conditions of the stomach. The increased pH and larger surface area of the small intestine causes aspirin to be absorbed more slowly there, as more of it is ionised. Owing to the formation of concretions, aspirin is absorbed much more slowly during overdose, and plasma concentrations can continue to rise for up to 24 hours after ingestion.[152][153][154] About 50-80% of salicylate in the blood is bound to albumin protein, while the rest remains in the active, ionized state; protein binding is concentration-dependent. Saturation of binding sites leads to more free salicylate and increased toxicity. The volume of distribution is 0.1-0.2 L/kg. Acidosis increases the volume of distribution because of enhancement of tissue penetration of salicylates.[154] As much as 80% of therapeutic doses of salicylic acid is ...
The drug is clear with a pH of 10.[7] Its production is inhibited indirectly by NSAIDs, which inhibit the cyclooxygenase enzymes COX1 and COX2. These convert arachidonic acid to prostaglandin H2 (PGH2), the immediate precursor of prostacyclin. Since thromboxane (an eicosanoid stimulator of platelet aggregation) is also downstream of COX enzymes, one might think that the effect of NSAIDs would act to balance. However, prostacyclin concentrations recover much faster than thromboxane levels, so aspirin administration initially has little to no effect but eventually prevents platelet aggregation (the effect of prostaglandins predominates as they are regenerated). This is explained by understanding the cells that produce each molecule, TXA2 and PGI2. Since PGI2 is primarily produced in a nucleated endothelial cell, the COX inhibition by NSAID can be overcome with time by increased COX gene activation and subsequent production of more COX enzymes to catalyze the formation of PGI2. In contrast, TXA2 is ...
... is a natural compound coming from plants like the common fig, but it can also be synthesized. Most syntheses of linear furanocoumarins involve starting with a central aromatic unit and adding two heterocyclic rings. Alternate routes of synthesis are desirable to avoid regiochemical problems and moderate yields. The synthesis described here involves Iodine as a removable group to insure regiochemical integrity and convergence.[13] As shown in the diagram, phloroglucinol (compound 1) was the starting material. Mono-methylation was conducted followed by a reaction with ethyl propiolate in the presence of ZnCl2 to yield 7-hydroxy-5-methoxycoumarin (product 3, not shown) with 68% yield. The 8-position of 7-hydroxy-5-methoxycoumarin was then protected by iodine to avoid the formation of an angular furanocoumarin. Product 4 in the diagram is the result of that iodine protection. Product 5 was the result of the allylation of product 4. Osmium tetraoxide and sodium metraperiodate were used to ...
Sinthrome tablets contain the active ingredient acenocoumarol (previously known as nicoumalone in the UK), which is a type of ... The following medicines may also alter the effect of acenocoumarol and your dose of acenocoumarol may need to be adjusted up or ... Sinthrome (acenocoumarol). Sinthrome tablets contain the active ingredient acenocoumarol (previously known as nicoumalone in ... Acenocoumarol works by preventing the vitamin K dependent production of the clotting factors described above. Acenocoumarol ...
Acenocoumarol is an anticoagulant that functions as a vitamin K antagonist (like warfarin). It is a derivative of coumarin and ... Drugs.com Drugs.com international listings for acenocoumarol Diseases Database (DDB): 29202 Cesar J, García-Avello A, Navarro J ... Lengyel M; SPORTIF-III Altanulmány Vizsgálói (2004). "Warfarin or acenocoumarol is better in the anticoagulant treatment of ... Ufer M (2005). "Comparative pharmacokinetics of vitamin Kd antagonists: warfarin, phenprocoumon and acenocoumarol". Clin ...
If you have an allergy to acenocoumarol or any other part of this drug. ...
Si es alérgico al acenocoumarol o cualquier otro componente de este medicamento. ...
Acenocoumarol is an anticoagulant that functions as a vitamin K antagonist (like warfarin). It is a derivative of coumarin and ... Cesar J, García-Avello A, Navarro J, Herraez M (2004). "Aging and oral anticoagulant therapy using acenocoumarol". Blood Coagul ... Lengyel M; SPORTIF-III Altanulmány Vizsgálói (2004). "Warfarin or acenocoumarol is better in the anticoagulant treatment of ... Ufer M (2005). "Comparative pharmacokinetics of vitamin Kd antagonists: warfarin, phenprocoumon and acenocoumarol". Clin ...
Genetic determinants of acenocoumarol and phenprocoumon maintenance dose requirements.. Cadamuro J1, Dieplinger B, Felder T, ... Acenocoumarol (AC) and phenprocoumon (PC) are coumarin derivates widely prescribed in European countries for the prevention and ...
As a vitamin K antagonist, acenocoumarol inhibits vitamin K epoxide reductase, thereby inhibiting the reduction of vitamin K ... acenocoumarol A 4-hydroxycoumarin derivative with anticoagulant activity. As a vitamin K antagonist, acenocoumarol inhibits ... Compared to other coumarin derivatives, acenocoumarol has a short half-life. Check for active clinical trials using this agent ...
Stable treatment with acenocoumarol Patients in stable anticoagulant treatment with acenocoumarol for auricular fibrillation, ... Pharmacogenetic Dosage Algorithm for Acenocoumarol. The safety and scientific validity of this study is the responsibility of ... Genetic: Acenocoumarol A blood sample was collected for CYP2C9, VKORC1, CYP4F2, APOE and 2 variants of POR genotypes. ... Creation of a pharmacogenetic algorithm of dosage for acenocoumarol [ Time Frame: Up to 5 years ]. ...
Validation of the acenocoumarol EU-PACT algorithms: similar performance in the Rotterdam Study cohort as in the original study ... A randomized trial of genotype-guided dosing of acenocoumarol and phenprocoumon. N Engl J Med. 2013 Dec 12;369(24):2304-12. doi ... Long-term anticoagulant effects of the CYP2C9 and VKORC1 genotypes in acenocoumarol users. J Thromb Haemost. 2012 Apr;10(4):606 ... Evaluation of the effect of statin use on the acenocoumarol and phenprocoumon maintenance dose. Drug Metabol Drug Interact. ...
Leflunomide may increase the anticoagulant effect of acenocoumarol.. Trimetrexate. The anticoagulant effect of Acenocoumarol, a ... The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Acenocoumarol by decreasing Acenocoumarol ... The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Acenocoumarol by decreasing Acenocoumarol ... Thiopental may increase the metabolism of the Vitamin K antagonist, Acenocoumarol. Acenocoumarol dose adjustment may be ...
... acenocoumarol and phenprocoumo were found in PRIME PubMed. Download Prime PubMed App to iPhone, iPad, or Android ... AcenocoumarolAlgorithmsAnticoagulantsClinical Trials as TopicCost-Benefit AnalysisCytochrome P-450 CYP2C9Drug Dosage ... Pharmacogenetic-guided dosing of coumarin anticoagulants: algorithms for warfarin, acenocoumarol and phenprocoumon. Br J Clin ... Pharmacogenetic-guided Dosing of Coumarin Anticoagulants: Algorithms for Warfarin, Acenocoumarol and Phenprocoumon. Br J Clin ...
... acenocoumarol explanation free. What is acenocoumarol? Meaning of acenocoumarol medical term. What does acenocoumarol mean? ... Looking for online definition of acenocoumarol in the Medical Dictionary? ... acenocoumarol. Also found in: Encyclopedia, Wikipedia. Acenocoumarol. A fast-acting vitamin K-antagonist anticoagulant. In ... acenocoumarol. A fast-acting vitamin K-antagonist anticoagulant. acenocoumarol, acenocoumarin. a warfarin derivative used as an ...
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The mean absolute error of the predicted acenocoumarol dose (mg/week) obtained with the pharmacogenetic algorithm was 3.63 vs. ... We ascertained the influence of clinical and genetic variables on the stable acenocoumarol dose by multiple linear regression ... and some pharmacogenetic-guided dosing algorithms for warfarin and acenocoumarol have been developed for mixed populations. We ...
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... method for the determination of R-acenocoumarol and S-acenocoumarol in human plasma was developed and validated at IPRC ... The method was validated over a linear range of 0.40 - 40.00 ng/ml for R-acenocoumarol and 0.20 - 20.00 ng/ml for the S- ... The method was successfully applied for the determination of R and S-acenocoumarol in plasma samples of 28 healthy subjects who ... acenocoumarol. Method validation covered different parameters such as linearity, accuracy, precision and stability. ...
Acenocoumarol is effective and safe in all age groups. It offers an advantage over warfarin in terms of better stability of ... Acenocoumarol is mono-coumarin derivative with racemic mixture of R (+) and S (-) enantiomers. Efficacy and safety of ... Due to its economic advantage acenocoumarol may be suitable oral anticoagulant for long term use in countries like India. ... acenocoumarol has been evaluated in atrial fibrillation, cardiac valve replacement, after myocardial infarction, treatment of ...
acenocoumarol after adjustment for the CHA2DS2-VASc score [hazard ratio (HR)dabigatran = 0.72, 95% CI: 0.20-2.63, P = 0.61]. ... 3.7%/year acenocoumarol-treated patients. The actual incidence rate of stroke or systemic embolism was 0.8%/year [95% ... acenocoumarol (vitamin K antagonist) in patients with atrial fibrillation (AF) in daily clinical practice. ... 4.3%/year (95% CI: 2.9-6.2) in acenocoumarol. This over 50% reduction remained significant after adjustment for the HAS-BLED ...
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Acenocoumarol inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K ... Acenocoumarol inhibits the reduction of vitamin K by vitamin K reductase. This prevents carboxylation of certain glutamic acid ... Both the extrinsic (via factors VII, X and II) and intrinsic (via factors IX, X and II) are affected by acenocoumarol. ... LGM Pharma is a Acenocoumarol CAS# 152-72-7 API supplier distributor based in the USA. Inquire about DMF, cGMP, price, ...
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  • Genetic determinants of acenocoumarol and phenprocoumon maintenance dose requirements. (nih.gov)
  • Acenocoumarol (AC) and phenprocoumon (PC) are coumarin derivates widely prescribed in European countries for the prevention and treatment of thromboembolic events. (nih.gov)
  • Objective: To determine whether a dosing algorithm containing genetic information increases the time within therapeutic INR range during anticoagulation therapy with each of warfarin, acenocoumarol and phenprocoumon compared to a dosing regimen that does not contain this information. (clinicaltrials.gov)
  • In one arm (intervention) patients commencing anticoagulation therapy with either warfarin, acenocoumarol or phenprocoumon will be dosed according to a drug-specific genotype-guided dosing algorithm, which is based on genetic information, clinical data and (in the monitoring phase) previous INR. (clinicaltrials.gov)
  • Study population: Newly diagnosed patients of both genders and at least 18 years old who need anticoagulant treatment with either acenocoumarol, phenprocoumon or warfarin within the low intensity INR range will be included in the trial. (clinicaltrials.gov)
  • Pharmacogenetic-guided dosing of coumarin anticoagulants: algorithms for warfarin, acenocoumarol and phenprocoumon. (unboundmedicine.com)
  • Coumarin derivatives, such as warfarin, acenocoumarol and phenprocoumon are frequently prescribed oral anticoagulants to treat and prevent thromboembolism. (unboundmedicine.com)
  • Although the current treatment for stroke - vitamin K antagonists, acenocoumarol and phenprocoumon - can be effective, they are also associated with a number of drawbacks and are currently underused, particularly in elderly patients who are at greatest risk of stroke. (thefreedictionary.com)
  • Drug interactions as a cause of overanticoagulation on phenprocoumon or acenocoumarol predominantly concern antibacterial drugs. (thefreedictionary.com)
  • The risk of overanticoagulation in patients with cytochrome P450 CYP2C9*2 or CYP2C9*3 alleles on acenocoumarol or phenprocoumon. (ox.ac.uk)
  • However, an effect on acenocoumarol dose requirements appears to be absent for the CYP2C9*2 allele and the consequences for the metabolism of phenprocoumon have not yet been established. (ox.ac.uk)
  • We investigated CYP2C9 polymorphisms in relation to the international normalized ratio (INR) during the first 6 weeks of treatment and its effect on the maintenance dose in a cohort of 1124 patients from the Rotterdam Study who were treated with acenocoumarol or phenprocoumon. (ox.ac.uk)
  • The drug-drug interaction between oral anticoagulants (especially warfarin) and acetaminophen has been described, but evidence is conflicting and evidence for a similar interaction between acenocoumarol or phenprocoumon and acetaminophen is limited. (springer.com)
  • Therefore, a study was performed to determine the influence of acetaminophen on oral anticoagulation with acenocoumarol or phenprocoumon in everyday practice. (springer.com)
  • Acenocoumarol is an oral anticoagulant of the coumarin series, synthesized and developed in the Geigy laboratoires in the late 1960s and sold in the United States under the brand name of Sintrom . (blogspot.com)
  • entitled to a copy of this authorization form for my records, for instance, acenocoumarol sintrom. (tripod.com)
  • SINTROM : · Cardiopathies emboligènes : prévention des complications thrombo-emboliques en rapport avec certains. (saverxcanada.to)
  • Acenocoumarol is an anticoagulant that functions as a vitamin K antagonist (like warfarin). (wikipedia.org)
  • Warfarin or acenocoumarol is better in the anticoagulant treatment of chronic atrial fibrillation? (wikipedia.org)
  • Acenocoumarol is a coumarin that is used as an anticoagulant, with actions and uses similar to warfarin . (guidetopharmacology.org)
  • Human liver microsomal metabolism of the enantiomers of warfarin and acenocoumarol: P450 isozyme diversity determines the differences in their pharmacokinetics. (semanticscholar.org)
  • Since thrombosis is the most relevant clinical manifestation of this disorder, its treatment relies almost exclusively on anticoagulant therapy with warfarin, acenocoumarol and heparin-based regimens. (frontiersin.org)
  • Compared to other coumarin derivatives, acenocoumarol has a short half-life. (cancer.gov)
  • His fever subsided, and he was discharged a few days later while continuing to receive acenocoumarol , an oral coumarin anticoagulant. (thefreedictionary.com)
  • Acenocoumarol is mono-coumarin derivative with racemic mixture of R (+) and S (-) enantiomers. (semanticscholar.org)
  • For acenocoumarol, the most frequently used coumarin in many countries worldwide, pharmacodynamic influences are expected to be comparable. (cdc.gov)
  • Acenocoumarol (AC) is a coumarin, vitamin K derivate with antagonistic activity, used as anticoagulant therapy mainly in Central Europe and Latin America. (cdc.gov)
  • VKORC1 and CYP2C9 genotypes and acenocoumarol anticoagulation status: interaction between both genotypes affects overanticoagulation. (thefreedictionary.com)
  • Cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) genotypes as determinants of acenocoumarol sensitivity. (thefreedictionary.com)
  • Of various cDNA-expressed human CYPs, only CYP2C9 hydroxylated (S)-acenocoumarol. (semanticscholar.org)
  • Impact of CYP2C9 polymorphisms on the vulnerability to pharmacokinetic drug-drug interactions during acenocoumarol treatment. (semanticscholar.org)
  • Finally, CYP2C9 phenotype was evaluated after a single oral dose of 4 mg of acenocoumarol. (uclouvain.be)
  • The haplotype that contains the CYP2C9*3 allele was the only one influencing acenocoumarol pharmacodynamics, explaining 14.3% of its interindividual variability. (uclouvain.be)
  • CONCLUSION: Overall, CYP2C9-related genetic variability accounts for 14% of the interindividual variability in acenocoumarol pharmacodynamic response. (uclouvain.be)
  • Thus we confirmed earlier findings that acenocoumarol dosage mainly depends on polymorphisms in the VKORC1 and CYP2C9 genes. (cdc.gov)
  • Besides age, gender, body mass index and target INR, one polymorphism within each of the VKORC1, CYP2C9, CYP4F2 and CYP2C18 genes could explain 48.8% of acenocoumarol dosage variation. (cdc.gov)
  • Individuals with one or more CYP2C9*2 or CYP2C9*3 allele(s) require a significantly lower dose of acenocoumarol compared to wild-type patients. (ox.ac.uk)
  • T and the CYP2C9*3 polymorphisms, could thus predict a high risk of overdose before initiation of anticoagulation with acenocoumarol, and provide a safer and more individualized anticoagulant therapy. (uclouvain.be)
  • As a vitamin K antagonist, acenocoumarol inhibits vitamin K epoxide reductase, thereby inhibiting the reduction of vitamin K and the availability of vitamin KH2. (cancer.gov)
  • The aim of this study was to assess the effectiveness and safety of dabigatran (direct thrombin inhibitor) vs. acenocoumarol (vitamin K antagonist) in patients with atrial fibrillation (AF) in daily clinical practice. (ovid.com)
  • Immunomodulatory effects in vitro of vitamin K antagonist acenocoumarol. (nih.gov)
  • Your doctor will take regular blood samples and adjust your dose of acenocoumarol as necessary to make your INR fall into the range that has been shown to be effective at preventing blood clots in your particular condition. (netdoctor.co.uk)
  • You will probably need your INR checking after any changes to your acenocoumarol dose, if you become ill suddenly, or if you are prescribed certain other medicines. (dxline.info)
  • A clear genotype-dose relationship was found for acenocoumarol-treated patients. (ox.ac.uk)
  • The aim of the study is to explore the contribution of genetic factors related either to drug metabolism (cytochrome P450 2C9) or to drug target (vitamin K epoxide reductase) to variability in the response to acenocoumarol among 222 healthy volunteers after a single oral dose. (uclouvain.be)
  • Sinthrome tablets contain the active ingredient acenocoumarol (previously known as nicoumalone in the UK), which is a type of medicine called an oral anticoagulant. (netdoctor.co.uk)
  • Our organization, Shreeji Pharma International, has marked a distinct position in this industry and is engaged in manufacturing, exporting & supplying quality assured Acenocoumarol (Nicoumalone) . (shreejiexports.net)
  • Acenocoumarol (also called nicoumalone) is used to prevent and treat harmful blood clots, reducing the risk of a stroke or heart attack. (shreejiexports.net)
  • Acenocoumarol works by preventing the vitamin K dependent production of the clotting factors described above. (netdoctor.co.uk)
  • Acenocoumarol prevents the production of these clotting factors by inhibiting the action of vitamin K. Without the clotting factors fibrinogen cannot be converted into fibrin and blood clots are therefore less likely to occur. (netdoctor.co.uk)
  • Acenocoumarol inhibits the reduction of vitamin K by vitamin K reductase. (nextbio.com)
  • Acenocoumarol inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). (nextbio.com)
  • Pharmacogenetics of acenocoumarol pharmacodynamics. (uclouvain.be)
  • Potentiation of the acenocoumarol anticoagulant effect by acetaminophen. (springer.com)
  • Patients in stable anticoagulant treatment with acenocoumarol for auricular fibrillation, venous thromboembolic disease and/or cardiac valve replacement. (clinicaltrials.gov)
  • Patients' consent was requested for the preservation of their DNA sample, in case of new genes related to the pharmacokinetics or pharmacodynamics of acenocoumarol are discovered in the future. (clinicaltrials.gov)
  • Patients receiving stable anticoagulant treatment with acenocoumarol for auricular fibrillation, venous thromboembolic disease and/or cardiac valve replacement in Hospital La Paz and Barrio del Pilar primary care center. (clinicaltrials.gov)
  • Patients with Auricular fibrillation, venous thromboembolic disease and cardiac valve replacement receiving acenocoumarol. (clinicaltrials.gov)
  • This was demonstrated in a cohort of 112 Dutch patients treated with acenocoumarol who received an NSAID (diclofenac, naproxen, or ibuprofen). (thefreedictionary.com)
  • 2,3) We studied the outcomes in patients treated with acenocoumarol for more than 6 months in a series of consecutive outpatients with VTD from a rural Spanish area. (thefreedictionary.com)
  • In total, 920 consecutive AF patients were enrolled (442 dabigatran, 478 acenocoumarol), of which 2 × 383 were available for analysis after propensity score matching. (ovid.com)
  • The mean calculated stroke risk according to the CHA2DS2-VASc score was 3.5%/year in dabigatran vs. 3.7%/year acenocoumarol-treated patients. (ovid.com)
  • In 'real-world' patients with AF, dabigatran appears to be as effective, but significantly safer than acenocoumarol. (ovid.com)
  • Reliability of thromboelastometry for detecting the safe coagulation threshold in patients taking acenocoumarol after elective heart valve replacement. (nextbio.com)
  • To assess effects of the ABCB1 pilymorphisms on safety profile and dosing regimen of acenocoumarol in the patients with valvular atrial fibrillation. (cdc.gov)
  • All patients received acenocoumarol at doses of 1-6 mg daily with a target international normalized ratio (INR) of 2.0 to 3.0. (cdc.gov)
  • Is it safe to perform joint infiltrations or aspirations in patients anticoagulated with acenocoumarol? (medscape.com)
  • The method was successfully applied for the determination of R and S-acenocoumarol in plasma samples of 28 healthy subjects who participated in a pharmacokinetics study. (scirp.org)
  • Acenocoumarol takes about three days to produce its full anticoagulant effect because, while it prevents the production of new clotting factors, it takes about this long for clotting factors that have already been produced to be used up. (netdoctor.co.uk)
  • The anticoagulant effect of acenocoumarol is measured in terms of the prothombin time, which is the time taken for blood clotting to occur in a sample of blood to which calcium and a substance known as thromboplastin have been added. (netdoctor.co.uk)
  • OBJECTIVE: The aim of this study was to investigate the respective contribution of the different cytochrome P450 (CYP) 2C9 genetic polymorphisms to the interindividual variability of acenocoumarol pharmacodynamic response. (uclouvain.be)
  • We aimed to confirm known or identify new genetic variants contributing to interindividual variation on stabilized acenocoumarol dosage by a GWAS. (cdc.gov)
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  • Cesar JM, Garcia-Avello A, Navarro JL, Herraez MV: Aging and oral anticoagulant therapy using acenocoumarol. (lgmpharma.com)
  • Multivariable analysis confirmed this lower but non-significant risk in dabigatran vs. acenocoumarol after adjustment for the CHA2DS2-VASc score [hazard ratio (HR)dabigatran = 0.72, 95% CI: 0.20-2.63, P = 0.61]. (ovid.com)
  • Actual incidence rate of major bleeding was 2.1%/year (95% CI: 1.0-3.8) in the dabigatran vs. 4.3%/year (95% CI: 2.9-6.2) in acenocoumarol. (ovid.com)
  • The objective of the study was to establish the cytochrome P450 (CYP) enzymes catalyzing the hydroxylations of the acenocoumarol enantiomers. (semanticscholar.org)
  • We compared the average doses of acenocoumarol in groups identified according to their genotypes: CC (3.45 mg/day), CT (2.64 mg/day), TT (3.07 mg/day) and found no significant differences. (cdc.gov)
  • On chromosome 10, we further identified genetic variation in the cytochrome P450 2C18 (CYP2C18) gene contributing to variance of acenocoumarol dosage. (cdc.gov)
  • From polymorphisms tested for association with acenocoumarol dosage, 35 single nucleotide polymorphisms (SNPs) on chromosome 16 and 18 SNPs on chromosome 10 reached genome-wide significance. (cdc.gov)
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  • Factor VII coagulant activity was measured before and 24 hours after acenocoumarol intake. (uclouvain.be)
  • Body weight explained 5% of acenocoumarol pharmacodynamic variability, whereas the NQO1*2 allele had no significant effect. (uclouvain.be)