Acenocoumarol
Vitamin K Epoxide Reductases
International Normalized Ratio
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.
Drug Dosage Calculations
Steroid 16-alpha-Hydroxylase
Pharmacogenetics
Aryl Hydrocarbon Hydroxylases
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.
Warfarin
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.
Prothrombin Time
Vitamin K
A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
Heart Valve Prosthesis
Aortic Valve
Heart Valves
Heart Valve Prosthesis Implantation
Vitamin K 1
A family of phylloquinones that contains a ring of 2-methyl-1,4-naphthoquinone and an isoprenoid side chain. Members of this group of vitamin K 1 have only one double bond on the proximal isoprene unit. Rich sources of vitamin K 1 include green plants, algae, and photosynthetic bacteria. Vitamin K1 has antihemorrhagic and prothrombogenic activity.
Vitamin K Deficiency
Vitamin K 2
Vitamin A
Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of CAROTENOIDS found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products.
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)
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Cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) genotypes as determinants of acenocoumarol sensitivity.
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SintromPhenprocoumon and acenocoumarolNicoumaloneAntagonistsVKORC1Warfarin or acenocoumarolAnticoagulantsAnticoagulant acenocoumarolAntagonistTherapeuticAnticoagulationDoseAnisindioneVitaminApixabanAtrial fibrillationPolymorphismsBloodDosesMetabolismSevereDrugGenesTabletOralStableEffectIncreaseInternationalTimeHuman
Sintrom3
- Comparative study of the clinical effect of acenocoumarol (Sintrom) and phenprocoumon (Marcoumar) in myocardial infarction and angina pectoris. (semanticscholar.org)
- Manufacturer Cipla, India your acenocoumarol Sintrom ipratropium, in a method head to. (ncld.org)
- Acenocoumarol (Sintrom) - This is a drug used to slow blood clotting. (medicineclue.com)
Phenprocoumon and acenocoumarol1
- Liver injury is more common with other coumarin derivatives such as phenprocoumon and acenocoumarol, which are available in other countries but not in the United States. (richardvigilantebooks.com)
Nicoumalone2
- Acitrom (Acenocoumarol or Nicoumalone) 1mg Tablet is an oral anticoagulant that helps prevent harmful blood clots in the legs, lungs, brain, and heart. (biopharmzpharma.in)
- Acenocoumarol (Nicoumalone) The t½ of acenocoumarol as such is 8 hours, but an active metabolite is produced so that overall t½ is about 24 hours. (pharmacy180.com)
Antagonists4
- In the United States, approximately 2.7-6.1 million patients had atrial fibrillation (AF) in 2010, and this number is expected to gradually increase to approximately 5.6 to 12 million by 2050.1, 2 ) The vitamin K antagonists (VKAs), warfarin and acenocoumarol, are prescribed for the treatment or prophylaxis of embolic AF or deep vein thrombosis (DVT). (ekjcp.org)
- Increased coagulation tests (prothrombin time/INR) and/or bleeding w/ vit K antagonists (e.g. warfarin, acenocoumarol, fluindione). (medicscientist.com)
- Increased coagulation tests (prothrombin time/INR) and/or bleeding with vit K antagonists (e.g. warfarin, acenocoumarol, fluindione). (com.bd)
- Vitamin K: 'The product should not be consumed by people taking anticoagulants containing vitamin K antagonists (e.g. warfarin and acenocoumarol). (colwayinternational.com)
VKORC16
- The required acenocoumarol dose and the risk of underanticoagulation and overanticoagulation are associated with the CYP2C9 and VKORC1 genotypes. (eur.nl)
- Patients with polymorphisms in CYP2C9 and VKORC1 had a higher risk of overanticoagulation (up to 74%) and a lower risk of underanticoagulation (down to 45%) in the first month of treatment with acenocoumarol, but this effect diminished after 1-6 months. (eur.nl)
- Intr-un studiu efectuat in Franta s-a constatat ca testarea farmacogenetica poate sa identifice un risc crescut de supradozare la 25% dintre persoanele care vor incepe terapia cu acenocoumarol (purtatorii alelei VKORC1 1639A si CYP2C9*3). (lamedic.ro)
- Variants in CYP2C9 and VKORC1 have been associated with acenocoumarol maintenance dose. (udl.cat)
- 11 ) Similarly, the maintenance dose of acenocoumarol is also affected by VKORC1 and CYP2C9 genes. (ekjcp.org)
- A pharmacokinetic-pharmacodynamic model for predicting the impact of CYP2C9 and VKORC1 polymorphisms on fluindione and acenocoumarol during induction therapy. (cdc.gov)
Warfarin or acenocoumarol3
- Warfarin or acenocoumarol is better in the anticoagulant treatment of chronic atrial fibrillation? (wikipedia.org)
- A prespecified pooled analysis of the EINSTEIN-DVT and EINSTEIN-PE studies compared the efficacy and safety of rivaroxaban (15 mg twice-daily for 21 days, followed by 20 mg once-daily) with standard-therapy (enoxaparin 1.0 mg/kg twice-daily and warfarin or acenocoumarol). (biomedcentral.com)
- If you take medicines that thin the blood to prevent blood clots, e.g. warfarin or acenocoumarol, the risk of bleeding may be increased. (zeepedia.com)
Anticoagulants2
Anticoagulant acenocoumarol1
- Biobarcode assay for the oral anticoagulant acenocoumarol. (cocites.com)
Antagonist3
- Acenocoumarol is an anticoagulant that functions as a vitamin K antagonist (like warfarin). (wikipedia.org)
- Immunomodulatory effects in vitro of vitamin K antagonist acenocoumarol. (semanticscholar.org)
- The androgen, Testolactone, may incrase the anticoagulant effect of the Vitamin K antagonist, Acenocoumarol. (genelabs.com)
Therapeutic2
- Nanoplasmonic biosensor device for the monitoring of acenocoumarol therapeutic drug in plasma. (semanticscholar.org)
- Monitor for changes in the therapeutic effect of Acenocoumarol if Testolactone is initiated, discontinued or dose changed. (genelabs.com)
Anticoagulation4
- 1 There is a growing interest in the identification of genetic variants of cytochrome P450 CYP2C9, which can modify its ability to inactivate warfarin and acenocoumarol, since a reduced CYP2C9 activity on these drugs would put patients at risk of over anticoagulation and subsequent bleeding complications. (ashpublications.org)
- Patients with acute pulmonary embolism and no contraindication to anticoagulant therapy were randomly assigned - by card draw no less, demonstrating how far trial randomization has come in subsequent years - to receive anticoagulation with heparin and the coumarin-derivative acenocoumarol, or no anticoagulant. (nature.com)
- Besides this, he was managed conservatively with anticoagulation using enoxaparin and acenocoumarol and followed up with echocardiographic evaluation of IVC and RA thrombus and INR monitoring. (austinpublishinggroup.com)
- Individuals with PM phenotype (i.e. genotypes with homozygous or compound heterozygous *2 or *3 alleles) are at greater risk of severe bleeding during coumarin-based anticoagulation therapy with warfarin, acenocoumarol and phenprocoumon. (goffinmoleculartechnologies.com)
Dose2
- The dose of acenocoumarol is individualized by your doctor according to blood clotting time as determined by laboratory tests, called an INR, performed at regular intervals. (pharmachoice.com)
- Acenocoumarol is an oral anticoagulant with significant interindividual dose variations. (udl.cat)
Anisindione1
- Prescription medications (for treating interact with acenocoumarol, anisindione, bupropion, dicumarol rule provided an opportunity for all interested persons to submit their comments on or before January 23, 2012. (redlightoflove.com)
Vitamin1
- Acenocoumarol works by partially blocking the reuse of vitamin K in your liver. (pharmachoice.com)
Apixaban1
- Both apixaban and acenocoumarol can increase the risk of bleeding. (goldwestafrica.com)
Atrial fibrillation1
- Acenocoumarol is prescribed to prevent unwanted clots from forming if you have a condition that puts you at risk of this happening, such as atrial fibrillation, or if you have had a heart valve replacement . (lazoi.com)
Polymorphisms2
- In the present study, the effects of these polymorphisms on the risk of underanticoagulation and overanticoagulation over time after the start of acenocoumarol were investigated. (eur.nl)
- Conclusions These results suggest that Acenocoumarol rs9652490 and rs11856808 polymorphisms are not related with risk for MS. This study adds to other published evidence indicating that, to date, the SNPs studied here could be useful risk biomarkers of developing essential tremor, but not other movement disorders. (seatra.org)
Blood5
- Acenocoumarol is a blood thinner agent prescribed to treat or prevent the formation of blood clots or thrombus in the blood vessels helps by dissolving the blood clots and reducing the complication of thromboembolic disorders. (medindia.net)
- Acenocoumarol is used to prevent and treat blood clots in blood vessels e.g. (lazoi.com)
- Acenocoumarol is used to treat and prevent blood clots in the veins by preventing blood clots from forming or from getting bigger, but it does not dissolve blood clots. (pharmachoice.com)
- Some products that may interact with this drug include: "blood thinners" (such as acenocoumarol, warfarin), strontium. (parspharmed.com)
- Concomitant use of Monk Cv Dry Syrup with blood thinners such as warfarin, acenocoumarol increases the risk of bleeding. (pharmeasy.in)
Doses1
- METHODS: In order to investigate the choice of the best molecule and treatment regimen for a given noncompliance pattern, we performed an in silico study with two oral anticoagulant agents, warfarin and acenocoumarol, each taken in one or two daily doses. (archives-ouvertes.fr)
Metabolism1
- The metabolism of Acenocoumarol can be decreased when combined with Entecavir. (drugbank.com)
Severe2
- Acenocoumarol can also lead to severe allergic reactions including pale red, dizziness, severe headache, itchy skin rash however, these are rare. (lazoi.com)
- A 59-year-old patient with chronic obstructive pulmonary disease (emphysema) operated upon in childhood due to coarctation of the aorta, with aortic valve replacement surgery due to severe stenosis (anticoagulated with acenocoumarol), reported for two-lung transplantation. (medintensiva.org)
Drug3
- Tous les résultats de la recherche seront tirés du « National Drug Schedules » du site Web en anglais. (napra.ca)
- L-carnitine, the active ingredient in the drug, can increase the effects of acenocoumarol, which may increase the chance of bruising or bleeding. (medicineclue.com)
- RESULTS: Considering different patterns of noncompliance (including timing errors in drug intake and the phenomenon of drug holidays) and comparing warfarin with acenocoumarol, we identified different situations in which one agent (prescribed once or twice daily) could clearly minimise both the thromboembolic and haemorrhagic risks. (archives-ouvertes.fr)
Genes1
- The authors comment that CYP2C18 is only included in three PharmGKB pathways (there are actually four: clobazam, diclofenac, warfarin and acenocoumarol), while the other genes of the CYP2C locus are in many. (blogspot.com)
Tablet2
- Each peach coloured, biconvex, round tablet contains acenocoumarol 1 mg. (pharmachoice.com)
- Each white, flat-faced tablet, debossed with Paladin shield on one side and double scored on the other, contains acenocoumarol 4 mg. (pharmachoice.com)
Oral1
- Warfarin and acenocoumarol are commonly prescribed oral anticoagulant drugs that are used in the prevention and treatment of thromboembolic disorders across the world. (innovareacademics.in)
Stable1
- This case report highlights an instance wherein warfarin proved to provide a much more stable anticoagulant cover, as compared to that provided by acenocoumarol. (innovareacademics.in)
Effect1
- Anti-coagulant effect of acenocoumarol and warfarin enhanced by clarithromycin. (pharmacia1.com)
Increase1
- Oxytetracycline may increase the anticoagulant activities of Acenocoumarol. (drugbank.com)
International1
- Drugs.com Drugs.com international listings for acenocoumarol Diseases Database (DDB): 29202 Cesar J, García-Avello A, Navarro J, Herraez M (2004). (wikipedia.org)
Time1
- Take acenocoumarol at the same time each day. (pharmachoice.com)
Human1
- Cytochrome P450 CYP2C9 is the principal catalyst of warfarin and acenocoumarol hydroxilation reactions in human liver microsomes. (ashpublications.org)