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PubMed1990

Interaction of the combined medication with the new low-molecular-weight heparinoid Lomoparan (Org 10172) and acenocoumarol.

A high intravenous dose of the low-molecular-weight heparinoid Lomoparan (Org 10172) was administered to 6 healthy males in a steady state of anticoagulation (Thrombotest) by acenocoumarol. Prothrombin time, activated partial thromboplastin time and Stypven time were prolonged to a degree which was greater than that expected on the base of the summation of the effects by each drug alone. This effect was observed for a period of up to 1 h. The Thrombotest was affected for up to 5 h after the intravenous administration of Org 10172, therefore it is deemed unsuitable for monitoring the combined effects of these two anticoagulants during this period. Acenocoumarol did not affect the pharmacokinetic parameters of Org 10172 with the exception of a slight reduction of the clearance of plasma anti-Xa activity.

Acenocoumarol↗
PubMed2005

Cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) genotypes as determinants of acenocoumarol sensitivity.

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 allele is independent of the VKORC1 gene effect. These 2 polymorphisms account for up to 50% of the interindividual variability. The simple genotyping of 2 single-nucleotide polymorphisms (SNPs), VKORC1 -1639G>A or 1173C>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.

Acenocoumarol↗
PubMed1999

[Plasma concentrations of vitamin K1 and acenocoumarol related to international normalized ratios].

Reduced vitamins K are acting as cofactors of glutamic carboxylation of procoagulant factors (II, VII, IX and X). The reduction of these vitamins is inhibited by oral anticoagulants. The response to antivitamins K is individual and may change during the treatment of a patient. The determinations of plasmatic vitamin K and acenocoumarol may help to explain the mechanism of a resistance to the anticoagulant therapy. Quantifications of vitamin K1 are realized after liquid-liquid extraction with liquid chromatography and fluorescence detection after post-column reduction. For acenocoumarol, plasma concentration is measured, after liquid-liquid extraction, by liquid chromatograph, with ion trap mass spectrometer detector.

Acenocoumarol↗
PubMed2001

The effect of acenocoumarol on hemorheological parameters.

The effect of acenocoumarol on hemorheological variables was measured in 35 non-valvular chronic atrial fibrillation patients before starting oral anticoagulant therapy (basal) and one and two months after beginning treatment (INR-2,3). Fibrinogen increased significantly from the basal situation: 332+/-99 mg/dl to 386+/-96 mg/dl in the second month (p<0.05). However, this small increase in fibrinogen is not large enough to mediate other rheological changes, and whole blood filterability, blood viscosity, plasma viscosity and erythrocyte deformability and aggregability remained unchanged after treatment. These results suggest that acenocoumarol does not affect rheological parameters and can therefore be used as a "neutral drug" for rheological studies in cardiovascular patients under oral anticoagulant therapy.

Acenocoumarol↗
PubMed2002

Overanticoagulation associated with combined use of antibacterial drugs and acenocoumarol or phenprocoumon anticoagulants.

BACKGROUND: Several case reports associated combined use of coumarins and antibacterial drugs with overanticoagulation. Despite the fact that these drugs are frequently prescribed concurrently, there is little quantitative information on the risks of such complications. OBJECTIVE: To study which antibacterial drugs are associated with overanticoagulation during therapy with coumarins. DESIGN: Population-based cohort study in a sample of the Rotterdam Study. SUBJECTS: All patients who were treated with acenocoumarol or phenprocoumon in the study period from April 1, 1991 through December 31, 1998 and for whom INR data were available. METHODS: Patients were followed until an INR >/= 6.0, the end of their treatment, death or end of the study period. Proportional hazards regression analysis was used to estimate the risk of an INR >/= 6.0 in relation to concomitant use of an oral anticoagulant and antibacterial drugs after adjustment for several potentially confounding factors such as age, gender, hepatic dysfunction, malignancies, and heart failure. RESULTS: Of the 1,124 patients in the cohort, 351 developed an INR >/= 6.0. The incidence rate was 6.9 per 10,000 treatment days. Sulfamethoxazole combined with trimethoprim most strongly increased the risk of overanticoagulation with an adjusted relative risk of 20.1 (95% CI: 10.7-37.9). Stratification showed that the induction period of overanticoagulation varied between different antibacterial drugs. CONCLUSION: In this study among outpatients of an anticoagulation clinic using acenocoumarol or phenprocoumon, several antibacterial drugs strongly increased the risk of overanticoagulation. Awareness of these drug interactions and more frequent monitoring of INR values during the initial stages of antibacterial drug therapy are warranted to minimize the risk of bleeding complications.

Acenocoumarol↗
PubMed2004

Stability of the complexes of some lanthanides with coumarin derivatives. II. Neodymium(III)-acenocoumarol.

A complex of neodymium(III) with 4-hydroxy-3[1-(4-nitrophenyl)-3-oxobutyl]-2H-1-benzopyran-2-one (acenocoumarol) was synthesized by mixing water solutions of neodymium(III) nitrate and the ligand (metal to ligand molar ratio of 1:3). The complex was characterized and identified by elemental analysis, conductivity, IR, 1H NMR and mass spectral data. DTA and TGA were applied to study the composition of the compound. Elemental and mass spectral analysis of the complex indicated the formation of a compound of the composition NdR3 x 6H2O, where R = C19H14NO6-) The reaction of neodymium(III) with acenocoumarol was studied in detail by the spectrophotometric method. The stepwise formation of three complexes, vis., NdR2+, NdR2+ and NdR3 was established in the pH region studied (pH 3.0-7.5). The equilibrium constants for 1:1, 1:2 and 1:3 complexes were determined to be log K1 = 6.20 +/- 0.06; log K2 = 3.46 +/- 0.07 and log K2) = 2.58 +/- 0.05, respectively.

Acenocoumarol↗
PubMed2004

[Warfarin or acenocoumarol is better in the anticoagulant treatment of chronic atrial fibrillation?].

UNLABELLED: A SPORTIF-III substudy. BACKGROUND: Warfarin has been considered to provide more stable anticoagulant effect than acenocoumarol due to its longer half-life. OBJECTIVE: The aim of this SPORTIF-III substudy was to compare acenocoumarol (A) with warfarin (W) in the same group of 74 patients, with chronic atrial fibrillation who started with W and then changed to A. METHODS: We compared prospectively a 3 months period on W with a 3 months period on A. RESULTS: The mean number of INR measurements per patient was 5.7 +/- 1.2 and 5.4 +/- 1.6 resp (NS). The mean percentage of INR-s in the therapeutic range of 2-3 was 49 +/- 22.6% for W and 56 +/- 26.8% for A (p < 0.05), the percentage of subtherapeutic values were not different, the supratherapeutic values however occurred more frequently on W (28 +/- 20%) than on A (19 +/- 19%), p < 0,001. There was a good correlation between A and W doses (r = 0.65, p < 0.001), the mean W dose was 5.03 +/- 1.99 mg, the mean A dose was 2.5 +/- 1.3 mg, the W/A dose ratio was computed to be 2.18 +/- 0.78. CONCLUSIONS: 1. anticoagulation effect stability was superior for A compared to W; 2. W/A dose ratio was 2.18.

Acenocoumarol↗
PubMed1989

Acenocoumarol and pentoxifylline in intermittent claudication. A controlled clinical study. The APIC Study Group.

The efficacy and safety of pentoxifylline (400 mg tid orally) and acenocoumarol, administered singly or in combination, in the treatment of intermittent claudication associated with chronic occlusive arterial disease were evaluated in a multi-center, randomized, factorial, blind clinical trial involving 146 patients. The response to treatment was assessed by measuring pain-free walking time on the treadmill and by Doppler ankle/arm systolic pressure ratio at rest and after treadmill. Both pentoxifylline and acenocoumarol were significantly more effective than placebo in increasing the proportion of patients who improved their performance on the treadmill after one year of treatment. Benefit from active treatment was also apparent from the results of Doppler examinations performed after physical exercise. No significant differences were observed in comparing the effect of one active drug versus the other or versus the combined treatment. Five major hemorrhagic complications were registered in anticoagulated patients, two fatal cerebral hemorrhages and one gastrointestinal bleeding occurring in the group treated with both active drugs. The investigators conclude that (1) pentoxifylline is effective and safe in the treatment of patients with intermittent claudication (2) the benefits of oral anticoagulant therapy are outweighed by the risk of serious bleeding, and (3) the risk of bleeding is probably increased by the combined treatment with pentoxifylline.

Acenocoumarol↗
PubMed1988

Effect of benazepril, a converting enzyme inhibitor, on plasma levels and activity of acenocoumarol and warfarin.

The effect of benazepril (CGS 14824), 20 mg/day orally, on the steady-state pharmaco-dynamics and plasma levels of the anticoagulants, warfarin and acenocoumarol, was studied in healthy volunteers. The anticoagulant activity of acenocoumarol was not affected by benazepril; there was an apparent slight but statistically significant reduction of the anticoagulant effect of warfarin. The magnitude of the inhibitory effect was considered not to be clinically important. There was no effect of benazepril on plasma steady-state levels of either anticoagulants.

Acenocoumarol↗
PubMed1979

[Interaction between anti-aggregating and anticoagulant agents. A double blind study on the concomitant administration of nicergoline and acenocoumarols].

A double blind study was carried out comparing 10-methoxy-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate) (nicergoline, Sermion) and placebo in 60 thromboembolic patients on long-term controlled acenocoumarol treatment. Aim of the trial was to assess the hypothesis of an interaction on both the coagulatory parameters and the clinical findings. No significant variations of the acenocoumarol daily dose were required in nicergoline treated group and no interaction was demonstrated in coagulatory parameters. Prothrombin activity and thrombo-test evaluated fortnightly were not statistically different in nicergoline and placebo groups while the platelet antiaggregating activity of nicergoline was confirmed after a three months' treatment. Bleeding time was unaffected. Minor differences in clinical findings were observed in the two groups.

Acenocoumarol↗
PubMed1993

Stereoselective distribution of acenocoumarol enantiomers in human plasma: chiral chromatographic analysis of the ultrafiltrates.

Stereoselectivities for the binding of rac-acenocoumarol to human serum albumin (HSA), alpha 1-acid glycoprotein (AGP), and human plasma were determined by chiral HPLC analysis of the ultrafiltrates on a Chiral-AGP column. The results confirmed the previously detected inverse stereoselectivities; for HSA the ratio of the enantiomeric constants was KR/KS approximately 2, while for AGP it was KR/KS approximately 0.3. In plasma the contribution of HSA dominates, although in pathological states, elevated AGP levels may compensate for stereoselective distribution.

Acenocoumarol↗
PubMed1989

A prospective randomized trial of low molecular weight heparin-DHE and conventional heparin-DHE (with acenocoumarol) in patients undergoing gynaecological surgery.

The antithromboembolic efficacy of once a day low molecular weight heparin in fixed combination with dihydroergotamine (LMWH-DHE) was compared with conventional heparin-DHE in combination with Acenocoumarol (heparin-DHE/A) in 191 patients undergoing gynaecological surgery. LMWH-DHE proved equally effective in preventing thromboembolic complications, with a similar incidence of postoperative bleeding and side effects. Deep vein thrombosis occurred once in each group and one non-fatal pulmonary embolism occurred in the LMWH-DHE group. The main advantage of LMWH-DHE was significantly better patient acceptance of the single daily subcutaneous injection as compared with the two injections of conventional heparin-DHE (P = 0.02). On the other hand, LMWH-DHE was associated with significantly increased incidence of intraoperative bleeding (P less than 0.02). The bleeding did not, however, cause any clinical problems. Discontinuation of therapy due to bleeding or pain at the site of injection occurred three times in each group. We consider the use of LMWH-DHE to be an attractive, economic and safe method of thromboembolic prophylaxis.

Acenocoumarol↗
PubMed1986

The in vivo effects of acenocoumarol, phenprocoumon and warfarin on vitamin K epoxide reductase and vitamin K-dependent carboxylase in various tissues of the rat.

In rats the in vivo effects of a chronic low-dose treatment (+/- 60 micrograms/rat per day) with different coumarins (acenocoumarol, phenprocoumon and warfarin) on hepatic and non-hepatic vitamin K-dependent enzyme systems were compared. The plasma concentrations of the three coumarins differed largely but these differences were not reflected in the microsomal coumarin contents. The non-hepatic microsomes contained less than 20% of the coumarins found in liver microsomes. No substantial differences were observed between the following effects of the three anticoagulant treatments. The blood coagulation factor activities were about 10% of normal. The hepatic microsomal vitamin K epoxide reductase activity was diminished to about 35% of control values. The vitamin K epoxide reductase activities present in kidney, lung, spleen, testis and brain microsomes were less influenced by the coumarin treatments; activities ranged between 45 and 65% of normal. In the liver microsomes a 15-fold accumulation of non-carboxylated precursor proteins was found; in the non-hepatic microsomes this effect was less pronounced but still present. The hepatic vitamin K-dependent carboxylase activity was enhanced but the corresponding non-hepatic enzyme activities were slightly or not affected. In addition, the effects of a chronic low-dose warfarin treatment were compared with those after an acute high dose of the drug.

4-Hydroxycoumarins↗
PubMedDate not supplied

Upper airway obstruction by sublingual hematoma: a complication of anticoagulation therapy with acenocoumarol.

Upper airway obstruction secondary to the use of oral anticoagulants has been reported. In most of the cases, it is produced by retropharyngeal and laryngeal hematomas. The sublingual space is an extremely rare site for bleeding, but this constitutes a life-threatening complication, it must be considered as an emergency situation, and the main priority is to secure patient's airway. We recommend immediate reversal of the anticoagulation therapy, preferably with fresh frozen plasma. The surgical drainage usually is not recommended. We present what is to our knowledge the 10th case reported of an airway obstruction due to sublingual hematoma after the administration of oral anticoagulants, and the third one due to the use of acenocoumarol.

Acenocoumarol↗
PubMedDate not supplied

[Treatment by lepirudin and acenocoumarol of heparin induced thrombocytopenia after valvular surgery: a word of caution].

The diagnosis and treatment of type II heparin-induced thrombocytopenia (HIT) after valvular surgery raise difficult issues due to the substitution of heparin by other anticoagulants. A 50-year-old man with hepatic cirrhosis and acute infective endocarditis underwent aortic valve replacement. On the 4th postoperative day platelet count decreased to 50 g/l. Platelet aggregation was demonstrated in vitro with unfractioned and low molecular weigh heparins and danaparoid sodium. As serum creatinine was 94 micromol/l, lepirudine (r-hirudin) was administered at recommended doses. However, six hours later hirudinaemia estimated by ecarin-clotting time was 3 mg/l and lepirudine dose had to be divided by 15 in order to reach therapeutic levels. Similarly, INR increased up to 6,7 on the 11th postoperative day after acenocoumarol 1 mg daily was administered. Despite the presence of oesophageal, gastric and duodenal lesions at risk of haemorrhage no bleeding was detected. The reasons for overdosage are discussed. The necessity of measurement or calculation of creatinine clearance before lepirudine prescription and frequent hirudinaemia during treatment is emphasized.

Acenocoumarol↗
PubMed2006

VKORC1 and CYP2C9 genotypes and acenocoumarol anticoagulation status: interaction between both genotypes affects overanticoagulation.

OBJECTIVE: Our objective was to assess the effects of VKORC1 and CYP2C9 genotypes on severe overanticoagulation and time to achieve stability and their contributions to dose requirement during the initial phase of acenocoumarol treatment. METHODS: A prospective follow-up study was conducted at 2 anticoagulation clinics in The Netherlands. We assessed the CYP2C9 genotype (CYP2C9*2 and CYP2C9*3 polymorphisms) and the VKORC1 C1173T genotype of the subjects and collected data on international normalized ratio, dose, comedication, and comorbidity. RESULTS: Of the 231 patients in the cohort, 150 (64.9%) had a VKORC1 C1173T polymorphism and 84 (36.4%) had a CYP2C9*2 or CYP2C9*3 allele. Only carriers of a combination of a CYP2C9 polymorphism and a VKORC1 polymorphism had an increased risk of severe overanticoagulation compared with subjects with no polymorphism or only 1 polymorphism (hazard ratio, 3.83 [95% confidence interval, 1.62-9.05]). The time to achieve stability was associated with the possession of the CYP2C9 genotype, not with the VKORC1 genotype (hazard ratio for CYP2C9*3 allele compared with CYP2C9 wild type, 0.59 [95% confidence interval, 0.40-0.87]). Patients with a VKORC1 polymorphism required significantly lower doses than VKORC1 CC wild-type patients. A larger part of the variability in dose requirement was explained by the VKORC1 genotype than by the CYP2C9 genotype (21.4% and 4.9%, respectively). CONCLUSION: Being a carrier of a combination of polymorphisms of VKORC1 and CYP2C9, rather than of one of these polymorphisms, is associated with severe overanticoagulation. The time to achieve stability is mainly associated with the CYP2C9 genotype.

Acenocoumarol↗
PubMed1997

Evolution of blood coagulation and fibrinolysis parameters after abrupt versus gradual withdrawal of acenocoumarol in patients with venous thromboembolism: a double-blind randomized study.

A double-blind randomized trial was conducted to research a hypercoagulable state rebound after abrupt versus gradual withdrawal of acenocoumarol, 20 patients were included: 10 in the abrupt withdrawal group (AW) and 10 in the gradual withdrawal group (GW). Between days 1 and 15,F1 + 2 was higher in group AW (P < 0.002). A significant increase of D-dimer with time was found (P < 0.001) without difference between the two groups, tPA and PAI-1 levels remained stable throughout without difference between the two groups. No rebound phenomenon was observed. Four thrombotic recurrences were observed: group AW: 1, group GW: 3 (P = 0.29). There is neither clinical nor biological support for a gradual anticoagulation withdrawal.

Acenocoumarol↗