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PubMed2000

Low molecular weight heparin (enoxaparin) versus oral anticoagulant therapy (acenocoumarol) in the long-term treatment of deep venous thrombosis in the elderly: a randomized trial.

This study aims to establish the relative effectiveness and safety of low molecular weight heparin in elderly patients with venous thrombosis in order to find an alternative to oral anticoagulant therapy with less bleeding complications in the long-term treatment of deep venous thrombosis (DVT). One hundred consecutive elderly patients (>75 years old) with venographically demonstrated proximal DVT were included in a randomized trial. All patients were treated for ten days with adjusted doses of intravenous heparin. Informed consent was obtained and on the eight day, patients were randomly allocated to receive acenocoumarol (INR 2.0-3.0) or subcutaneous enoxaparin (4000 anti-Xa units once a day) for three months. All patients were followed-up clinically and venographically for a one year period. The results were analyzed with Fisher's exact test or chi-square test as appropriate. During the treatment and surveillance period, 6 of the 50 patients (12%) who received acenocoumarol and 8 of the 50 patients (16%) who received enoxaparin had new episodes of venous thromboembolism confirmed by objective testing (p = 0.6; 95% CI for the difference: -19.5 to 11.5). Hemorrhagic complications occurred in six of the 50 patients (12%) who received acenocoumarol and in one (2%) of those on enoxaparin (p = 0.1; 95% CI for the difference: -1.8 to 21.8). Vertebral fractures developed in 2 patients (4%) in the enoxaparin group (p = 0.5; 95% CI for the difference: -11.4 to 3.4). These results show that fixed dose enoxaparin seems to be effective and safe in the long-term treatment of proximal DVT in the elderly. In comparison with oral anticoagulants, the findings are inconclusive due to the wide confidence intervals for differences between outcomes, however they suggest that the former may have less bleeding complications with similar efficacy.

Acenocoumarol↗
PubMed2006

[Partial resistance to acenocoumarol and phenprocoumon caused by enzyme polymorphism].

A 78-year-old man was treated with coumarin derivatives following myocardial infarction. The international normalised ratio was not increased by using standard loading doses and dose adjustments for acenocoumarol and phenprocoumon. The desired level of anticoagulation was achieved with a high dosage of phenprocoumon (18-21 mg daily). This dose was associated with a phenprocoumon serum concentration that was ten times higher than the normal therapeutic concentration. The serum concentration of vitamin K1 was low. After exclusion of alternative causes, we concluded that the exceptionally high dose of phenprocoumon needed was due to partial resistance to coumarin derivatives. Partial resistance is related to a polymorphism of the gene coding for the enzyme vitamin K epoxide reductase. The patient was successfully treated with chronic high-dose phenprocoumon. Resistance to coumarin derivatives caused by a congenital polymorphism in the vitamin K reductase gene is a rare phenomenon. Resistance is seldom absolute. The desired anticoagulation effect can be achieved with doses that are 10-20 times higher than standard doses. Phenprocoumon is advantageous in this situation because it requires fewer tablets than acenocoumarol. Determination of serum concentrations of acenocoumarol and phenprocoumon can be used to exclude other causes of treatment resistance.

Acenocoumarol↗
PubMed1995

[Hemorrhagic incidents during prolonged ambulatory treatment with acenocoumarol].

BACKGROUND: To analyze hemorrhagic complications in a series of outpatients treated with acenocoumarol in an anticoagulant specialized unit by a prospective observational clinical study. PATIENTS AND METHODS: 1,200 outpatients (682 women/518 men, mean age 54.6 +/- 15.8 yrs.) treated with acenocoumarol for at least 6 weeks, with a total follow-up of 2,795 patients-yr. Prevalence and incidence of bleeding was analyzed. The episodes that were potentially life-threatening, or forced to blood transfusion or hospital patient admittance were considered as major bleedings, and the remainder episodes were minor. RESULTS: There were 379 minor bleedings in 258 patients (incidence 13.56/100 patients-yr.), 45 major bleedings (1.61/100 patients-yr.) and 2 lethal bleedings (0.07/100 patients-yr.). Minor bleedings correlated with more advanced age (57.3 +/- 11.8 vs. 53.9 +/- 16.7 yrs., p = 0.002), with the first two months in treatment in the 511 patients who start the treatment during the study (31.09 vs. 13.04/100 patients-yr., p < 0.001), and with a worse achievement of the desired anticoagulation (72.4% vs. 81.6%; p = 0.002). Major bleeding was associated with local causes in 48.9%, and with an excessive anticoagulation in 35.6%. CONCLUSIONS: Bleeding is relatively frequent during acenocoumarol therapy, mainly in patients with worse control, but only in a few of these episodes is severe, and is usually associated with local lesions.

Acenocoumarol↗
PubMed1995

[Adverse effects of combined use of acenocoumarol and acetylsalicylic acid after myocardial infarct and unstable angina].

The authors examined the bleeding complications in 75 patients who received acenocoumarol and acetylsalicylic acid combined therapy. The studied population suffered from either acute myocardial infarction or unstable angina. Among the 75 patients in two cases (2.7%) appeared serious bleeding and in another 25 cases (33.3%) mild bleeding complications. There were no fatal cases. Comparing these data with literary data, the authors stated that in the study group the proportion of serious complications didn't increase in comparison with patients who received either acenocoumarol, warfarin or acetylsalicylic acid but mild bleeding appeared more frequently. This finding suggests that in high risk patients the combined acenocoumarol-acetylsalicylic acid therapy can be considered under strict control.

Acenocoumarol↗
PubMed1999

Low molecular weight heparin versus acenocoumarol in the secondary prophylaxis of deep vein thrombosis.

The aim of this study was to determine the efficacy and safety of subcutaneous weight-adjusted dose low molecular weight heparin (LMWH) compared with oral anticoagulant (OA) in the prevention of recurrent venous thromboembolism. In a prospective multicenter trial, 202 patients with symptomatic proximal deep vein thrombosis (DVT) were included. As soon as the diagnosis of DVT was confirmed by phlebography, 101 were randomly assigned to receive LMWH (nadroparin) for secondary prophylaxis and 101 to receive OA (acenocoumarol). Patients in both groups were initially treated with nadroparin in a dose of 85 anti-Xa IU/kg s.c. every 12 h. Secondary prophylaxis with either nadroparin, 85 anti-Xa IU/kg s. c. once daily, or acenocoumarol was continued for at least 3 months. Three patients in the LMWH group and 6 in the OA group were excluded from analysis for various reasons. During the one-year combined secondary prophylaxis and surveillance period, 7 of of the 98 evaluable patients (7.1%) in the LMWH group and 9 of the 95 evaluable patients (9.5%) in the OA group had a documented recurrence of venous thromboembolism (Fisher's exact test, p = 0.61). Of these, 2 patients who received LMWH and 7 patients on acenocoumarol had recurrences in the 3-month period of secondary prophylaxis. Four patients (4.1%) in the LMWH group developed bleeding complications during this study period, as compared with 7 (7.4%) in the OA group (Fisher's exact test, p = 0.37). There were two major bleedings, one in the LMWH group and one in the OA group. Eleven patients died, 5 (5.1%) in the LMWH group and 6 (6.3%) in the OA group. It is concluded that nadroparin in a dose of 85 anti-Xa IU/kg s.c. once daily provides an effective and safe alternative to oral anticoagulants in the secondary prophylaxis of DVT.

Acenocoumarol↗
PubMed1996

[Comparative study of the stability of oral anticoagulant treatments (warfarin vs acenocoumarol)].

PURPOSE: To compare the stability of the effect of two oral anticoagulants, one of them (acenocoumarol) with a short half life and the other one with a long half life (warfarin) in patients in the stable phase of treatment (at least 2 months with treatment before entering the study). PATIENTS AND METHODS: During a year period (January-December 1993) a comparative study of two groups of 53 patients each was performed: group 1 patients were treated with warfarin and group 2 with acenocoumarol. Both groups were paired with respect to age, sex, diagnosis for anticoagulant therapy and desired therapeutic range (INR 3-4.5). The mean value of controls per patient, the dosage changes, the evolutive controls and the incidence of haemorrhagic and thromboembolic episodes were studied. RESULTS: The controls performed in group 1 were 728 in total with a mean value of 13.74 per patient and 800 in group 2 with a mean value of 15.09 per patient. A change in the dosage was performed in 214 controls in patients of group 1 and in 269 of group 2. Seventeen patients had 38 haemorrhagic episodes (2 major and 36 minor) in group 1, and 6 of group 2 had 20 episodes (2 major and 18 minor). Significant differences were observed in the mean value of controls (p = 0.04), the evolutive controls (p < 0.001), the global incidence of haemorrhages (p = 0.008) and incidence of minor ones (p = 0.006). No significant differences in dosage were observed. In both groups no thromboembolic episodes during the period of study were reported. CONCLUSIONS: Anticoagulant treatment with warfarin is more stable than with acenocoumarol. The total controls and the mean value of controls per patient are decreased. Nevertheless with warfarin we have observed a greater incidence of haemorrhagic episodes.

Adult↗
PubMed2000

Bleeding risk factors in chronic oral anticoagulation with acenocoumarol.

We studied major bleeding complications, death related to hemorrhage, and tried to identify predisposing factors for bleeding in outpatients treated with acenocoumarol. We evaluated 811 outpatients attending a specialized anticoagulant therapy unit. The intended INR range was 3.5-4.5 for mechanical heart valve replacement (N= 384) and 2.0-3.0 for other indications (N= 427). The variability of INR for the total follow-up and the 2 months before the hemorrhage was calculated. The total follow-up was 1,963.26 years with 27,321 control tests. We observed 47 major bleeding episodes, including 2 fatal (central nervous system hemorrhages), in 37 patients. 49.5% of the patients had underlying diseases. The rate of major and fatal hemorrhage was 2.39 and 0.10 episodes per 100 patients year, respectively. Hemorrhagic complications were more frequently observed in patients with a more intense intended range (8.2% in the INR 3.5-4.5 group vs. 1.5% in the 2.0-3.0 INR group). The risk of major bleeding increased in patients with an achieved INR higher than 6 and in those with higher INR variability during follow-up. The estimated probability of bleeding also increased with time: it was 0.102% at 78 months, and at the beginning of therapy it was 0.006% and 0.007% at 1 and 4 months, respectively. The intensity of anticoagulation and the deviation of the INR from the target are the most important risk factors for bleeding in patients taking acenocoumarol. Monitoring the variability of INR can help identifying patients predisposed to bleeding. However, the screening for underlying disease should always be performed.

Acenocoumarol↗
PubMed1977

Determination of acenocoumarol in plasma and urine by double radioisotope derivative analysis.

Acenocoumarol, to which a 14C-labeled internal standard has been added, is extracted at pH 4 into ethyl acetate-heptane (20:80 v/v), back-extracted into aqueous sodium hydroxide solution after solvent washing with a pH 7 buffer, and reextracted after acidification in the solvent mixture. It is then acetylated with 3H-acetic anhydride. The acenocoumarol acetyl derivative is separated from the metabolite derivatives by TLC, and its radioactivity is measured. The method is specific and sensitive to a concentration of 8 ng/ml.

Acenocoumarol↗
PubMed1988

[Observation of acenocoumarol-induced granulocytosis].

A male patient had been treated with acenocoumarol for 9 years. Raised white cell count returned to normal, when acenocoumarol was substituted by heparin, but rose again after reexposure. An analysis of variance showed that this effect is mediated by neutrophils only. The rise is quick and may therefore be caused by a redistribution of white cells rather than by increased cell production.

Acenocoumarol↗
PubMed2004

Acenocoumarol stabilization is delayed in CYP2C93 carriers.

OBJECTIVE: Our objective was to assess whether there is an association between the presence of allelic variants of the gene for cytochrome P450 (CYP) 2C9 and anticoagulation problems during the initial 3 to 6 months of acenocoumarol treatment. METHODS: A prospective follow-up study was performed at 2 anticoagulation clinics in the Netherlands. Included subjects started with a standard dose regimen as follows: 6 mg on the first day, 4 mg on the second day, and 2 mg on the third day. CYP2C9 genotypes were assessed, and data on international normalized ratio (INR), comedication, and comorbidity were collected. RESULTS: The CYP2C9 genotype of 231 subjects was assessed. Of these, 147 (63.6%) were wild-type subjects (CYP2C9*1/*1), 38 (16.5%) were carriers of CYP2C9*2, and 46 (19.9%) were carriers of CYP2C9*3. Compared with wild-type subjects, carriers of the CYP2C9*3 allele had (1) a lower chance to achieve stability in the first 6 months of therapy (hazard ratio, 0.62; 95% confidence interval, 0.42-0.91; P <.05) and (2) an increased risk of severe overanticoagulation (INR >6.0) (hazard ratio, 3.80; 95% confidence interval, 1.54-9.39; P <.01). For both outcomes, there was no significant difference between carriers of the CYP2C9*2 allele and wild-type subjects. CONCLUSION: In carriers of the CYP2C9*3 allele more difficulties in terms of stabilization and overanticoagulation were found as compared with wild-type subjects or CYP2C9*2 carriers. CYP2C9 genotyping could be useful to identify potential candidates for more frequent INR controls to minimize problems with acenocoumarol anticoagulation status.

Acenocoumarol↗
PubMed2001

[Risk factors of a new cardio-embolic cerebral accident in non-valvular atrial fibrillation treated with acenocoumarol].

OBJECTIVES: To investigate the risk factors determining the appearance of a new cardio-embolic cerebral accident on secondary thrombophylaxis of non-valvular auricular fibrillation (NVAF). DESIGN: Controlled observational study on a series of patients treated with acenocoumarol for a period of 2.8 years. SETTING: Anticoagulation Unit of the La Paz Hospital and patients from Madrid Area 5. PARTICIPANTS: 172 patients with NVAF, over 55 and with fibrillation for at least a year, and who had suffered at least one ischaemic cerebral accident. All were treated with acenocoumarol and controlled at an INR of 2.5. The risk factors were determined and the appearance of new cardio-embolic phenomena was watched during the study period. MEASUREMENTS AND MAIN RESULTS: 12 cardio-embolic phenomena were recorded (11 CVA and one peripheral embolism). The univariate study showed there was a significant association between patients who suffered a new ictus and those who suffered heart failure (p < 0.05) and had a history of more than one ictus before the start of the study (p < 0.05). Multivariate analysis found that what had independent predictive value was having suffered more than one ictus. CONCLUSIONS: The greatest threat for developing a new ischaemic CVA during anticoagulation in NVAF is having a history of two or more previous ictus, as if the tendency to recur was due to these patients having more extensive atherosclerosis.

Acenocoumarol↗
PubMed2002

[Acenocoumarol (Sintrom) and fluinidione (Previscan) in pediatrics after cardiac surgical procedures].

PATIENTS AND METHODS: Between 1997 and 2001, 150 children (one month to 16 years of age) were treated with oral anticoagulants after cardiac surgery (Fontan's operations and congenital heart diseases without valvulopathy: 62%, valvular prosthesis: 20%, arrhythmia: 4.6%, thrombosis: 4%, other: 9.4%). They were first treated by either unfractionated heparin (49%) or nadroparin (51%), then by acenocoumarol (n1 = 114) or fluindione (n2 = 36) until steady state. RESULTS: The retrospective analysis of data (age, body weight, international normalized ratio, loading and maintenance doses, time to achieve the steady state) led to the building of a dosage nomogram usable in pediatrics. CONCLUSION: We demonstrated that the mean maintenance dose depended on age and weight. After three years, that dose (mg/kg) was getting close to adult values; it was higher before three years of age, especially before 12 months (p < 0.01), and very variable from a child to another. The recommended loading dose should be as close as possible to the effective maintenance dose: within that cohort, about 0.14 and 0.05 (acenocoumarol) or 1.1 and 0.40 mg kg-1 day-1 (fluindione), before 12 months and after three years respectively.

Acenocoumarol↗
PubMed2004

Acenocoumarol associated priapism: report of a case.

We report on a 20-year-old man presenting with priapism while receiving oral acenocoumarol for the treatment of deep vein thrombosis. To the authors' knowledge, it is the first reported case of acenocoumarol-associated priapism.

Acenocoumarol↗
PubMed2001

Drug interactions as a cause of overanticoagulation on phenprocoumon or acenocoumarol predominantly concern antibacterial drugs.

BACKGROUND: The risk of hemorrhage when coumarin anticoagulants are used sharply increases when the international normalized ratio (INR) is > or = 6.0. Such overanticoagulation may be caused by drug interactions. We performed a case-control study among previously stable outpatients of an anticoagulation clinic using phenprocoumon or acenocoumarol to identify changes in the use of potentially interacting drugs related to overanticoagulation. METHODS: Three hundred case patients with INR values > or = 6.0 were compared with 302 randomly selected matched control subjects with INR values within the target zone. Information on changes in the use of 87 potentially interacting drugs in the 4 weeks before the index day was collected by interviewing patients and by reviewing the anticoagulant medical record. RESULTS: Forty-five potentially interacting drugs were not used in the 4-week study period, and only 15 drugs were used by at least 10 patients. For a number of drugs, too few patients had a relevant change in use to judge their association with overanticoagulation. A course of a combination product of sulfamethoxazole and trimethoprim strongly increased the risk of overanticoagulation (adjusted odds ratio, 24.2; 95% confidence interval [CI], 2.8 to 209.1; population attributable risk percentage [PAR%], 5.7%), especially in patients receiving acenocoumarol. Penicillins were associated with a risk of overanticoagulation of 2.4 (95% CI, 1.00 to 5.5); the corresponding PAR% was 3.4%. The effect was confined to amoxicillin (INN, amoxicilline) plus clavulanic acid. CONCLUSION: Drug interactions as a cause of overanticoagulation predominantly concerned antibacterial drugs. If possible, the use of sulfamethoxazole-trimethoprim and amoxicillin plus clavulanic acid should be avoided in patients receiving coumarins. If there is no therapeutic alternative available, increased monitoring of INR values is warranted to prevent overanticoagulation and potential bleeding complications.

Acenocoumarol↗
PubMed2003

Early overanticoagulation with acenocoumarol due to a genetic polymorphism of cytochrome P450 CYP2C9.

We report the case of a young healthy woman who presented an early overanticoagulation when receiving acenocoumarol for a first thromboembolic episode. The patient had none of the risk factors known to influence the response to the coumarinic derivative except that she carried the rare *3 allelic variant of the cytochrome P450 CYP2C9 in a homozygous status. This case illustrates the role of the *3 polymorphism of the cytochrome P450 CYP2C9 as an independent risk factor modulating the sensitivity of patients to the anticoagulant effect of acenocoumarol. The usefulness of CYP2C9 genotyping before starting coumarinic treatments is discussed.

Acenocoumarol↗
PubMed2001

Early acenocoumarol overanticoagulation among cytochrome P450 2C9 poor metabolizers.

Cytochrome P450 2C9 (CYP2C9) is the enzyme that terminates the anticoagulant effect of warfarin. The heterozygous carriers of the two allelic variants CYP2C9*2 and CYP2C9*3 have been associated with impaired warfarin metabolism and a higher risk of haemorrhage. Only three CYP2C9 poor metabolizers (CYP2C9*3/CYP2C9*3) initiating warfarin treatment have so far been identified, all of them with a dramatic overdose occurring a few days after treatment initiation. Acenocoumarol, another coumarinic anticoagulant, has recently been shown to be metabolized by CYP2C9. We report, for the first time, two cases of dramatic overanticoagulation occurring in patients starting acenocoumarol treatment while taking recommended doses (4 mg/day). In both cases, the overdose was discovered at the first INR control with values above 9. Genotyping revealed that the two patients were homozygous for the CYP2C9*3 allele. Our report highlights the need for CYP2C9 genotyping before starting oral anticoagulants in order to prevent early overanticoagulation episodes.

Acenocoumarol↗
PubMedDate not supplied

A prospective controlled study of a computer-assisted acenocoumarol dosage program.

The increase in oral anticoagulant (OA) treatment has led to development of new strategies for its control. We tested the efficacy of the GAO software (Dade Behring) in providing adequate acenocoumarol dosages for patients whose international normalised ratios (INRs) were no more than 0.5 points out of range. From December 1998 to August 1999, all outpatients in this setting were randomly assigned to receive computer-generated or traditionally fixed OA doses. Patients in their first 4 weeks of treatment were excluded. Overall, 8352 dosages were calculated by the computer and 7586 by the medical staff. The main endpoint of the study was the time spent in target INR range. The computer matched the traditional dosing, achieving a small but statistically significant greater efficacy in maintaining patients within the INR target range. The percentage of INR determinations over 5.5 was very low in both groups. Our results validate the computerised acenocoumarol dosing in our centre, achieving at least similar levels of effectiveness and safety compared with traditional dosage by medical staff.

Acenocoumarol↗
PubMed1993

Probable acenocoumarol-amoxycillin interaction.

We present the case of a woman undergoing treatment with acenocoumarol for deep vein thrombosis, who maintained an international normalized ratio (INR) of between 2.5 and 4 for 2 months. Seven days after the introduction of amoxycillin (500 mg/8 h) for a probable respiratory infection, the patient developed spontaneous bruising, with an INR of 7.1. Treatment with amoxycillin was discontinued, and 3 weeks later the INR had returned to previous values. In this case, the increase in the INR value with associated bruising after the addition of amoxycillin suggests a drug interaction between acenocoumarol and amoxycillin, other possible causes having been eliminated.

Acenocoumarol↗