Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACENOCOUMAROL”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources
PubMed2000

[Acute necrotizing hepatitis: an unusual side effect of oral anticoagulants].

We report the case of a severe relapsing phenprocoumon-induced hepatitis. The first episode of hepatitis was thought to be caused by another drug (Verapamil). The anticoagulation with Phenprocoumon was therefore continued after healing of liver inflammation. The relapse typically developed after a shorter exposition-time supporting the hypothesis of an allergic etiology. Fortunately we didn't find any cross-reaction between Phenprocoumon and Acenocoumarol. The patient could thus be anticoagulated orally without complications. If long term anticoagulation is absolutely essential, it is reasonable to prescribe a different Coumarin-derivate. In the case of a cross-reaction, the therapy should be continued with low-molecular weight heparin.

Administration, Oral↗
PubMed1976

Suicide with aprindine and digoxin.

A 48 year old man with severe coronary artery disease died approximately 33 hours after swallowing unknown amounts of aprindine, digoxin, furosemide, acenocoumarol, flurazepam, nitrazepam and lorazepam. Blood analysis carried out 40 min. before death showed no hydric or ionic imbalance; blood gases were normal. Serum digoxin concentration was 3.9 ng/ml; plasma concentration of aprindine was 2.5 mug/ml and plasma concentration of desethylaprindine was 386 ng/ml. Patient was profoundly comatose, hypotensive, and the electrocardiogram showed broad and bizarre QRS complexes; patient ultimately died in irreversible secondary ventricular fibrillation and asystole. Aprindine probably played a decisive role in the fatal outcome of this complex drug intoxication.

Aprindine↗
PubMed2001

Costs of outpatient anticoagulant treatment in patients with cerebral and peripheral arterial occlusive disease.

BACKGROUND AND OBJECTIVE: Knowledge of the costs of oral anticoagulant (AC) treatment may be relevant for resource allocation. Also, the incremental costs may be compared with other treatments for health care policy decisions. In this report, we have assessed actual costs of anticoagulant therapy in anticoagulation clinics (AC-clinic) in three different settings in the Netherlands. METHODS: Costs of anticoagulant drug supply and costs as a result of INR-adjustment procedures were estimated. We compared the total costs of treatment in patients treated after minor cerebral ischaemia in the Stroke Prevention in Reversible Ischemia Trial (SPIRIT) and in patients treated because of peripheral arterial occlusive disease in the Dutch Bypass Oral anticoagulants or Aspirin Trial (BOA). RESULTS: Costs of monitoring ranged between Euro 6.44 and Euro 9.87 per visit for monitoring at the AC-clinic and at home, respectively. The annual costs of administering anticoagulant drugs ranged between Euro 83 (phenprocoumon) and 107 (acenocoumarol). Variation in the overall actual annual costs of AC treatment was caused by the number of monitoring visits, the distribution of home and clinic visits and, to a lesser extent, the medication used. Annual costs of AC therapy for patients in SPIRIT was Euro 239 and for patients in BOA Euro 312. Overall costs of anticoagulant therapy were about 3 to 4-fold higher than standard treatment with aspirin. CONCLUSIONS: Although the actual costs of anticoagulant therapy may be substantially higher than that of other antithrombotic therapies, its cost-effectiveness depends highly on efficacy.

Aged↗
PubMed2001

Pharmacokinetic evaluation of recombinant, activated factor VII in patients with inherited factor VII deficiency.

BACKGROUND AND OBJECTIVES: Recombinant factor VIIa (rFVIIa) has been widely used in the treatment of bleedings occurring in hemophiliacs with inhibitors. Very few reports exist on the use of rFVIIa in patients with inherited FVII deficiency. Pharmacokinetic studies on rFVIIa have been performed exclusively in hemophiliacs, patients with cirrhosis or volunteers pretreated with acenocoumarol. The aim of this study was to evaluate the kinetics of rFVIIa in patients naturally deficient of FVII. DESIGN AND METHODS: A single dose kinetic study with rFVIIa was performed in 5 patients affected by severe congenital deficiency of factor VII in order to evaluate the true kinetic parameters of rFVIIa without the interference of FVII. Two dosages, 15 and 30 microg/kg, were used in a crossover schedule. FVII:C and FVIIa concentration/time curves were analyzed by a model-independent method. Antithrombin (AT), prothombin fragment 1+2 (F1+2) and tissue factor pathway inhibitor (TFPI) were assayed. RESULTS: No differences emerged between the dosages with respect to dose-independent parameters [total body clearance (CL), volume of distribution area (VdArea), mean residence time (MRT)]. No significant changes of AT, TFPI, and F1+2 were observed. Comparing the results with those of other studies performed in adult hemophiliacs, in patients affected by cirrhosis or in volunteers on oral anticoagulant therapy (OAT), CL and VdArea of rFVIIa were definitely higher and in vivo recovery was lower. INTERPRETATION AND CONCLUSIONS: These findings suggest that the kinetics of rFVIIa are not dose-dependent. In the absence of FVII, the changes of VdArea and CL may be in agreement with a mechanism of competition between FVII and rFVIIa for tissue factor binding.

Adult↗
PubMed2000

[Thrombectomy in a patient with a mobile clot in the inferior vena cava--case report].

Switching from heparin to acenocoumarol was complicated by severe retroperitoneal bleeding in a 50-years old patient with massive pulmonary embolism and deep venous thrombosis. The haematomas were evacuated by surgical procedure. Planned insertion of a vena cava filter was abandoned because of a mobile clot in inferior vena cava (IVC) reaching above renal veins as evidenced by spiral computed tomography (SCT). Patient was transferred to the Surgical Department of Medical Academy in Warsaw where thrombectomy was performed. In spite of mechanical and pharmacological methods of venous thrombosis prophylactic, thrombectomy was complicated by massive proximal deep venous thrombosis of right leg and distal part of IVC. Patient was successfully treated with UFH i.v. followed by low molecular weight heparins. No bleeding complications were observed. Screening for thrombophilia and cancer were negative. This case report is an example of difficulties in clinical management in a patient who has both life-threatening thromboembolic disease and bleeding.

Heparin, Low-Molecular-Weight↗
PubMed2000

[Recombinant hirudine in suspected heparin induced thrombocytopenia--case report of pulmonary embolism].

A case of 68 years old women suffering from chronic anemia, myelodysplastic syndrome and treated with progestogen due to endometrial hypertrophy is presented. Initially she was admitted to a regional hospital because of progressive weakness and exertional dyspnea. Three months earlier she reported an episode of acute dyspnea and chest pain. On the basis of clinical symptoms and perfusion lung scintigraphy pulmonary embolism (PE) was diagnosed. Patient received i.v. heparin which was changed to s.c. nadroparine subcutaneously. Platelet count dropped to 55,000'/ml on fifth day of treatment from initial level of about 200,000'/ml. Heparin induced thrombocytopenia was diagnosed, heparin was stopped and ticlopidine was recommended. After 3 weeks symptoms suggesting recurrent PE were observed. The patient was transferred to National Tuberculosis and Lung Diseases Research Institute. Recombinant hirudine (Refludan) was administrated (bolus 0.4 mg/kg and initial dose of infusion 0.1 mg/kg/h) overlapping with acenocoumarol from second day. Dose of r-hirudine was adjusted to achieve APTT prolongation 1.5 to 2.5 times of mid-normal range. During treatment with r-hirudine no bleeding and new thromboembolic complications occurred. Platelets count remained within normal range. After 14 days clinical improvement was observed, though symptoms of right ventricular overload and hypoxemia were still present after 6 months of treatment with oral anticoagulants suggesting chronic thromboembolic pulmonary hypertension.

Aged↗
PubMed2001

[Atrial fibrillations: daily occurrence possibly leading to embolism in an extremity].

A 64-year old woman had been tired and short of breath for the previous few months. During the past few days she had experienced disruptions in the movement and feeling of the right arm and both feet as well as a loss of strength and a heavy feeling in her right leg. Due to atrial fibrillation she had recently started using digoxin and due to possible arterial embolisms in the extremities she had recently started using acenocoumarol. Further investigations revealed one large thrombus in the left atrium, two large thrombi in the left auricle and a serious constriction in the right iliac artery. The thrombi were treated with heparin and oral anticoagulants; the ischaemia which probably occurred as a result of this was successfully treated with embolectomy. After the cardiac thrombi had disappeared, the patient was electrically converted to sinus rhythm. One month later, the patient was still in sinus rhythm and her clinical picture had improved. As she does not feel the atrial fibrillation, she will be permanently maintained on oral anticoagulants. In patients with atrial fibrillations, the possibility of an embolisation towards the extremities deserves serious consideration.

Anticoagulants↗
PubMed2001

Characteristics of anticoagulant therapy and comorbidity related to overanticoagulation.

The risk of hemorrhage when using coumarin anticoagulants sharply increases when the International Normalised Ratio (INR) is > or =6.0. We performed a prospective cohort study with a nested case-control design among 17,056 outpatients of an anticoagulation clinic to determine the incidence of overanticoagulation and to study the association between overanticoagulation and characteristics of anticoagulant therapy and comorbidity. The incidence rate of an INR > or =6.0 was 7.8 per 10,000 treatment days in prevalent users on the starting date and 22.5 per 10,000 treatment days in incident users during the study period. 300 cases with an INR > or =6.0 were compared with 302 randomly selected matched controls with an INR within the target zone. Patients on acenocoumarol had an increased risk of an INR > or =6.0 compared to patients on phenprocoumon. Regarding comorbidity, impaired liver function, congestive heart failure, diarrhea and fever were risk factors for overanticoagulation. Increased monitoring of INR values if risk factors are present or avoidance of risk factors could prevent excess anticoagulation and potential bleeding complications.

Aged↗
PubMed1985

Electroconvulsive Therapy During Anticoagulant Therapy.

The safety of ECT in patients receiving anticoagulants is reviewed. In patients who failed to respond to drug therapy and in some whose cardiovascular conditions precluded the use of antidepressant drugs, the authors successfully carried out five courses of ECT in depressed patients maintained on anticoagulants. In three cases, heparin was used, blood coagulation values were closely monitored, and the dose of succinylcholine employed was increased to provide almost complete muscular paralysis during the seizure. In one patient, acenocoumarol was sustained. The authors conclude that ECT may be safely administered in the presence of anticoagulant drug therapy.

Journal Article↗
PubMed2003

[Excess antivitamin K in elderly hospitalised patients aged over 70. A one-year prospective survey].

INTRODUCTION: Antivitamin K treatments (AVK) are related to increased morbidity and mortality, notably in elderly patients. The International Normalized Ratio (INR) should be well controlled and its stabilisation within the therapeutic range help to prevent the haemorrhagic complications. METHODS: A one-year prospective survey on all the cases of excess AVK was conducted in hospitalised patients aged over 70. RESULTS: During the study period, 225 hospitalised patients treated with AVK (mean age 84 years) were identified: 62% received warfarin, 19% fluindione, 8% acenocoumarol and 11% received several successive AVK. During this period, 1.904 INR measurements were recorded: 97 (5.1%) were > or =5.0 and 12 (0.63%) were > or =9.0. In all, 59 patients (23.1%) exhibited one or several episodes of excess AVK (INR > or =5.0) and 57 exhibited a target INR of 2.5. Three patients died of accidental haemorrhage--two of them due to intra-cerebral bleeding--among the 59 patients with excess AVK. In three cases, the INR was greater than 7.0 at the time of the accident. DISCUSSION: In half of the cases of excess, the episode occurred during the month following initiation of treatment with AVK. In nearly two thirds of cases, a change had been made in drug therapy in the 10 days preceding the excess, with the prescription of a drug enhancing the effect of the AVK: anti-infection agents (antibiotics and anti-fungals) and amiodarone were the drugs most frequently involved. Oral or intravenous vitamin K1 was administered in only 19% of cases. CONCLUSION: In very old patients treated with oral anticoagulants, certain risk factors must be identified: the initiation period of treatment, the occurrence of an intercurrent disease and the subsequent change in the drug therapy. INR monitoring should be intensified in order to detect any excess and, if detected, ensure the optimal management of the patient.

4-Hydroxycoumarins↗
PubMed2003

[Bradycardia-tachycardia syndrome during spinal anesthesia].

A 78-year-old man developed bradycardia with decreased level of consciousness followed by sinus arrest during femoropopliteal bypass surgery under subarachnoid anesthesia. Early in the recovery period, a similar clinical picture developed, with bradycardia but no change in level of consciousness. Sinus node automaticity or sinoatrial conduction abnormalities were suspected, and a 24-hour Holter electrocardiogram revealed bradycardia-tachycardia syndrome. The patient was prescribed amiodarone and anticoagulant therapy with acenocoumarol; no further episodes occurred during hospitalization. Bradycardia-tachycardia syndrome is a sinus node disorder that manifests intermittently. It can become apparent during or shortly after surgery, leading to problems of differential diagnosis.

Aged↗
PubMed2004

Management of coumarin-associated coagulopathy in the non-bleeding patient: a systematic review.

BACKGROUND AND OBJECTIVES: Excessive anticoagulation is a frequent complication of anticoagulant therapy. The risk of hemorrhage approximately doubles for each one point increase in the International Normalized Ratio (INR) above 3.0. Reducing a prolonged INR to within the desired therapeutic range requires that oral anticoagulants be withheld. In addition, vitamin K may be administered. Since this latter treatment can produce rapid reductions in the INR, it must be carefully tailored to meet individual needs, balancing the risk of bleeding against the potential risk of causing thromboembolism. METHODS: To review available literature on the management of coumarin-associated coagulopathy in asymptomatic patients, a Medline search was carried out and papers published in English from 1966 and 2003 were identified. All available information on the management of asymptomatic patients presenting with coumarin-associated coagulopathy was analyzed. RESULTS: Following the results of clinical studies that only used an elevated INR as a surrogate end-point for the risk of bleeding, low dose oral vitamin K appears as the preferable strategy for rapidly restoring therapeutic INR levels in asymptomatic patients who present with an excessively prolonged INR due to warfarin therapy. For the treatment of patients with asymptomatic acenocoumarol-induced coagulopathy, vitamin K does not add any benefit to the strategy of simply withholding oral anticoagulant treatment. INTERPRETATION AND CONCLUSIONS: Large randomized trials using clinical end-points are now required to provide evidence-based treatment recommendations for patients with coumarin-associated coagulopathy.

Anticoagulants↗
PubMed2004

[Periorbital swelling caused by carbasalate calcium].

A 61-year-old man presented with visual problems due to a marked two-sided periorbital swelling that had started three years earlier. There was no obvious underlying cause and he had persistent rhinoconjunctival symptoms. At the time the swelling started he was already suffering from xanthelasmata palpebrarum and chronic obstructive pulmonary disease. He had been taking simvastatin and salmeterol-fluticason for a year and carbasalate calcium for two years. There was marked periorbital swelling accompanied by xanthelasmata palpebrarum and slight chemosis and erythema of the eyelids. After exclusion of other potential causes for the swelling, acenocoumarol was prescribed in place of carbasalate calcium. This resulted in a quick recovery from the swelling and rhinoconjunctival symptoms. Provocation with acetyl salicylic acid led to renewed swelling of both eyelids. Periorbital angio-oedema, a relatively uncommonly reported side effect of acetyl salicylic acid and its derivates, can occur even after previous long-term medication use.

Aspirin↗
PubMedDate not supplied

Efficacy and safety of oral amiodarone in controlling heart rate in patients with persistent atrial fibrillation who have undergone digitalisation.

INTRODUCTION: Oral amiodarone has been suggested by some authors for rate control in patients with persistent atrial fibrillation. In this study we evaluated the efficacy and safety of oral amiodarone versus placebo for rate control during exercise and daily activities in patients with chronic atrial fibrillation who had undergone digitalisation. METHODS: The study group consisted of 53 patients (35 men, mean age 65 +/- 9 years) with persistent atrial fibrillation (mean duration 17 +/- 7 months). All patients had therapeutic levels of digitalis and were under anticoagulation treatment with acenocoumarol. Twenty-eight of them were treated with amiodarone (200 mg per day orally) and 25 received placebo. All patients were assessed with 24-hour ECG monitoring, a maximal symptom-limited cardiopulmonary exercise test and evaluation of adverse events. RESULTS: The mean exercise duration was similar in both groups. Amiodarone produced a lower heart rate than placebo at all exercise levels (p<0.0001 for all). VO2 was similar in both groups whereas O2 pulse was higher in the amiodarone group at all exercise levels. During daily life, heart rate showed a significant circadian pattern in both groups, with higher values during the day than at night (time effect for both p<0.001). The mean value of heart rate under amiodarone was lower than for placebo (75 +/- 10 vs. 86 +/- 12/min, p<0.001) but this difference was due to a significant difference during the day (p<0.001) that was not present during the night (p =0.48). CONCLUSIONS: Oral amiodarone is very effective when combined with digoxin for control of heart rate in patients with chronic atrial fibrillation and it should be considered as an alternative treatment when more traditional drugs, such as Ca(+2) inhibitors or b-blockers have proven ineffective or are contraindicated.

Aged↗
PubMed2006

[Pharmacogenetics and interindividual variability in drug response: cytochrome P-450 2C9 and coumarin anticoagulants].

Pharmacogenetics, a discipline still in its infancy, is the study of genetically determined variations in how individuals respond to drugs. Mutations may affect drug metabolism, transmembrane transport into cells, or target receptors. Genetic polymorphisms affecting drug metabolism were the first to be identified. Genetic factors control the activity of phase I reactions involving cytochrome (CYP) P450 isoenzymes. Three CYP families catalyze drug metabolism in humans. Their genes have been identified and polymorphisms have been described in various populations, leading to either high activity ("extensive metabolizer" phenotype) or low activity ("poor metabolizer" phenotype). The CYP2C9 polymorphism illustrates the potential clinical importance of pharmacogenetics. This enzyme catalyzes the metabolism of the coumarinic oral anticoagulants acenocoumarol and warfarin. The homozygous mutant genotype CYP 2C9 *31*3, present in 0, 7% of Caucasians, leads to low enzyme activity and thus to the accumulation of these drugs in the body; this in turn increases the anticoagulant activity and induces a higher risk of bleeding. In three clinical studies of patients and healthy volunteers, we found that this CYP2C9 *3 mutant allele was responsible for 14% of the variability in the response to these drugs. Then, by studying the genetic polymorphism of the receptor site of oral anticoagulants--the vitamin K epoxide reductase multiprotein complex--we showed that a combination of the two genetic variants (CYP2C9 and the receptor site) was responsible for 50% of the variability. These data suggest that patients who have both genetic polymorphisms could be at an increased risk of bleeding during oral anticoagulant therapy.

Aryl Hydrocarbon Hydroxylases↗
PubMed1965

[Effect of the activity of an indirect anticoagulant by a monoamine oxidase inhibitor].

The combinations of some anticoagulants (phenindione, chlorphenadione, diphenadione, phenprocoumon, 3-[1-(p-chlorophenyl)propyl]-4-hydroxycoumarin, cumachlor and acenocoumarol) with MAO-inhibitors (phenylcyclopropylamino hydrochloride, isocarboxazid, iproniazid, nialamide and p-chloro-N'-[2-(isopropylcarbamoyl)-1-methylethyl]benzohydrazide) were investigated with regard to modification of the anticoagulant activity in the rat. The activity of some anticoagulants like phenindione may be enhanced by the addition of MAO-inhibitors, whereas others (chlorphenadione, phenprocoumon) are only slightly or not at all influenced. The MAO-inhibitors phenylcyclopropylamino hydrochloride and nialamide show enhancement of activity in most combinations whereas iproniazid never does. The other MAO-inhibitors lie between these two extremes.

Animals↗
PubMedDate not supplied

A computerized regulation of dosage in oral anticoagulant therapy.

The results of a cooperative study on the quality of treatment of patients with prosthetic heart valves (PHV) on long-term oral anticoagulants (OA) are reported. The study was carried out on 695 patients bearing PHV (with an overall 8,340 checks carried out in 1988) through a computer-assisted system for monitoring the laboratory and treatment follow-up. The specifications of the software are described in detail in the text. The mean INR slightly differed in the two participating centers (Rome and Parma) (3.25 vs 3.19) as did the weekly mean dosage (18.2 vs 20.7 mg) of oral anticoagulant, which was always Acenocoumarol. More than 70% of the checks were within the range in both centers as evaluated by a check randomly chosen once a month for each single patient. Considering the whole bunch of data, about 80% of the patients had greater than 50% of their checks within the therapeutic range and more than 30% had greater than 75% of the checks within the range. This study demonstrates that the availability of a computerized program for monitoring oral anticoagulant therapy allows to perform multicenter studies and to obtain data which can improve the quality of treatment of patients on OA.

Administration, Oral↗
PubMed1988

[Risk of thrombosis in irradiation of uterine cancer. A review with new results of studies].

Malignomas of the uterus predispose to thromboembolism. Local application of radium increases the activation of hemostasis. In newer examinations there are hints, that impairment to thrombocyte function and prostacyclin metabolism may have a pathogenetic meaning. Thrombocyte aggregation and prostacyclin sensitivity of thrombocytes have been examined in two groups of patients: 21 patients following hysterectomy because of endometrium cancer stage I, treated with one vaginal application for the vaginal cuff and 10 patients with cervical carcinoma Stage IIa-IIIb treated combined intrauterine-intravaginally. The first group was prophylactically treated with low-dose-heparin, the second one with acenocoumarol (Sintrom). A slight, but significant increase of thrombocyte aggregation by 4.8 per cent respectively 5.0 per cent could be observed in both groups. Prostacyclin sensitivity of thrombocytes (PST) was significantly reduced by 20 per cent before irradiation in all patients compared with patients without carcinomas. In cases of intravaginal radium application we saw immediately after removal of the radioactive source a further reduction of PST by 12.5 per cent. 24 hours later a significant decrease of PST by 18.5 per cent could be observed. Contrary to this no significant changes were induced by combined intrauterine and intravaginal radium insertion. Therefore reduction of PST may be interpreted as a possible change of thrombocyte function in vivo caused by irradiation. It may be likely that these disturbances of thrombocyte function combined with radiogenic vessel wall damages and plasmatic hypercoagulability are responsible for the high thromboembolic risk of radium therapy. These patients should be treated prophylactically. Probably the efficiency of this prophylaxis can be improved by additional application of selective inhibitors of thrombocyte aggregation or inductors of prostacyclin synthesis.

Brachytherapy↗