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PubMed1983

Plasma hypercoagulability after termination of oral anticoagulants.

The effect of discontinuation of a long term oral anticoagulant therapy with phenprocoumon on blood clotting parameters has been evaluated in patients in a controlled prospective trial. After termination of phenprocoumon the prothrombin time normalized within 15 days and the thrombotest coagulation value within 57 days. Fibrinopeptide A (FPA) increased significantly during the observation period. FPA release in vitro also rose after discontinuation of anticoagulants. In control patients on a phenprocoumon maintenance therapy no alterations of the above mentioned parameters occurred within the same period. The data indicate that plasma hypercoagulability is found in many patients, orally anticoagulated because of myocardial infarction, when the anticoagulant therapy is discontinued.

4-Hydroxycoumarins↗
PubMed1991

[The clinical course of coumarin-induced necrosis].

In three patients painful reddening of a well-circumscribed area of the skin occurred within five days of starting anticoagulant treatment with phenprocoumon (Marcumar), and within a short time it developed into a full-blown picture of coumarin necrosis. The indication for phenprocoumon was, in the first patient (a 29-year-old mother lying-in after her second child had been born) an increased platelet count and the presence of high risk factors for thromboembolism. In the second patient (25-year-old man) and the third one (45-year-old woman) it was secondary prophylaxis after pulmonary embolus and deep-vein thrombosis, respectively. All three patients were very obese and had a drug allergy, as well as other allergies (bronchial asthma in Cases 1 and 2; allergic rhinitis in Case 3). Phenprocoumon was at once discontinued in all three patients and low-dose heparin administration (Cases 1 and 3) or dextran infusion (Case 2: heparin intolerance) started. All three needed excision of the necrotic tissue with grafting to the skin defect. The coexistence of obesity and allergic diathesis may thus present an especially high risk for coumarin necrosis.

Adult↗
PubMed2005

The effect of oral anticoagulation on clotting during hemodialysis.

BACKGROUND: Between 5% and 10% of hemodialysis patients are treated with oral anticoagulants. It is currently unknown whether additional anticoagulation with heparin or low-molecular-weight heparin (LMWH) is needed to prevent clotting during hemodialysis. METHODS: In this prospective, randomized, cross-over study 10 patients treated with oral anticoagulants (phenprocoumon) received either no additional anticoagulation or low dose dalteparin (bolus of 40 IU/kg body weight) before dialysis. Efficacy of hemodialysis was measured by normalized weekly Kt/V and urea reduction rate (URR). Thrombus formation was evaluated by measurement of D-dimer and inspection of air traps and dialyser. RESULTS: The median international normalized ratio (INR) did not differ between both observation periods (phenprocoumon 2.2(2 to 3) vs. dalteparin 2.1(2 to 2.9). The anti-Xa level in dalteparin patients was 0.33 (0.27 to 0.38) IU/mL after 2 hours and 0.16 (0.03 to 0.23) IU/mL after 4 hours of hemodialysis. The median increase of D-dimer was significantly higher in patients without additional dalteparin therapy during hemodialysis (DeltaD-dimer 0.23 microg/mL vs. 0.03 mug/mL) (P= 0.0004). Complete thrombosis of the dialyser membrane occurred in one patient in the phenprocoumon group but in none with combined treatment. The extent of thrombosis in the arterial and venous air trap and dialyser was significantly less in patients with additional dalteparin therapy (P= 0.0014, P= 0.0002, and P= 0.0005, respectively). Weekly Kt/V and URR was similar in both groups. CONCLUSION: Standard oral anticoagulation with an INR between 2 and 3 is insufficient to prevent clotting during hemodialysis. Additional low dose anticoagulation with a LMWH or heparin is necessary to facilitate treatment.

Administration, Oral↗
PubMed2005

A C1173T dimorphism in the VKORC1 gene determines coumarin sensitivity and bleeding risk.

BACKGROUND: A C1173T polymorphism in intron 1 of the VKORC1 gene has been claimed to determine the interindividual variability in the response to vitamin K antagonist therapy (VKA), but it is unknown whether it also influences bleeding risk. We aimed to confirm the relationship between C1173T status and phenprocoumon or acenocoumarol use, and to examine the risk of severe bleeding for the various genotypes. METHODS AND FINDINGS: We studied this in a case-control study of 110 patients who bled during VKA therapy and 220 control patients free of bleeding under the same therapy. To achieve the same target INR, CT genotype and TT genotype control patients required less phenprocoumon (CC genotype 2.9 mg/d [95% confidence interval (CI): 2.6-3.2], CT genotype 2.6 mg/d [95% CI: 2.1-3.1], TT genotype 1.4 mg/d [95 % CI: 1.1-1.7]) or acenocoumarol (CC genotype 3.2 mg/d [95% CI: 2.9-3.5], CT genotype 2.3 mg/d [95% CI: 2.1-2.5], TT genotype 1.7 mg/d [95% CI: 1.3-2.1]) than CC genotype control patients. Compared with CC genotype individuals, carriers of at least one T allele had an increased risk of bleeding in the phenprocoumon users (crude odds ratio = 2.6, 95% CI: 1.2-5.7), but not in acenocoumarol users (crude odds ratio = 1.2, 95% CI: 0.6-2.3). CONCLUSION: These findings encourage taking further steps towards the evaluation of the use of VKORC1 genetic testing for bleeding prevention in individuals who receive VKA therapy.

Acenocoumarol↗
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↗
PubMed2002

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

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.

4-Hydroxycoumarins↗
PubMed1988

4-Hydroxycoumarin oral anticoagulants: pharmacokinetics-response relationship.

The blood coagulating factors II and VII and prothrombin times (Thrombotest) were followed during a dosage interval (= 24 h) in patients on acenocoumarol (n = 6) and on phenprocoumon (n = 6) therapy. The patients were on stable anticoagulation (%TT: 7-13%) for at least 6 months. The study was performed to investigate the concentration-response relationship of the 4-hydroxycoumarin-type oral anticoagulants. The three parameters were stable during the 24-h interval for patients on phenprocoumon therapy. Patients on acenoumarol showed fluctuations in their factor VII levels; peak activities were observed at about 2 h, trough activities at about 16 h after acenocoumarol intake. Factor II and Thrombotest activities were stable. Plasma levels of phenprocoumon were stable during daytime whereas acenocoumarol levels declined exponentially (t1/2 about 12 h). The results indicate the oral anticoagulants to exhibit a concentration-response relationship common to drug-receptor interactions. The results also suggest that for stable and long-lasting anticoagulant therapy oral anticoagulants with half-lives beyond the dosage interval (t1/2 greater than 24 h) should be preferred.

4-Hydroxycoumarins↗
PubMed1985

[Is optimal anticoagulation possible in ambulatory practice? Report on a retrospective 5-year study of a cardiology practice].

In a 5-year retrospective study (1982-1978) in a well defined population of 332 patients (representing greater than or equal to 2140 anticoagulation years) from a heart specialist's practice, the question was studied whether optimum anticoagulation (Quick test between 18-29%, INR 4.0-2.75, Geigy thromboplastin, capillary blood method) with minimum complications could be achieved. In the qualitative study it was found that 75% of Quick determinations were in the optimum range for phenprocoumon, 71.6% for clorindion, 62% for acenocoumarol and 72% for all anticoagulants. 77% of phenprocoumon patients were optimally anticoagulated for more than 3 years. With phenprocoumon there was no difference in intensity of anticoagulation between the oldest and youngest patient groups, as all mean Quick values ranged over 20% (means Q% 1982-1978 = 25, INR = 3.0). It was also shown that after 6 months' anticoagulant therapy it is clearly recognizable whether optimum anticoagulation is feasible or not: at that moment the criteria for halting or continuing anticoagulant therapy can and should be reviewed.

Aged↗
PubMed1980

[Controlled, double blind study of a possible interaction between acemetacin and a concomitant anticoagulant therapy].

In a controlled double blind study, 20 patients undergoing long-term anticoagulant therapy with phenprocoumon received [1-(p-chlorobenzoyl)-5-methoxy-2-methylindole-3-acetoxy]acetic acid (acemetacin, TV 1322, Rantudil) concomitantly to establish whether there was any risk of an interaction. Neither the placebo dose nor the concomitant medication with 3 x 60 mg acemetacin had any statistically important influence on thromboplastin value, fibrinogen, phenprocoumon consumption or platelet aggregation. Accordingly, no clinically relevant interaction is to be expected by the concomitant therapy with 3 x 60 mg acemetacin/d and phenprocoumon, or in all probability, with any coumarin compound.

4-Hydroxycoumarins↗
PubMed1980

Coumarin-associated hepatitis. Report of two cases.

We investigated two cases of recurrent jaundice, both involving repeated exposure to phenprocoumon and suggestive of coumarin-induced hepatitis. The first patient showed the histologic picture of cholestasis during the second bout of jaundice, the other that of chronic aggressive hepatitis. In both patients, the hepatitis appearance disappeared after termination of the first exposure to the coumarin drug, in the first case without additional drug therapy. In the second case, prednisone therapy was instituted when phenprocoumon administration was withdrawn. In both cases, hepatopathy recurred after reexposure to the drug. In one of these patients, and with his consent, a third bout of jaundice was provoked with phenprocoumon.

4-Hydroxycoumarins↗
PubMed2002

The potential interaction between oral anticoagulants and acetaminophen in everyday practice.

OBJECTIVE: The drug-drug interaction between oral anticoagulants (especially warfarin) and acetaminophen has been described, but evidence is conflicting and evidence for a similar interaction between acenocoumarol or phenprocoumon and acetaminophen is limited. Therefore, a study was performed to determine the influence of acetaminophen on oral anticoagulation with acenocoumarol or phenprocoumon in everyday practice. METHOD: Included were patients from two Dutch anticoagulant clinics who had used oral anticoagulants for at least three months and who started with acetaminophen (case group) or benzodiazepines (control group). RESULTS: Fifty-four patients were included who had a first prescription of acetaminophen in their pharmacy record (during oral anticoagulant use) and twenty patients with a first prescription of a benzodiazepine (during oral anticoagulant use). The INR (International Normalized Ratio) difference before and after acetaminophen use was not statistically significant between the two groups and showed no dose dependency. CONCLUSION: These data do not demonstrate that acetaminophen, in the dosages used in everyday practice, has a clinically relevant influence on the INR in patients using acenocoumarol or phenprocoumon.

Acetaminophen↗
PubMed2002

[Complicated antiphospholid antibody syndrome].

HISTORY AND CLINICAL FINDINGS: A 51-year-old female patient suffered from recurrent ischemic strokes and venous thromboembolism although treated with ASS and phenprocoumon, which mainly occurred after diagnosis and treatment of an invasive-ductal mamma carcinoma. The severely ill patient presented with right-sided hemiparesis and dysarthria, a swollen leg, a painful necrotic-ulcerative lesion at the left-lateral ankle and a systolic heart murmur. INVESTIGATIONS: Laboratory data revealed a haemoglobin of 8,4 g/dl, a leucocyte count of 3,1 x 10 (9)/l and a platelet count of 87 x 10 (9)/l. C-reactive protein, ESR and plasma fibrinogen were markedly increased. Levels of antinuclear, IgG-anticardiolipin and anti-doublestranded-DNA antibodies were excessively elevated. A test for lupus anticoagulant was strongly positive. Sonographic examinations showed deep vein thrombosis and significant mitral valve regurgitation. Suspected pulmonary embolism was demonstrated by CT scan. We diagnosed systemic lupus erythematosus with secondary antiphospholipid antibody syndrome (APAS). TREATMENT AND COURSE: Phenprocoumon was stopped and full-dose anticoagulation with low-molecular-weight heparin initiated. Additional immunosuppressive therapy consisted of cyclophosphamide, azathioprin and prednisone resulting in prevention of further thromboembolism and significant improvement of clinical symptoms. The observed severe interference of LA with the prothrombin time after cessation of phenprocoumon (INR 3,6; FII activity 81 %) suggested that the effect of oral anticoagulation had been overestimated in the past. CONCLUSION: APAS may present as an acute and life-threatening disorder. In this case interdisciplinary co-operation and a highly individualised treatment strategy are mandatory.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1977

The influence of age on the response to anticoagulants.

1 A group of 114 patients on long-term anticoagulant therapy was studied. The daily maintenance dose of both phenprocoumon, bishydroxycoumarin and warfarin was found to be significantly lower in patients aged between 61 and 70 years than in the those between 50 and 60 years of age. The mean daily dose of bishydroxycoumarin, hower, when expressed on a weight basis, was not significantly lower in the elderly. 2 For bishydroxycoumarin but not for phenprocoumon and warfarin there was found a statistically significant correlation between the daily maintenance dose and the weight of the patient. 3 The mean daily dose of both bishydroxycoumarin and warfarin was 30-40% lower than that recommended in the literature. 4 'Correction' was made for potential drug interference by excluding patients in continuous medication with order drugs known to influence the treatment with orally administered anticoagulants. The interindividual variation in dosage requirements of coumarin drug was thereby reduced in the age groups above 60 years. 5 The level of vitamin-k dependent coagulation factors, measured by Owren's 'P and P' method (PP%) was significantly lower (P less than 0.001) in patients of advanced age (between 61 and 70 years) than in younger patients (between 50 and 60 years). 6 The plasma concentration of albumin was significantly lower in patients over 60 years than in those under that age. 7 Correlation (P less than 0.01) was found between the daily maintenance dose of phenprocoumon and the plasma concentraction of albumin.

Aged↗
PubMed2005

[Severe intrahepatic cholestasis in a 66-year old male patient with medically treated atrial fibrillation].

A 66-year-old male was admitted to hospital due to painless jaundice. Because of ischemic cardiomyopathy with paroxysmal atrial fibrillation as well as recurrent ventricular tachycardias and fibrillation he was treated with phenprocoumon and amiodarone (200 mg per day) for 2 years. Laboratory tests revealed significant elevation of the parameters of cholestasis and aminotransferase activity. Serological tests excluded infectious, autoimmune or metabolic liver diseases. Abdominal ultrasound and ERCP showed no mechanic cholestasis nor tumor of the pancreas. Cardiac congestive disease was also excluded. Severe intrahepatic cholestasis, consistent with drug-induced hepatotoxic damage, was diagnosed histologically. After discontinuing phenprocoumon the liver enzymes further increased. When amiodarone was stopped, however, laboratory parameters showed a continuous downward tendency. For prevention of malignant cardiac arrhythmia the patient received an atrioventricular defibrillator. Intrahepatic cholestasis is a rare presentation of amiodarone-induced hepatic toxicity. Liver damage can even occur after the drug has been taken for prolonged periods without any problems.

Aged↗
PubMed2002

[Increased thrombocyte activation in dilated cardiomyopathy: a risk factor for development of ventricular thrombosis despite anticoagulant therapy?].

HISTORY AND CLINICAL FINDINGS: A 48-year-old patient with dilated cardiomyopathy complained of dyspnea at rest, severe sleeplessness and a slight pain in the stomach. The clinical examination was normal except for a murmur at the apex of the heart. There was no evidence of edema or congestion of the jugular veins. INVESTIGATION: The echocardiography demonstrated a dilated left ventricle with severely compromised function. No ventricular thrombi were present at this time. Coronary artery disease was excluded by coronary angiography. Endomyocardial biopsies were obtained from the right ventricular septum. The immunohistological analysis of the endomyocardial biopsy specimens revealed pathologically increased lymphocytic infiltrates and increased expression of interstitial and endothelial MHC I and II antigens. Flow cytometric analysis of platelets surface antigens (P-selectin, GP53, thrombospondin) was performed as a measure for intravasal platelet activation. Our patient compared to a healthy control group (> 4 SD) and to other patients with dilated cardiomyopathy (> 2 SD). A high grade increase of platelet activation was found. TREATMENT AND COURSE: ACE inhibitor, diuretics, spironolactone and digitalis were used to treat the heart insufficiency. Due to the severe left ventricular dysfunction phenprocoumone and aspirin were also prescribed. A follow-up echocardiography was performed 6 months later. Comparable to the first examination left ventricular contractility was found to be severely reduced. In addition, a marginal thrombus was now present in the left ventricle despite antithrombotic therapy. DISCUSSION: An increased platelet activation was found in the peripheral circulation of our patient with dilated cardiomyopathy. After 6 months, ventricular thrombi were found in the dilated ventricle, although aspirin and phenprocoumone had been administred. We speculate that an additional thrombotic treatment with clopidogrel is necessary in patients with dilated cardiomyopathy and increased platelet activation.

Anticoagulants↗
PubMed1998

[Long term effects of 50 mg acetylsalicylic acid alone and in combination with dipyridamole on platelet function after coronary bypass surgery].

In a prospective randomized trial in 42 patients undergoing coronary artery bypass surgery, we analyzed the long term platelet inhibiting effects of 50 mg acetylsalicylic acid (ASA) by itself and in combination with dipyridamole (2 x 200 mg), in comparison with phenprocoumon. Three and six months therapy led to significant inhibition of maximum aggregation induced by collagen 1 microgram/ml in platelet rich plasma (PRP) by more than 50% (p < or = 0.05). In PRP stimulated with 5 micrograms/ml collagen maximum inhibition amounted to nearly 20% (n.s.). The groups treated with ASA/ASA + dipyridamole showed an ADP threshold concentration 2.5 times higher than the group treated with phenprocoumon (p < or = 0.05). After stimulation with collagen 1 microgram/ml and 5 micrograms/ml thromboxane B2 synthesis in vitro in both groups treated with ASA was reduced to 1% of the base line values (p < or = 0.01). Inhibition of aggregation in whole blood appeared evident, but was not statistically significant due to considerable fluctuation of measurement. An additional effect of dipyridamole was not detectable. In conclusion, treatment with 50 mg ADA/d results in a lasting, effective inhibition of aggregation of platelets in patients with coronary artery bypass surgery. There is no synergistic effect of additional dose of 400 mg dipyridamole/d.

Anticoagulants↗
PubMed2002

Low molecular weight heparin for prevention of thromboembolic complications in cardioversion--rationale and design of the ACE study (Anticoagulation in Cardioversion using Enoxaparin).

The modality and duration of anticoagulation before, during, and after cardioversion of atrial fibrillation--either with or without guidance by transesophageal echocardiography (TEE)--is still an unresolved issue. Intravenous infusion of unfractionated heparin until effective anticoagulation with phenprocoumon or warfarin is used as the standard therapy. However, this approach may be associated with several days of hospitalization because of the necessity for intravenous heparin administration. Moreover, there may be an increased risk of bleeding complications or, conversely, episodes of undercoagulation. Low-molecular weight heparin is an attractive alternative as it not only provide a safe and predictable level of anticoagulation with fewer side effects but can also be administered safely on an outpatient basis. In addition, no anticoagulation monitoring is needed. The ACE study (Anticoagulation in Cardioversion using Enoxaparin) is a randomized, prospective, open-label multicenter trial comparing the safety and efficacy of subcutaneous enoxaparin with intravenous heparin/oral phenprocoumon before and after cardioversion (stratified to TEE guidance or no TEE guidance). This article presents the rationale, design and status of the ACE study.

Administration, Oral↗
PubMed2000

Managing the therapeutic dilemma: patients with spontaneous intracerebral hemorrhage and urgent need for anticoagulation.

Physicians face a therapeutic dilemma in patients with acute hemorrhagic stroke requiring long-term, high-intensity anticoagulants because this treatment increases the risk of intracranial hemorrhage (ICH) 8- to 11-fold. We retrospectively studied 15 patients with ICH which occurred under anticoagulation with phenprocoumon, with an international norrmalized ratio (INR) of 2.5-6.5 on admission. Hemispheric, thalamic, cerebellar, intraventricular, or subarachnoid hemorrhage without aneurysm occurred. Absolute indications for anticoagulation were double, mitral, or aortic valve replacement, combined mitral valve failure with atrial fibrillation and atrial enlargement, internal carotid artery-jugular vein graft, frequently recurring deep vein thrombosis with risk of pulmonary embolism, and severe nontreatable ischemic heart disease. As soon as the diagnosis of ICH was established, INR normalization was attempted in all patients by administration of prothrombin complex, fresh frozen plasma, or vitamin K. After giving phenprocoumon antagonists (and neurosurgical therapy in four patients) heparin administration was started. Nine patients received full-dose intravenous and six low-dose subcutaneous heparin. The following observations were made: (a) All patients with effective, full-dose heparin treatment with a 1.5- to 2-fold elevation in partial thromboplastin time after normalization of the INR were discharged without complication. (b) Three of four of the patients with only incomplete correction of the INR (> 1.35) experienced relevant rebleeding within 3 days (all patients with an INR higher than 1.5), two of whom were on full-dose heparin. (c) Three of seven of the patients with normalized INR and without significant PTT elevation developed severe cerebral embolism. Although our data are based on a retrospective analysis, they support treatment with intravenous heparin (partial thromboplastin time 1.5-2 times baseline value) after normalization of the INR in patients with an ICH and an urgent need for anticoagulation.

Aged↗