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PubMed2006

Arterial ischemic stroke and cerebral venous thrombosis in children: a 12-year Argentinean registry.

Over a 12-year period, 112 consecutive children with arterial ischemic stroke (AIS) and 38 children with cerebral venous thrombosis (CVT) were prospectively recruited at a single pediatric center in Argentina. One or more underlying clinical conditions were identified in most patients (55%) with AIS and in almost all patients with CVT. Inherited and/or acquired prothrombotic disorders were detected in 17% of the patients with AIS and in 34% of the children with CVT. No associations between factor V Leiden or prothrombin G20210A mutation and children with AIS or CVT were found. Antithrombotic agents (i.e., aspirin, low-molecular-weight heparin and acenocoumarol) were administered without major hemorrhagic complications. In our cohorts, mortality due to the thrombotic episode was 1.8% in children with AIS. No child with CVT died from his or her thrombotic episodes. Three children (3.2%) and 1 adolescent (1.1%) with AIS had thrombotic progression and recurrence, respectively. A large percentage of children with AIS (68%) and CVT (32%) have had some kind of sequels that caused serious disability in approximately half the cases.

Adolescent↗
PubMedDate not supplied

Vitamin K metabolism in a patient resistant to vitamin K antagonists.

We investigated various pharmacokinetic and pharmacodynamic parameters in a 63-year-old man, resistant to warfarin, fluindione, acenocoumarol and phenprocoumon. Daily doses of up to 30 mg of the long-acting phenprocoumon yielded a drug concentration of 85 mg/l (usual range 1-5 mg/l) but the international normalized ratio remained around 1. The plasma half-life of phenprocoumon was approximately 350 h (normal 120-150 h). Thus, the resistance was not due to malabsorption or to an accelerated metabolism of the drug. The level of vitamin K1 (1,202 ng/l) was insufficient to induce resistance. Decarboxyprothrombin concentrations were low, demonstrating that the gamma-carboxylation of the precursors of the vitamin K-dependent coagulation factors was not effectively reduced. The concentration of vitamin K epoxide, normally increased under oral anticoagulation, correlated to the vitamin K concentration (r2 = 0.77) but the quotient epoxide/vitamin K remained 4-fold lower than that of 22 warfarin-sensitive patients, suggesting an absence of blockade of the vitamin K reductase by phenprocoumon. This resistance to all the molecular forms of the vitamin K antagonists is most likely due to a reduced affinity of the drugs to a mutant vitamin K reductase.

Drug Resistance↗
PubMed1987

Rheological and anticoagulant therapy of patients with chronic peripheral occlusive arterial disease (COAD).

In the course of a six-month study, a three-subgroup cohort of 113 patients (103 m, 10 f, mean age 58 +/- 8 years) with angiographically proven occlusive peripheral arterial disease (COAD) Fontaine stage II was analyzed regarding the therapeutic (improvement of walking performance) and prophylactic (prevention of new vascular events) effects of oral treatment with three different drug regimens. Group A (38 patients) was treated with the anticoagulants phenprocoumon or acenocoumarol; group B (32 patients), with the same anticoagulants plus pentoxifylline--800-1200 mg per day; and group C (43 patients) received irregular treatment with various vasodilators, such as xanthinolnicotinate, naftidrofuryl, pyridylmethanol, and others. At the end of the trial period a significant increase in systolic ankle pressure index and walking distance was observed in group B whereas the two other groups showed minor changes only. The elevated plasma fibrinogen concentration in group B was also significantly decreased. The percentage of atherosclerotic complications such as new arterial thrombosis in the lower limbs, newly appeared stenocardia, myocardial infarction, transient ischemic attack (TIA), and stroke was highest in group C (20%), relatively lower in group A (10%), and lowest in group B (3%). The percentage of hemorrhagic complications was minimal, with no significant differences between group A and group B. These complications were mild and disappeared quickly. The combined therapy with anticoagulants and pentoxifylline had a marked therapeutic and probably prophylactic effect as regards thromboembolic complications in patients with COAD and other localizations of atherosclerosis.

Aged↗
PubMed2000

Familial antithrombin-III deficiency during cardiopulmonary bypass: a case report.

The serine protease inhibitor antithrombin-III (AT-III) is the principal in vivo inhibitor of blood coagulation, inactivating mainly thrombin, but also other serine proteases. Binding of AT-III to heparin dramatically increases its inhibitory effect. AT-III deficiency during cardiopulmonary bypass (CPB) can lead to insufficient anticoagulation which cannot be treated by higher doses of heparin. A 60-year-old male with familial AT-III deficiency was admitted to our hospital for coronary artery bypass surgery and aortic valve replacement. Four days before the operation, acenocoumarol was stopped and anti-Xa nadroparincalcium (Fraxiparine) was started. AT-III activity at that time was 56%. Two hours before the operation, a single dose of 4500 IU AT-III concentrate was administered. Heparinization was performed with 400 IU/kg of porcine mucosal heparin, increasing the activated coagulation time (ACT) from a baseline of 115 to 549 s. AT-III activity at that time was above 100% and the plasma D-dimer concentration was 230 ng/l. ACTs during CPB remained above 999 s, whereas the AT-III activity dropped to 54% and the D-dimer increased up to 500 ng/l at the end of CPB. CPB was terminated uneventfully. Heparin was reversed with 3 mg/kg protamine chloride, decreasing the ACT to 155 s. In the intensive care unit (ICU), the patientreceived prophylactic Fraxiparine and 1500 IU AT-III, increasing the AT-III activity to 84%. Postoperatively, there was continued blood loss, which necessitated the administration of whole blood and eventually re-exploration. The case presented illustrates an uneventful treatment of a patient with a hereditary AT-III deficiency undergoing CPB. In spite of an uneventful treatment with AT-III pre-CPB, administration of prophylactic AT-III concentrate after surgery should be considered with caution, as this might increase the postoperative morbidity.

Animals↗
PubMed1978

The chemistry, pharmacology and clinical pharmacology of diflunisal.

Studies are reviewed on diflunisal, a new analgesic agent with an improved therapeutic index, compared with acetylsalicylic acid, in animals and humans. Pharmacokinetic data indicate that a twice-daily dosage regimen of diflunisal is adequate for therapeutic purposes. Diflunisal inhibits prostaglandin E synthesis, but in humans at clinically effective doses it does not alter bleeding time or platelet aggregation. Diflunisal is uricosuric at clinically effective doses. No clinically important drug interactions with diflunisal have been found to date, although some slight alterations in blood and urine drug levels have been noted. The slight increase in prothrombin time seen when diflunisal and acenocoumarol were co-administered is not considered to be of major clinical importance.

Animals↗
PubMed2003

Multivariate relationships between international normalized ratio and vitamin K-dependent coagulation-derived parameters in normal healthy donors and oral anticoagulant therapy patients.

BACKGROUND AND OBJECTIVES: International Normalized Ratio (INR) is a world-wide routinely used factor in the monitoring of oral anticoagulation treatment (OAT). However, it was reported that other factors, e. g. factor II, may even better reflect therapeutic efficacy of OAT and, therefore, may be potentialy useful for OAT monitoring. The primary purpose of this study was to characterize the associations of INR with other vitamin K-dependent plasma proteins in a heterogenous group of individuals, including healthy donors, patients on OAT and patients not receiving OAT. The study aimed also at establishing the influence of co-morbid conditions (incl. accompanying diseases) and co-medications (incl. different intensity of OAT) on INR. DESIGN AND METHODS: Two hundred and three subjects were involved in the study. Of these, 35 were normal healthy donors (group I), 73 were patients on medication different than OAT (group II) and 95 were patients on stable oral anticoagulant (acenocoumarol) therapy lasting for at least half a year prior to the study. The values of INR and activated partial thromboplastin time (APTT) ratio, as well as activities of FII, FVII, FX, protein C, and concentration of prothrombin F1+2 fragments and fibrinogen were obtained for all subjects. In statistical evaluation, the uni- and multivariate analyses were employed and the regression equations describing the obtained associations were estimated. RESULTS: Of the studied parameters, three (factors II, VII and X) appeared as very strong modulators of INR, protein C and prothrombin fragments F1+2 had moderate influence, whereas both APTT ratio and fibrinogen had no significant impact on INR variability. Due to collinearity and low tolerance of independent variables included in the multiple regression models, we routinely employed a ridge multiple regression model which compromises the minimal number of independent variables with the maximal overall determination coefficient. The best-fitted two-component model included FII and FVII activities and explained 90% of INR variability (compared to 93% in the 5-component model including all vitamin K-dependent proteins). Neither the presence of accompanying diseases nor the use of OAT nor any other medication (acetylsalicylic acid, statins, steroids, thyroxin) biased significantly these associations. CONCLUSION: Among various vitamin K-dependent plasma proteins, the coagulation factors II, VII and X showed the most significant associations with INR. Of these variables, the two-component model, including factors II and VII, deserves special attention, as it largely explains the overall variability observed in INR estimates. The statistical power of this model is validated on virtue of the estimation that the revealed associations are rather universal and remain essentially unbiased by other compounding variables, including clinical status and medical treatment. Further, much broader population studies are needed to verify clinical usefulness of methods alternate or compounding to INR monitoring of OAT.

Journal Article↗
PubMed1994

Clinically significant drug interactions with the oral anticoagulants.

Oral anticoagulants were introduced in the late 1940s and remain widely used today. Indications include prevention of thrombosis associated with atrial fibrillation, structural cardiac diseases and following prosthetic valvular replacement. They have been used for both treatment and prophylaxis of deep venous thrombosis and in efforts to decrease the frequency and rate of second myocardial infarction. These compounds include the coumarin derivatives [dicoumarol (bishydroxycoumarin), phenprocoumon, nicoumalone (acenocoumarol)] and the indanedione derivatives (diphenadione, phenindione, anisindione) which, because of adverse reactions, are largely unavailable. The oral anticoagulants, and warfarin in particular, are highly interactive with other drugs. Mechanisms of those interactions include both pharmacokinetic and pharmacodynamic mechanisms and may result in either hyper- or hypoprothrombinaemia. Because their principal adverse reaction is haemorrhage, and interactions are widespread across many therapeutic specialties, it becomes imperative for the practising physician to be aware of the possibility of interaction whenever these agents are coadministered with other drugs.

Administration, Oral↗
PubMed1996

Cisapride. Drug interactions of clinical significance.

Cisapride is a prokinetic agent which restores motility of the gastrointestinal tract in conditions of decreased bowel transit. It may also alter the absorption of coadministered drugs. The absorption of morphine, diazepam, cyclosporin, alcohol (ethanol) and levodopa are increased. Initial absorption of cimetidine and raniditine is also increased, but overall absorption is lower due to increased bowel transit. The absorption of digoxin, propranolol and the anticoagulants warfarin and phenprocoumon appears unaffected by cisapride, although increase thrombotest values were seen with acenocoumarol (nicoumalone). Drug interactions leading to increased plasma concentrations of cisapride may produce an increase in adverse effects. The most important of these is QT interval prolongation and ventricular arrhythmias. Phenytoin does not appear to affect protein binding of cisapride. Cisapride metabolism is inhibited by the antifungals ketoconazole, fluconazole, itraconazole and miconazole, and by the antibacterials erythromycin, troleandomycin and clarithromycin. Cisapride should not be coadministered with these drugs. Cimetidine produces a small increase in cisapride plasma concentrations, which may be due to inhibition of metabolism. Cisapride absorption is unaffected by other antacids. Atropine may reverse the cisapride-induced increase in peristalsis. Prescribers should remain vigilant to the presence of these and other, as yet unreported, reactions.

Cisapride↗
PubMed2005

Cognitive impairment as determinant for sub-optimal control of oral anticoagulation treatment in elderly patients with atrial fibrillation.

BACKGROUND AND OBJECTIVE: Atrial fibrillation is an indication for oral anticoagulation treatment. Maintaining the International Normalized Ratio (INR) within the therapeutic range minimises thromboembolic and bleeding complications. We have investigated whether cognitive capacity affects control of anticoagulation in elderly patients with atrial fibrillation. PATIENTS AND METHODS: A retrospective study was conducted to investigate the association between cognitive impairment and control of anticoagulation. Patients > or =70 years of age with atrial fibrillation using acenocoumarol (nicoumalone) as anticoagulant were included. All patients were monitored by the Anticoagulation Clinic in the Midden-Brabant region in the Netherlands. The cognitive function of all patients was assessed using the Mini-Mental State Examination (MMSE) on the index date. INR values were obtained from the year preceding the index date. Patients with an MMSE score <23 were defined as cognitively impaired. The primary outcome of the study was the incidence of an INR value within the therapeutic range of 2.0-3.4 during < or =70% of treatment time in the year prior to the cognitive function assessment. The secondary endpoint was the number of patients with an INR <2.0 or > or =6.0 at least once during this year. Logistic regression analysis was used to evaluate the association between cognitive function and control of anticoagulation. RESULTS: A total of 152 patients were included in the study. An MMSE score <23 was associated with an inadequate INR control (odds ratio [OR] 2.77; 95% CI 1.13, 6.74). After correction for hospital admission and change of possibly interacting medication (both also associated with inadequate INR control), this association remained statistically significant. Significantly more patients with an MMSE score <23 had one or more INR values of six or higher (OR 3.06; 95% CI 1.14, 8.18). CONCLUSION: In elderly people with atrial fibrillation using oral anticoagulation, an MMSE score <23 is independently associated with an inadequate INR control, mainly because of an increased number of supratherapeutic INR values. This finding should be taken into account when making decisions about use of oral anticoagulants in the elderly.

Administration, Oral↗
PubMed1994

Pharmacokinetics of oxicam nonsteroidal anti-inflammatory agents.

Oxicam nonsteroidal anti-inflammatory drugs (NSAIDs) are a group of structurally closely related substances with anti-inflammatory, analgesic and antipyretic activities. They have a weakly acidic character and are extensively bound to plasma proteins. Piroxicam, the most widely used oxicam, is well absorbed after oral administration. Peak plasma concentrations (Cmax) of the drug are reached within 2 to 4 hours. Piroxicam has a small volume of distribution and a low plasma clearance. It undergoes hepatic metabolism and only 5 to 10% is excreted unchanged in urine. The elimination half-life varies between 30 and 70 hours. Age of the patient and renal or hepatic dysfunction do not seem to have any major effect on the pharmacokinetics of piroxicam. The drug reduces the renal excretion of lithium to a clinically significant extent, but the clinical significance of piroxicam-aspirin (acetylsalicylic-acid) and piroxicam-acenocoumarol interaction has not been established. Ampiroxicam, droxicam and pivoxicam are prodrugs of piroxicam that have been synthesised to reduce piroxicam-related gastrointestinal irritation. All prodrugs are well absorbed, but Cmax values are reached later than those following administration of piroxicam. Tenoxicam is used in the management of rheumatic and inflammatory diseases. Mean Cmax values are achieved 2 hours postdose. Food reduces the rate but not the extent of absorption. The oral bioavailability of tenoxicam is 100% and rectal bioavailability is 80%. Like piroxicam, tenoxicam has a low volume of distribution and low plasma clearance. It is eliminated through hepatic metabolism. The mean elimination half-life is 60 to 75 hours. The pharmacokinetics of tenoxicam are independent of patient age, or concurrent liver or renal diseases. High doses of aspirin have been shown to increase the elimination of tenoxicam, but this has little clinical significance. Isoxicam was in widespread clinical use until its worldwide marketing was suspended because of fatal skin reactions. Isoxicam is completely absorbed, but Cmax values are not reached until 10 hours postdose. It has a low plasma clearance, approximately 5 ml/min (0.3 L/h), and low volume of distribution. The mean elimination half-life is 30 hours and does not appear to be affected by the age of the patient. Isoxicam potentiated the anticoagulant effect of warfarin, necessitating a 20% dosage reduction. Lornoxicam differs from other oxicam NSAIDs because it has a short elimination half-life of 3 to 4 hours. On the basis of limited data, some individuals seem to eliminate lornoxicam very slowly, suggesting the presence of polymorphic metabolism. The pharmacokinetics of cinnoxicam and sudoxicam have not been studied thoroughly.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed2004

The use of vitamin K in patients on anticoagulant therapy: a practical guide.

Anticoagulation with antivitamin K (AVK) is very effective for primary and secondary prevention of thromboembolic events. However, questions persist about the risks and management of over-anticoagulation. For reversal of excessive anticoagulation by warfarin, AVK withdrawal, oral or parenteral vitamin K administration, prothrombin complex or fresh frozen plasma may be used, depending on the excess of anticoagulation, the existence and site of active bleeding, patient characteristics and the indication for AVK. In over-anticoagulated patients, vitamin K aims at rapid lowering of the international normalized ratio (INR) into a safe range to reduce the risk of major bleeding and therefore improving patient outcome without exposing the patient to the risk of thromboembolism due to overcorrection, resistance to AVK, or an allergic reaction to the medication. The risk of bleeding increases dramatically when the INR exceeds 4.0-6.0, although the absolute risk of bleeding remains fairly low, <5.5 per 1000 per day. Patient characteristics, including advanced age, treated hypertension, history of stroke, and concomitant use of various drugs, affect the risk of bleeding. The absolute risk of thromboembolism associated with overcorrection appears to be in the same range as the risk of bleeding due to over-anticoagulation. The use of vitamin K in patients with warfarin over-anticoagulation lowers excessively elevated INR faster than withholding warfarin alone; however, it has not been clearly demonstrated that vitamin K treatment does, in fact, lower the risk of major hemorrhage. As vitamin K administration via the intravenous route may be complicated by anaphylactoid reactions, and via the subcutaneous route by cutaneous reactions, oral administration is preferred. A dose of 1-2.5mg of oral phytomenadione (vitamin K(1)), reduces the range of INR from 5.0-9.0 to 2.0-5.0 within 24-48 hours, and for an INR >10.0, a dose of 5mg may be more appropriate. Overcorrection of the INR or resistance to warfarin is unlikely if the above doses of vitamin K are used. Vitamin K is less effective for over-anticoagulation after treatment with acenocoumarol or phenprocoumon than after treatment with warfarin.

Anticoagulants↗
PubMed1996

Anticoagulant therapy in pregnancy. Report of 54 cases.

BACKGROUND: To investigate the adverse effects of anticoagulant therapy during pregnancy in a tertiary care center. MATERIAL AND METHODS: A prospective study was carried out between 1 January 1977 and 31 December 1994 and included 54 pregnancies in 50 women treated with anticoagulants. In Group I (n=43) oral anticoagulants were replaced for heparin from the sixth until the end of the twelfth week of gestation and acenocoumarol was not substituted. All patients received vitamin K antagonists during the second and third trimesters. Heparin was given after 36 weeks of pregnancy until the tenth day in the postpartum period. Statistical comparisons used Chi square test (with the Yates correction when appropriate) and Student t test. RESULTS: Mechanical heart valve prosthesis was the most frequent indication (68%). There was one artificial heart valve thrombosis during first trimester in Group I and none in Group II (p=0.45). One spontaneous abortion occurred in each group (p=0.86). Seven cardiac complications (13.7%) occurred during the second and third trimesters. We recorded no thrombotic episode of an artificial heart valve after the first trimester of pregnancy. Hemorrhagic complications occurred in mid-pregnancy (one case=2%) and during peripartum (eight cases=16%). Two maternal deaths occurred in the postpartum period, both were linked with the anticoagulant therapy. There was one coumarin embryopathy (Group II: 9%),but no neonatal mortality. CONCLUSIONS: (1) Hemorrhagic complications occur among 16% of patients receiving anticoagulant therapy during pregnancy. (2) Delivery and postpartum are the most critical periods.

Adult↗
PubMed2006

Treatment of hirudin overdosage in a dialysis patient with heparin-induced thrombocytopenia with mixed hemodialysis and hemofiltration treatment.

We report a patient who developed type II heparin-induced thrombocytopenia (HIT) and accidentally received a recombinant hirudin (r-hirudin) overdosage. Treatment with hemodialysis (HD) using high-flux polysulfone dialyzer and hemofiltration was performed. Length of treatment was adjusted, monitoring activated partial thromboplastin time (aPTT) to 1.5-2.5 times the mean of the normal range. She developed deep venous thrombosis and occlusion of vascular access. Only after cessation of heparin lock catheter, platelet count began to increase. After one year of treatment with acenocoumarol and additional low-dose r-hirudin, neither bleeding nor thrombotic episodes have been reported.

Aged↗
PubMed1995

Comparing subcutaneous danaparoid with intravenous unfractionated heparin for the treatment of venous thromboembolism. A randomized controlled trial.

OBJECTIVE: To compare the efficacy and safety of two subcutaneous doses of danaparoid with that of continuous intravenous administration of unfractionated heparin in the treatment of venous thromboembolism. DESIGN: An open-label, randomized, multicenter clinical trial. SETTING: One university hospital and two university-affiliated hospitals. PATIENTS: 209 patients suspected to have venous thromboembolism. Of these, 188 had a confirmed diagnosis (by ventilation-perfusion lung scan and ultrasonography or contrast venography of the leg) and received study medication. INTERVENTIONS: Patients were randomly assigned to either low-dose danaparoid (intravenous loading dose of 1250 U followed by 1250 U administered subcutaneously twice daily [n = 65]); high-dose danaparoid (intravenous loading dose of 2000 U followed by 2000 U administered subcutaneously twice daily [n = 63]); or unfractionated heparin (intravenous loading dose of 2500 U followed by dose-adjusted continuous infusion [n = 60]). Treatment lasted at least 5 days and was continued until anticoagulation (achieved with acenocoumarol) was adequate. MEASUREMENTS: Efficacy determined clinically and by repeated imaging tests on treatment days 5 to 8; safety determined by daily assessment for bleeding. RESULTS: Two lung scans were done in each of 179 patients; ultrasonography or venography of the leg was done twice in each of 173 patients; and both repeated leg and lung tests were done in 166 patients. A significant reduction in recurrence or extension of venous thromboembolism was seen in patients receiving high-dose danaparoid (8 of 63 [13%]) compared with patients receiving intravenous unfractionated heparin (17 of 60 [28%]; relative risk, 0.45 [95% CI, 0.21 to 0.96]). Four of 61 patients receiving high-dose danaparoid (7%) and 14 of 58 patients receiving unfractionated heparin (24%) had recurrence of pulmonary embolism (relative risk, 0.27 [CI, 0.09 to 0.78]); 3 of 58 patients receiving high-dose danaparoid (5%) and 6 of 54 patients receiving unfractionated heparin (11%) had recurrence of deep venous thrombosis (relative risk, 0.47 [CI, 0.12 to 1.77]). Occurrence of major and minor bleeding was similar in the three groups; major bleeding occurred in 1 patient receiving low-dose danaparoid, 1 patient receiving high-dose danaparoid, and 2 patients receiving heparin. CONCLUSIONS: Our results suggest that high-dose danaparoid is safer and more effective than unfractionated heparin for the treatment of venous thromboembolism.

Adult↗
PubMed1999

Effects of aspirin or picotamide, an antithromboxane agent, in combination with low-intensity oral anticoagulation in patients with acute myocardial infarction: a controlled randomized pilot trial.

BACKGROUND AND OBJECTIVE: Combined treatment with antiplatelet drugs and oral anticoagulants seems more effective than monotherapy in the reduction of thrombotic episodes in patients with ischemic heart diseases. We compared the safety and efficacy of two different antiplatelet drugs, aspirin (asa) and picotamide (pico)--a dual antithromboxane agent--in combination with low-intensity oral anticoagulation with warfarin or acenocoumarol in acute myocardial infarction (AMI). PATIENTS AND METHODS: Primary endpoint of the study was to compare the incidence of major events (death, reinfarction, postinfarction angina and heart failure) in AMI patients undergoing thrombolytic therapy. In a controlled randomized parallel group pilot study, 101 patients with AMI were enrolled and treated with asa 160 mg/die plus low-intensity oral anticoagulation (target INR: 1.5-2.5) (n = 51) or pico 300 mg/tid plus low-intensity oral anticoagulation (n = 50). Secondary endpoint of the study was to compare the cumulative incidence of major events plus major hemorrhagic episodes defined as macroscopic hematuria, nose bleeding and melena. RESULTS: The two groups were well matched regarding the main demographic and clinical variables. AMI location was anterior in 22 and 20 patients in the pico and asa group respectively, inferoposterior in 27 (pico) and 29 (asa) patients. At the end of the six-month period, major events were observed in 20 patients in the pico group and in 31 patients in the asa group (p < 0.05). The cumulative incidence of major clinical events plus major hemorrhagic episodes was significantly lower in the pico group in comparison with the asa group (28 vs 48; p < 0.001). CONCLUSION: The results of this pilot study suggest that combination therapy with picotamide and low-intensity oral anticoagulation could be a safe and effective alternative to aspirin in patient with AMI. This hypothesis should be confirmed by controlled randomized trial with an adequate sample size.

Administration, Oral↗
PubMed1999

Monitoring oral anticoagulant treatment from plasma stored for up to 48 hours and frozen plasma.

BACKGROUND AND OBJECTIVE: The number of patients being referred for lifelong anticoagulant treatment has increased markedly in the last years. The prothrombin time test is sometimes difficult to perform the same day as sample collection. The aim of this study is to determine International Normalized Ratio (INR) and vitamin-K dependent factor levels of frozen plasma and plasma stored for up 48 hours. DESIGN AND METHODS: The INR of 84 patients receiving acenocoumarol were determined fresh (0 hours), on samples stored between 2 degrees C and 8 degrees C for 24 hours and 48 hours, and on frozen samples (-40 degrees C) using 4 different thromboplastin reagents (Thromboplastin IS; Thromborel; Simplastin; and Thromboplastin D+G). In addition, factors II, VII, IX, X were determined in 34 of these patients in all these situations. We used the interclass correlation coefficient to compare the results obtained at 0 hours and the results obtained in the subsequent measurements. Both measurement and proportional errors were also estimated by linear regression analysis. RESULTS: The correlation coefficient of the INR between fresh and frozen plasma was 0.98, 0.98, 0.92 and 0.97 for IS, Thromborel, Simplastin and D+G respectively. The correlation between 0 and 24 hours was 0. 98, 0.91, 0.95 and 0.85 for IS, Thromborel, Simplastin and D+G respectively. By 48 hours although IS still had r=0.94, Thromborel, Simplastin, and D+G had r=0.55, r=0.50 and r=0.81, respectively. By 24 hours in stored plasma and in frozen plasma the activity of vitamin-K dependent factors was slightly reduced (r=0.97 at 24h/r=0. 94 with frozen plasma for factor II, r=0.92/0.96 for factor VII, r=0. 83/0.98 for factor IX, and r=0.98/0.95 for factor X). By 48 hours however, significant reductions were noted in the activity of these factors (r=0.94 for factor II, r=0.88 for factor VII, r=0.70 for factor IX, and r=0.98 for factor X). INTERPRETATION AND CONCLUSIONS: The INR can be reliable determined in frozen plasma and in plasma stored at 2-8 degrees C for up to 24 hours.

Administration, Oral↗
PubMed1999

[Hemorrhagic complications from anticoagulant treatment: analysis of predictive risk factors].

UNLABELLED: Anticoagulant therapy has shown its efficacy in the prevention of thromboembolic complications but it is not devoid of bleeding complications. Although the thromboembolic risk of some cardiac diseases may be extrapolated from well-organized clinical trials, the risk of bleeding complications should be determined in the context of the environment in which it is carried out. OBJECTIVE: To determine the complications of the patients in anticoagulant therapy, in our environment, and to analyse the of risk factors. PATIENTS AND METHODS: We have studied the complications suffered by 300 patients who underwent anticoagulation for cardiac diseases, between March-94 and March-96 retrospectively. We have classified the complications in two groups: a) Fatal or intracranial with sequelae. b) Those requiring hospitalization and/or transfusion. Univariate and multivariant analyses were conducted to identify predictors of complications, including the following factors: age, sex, diabetes, hypertension, length of therapy, distance from our Center to their place of residence, INR (> 3 vs 2 to 3) and number of drugs associated with Acenocoumarol (> or = 3 vs 2 or less). RESULTS: During the follow-up 24 patients died due to non haemorrhagic complications; 3 left the treatment on their cardiologist recommendation; 2 moved their place of residence and 1 was lost in the follow-up. Of 270 remaining 3 (0.55/100 patients-year) had complications of group a and 21 (3.88/100 patients-year) of grub b. INR > 3 and multiple medications were shown as predictors of complications when including some of the complications considered. CONCLUSIONS: 1) During two years of follow-up 1.1% (0.55/100 patients-year) of patients in anticaogulant therapy had bleeding complications resulting in death or neurological sequelae. 2) When including some of the complications considered the percentage rises to 4.44/100 patients-years. 3) Although there were no differences statistically significant, INR > 3 and polymedication have been found as predictors risk factor. 4) Patients with INR of 2 to 3 and non polymedicated presented a low risk of bleeding complications (1.66/100 patients-year).

Adolescent↗
PubMed2000

[Deep venous thrombosis of the arm: etiology, diagnosis and treatment].

Thrombosis of the upper extremity is frequently (30-52%) related to the use of an indwelling venous catheter, but it can also occur in healthy individuals after exercise. In the past it was considered a relatively benign thrombotic event, which was treated conservatively, sometimes even without anticoagulant therapy. Recent studies have shown that complications of deep venous thrombosis of the upper extremity occur frequently: pulmonary embolism (8-36%), recurrence thrombosis after cessation of anticoagulant treatment (2-15%) and post-thrombotic syndrome (up to 50%). Therefore when thrombosis of the upper extremity is clinically suspected, it should be objectively diagnosed by compression echography followed if negative by phlebography, with anticoagulant treatment directly afterward, preferably with low-molecular heparin and then acenocoumarol or phenprocoumon.

Anticoagulants↗