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PubMed1977

[Hemarthroses complicating anticoagulant therapy (heparin, oral anticoagulants)].

Three patients with hemarthrosis complicating anticoagulant therapy are described. Two had acute hemarthrosis of the knee joint occurring during long term oral anticoagulant therapy for cardiovascular disorders. Joint symptoms disappeared rapidly after arthrocentesis and diminution of the dose of oral anticoagulant medication. The third patient has been on chronic hemodialysis for the last three years. After 2 years of this therapy he developed periarthritis of the right shoulder, followed suddenly by hemarthrosis of the right shoulder which remained symptomatic for 9 months in spite of several joint aspirations and reduction in the dosage of heparin administered during hemodialysis. Resolution of the hemarthrosis of the right shoulder occurred only when the vascular access for the dialysis sessions was displaced from the right to the left forearm. It is assumed that there was communication in the venous draining territories of the arterio-venous fistula and the shoulder articulation.

Acenocoumarol↗
PubMed1996

[Anticoagulant therapy in patients with atrial fibrillation: the experience of the Centers of Surveillance. Study group of the "Italian Study on Complications of Oral Anticoagulant Therapy" (ISCOAT)].

The present study evaluated the anticoagulant course of 580 patients (21% of the total number of patients, 317 males, half of them aged > 70 years) with atrial fibrillation (AF) enrolled in the ISCOAT study. During the 469 patient-years of follow-up 35 bleeding (7.6%; 2 fatal, 8 major) and 17 thrombotic events (3.6%) occurred. Bleeding was more frequent when AF was associated with other cardiovascular diseases (9.8%) and occurred even if the anticoagulation level was low (9% when INR was < 2), probably due to the presence of individual risk factors. As expected, thrombotic events were also more frequent when INR level was < 2. We conclude that in patients with AF the recommended therapeutic range seems to be INR 2-3, since this range proved to be safe and more effective than lower anticoagulation levels.

Administration, Oral↗
PubMed1998

In vitro anticoagulant properties of a minimum functional fragment of human thrombomodulin and in vivo demonstration of its benefit as an anticoagulant in extracorporeal circulation using a monkey model.

Recently, we demonstrated that the last three consecutive epidermal growth factor-like structures of human thrombomodulin form the minimum functional fragment for protein C activating activity. In this study, the recombinant minimum functional fragment of human thrombomodulin (E456) had similar activities for protein C activation and clotting time compared to the recombinant extracellular domains of human thrombomodulin (rhsTM) previously described. E456 had a shorter half-life (6-9 min) in animals, compared to rhsTM (5 h). To evaluate whether or not E456 is a suitable anticoagulant for extracorporeal circulation, the effects of E456 were investigated in the extracorporeal circulation model in monkeys. The effect of E456 at a dose of 0.03 mg/kg plus 0.113 mg/kg/h on circuit pressure was as potent as that of low molecular weight heparin, Fragmin, at a dose of 30 IU/kg plus 15 IU/kg/h. E456, however, also more effectively suppressed an increase of thrombin-antithrombin III complex than Fragmin. Also the APTT quickly returned to the pre-treatment level following E456, but did not when using Fragmin. Moreover, E456 had no influence on the plasma free fatty acid levels, while Fragmin significantly increased them. Thus, E456 appears to have anticoagulant properties which make it more suitable anticoagulant in extracorporeal circulation than Fragmin.

Animals↗
PubMed1998

Changes of prothrombin fragment 1+2 (F 1+2) as a function of increasing intensity of oral anticoagulation--considerations on the suitability of F 1+2 to monitor oral anticoagulant treatment.

Plasma F 1+2 levels, the activation peptide originating from the factor Xa-mediated activation of prothrombin, increase in many clinical conditions associated with hypercoagulability and decrease in patients on oral anticoagulant treatment (OAT). However. the usefulness of F 1+2 measurement to monitor OAT has not yet been investigated in clinical studies. Before those studies are attempted, the plausibility of its implementation in the laboratory control of OAT should be evaluated. In this respect, a thorough investigation of the pattern of changes of F 1+2 as a function of increased intensity of anticoagulation expressed as International Normalized Ratio is essential. One hundred and thirty-two patients on long-term warfarin treatment were recruited to cover 8 ranges of anticoagulation from < 1.5 to 9.0 INR. F 1+2 was measured in batch on frozen plasma and INR was determined on fresh plasma. The relationship of F 1+2 vs. INR showed a hyperbolic pattern with F 1+2 levels decreasing progressively and significantly as a function of increasing INR up to 3.0. A further decrease in F 1+2 levels observed at INR up to 4.0 was not statistically significant. At INR greater than 4.0, F 1+2 reached a plateau, with mean levels not significantly different for patients at increasing INR up to 9.0. Since the risk of bleeding increases at INR greater than 4.5, our results suggest that F 1+2 is of little value to assess the hemorrhagic risk in patients on OAT.

Administration, Oral↗
PubMed1998

Effectiveness of anticoagulation among patients discharged from hospital on warfarin. The Newcastle Anticoagulation Study Group.

OBJECTIVES: To examine the effectiveness of anticoagulation among patients discharged from hospital on warfarin in the care of general practitioners (GPs). DESIGN AND SETTING: A historical cohort with questionnaires to patients discharged from a major metropolitan teaching hospital and their GPs. PARTICIPANTS: Patients discharged between 1 February 1995 and 31 January 1996 identified from hospital pharmacy records as being prescribed warfarin, and their treating GPs. MAIN OUTCOME MEASURES: Frequency of testing and levels of international normalised ratio of prothrombin time (INR) within six months of discharge; level of INR aimed at by GP; complication rates; and patient knowledge about anticoagulation. RESULTS: Replies were received from 242 (68%) patients and pathology records were examined for 195 (81%) of these. The median gap between INR measures was seven days. The median of the median INR level for each patient was 2.4 (rising to 2.7 in patients with an artificial heart valve); 24% of observed patient time was spent at an INR level of less than 2.0, 54% between 2.0 and 2.9, 18% between 3.0 and 3.9 and 4% at an INR level of 4.0 or more. There were five confirmed major complications (equivalent to 5 per 100 patient-years). Twenty-seven per cent of patients answered at least eight of the 10 knowledge questions correctly: education level predicted knowledge, but there was no relationship between knowledge and INR level. CONCLUSIONS: Among this unselected group of patients whose anticoagulation was managed by GPs, there was a high frequency of laboratory testing. INR levels were controlled safely and complication rates were comparable with those in published reports.

Anticoagulants↗
PubMed1996

Interference with anticoagulation monitoring by procainamide-induced lupus anticoagulant.

A patient scheduled for coronary revascularization was discovered to have elevated partial thromboplastin and activated clotting times. Preoperative testing revealed a lupus anticoagulant, probably secondary to long-term procainamide therapy. The resultant inability to use conventional anticoagulation monitoring for cardiopulmonary bypass was solved by direct measurement of heparin concentration. Operation and recovery were uneventful, and the patient was treated with long-term warfarin anticoagulation for this hypercoagulable state.

Aged↗
PubMed1990

The functional site of placental anticoagulant protein: essential histidine residue of placental anticoagulant protein.

Placental anticoagulant protein (PAP) rapidly lost its anticoagulant effect due to photooxidation in the presence of methylene blue at pH 7.9 and 8 degrees C. Photooxidized PAP failed to bind the phospholipid vesicle. It seemed unlikely that the protein underwent a change in molecular size during the photooxidation on the basis of its behavior in electrophoresis and gel filtration. Photooxidized PAP had significantly decreased histidine contents, whereas the contents of other amino acids remained essentially unchanged. The peptide, SHLRKV, was included in the functional site of PAP and still showed an anticoagulant activity. On the other hand, the peptide which substituted histidine by alanine, SALRKV, no longer showed the activity. It was shown that the histidine residue is involved in Ca2+ or the phospholipid binding site of the protein.

Amino Acid Sequence↗
PubMed1990

Studies of natural anticoagulant proteins and anticardiolipin antibodies in patients with the lupus anticoagulant.

Components of the natural anticoagulant system (NAS) and anticardiolipin antibodies were examined in 21 patients with lupus anticoagulant (LA), 13 of whom had past histories of thrombotic episodes. No relationship could be shown between the antigenic levels of protein C and S (PC, PS) and a history of thrombosis. Inhibition of the anticoagulant activity of activated protein C (APC) was observed using plasma from 20/21 patients when phospholipid vesicles were used as the surface for the coagulation reaction. This effect was not affected by the addition of PS. When platelet membranes were employed only 2/21 patients demonstrated inhibition of APC. Under the latter condition, PS functional activity was inhibited in 7/21 patients, six of whom had a past history of thrombosis. Reduced antithrombin III or heparin cofactor II levels were observed in a total of 4/21 patients and may have contributed to the development of thrombosis in three of these patients. Antibodies specifically directed against these proteins were not detected suggesting the possibility of an associated constitutional deficiency. Anticardiolipin antibodies, though elevated in 17/21 patients, did not serve as a useful marker for an increased risk of thrombosis, and the level did not correlate with inhibition of the activity of APC or PS. We conclude that the mechanism of thrombosis in patients with LA is multi-factorial. A subset of patients in whom LA specifically inhibits PS function may represent patients who are at significant risk from thrombosis.

Antibodies↗
PubMed1996

Anticoagulant response to Agkistrodon contortrix venom (ACV test): a new global test to screen for defects in the anticoagulant protein C pathway.

As specific assays used to identify defects in the protein C (PC) anticoagulant pathway are laborious and expensive, we describe here a global test to screen for these defects. This assay is expressed as the ratio of two activated partial thromboplastin times, one in the absence and one in the presence of 0,125 U/ml of the PC activator of Agkistrodon contortrix venom (ACV). Eight of the 168 healthy volunteers of the control group exhibited an ACV ratio below the lower normal limit of 3.37 [6 subjects with the mutation Arg 506 to Gln in their factor V gene (FV R506Q) and one with PS deficiency]. 128 patients who have had at least one episode of deep-vein thrombosis were retrospectively studied. All patients carrying FV Q506R (n = 48), PC deficiency (n = 14) or combined defects, i.e. FV Q506R and PC deficiency (n = 4) or FV Q506R and PS deficiency (n = 3), had ACV ratios < 3.37. PS deficient plasmas (n = 20) exhibited ACV ratios which overlapped normal range. ACV ratios of one out of seven patients with antithrombin deficiency, and 10% of patients without identified defect in the PC anticoagulant pathway (n = 30) were < 3.37. An ACV ratio raised to 3.70 could lead to a test identifying all patients with a defect in the PC anticoagulant pathway.

Adolescent↗
PubMed1998

Control of oral anticoagulation in patients with the antiphospholipid syndrome--influence of the lupus anticoagulant on International Normalized Ratio. Groupe Méthodologie en Hémostase du Groupe d'Etudes sur l'Hémostases et la Thrombose.

The recommended therapeutic range of International Normalized Ratio (INR) for oral anticoagulant treatment in patients with the antiphospholipid syndrome remains controversial. As a part of this controversy, it has been suggested that lupus anticoagulants (LA) could interfere with the determination of prothrombin time, thus questioning the validity of monitoring the treatment of these patients using INR. To clarify this point, we compared the values of INR obtained in the plasmas of two groups of patients, one without LA (n = 47), and the other with LA (n = 43). INR were determined using 8 different thromboplastin reagents on the same automated coagulation instrument. Chromogenic factor X, which is supposed to be insensitive to the presence of LA, was also measured. The results are the following: provided INR was calculated using calibrated reference plasmas, there was no significant difference between INR values obtained with the 8 reagents, both in the non-LA and in the LA groups (CV: 5.9 and 6.7%. respectively). Closer examination revealed that INR results obtained with one reagent (the recombinant thromboplastin Innovin) diverged from those of the 7 others, leading to an overestimation of INR, to a very large extent in some instances. However this effect was restricted to a subset of the patient population with LA (6 out of 43). Finally, the relationship between INR (average value obtained using the 8 reagents) and factor X was identical in non-LA and in LA patient groups. We conclude that, provided the reagents which display the LA interference are identified and excluded for this purpose, the INR system is valid for monitoring oral anticoagulant treatment in patients with LA.

Administration, Oral↗
PubMed2006

The full-length cDNA of anticoagulant protein infestin revealed a novel releasable Kazal domain, a neutrophil elastase inhibitor lacking anticoagulant activity.

Infestins are Kazal-type serine proteinase inhibitors found in the midgut of the Chagas' disease vector, Triatoma infestans. In previous studies, we characterized two double-headed infestins with potent anticoagulant activity; infestin 1-2, which inhibits thrombin and infestin 3-4, a factor XIIa inhibitor. In the present work, we have cloned the full-length cDNA of infestins' precursor. The translated cDNA predicted a polypeptide containing a signal peptide and seven Kazal-type domains, four domains from infestin 1-2 and infestin 3-4, and three new domains. Northern blot analysis confirmed that infestins are synthesized in a single transcript (approximately 1,800 bp) in the insect midgut, but not in salivary glands. Based on the cDNA sequence, the three new Kazal domains were named infestin 1R, 2R and 3R. Infestin 2R-3R has 77% amino acid sequence identity to infestin 1-2 and the same basic amino acid residue at P1 position in the inhibitory reactive site suggesting that these two proteins have a similar inhibitory specificity. In contrast, infestin 1R has two different characteristics when compared to the other infestins: i) a hydrophobic amino acid residue at P1 position in the inhibitory reactive site and ii) a prediction to be processed as a single Kazal domain. These two characteristics were experimentally demonstrated by the purification of native infestin 1R from T. infestans midgut. Native infestin 1R was shown to be processed as a single Kazal domain by mass spectrometry and it was able to inhibit neutrophil elastase, subtilisin A and chymotrypsin. To further characterize infestin 1R inhibitory activity, it was expressed as a recombinant protein in bacteria. Recombinant infestin 1R inhibited neutrophil elastase with the same K(i) of the native inhibitor. Moreover, it inhibited subtilisin A, chymotrypsin and proteinase K but did inhibit neither thrombin nor coagulation assays. In conclusion, unlike the other described infestins, infestin 1R did not present anticoagulant activity and is processed as a single Kazal domain with inhibitory specificity towards proteases that hydrolyze peptide bonds after hydrophobic amino acid residues.

Amino Acid Sequence↗
PubMed1998

Analysis for sites of anticoagulant action of plancinin, a new anticoagulant peptide isolated from the starfish Acanthaster planci, in the blood coagulation cascade.

1. Effects of plancinin, a new anticoagulant peptide, on the human blood coagulation cascade were investigated. 2. Plancinin prolonged both activated partial thromboplastin time and prothrombin time, and it significantly inhibited factor X activation by both intrinsic (factor IXa-factor VIIIa-phospholipids-Ca2+) and extrinsic (factor VIIa-tissue factor-phospholipids-Ca2+) tenase complexes and prothrombin activation by prothrombinase complex (factor Xa-factor Va-phospholipids-Ca2+) to 13.8%, 4.8% and 10.5% of control value, respectively. 3. Results indicate that sites of anticoagulant action of plancinin may be located in activation steps of prothrombin and factor X.

Animals↗
PubMed2000

Community impact of anticoagulation services: rationale and design of the Managing Anticoagulation Services Trial (MAST).

We describe the design of the Managing Anti-coagulation Services Trial (MAST), a practice-improvement trial testing whether anticoagulation services are a preferred method of managing anticoagulation for stroke prevention among patients with atrial fibrillation. Most randomized trials within the health care environment are designed as efficacy studies to determine what works under ideal conditions or ideal clinical practice. In contrast, effectiveness trials seek to generalize the results of efficacy studies by determining what works under more typical practice conditions. Practice-improvement trials are effectiveness trials that examine the management of a clinical problem in the context in which care is usually given. Noteworthy features of the MAST include defining the intervention in functional terms and collaboration with managed care organizations.

Aged↗
PubMed2004

Selective cleavage and anticoagulant activity of a sulfated fucan: stereospecific removal of a 2-sulfate ester from the polysaccharide by mild acid hydrolysis, preparation of oligosaccharides, and heparin cofactor II-dependent anticoagulant activity.

A linear sulfated fucan with a regular repeating sequence of [3)-alpha-L-Fucp-(2SO4)-(1-->3)-alpha-L-Fucp-(4SO4)-(1-->3)-alpha-L-Fucp-(2,4SO4)-(1-->3)-alpha-L-Fucp-(2SO4)-(1-->]n is an anticoagulant polysaccharide mainly due to thrombin inhibition mediated by heparin cofactor II. No specific enzymatic or chemical method is available for the preparation of tailored oligosaccharides from sulfated fucans. We employ an apparently nonspecific approach to cleave this polysaccharide based on mild hydrolysis with acid. Surprisingly, the linear sulfated fucan was cleaved by mild acid hydrolysis on an ordered sequence. Initially a 2-sulfate ester of the first fucose unit is selectively removed. Thereafter the glycosidic linkage between the nonsulfated fucose residue and the subsequent 4-sulfated residue is preferentially cleaved by acid hydrolysis, forming oligosaccharides with well-defined size. The low-molecular-weight derivatives obtained from the sulfated fucan were employed to determine the requirement for interaction of this polysaccharide with heparin cofactor II and to achieve complete thrombin inhibition. The linear sulfated fucan requires significantly longer chains than mammalian glycosaminoglycans to achieve anticoagulant activity. A slight decrease in the molecular size of the sulfated fucan dramatically reduces its effect on thrombin inactivation mediated by heparin cofactor II. Sulfated fucan with approximately 45 tetrasaccharide repeating units binds to heparin cofactor II but is unable to link efficiently the plasma inhibitor and thrombin. This last effect requires chains with approximately 100 or more tetrasaccharide repeating units. We speculate that the template mechanism may predominate over the allosteric effect in the case of the linear sulfated fucan inactivation of thrombin in the presence of heparin cofactor II.

Animals↗
PubMedDate not supplied

Anticoagulant poisoning in animals: a simple new high-performance thin-layer chromatographic (HPTLC) method for the simultaneous determination of eight anticoagulant rodenticides in liver samples.

The purpose of this study was to develop and evaluate a technique for the analysis of anticoagulant rodenticides in serum and liver samples using a new high-performance thin-layer chromatographic apparatus. Detection limits were estimated at 0.2 micrograms/g in liver extracts for eight different substances. Overall, this technique was repeatable and reproducible. The percent recovery was greater than 87% for each substance. Liver and serum samples of animals known to be exposed to one anticoagulant and showing clinical signs of poisoning were analyzed. Concentrations measured varied between 0.2 and 3 micrograms/g (liver extracts). Only blood samples from one dog could be analyzed. The concentration was 150 ng/mL the first day after admission and 140 ng/mL the following day. Analyses are technically easily and rapidly performed, and they are inexpensive. Therefore, this technique could be a valuable alternative to current high-performance liquid chromatographic methods.

4-Hydroxycoumarins↗
PubMed2001

Improved confirmation of weak lupus anticoagulants by employing sensitive and insensitive reagents to the lupus anticoagulant.

Detection of a lupus anticoagulant (LA) is of major importance to detect a thrombotic tendency. Confirmation of its phospholipid dependency may represent a tricky step in the diagnostic algorithm for LA, as several tests may yield borderline results of little diagnostic help. To improve on this point, we had previously employed a procedure comparing sensitive [rabbit brain kaolin (RBK)] and insensitive [soy bean phosphatides (SBP)] reagents to LA to screen and confirm LA at the same time in activated partial thromboplastin systems (aPTT). Here we compared its performance against a platelet neutralization procedure (PNP). To allow comparisons of our procedures with the PNP, a percentage ratio correction was calculated according to the following formula: [(RBK ratio - SBP ratio) x 100]/ RBK ratio. Similarly for the PNP: percentage ratio correction = [(buffer ratio - platelet phospholipid ratio) x 100]/buffer ratio. On 44 known LA plasmas, the PNP, expressed in seconds, yielded 15 (34%) negative or borderline results. After ratio transformation, the PNP still yielded 10 of 15 (66%) uncertain results, whereas the RBK/SBP procedure did not give any uncertain results (P = 0.0002). The mean percentage ratio correction was far superior for the RBK/SBP procedure than for the PNP (53.24 +/- 15.93 versus 20.28 +/- 12.15%, P < 0.0001). The use of sensitive and insensitive reagents to the lupus anticoagulant increases the confirmatory yield of LA in aPTT systems and may deserve inclusion amongst the confirmatory procedures for its diagnosis.

Anticoagulants↗
PubMed2006

The laboratory diagnosis of lupus anticoagulant in patients on oral anticoagulation.

Laboratory-specific cut-off lupus ratios (LR), above which a plasma is judged positive for lupus anticoagulant (LA), were established for both activated partial thromboplastin time-based and dilute Russell viper venom time-based methods. The validity of using these cut-off values to determine the presence of LA in patients on oral anticoagulation (OAC) was assessed. A cohort of 40 patients (23 male and 17 female), aged 22-84 years (mean 52 years) were tested for LA at the time of a thrombotic event. Repeated testing was performed after the same patients were treated with OAC (international normalized ratio 2.0-3.5). For 36 patients (90%), LA status was unchanged pre- and on-OAC. Thirteen of the 40 patients (32.5%) were positive for LA both pre- and on-OAC. Of the 27 patients negative for LA pre-OAC, 23 remained negative on-OAC. The four discordant results were interesting in that LA positivity was demonstrated only after the patient was stable on-OAC. In our cohort of 40 patients, there was a trend for LRs to decrease on-OAC, but this did not reach statistical significance. The subset (4) went against this trend and became positive after the thrombotic event.

Administration, Oral↗
PubMed2004

Patient self-management of oral anticoagulant care vs. management by specialized anticoagulation clinics: positive effects on quality of life.

BACKGROUND: Oral anticoagulant therapy (OAT) implies frequent blood checks and dose changes to prevent thromboembolic or hemorrhagic complications. This may interfere with patients' social and working circumstances in addition to the possible stress caused by the condition necessitating this treatment. We studied whether patient self-management could be a way to improve quality of life in these patients. METHODS: Within a multicenter randomized study performed by two Dutch anticoagulation clinics, designed to study the effect on treatment quality (time within target range) of different modalities of patient self-management, we looked at the effect of increased patient education (n = 28), self-monitoring of the International Normalized Ratio (INR) (n = 47) and full patient self-management (INR monitoring and dosing of the OAT) (n = 41) on the quality of life of the patients. This was done with the aid of a written questionnaire (32 questions, minimum score = 1, maximum score = 6) at baseline (n = 163), and after 26 weeks (n = 118). We compared the results after 26 weeks with those at baseline, as well as between groups. RESULTS: General treatment satisfaction was already high under routine care (5.11 on a scale of 1-6) and increased further through self-monitoring of the INR (+0.19) and full self-management (+0.32). Distress (-0.44), perceived daily hassles (-0.31) and strain on the social network (-0.21) were reduced through full self-management. Improved patient education was associated with increased distress (+0.33) and perceived daily hassles (+0.23). Comparison at 26 weeks between groups showed similar improvements on these outcomes for self-monitoring and self-management vs. routine care after education.

Adult↗