acenocoumarol has been researched along with Thrombophilia* in 22 studies
5 review(s) available for acenocoumarol and Thrombophilia
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Hemoptysis Associated With Therapeutic Doses of Acenocoumarol.
Topics: Acenocoumarol; Aged; Anticoagulants; Atrial Fibrillation; Comorbidity; Dose-Response Relationship, Drug; Drug Substitution; Factor Xa Inhibitors; Hemoptysis; Humans; International Normalized Ratio; Lung; Male; Pyrazoles; Pyridones; Thrombophilia; Tomography, X-Ray Computed | 2019 |
Extraperitoneal hemorrhagic rupture of a simple hepatic cyst. A case report and literature review.
Hemorrhagic rupture is a very rare complication of a simple hepatic cyst. We report the first case of a totally extraperitoneal rupture of a recurrent cyst, occurred in a 73-year-old man who presented with acute right hypochondralgia. Computed tomography revealed the rupture of a large hemorrhagic cyst in the right liver lobe and the formation of a voluminous hematoma in the retroperitoneal space. Despite the absence of hemoperitoneum, the entity of the bleeding led us to perform an urgent and successful surgical intervention. A review of the literature was conducted. To date, 9 cases of hemorrhagic rupture of simple hepatic cyst have been described and our case is the first one characterized by extraperitoneal bleeding. Our clinical management was in accordance with the majority of the other Authors. Different surgical procedures have been proposed and the best approach has not been established yet. However, the laparotomic approach should be preferred for a better control of the bleeding. In conclusion, the hemorrhagic rupture of a liver cyst is a life-threatening complication and a prompt surgery is necessary to prevent the hypovolemic shock.. Extraperitoneal rupture, Hemorrhagic rupture, Simple hepatic cyst.. Le cisti epatiche semplici sono patologie benigne di frequente riscontro nella popolazione generale, la cui incidenza è in progressivo aumento a seguito della larga diffusione di tecniche di imaging quali ecografia e TC addome. Tra le complicanze cui può andare incontro una cisti epatica, la rottura emorragica è sicuramente la più rara e temibile. Nel nostro lavoro riportiamo il caso di un paziente di 73 anni, giunto alla nostra osservazione per dolore ingravescente in ipocondrio destro. La TC dell’addome ha evidenziato la rottura emorragica di una voluminosa cisti del lobo epatico di destra, con formazione di un grossolano ematoma in sede retroperitoneale. L’instaurarsi di un iniziale quadro di instabilità emodinamica ha reso necessario l’esecuzione di un intervento chirurgico urgente, consistito nella resezione delle pareti cistiche e di parte del quinto segmento epatico da cui la cisti originava. Il decorso postoperatorio si è svolto in modo regolare ed il paziente è stato dimesso in sesta giornata postoperatoria. A dimostrazione della rarità dell’evento, abbiamo condotto una revisione della letteratura inglese. Ad oggi sono stati riportati 9 casi, incluso il nostro, di rottura emorragica di cisti epatica semplice. La peculiarità del caso da noi descritto, che lo rende unico in letteratura, è la rottura in sede extraperitoneale. Analizzando i pochi dati a disposizione, abbiamo cercato di individuare alcuni fattori di rischio per la rottura emorragica di una cisti epatica, riscontrando nell’età avanzata e nella terapia anticoagulante orale un ruolo predisponente. Riguardo al management clinico, la revisione della letteratura conferma il ruolo primario della chirurgia, riservando la gestione conservativa ai soli pazienti compromessi e non suscettibili di intervento. La rottura emorragica di una cisti epatica è infatti un evento “life-threatening”, che può indurre rapidamente uno scompenso emodinamico nel paziente. Secondo le nostre osservazioni, e in accordo con i dati estratti dalla letteratura, l’intervento chirurgico urgente si rende necessario al fine di prevenire lo shock ipovolemico. Topics: Acenocoumarol; Aged; Anticoagulants; Cysts; Drainage; Emergencies; Erythrocyte Transfusion; Hematoma; Hemostasis, Surgical; Humans; Liver Diseases; Male; Recurrence; Retroperitoneal Space; Rupture, Spontaneous; Thrombophilia; Tomography, X-Ray Computed; Ultrasonography | 2016 |
Deep vein thromboembolism after arthroscopy of the shoulder: two case reports and a review of the literature.
Deep vein thrombosis (DVT) has an incidence of 1 case per 1000 inhabitants in the general population and it is very rare after arthroscopy of the shoulder. Therefore, the current guidelines do not advise the administration of DVT prophylaxis in shoulder arthroscopy procedures.. We describe two cases of thrombosis of the arm after shoulder arthroscopy on a total of 10.452 shoulder arthroscopies performed during a period of ten years. One of two patients was further complicated by a bilateral pulmonary microembolism. In these two clinical cases the complication developed despite the absence of risk factors such as a concomitant neoplasm, thrombophilia, smoking habit, or a long duration of the procedure.. The DVT after shoulder arthroscopy procedure remain a very rare complication. However, in view of the growing number of patients undergoing this procedure, this figure is expected to rise. The clinician surgeon should take in mind this possible complication that normally appears in the first 3 weeks after surgery, so to perform anti-coagulant treatment. Further clinical studies are therefore warranted to assess the true risk of VTE. In fact, the presence of "minor" predisposing factors that are not routinely studied, as well as the postoperative immobilization period, are potential risk factors that, associated with the invasiveness of the arthroscopy procedure, could trigger a thromboembolism. Topics: Acenocoumarol; Anticoagulants; Arm; Arthroscopy; Axillary Vein; Dyspnea; Edema; Heparin, Low-Molecular-Weight; Humans; Hyperbaric Oxygenation; Male; Middle Aged; Perfusion Imaging; Postoperative Care; Postoperative Complications; Pulmonary Embolism; Risk Factors; Shoulder Joint; Thrombophilia; Ultrasonography, Doppler, Color; Venous Thrombosis; Young Adult | 2010 |
[The antiphospholipid syndrome, an update].
The antiphospholipid syndrome is an antibody mediated hypercoagulable state characterized by recurrent venous and arterial thromboembolic events. Several studies have determined that the frequency of antiphospholipid syndrome in patients presenting with a venous thromboembolic event is between 4% and 14%. Classical criteria include the presence of anticardiolipin antibody or lupus anticoagulant with typical complications of thrombosis or pregnancy loss. Other common associated manifestations include livedo reticularis, thrombocytopenia, valvular heart disease, and nephropathy with renal insufficiency, hypertension and proteinuria. Because of the high risk for recurrent thromboembolism in these patients, current recommendations suggest a longer, potentially lifelong, course of antithrombotic therapy following an initial event. For an initial venous thromboembolic event, a target INR of 2.0 to 3.0 is supported by two prospective, randomized clinical trials. In contrast, relatively limited data exist for an initial arterial thromboembolic event in patients who have the antiphospholipid syndrome, and therapeutic recommendations range from aspirin to warfarin with a high target INR. Recurrent thromboembolic events can be extremely difficult to treat, and some patients may benefit from the addition of immunosuppressive therapies. It is very important to evaluate in this setting additional, coincident prothrombotic risk factors. Topics: Abortion, Spontaneous; Acenocoumarol; Adult; Antibodies, Anticardiolipin; Anticoagulants; Antiphospholipid Syndrome; Aspirin; Enzyme-Linked Immunosorbent Assay; Female; Fibrinolytic Agents; Heparin; Humans; Lupus Coagulation Inhibitor; Male; Platelet Aggregation Inhibitors; Pregnancy; Prospective Studies; Randomized Controlled Trials as Topic; Recurrence; Risk Factors; Thrombophilia; Thrombosis; Warfarin | 2007 |
[Successful prophylaxis in a pregnancy with thrombophilic states].
It has been observed that the presence of antiphospholipid antibodies (aPL) is associated with a high incidence of fetal loss and this is thought to--a result from the vasculitis of placental circulation and subsequent thrombosis. A 38-year-old woman with second fetal loss had received oral anticoagulant after pulmonary embolism. APL were examined--anticardiolipin antibodies (aCA) were found. The third pregnancy was established and sintrom was stopped and replaced by fraxiparine 0.3 ml/24 h up to the end of the pregnancy even 20 days after delivery of a healthy baby. Topics: Acenocoumarol; Adult; Anticoagulants; Drug Therapy, Combination; Female; Gravidity; Humans; Nadroparin; Pregnancy; Pregnancy Complications, Hematologic; Pulmonary Embolism; Thrombophilia; Time Factors | 1999 |
4 trial(s) available for acenocoumarol and Thrombophilia
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Independent predictors of poor vitamin K antagonist control in venous thromboembolism patients. Data from the EINSTEIN-DVT and PE studies.
Vitamin K antagonists (VKA) are used to prevent recurrent disease in patients with venous thromboembolism (VTE). Their efficacy and safety depend on individual time in therapeutic range (iTTR) and variability of International Normalised Ratios (INR). We aimed to identify independent predictors of poor VKA control > 28 days. In a prospective cohort of 3825 VTE patients, separate logistic regression analyses were performed to identify predictors of low iTTR (first quartile) and instability (iTTR Topics: Acenocoumarol; Administration, Oral; Aged; Anticoagulants; Drug Therapy, Combination; Enoxaparin; Female; Hemorrhage; Humans; International Normalized Ratio; Male; Middle Aged; Neoplasms; Prognosis; Recurrence; Risk Factors; Thrombophilia; Treatment Outcome; Venous Thromboembolism; Vitamin K; Warfarin | 2015 |
Low adjusted-dose acenocoumarol therapy in sickle cell disease: a pilot study.
Vasoocclusion is a continuous process in sickle cell disease (SCD) and accumulates to significant end organ damage, mostly irrespective of the occurrence of manifest acute vasoocclusive events. As there are indications that reversing the hypercoagulable state may be of clinical benefit in sickle cell patients, we performed a randomized, double blind, placebo-controlled, cross-over pilot study to assess the efficacy and safety of low-adjusted dose acenocoumarol therapy (International Normalized Ratio: 1.6-2.0) in SCD. Treatment consisted of either acenocoumarol or placebo for 14 weeks, after which treatment was discontinued for a period of five weeks. Then, patients initially on acenocoumarol received placebo (and vice versa) for 14 weeks. Therapy efficacy was assessed by comparing the frequency of vasoocclusive complications, the occurrence of bleeding, and clotting activation between acenocoumarol and placebo treatment of each individual patient. Twenty-two patients (14 homozygous [HbSS] and 8 double heterozygous sickle-C [HbSC]; aged 20-59 years) completed the entire study. Acenocoumarol treatment did not result in a significant reduction of acute vasoocclusive events (three painful crises during acenocoumarol, five painful crises during placebo). There was a marked reduction of the hypercoagulable state (depicted by a decrease in plasma levels of prothrombin F1.2 fragments [P = 0.002], thrombin-antithrombin complexes [P = 0.003], and D-dimer fragments [P = 0.001]) without the occurrence of major bleeding. Even though no clinical benefit (pertaining to the frequency of painful crises) was detected in this pilot study, the value of low adjusted-dose acenocoumarol for preventing specific events (such as strokes) and as a long-term treatment of sickle cell patients should be subject of further study. Topics: Acenocoumarol; Adult; Anemia, Sickle Cell; Anticoagulants; Antifibrinolytic Agents; Dose-Response Relationship, Drug; Double-Blind Method; Humans; Middle Aged; Pilot Projects; Thrombophilia; Treatment Outcome | 2001 |
Abrupt versus gradual withdrawal of vitamin K antagonist treatment in patients with venous thromboembolic disease: assessment of hypercoagulability and clinical outcome.
It is yet unclear whether vitamin K antagonist treatment should be stopped abruptly or gradually after an episode of venous thromboembolism. The mode of withdrawal might influence a potential development of a hypercoagulable state, which could influence the risk for recurrent disease.. We prospectively studied 37 consecutive patients in whom acenocoumarol was discontinued either abrupt (18) or gradually (19) (2/3 and 1/3 of the initial dose for one week). Blood sampling was performed at various time points up to 18 days after complete withdrawal and was analysed for INR, prothrombin fragment F1 + 2 and D-dimer. All patients were clinically followed-up for the assessment of the association between hypercoagulability and occurrence of disease such as recurrent venous thromboembolism or malignancy.. An approximately fourfold increase was observed (median increase from 0.3 to 1.3 nmol/l) in the F1 + 2 levels after both abrupt and gradual withdrawal and in the D-dimer concentrations in the abrupt withdrawal group (0.10 to 0.44 mg/l), while those in whom acenocoumarol was discontinued gradually showed a less pronounced increase of the D-dimer levels (0.11 to 0.29 mg/L) (not significant). During follow-up one recurrent venous thromboembolic event occurred in each group, and a diagnosis of cancer was made four times. All these patients had the highest D-dimer concentrations measured in the entire study group.. This study indicates the potential for a hypercoagulable state after acenocoumarol discontinuation, which was not prevented by tapering the acenocoumarol dose. D-dimer, measured 2 to 3 weeks after acenocoumarol withdrawal, might be an important tool to identify patients at risk for recurrent venous thromboembolism and/or for the presence of an underlying malignancy. Topics: Acenocoumarol; Adolescent; Adult; Aged; Anticoagulants; Drug Administration Schedule; Female; Humans; Male; Middle Aged; Thromboembolism; Thrombophilia; Venous Thrombosis; Vitamin K | 2000 |
Warfarin or acenocoumarol: which is better in the management of oral anticoagulants?
Warfarin is employed more frequently than acenocoumarol because of its longer half-life (36 h), theoretically providing more stable anticoagulation, and avoiding factor VII fluctuations that potentially occur during acenocoumarol treatment (half-life 10 h). The aim of our study was to compare acenocoumarol with warfarin in the same group of 103 patients who started oral anticoagulation with acenocoumarol and then changed to warfarin. In these patients we compared the previous period of six months on acenocoumarol treatment (July-December 1996) with a new six-month period on warfarin (July-December 1997). We wished to know whether warfarin could improve the quality and the stability of oral anticoagulation of our patients and whether there was a difference between the two drugs in the weekly mean dose per patient. Moreover in order to detect the possible daily fluctuation of factor VII, we evaluated a further group of 54 patients. A subgroup of these patients was treated with warfarin while another received acenocoumarol. In the first group of patients, 1,158 and 1,064 PTs were carried out with acenocoumarol and warfarin, respectively. The percentage of PTs in the therapeutic range was 59% with acenocoumarol and 62% with warfarin (p=0.4). The mean number of visits per patient was 12 and 11, and the mean number of visits in the therapeutic range was 7 and 7, respectively. The last check in file method did not show any difference between the two drugs. Overdose states were 51 (4.4%) with acenocoumarol and 30 (2.8%) with warfarin (p=0.4). A good correlation (r=0.92) was found between the acenocoumarol and the warfarin weekly mean dose. The mean warfarin/acenocoumarol weekly dose ratio was 2.08 (range: 1.25-3.30; CI 95%: 1.99-2.16). In the second group of patients, factor VII levels with both drugs were higher 24 h after administration than 16 h after, showing that their daily fluctuation was independent of the drug's half-life, since factor VII levels in patients with a low vitamin K intake were not increased. Our results showed that warfarin did not appear to be better than acenocoumarol in the performance of an Anticoagulation Clinic in terms of PTs within the therapeutic range per patient. It seems that the behaviour of factor VII was affected by the intake of vitamin K rather than by the short half-life of acenocoumarol. Topics: Acenocoumarol; Administration, Oral; Adult; Aged; Anticoagulants; Cross-Over Studies; Dose-Response Relationship, Drug; Factor VII; Female; Humans; Male; Middle Aged; Prothrombin Time; Thrombophilia; Treatment Outcome; Vitamin K; Warfarin | 1998 |
13 other study(ies) available for acenocoumarol and Thrombophilia
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The pediatric acenocoumarol dosing algorithm: the Children Anticoagulation and Pharmacogenetics Study.
Essentials A pediatric pharmacogenetic dosing algorithm for acenocoumarol has not yet been developed. We conducted a multicenter retrospective follow-up study in children in the Netherlands. Body surface area and indication explained 45.0% of the variability in dose requirement. Adding the genotypes of VKORC1, CYP2C9 and CYP2C18 to the algorithm increased this to 61.8%.. Background The large variability in dose requirement of vitamin K antagonists is well known. For warfarin, pediatric dosing algorithms have been developed to predict the correct dose for a patient; however, this is not the case for acenocoumarol. Objectives To develop dosing algorithms for pediatric patients receiving acenocoumarol with and without genetic information. Methods The Children Anticoagulation and Pharmacogenetics Study was designed as a multicenter retrospective follow-up study in Dutch anticoagulation clinics and children's hospitals. Pediatric patients who used acenocoumarol between 1995 and 2014 were selected for inclusion. Clinical information and saliva samples for genotyping of the genes encoding cytochrome P450 (CYP) 2C9, vitamin K epoxide reductase complex subunit 1 (VKORC1), CYP4F2, CYP2C18 and CYP3A4 were collected. Linear regression was used to analyze their association with the log mean stable dose. A stable period was defined as three or more consecutive International Normalized Ratio measurements within the therapeutic range over a period of ≥ 3 weeks. Results In total, 175 patients were included in the study, of whom 86 had a stable period and no missing clinical information (clinical cohort; median age 8.9 years, and 49% female). For 80 of these 86 patients, genetic information was also available (genetic cohort). The clinical algorithm, containing body surface area and indication, explained 45.0% of the variability in dose requirement of acenocoumarol. After addition of the VKORC1, CYP2C9, and CYP2C18 genotypes to the algorithm, this increased to 61.8%. Conclusions These findings show that clinical factors had the largest impact on the required dose of acenocoumarol in pediatric patients. Nevertheless, genetic factors, and especially VKORC1, also explained a significant part of the variability. Topics: Acenocoumarol; Adolescent; Age Factors; Algorithms; Anticoagulants; Biological Variation, Individual; Biotransformation; Body Surface Area; Child; Child, Preschool; Cytochrome P-450 Enzyme System; Dose-Response Relationship, Drug; Female; Follow-Up Studies; Genetic Association Studies; Humans; Infant; Male; Models, Biological; Polymorphism, Single Nucleotide; Practice Guidelines as Topic; Retrospective Studies; Saliva; Thrombophilia; Vitamin K | 2018 |
Risk of thrombosis and hemorrhage in patients with polycythemia vera and atrial fibrillation treated with prophylactic oral anticoagulants.
Topics: Acenocoumarol; Administration, Oral; Aged; Aged, 80 and over; Anticoagulants; Atrial Fibrillation; Female; Follow-Up Studies; Hemorrhage; Humans; Male; Middle Aged; Polycythemia Vera; Proportional Hazards Models; Risk Factors; Smoking; Thrombophilia; Thrombosis; Warfarin | 2016 |
[Pulmonary embolism in a patient with familial thrombophilia due to homozygotic genetic mutation in 20209C>T].
Topics: Acenocoumarol; Aged, 80 and over; Anticoagulants; Fluid Therapy; Furosemide; Heparin; Homozygote; Humans; Male; Mutation; Polypharmacy; Promoter Regions, Genetic; Prothrombin; Pulmonary Embolism; Thrombophilia; Thrombophlebitis | 2015 |
[Quality control of oral anticoagulant therapy in Primary Care in Madrid City, Spain: CHRONOS-TAO study].
To determine quality control of patients with oral anticoagulant treatment recruited in Primary Care (PC) using the Rosendaal method to estimate time in therapeutic range (TTR) and comparing it with fraction of international normalized ratio (INR) in range and cross-sectional analysis (last INR registred).. A retrospective observational study based on electronic medical record in routine clinical practice.. PC centers (262) in Madrid. We included all patients with acenocumarol treatment, with an INR therapeutic range established between 2 and 3. We excluded patients with valvular pathology and disrupted clinical follow up in PC (<3 INR determinations in the studied period, a period of>90 days or ≥ 3 periods of>60 days between 2 determinations). The final population was 49,312 patients. The variables considered were all INR values and their respective dates. TTR was calculated by the 3 methods above mentioned. We considered "therapeutic range" INR between 2-3 and "adjusted range" INR between 1.8-3.2. Optimal control for each patient was considered TTR>60%.. By using Rosendaal method, TTR was 66.8% (81.7% adjusted), with a percentage of total INR in range was 58.8% (66.5% adjusted), and, with the cross-sectional analysis, it was 70.5% (76.8% adjusted). Mean TTR was 65% (standard deviation 20.3), and the percentage of patients with TTR>60% was 63.3% (88.1% adjusted).. The quality control of patients with oral anticoagulants in PC in Madrid is acceptable, similar or higher to other studies and pivotal trials of new anticoagulants. Compared to the Rosendaal method, total fraction of INR underestimates quality control, and cross-sectional analysis slightly overestimates it. Topics: Acenocoumarol; Administration, Oral; Adult; Aged; Aged, 80 and over; Anticoagulants; Comorbidity; Cross-Sectional Studies; Drug Monitoring; Drug Utilization; Female; Humans; International Normalized Ratio; Male; Middle Aged; Polypharmacy; Primary Health Care; Quality Control; Retrospective Studies; Spain; Thrombophilia; Urban Health; Warfarin | 2015 |
Atypical calciphylaxis secondary to treatment with acenocoumarol.
Topics: Acenocoumarol; Aged, 80 and over; Anticoagulants; Asthma; Atrial Fibrillation; Calciphylaxis; Calcium; Diabetes Complications; Female; Humans; Hypertension; Leg Ulcer; Livedo Reticularis; Polypharmacy; Thrombophilia | 2012 |
Late venous thrombosis of renal allograft: two cases with different treatment and outcome.
Topics: Acenocoumarol; Edema; Heparin; Heparin, Low-Molecular-Weight; Humans; Immunosuppression Therapy; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Polycystic Kidney, Autosomal Dominant; Polycythemia; Postoperative Complications; Recurrence; Renal Dialysis; Renal Veins; Thrombectomy; Thrombolytic Therapy; Thrombophilia; Thrombophlebitis; Time Factors; Treatment Outcome; Venous Thrombosis | 2011 |
[Necrotic leg ulcers induced by vitamin K antagonists: five cases].
Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing.. Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation.. Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted. Topics: Acenocoumarol; Activated Protein C Resistance; Aged; Aged, 80 and over; Anticoagulants; Diabetic Angiopathies; Factor V; Female; Humans; Hyperhomocysteinemia; Leg Ulcer; Male; Necrosis; Phenindione; Polyarteritis Nodosa; Postoperative Complications; Purpura; Thrombophilia; Varicose Ulcer; Vasculitis, Leukocytoclastic, Cutaneous; Vitamin K | 2011 |
[Anesthesia in a patient with homocystinuria and severe pulmonary embolism].
Topics: Acenocoumarol; Aggression; Anesthesia, General; Anesthetics; Anticoagulants; Contraindications; Enoxaparin; Hemodynamics; Homocystinuria; Humans; Hypoglycemia; Hypoxia; Intraoperative Complications; Male; Nitrous Oxide; Pulmonary Embolism; Seizures; Thrombophilia; Vena Cava Filters; Venous Thrombosis; Young Adult | 2009 |
JAK2 V617F-positive latent essential thrombocythemia and splanchnic vein thrombosis: the role of bone marrow biopsy for the diagnosis of myeloproliferative disease.
Splanchnic vein thrombosis (SVT) is a severe complication of essential thrombocythemia (ET). No clear explanation has been given for the occurrence of thrombosis in this unusual site in patients with ET, but the existence of a specific association between unexplained SVT and the JAK2 mutation has been reported.. The present study describes SVT (portal and splenic vein thrombosis) in a young woman as the first presenting symptom of latent ET. Extensive screening for thrombophilia was negative. Our patient in fact did not fulfill the WHO diagnostic criteria for myeloproliferative disease (MPD), while she had splenomegaly and developed features suggestive of latent ET during follow-up.. In these patients with SVT, the detection of JAK2(V617F) mutation is diagnostic for masked MPD as could be documented by bone marrow histopathology. The presence of JAK2(V617F) mutation should be considered per se a prothrombotic state for cerebral, coronary and peripheral microvascular disturbances and for SVT but not for deep vein thrombosis. Anticoagulation is the treatment of choice for all SVT and proper treatment of the MPD is recommended in patients with SVT associated with the JAK2(V617F) mutation. Topics: Abdominal Pain; Acenocoumarol; Adult; Anticoagulants; Biopsy; Bone Marrow; Bone Marrow Examination; Epilepsy; False Negative Reactions; Female; Heparin; Humans; Hydroxyurea; Janus Kinase 2; Polycystic Ovary Syndrome; Portal Vein; Splenic Vein; Splenomegaly; Thrombocythemia, Essential; Thrombophilia; Venous Thrombosis | 2009 |
[Aseptic cerebral venous thrombosis and multiple cerebral tuberculomas associated with pulmonary miliary tuberculosis].
Severe pulmonary tuberculosis may be complicated by deep vein thrombosis due to a state of hypercoagulability.. We report a case of pulmonary miliary tuberculosis associated with cerebral venous thrombosis and multiple intracranial tuberculomas. A 65-year-old woman developed a confusional syndrome one week after starting treatment for pulmonary military tuberculosis. Neuroimaging reveals a thrombus in the right lateral sinus and multiple silent intracranial tuberculoma.. The patient was given anticoagulants and fully recovered. Topics: Acenocoumarol; Aged; Anticoagulants; Antitubercular Agents; Confusion; Drug Therapy, Combination; Female; Heparin; Humans; Immunocompromised Host; Isoniazid; Lateral Sinus Thrombosis; Pyrazinamide; Radiography; Rifampin; Streptomycin; Thrombophilia; Tuberculoma, Intracranial; Tuberculosis, Miliary; Tuberculosis, Pulmonary | 2007 |
Interactions between thrombophilic genetic mutations and clinical bleeding in patients on chronic oral anticoagulant treatment.
We studied the prevalence of genetic thrombophilic mutations in patients on chronic oral anticoagulant treatment (OAT) who had bleeding complications. In a case-control study we found ten (12.8%) carriers of factor V Leiden and two (2.5%) carriers of the PT20210A mutation among 78 patients with a history of moderate-severe bleeding while on OAT, and seven (4.4%) and four (2.5%), respectively, among 156 matched patients with no bleeding while on OAT (odds ratio 3.1+/-1.6, p=0.026). In patients on chronic OAT, FV Leiden is a risk factor for moderate-severe bleeding. Topics: 3' Untranslated Regions; Acenocoumarol; Administration, Oral; Aged; Aged, 80 and over; Anticoagulants; Case-Control Studies; Factor V; Female; Follow-Up Studies; Gene Frequency; Hemorrhage; Hospitalization; Humans; International Normalized Ratio; Male; Middle Aged; Prevalence; Prothrombin; Sample Size; Thrombophilia; Warfarin | 2005 |
No effect of acenocoumarol therapy on levels of endothelial activation markers in sickle cell disease.
Sickle cell patients are characterized by a chronic inflammatory and hypercoagulable state, depicted by elevated levels of pro-inflammatory cytokines, endothelial adhesion molecules, and elevated markers of thrombin generation. We set out to determine whether anticoagulation with a coumadin derivative reduces inflammation in sickle cell disease. Therefore, serum levels of NFkappaB-regulated endothelial adhesion molecule soluble vascular cell adhesion molecule-1 and serum levels of non-NFkappaB-dependent markers of endothelial activation (soluble cellular fibronectin and von Willebrand factor antigen) were compared during treatment with acenocoumarol (INR 1.6-2.0) and placebo. No effect on circulating levels of the measured parameters was observed during treatment with acenocoumarol as compared to placebo. In the targeted INR range, anticoagulation of sickle cell patients with acenocoumarol does not seem to reduce endothelial activation. Topics: Acenocoumarol; Adult; Anemia, Sickle Cell; Anticoagulants; Biomarkers; Endothelium, Vascular; Female; Fibronectins; Humans; Inflammation; Male; Middle Aged; NF-kappa B; Peptide Fragments; Prothrombin; Solubility; Thrombophilia; Vascular Cell Adhesion Molecule-1; von Willebrand Factor | 2002 |
Hemorheological alterations and hypercoagulable state in deep vein thrombosis.
Deep vein thrombosis (DVT) seems to be related to a hypercoagulation and definite hemorheological alterations, but the importance of these alterations in the development of thrombotic events in the deep vein system has not been established. The present study examines both aspects in a group of 55 patients with DVT; the presence of a hypercoagulable state was assessed by quantifying the prothrombin fragment 1+2 (F1+2) and the thrombin-antithrombin III complex (T-AT), and the main hemorheological parameters were evaluated in the acute state and 6 and 12 months later. The results show marked hemorheological, F1+2, and TAT alterations in the acute phase. After 12 months the pattern shows a modest improvement, but erythrocyte aggregation, fibrinogen, F1+2 and T-AT remain increased with respect to the control group (8.51 +/- 1.43; 331 +/- 81 mg/dl; 1.33 +/- 0.60 nmol/l; 3.54 +/- 1.71 ng/ml vs. 8.10 +/- 1.40; 230 +/- 38; 0.94 +/- 0.40; 1.56 +/- 0.59, respectively). These data suggest that the thrombotic event could be influenced by the previous rheological situation and hypercoagulable state. Topics: Acenocoumarol; Acute Disease; Adult; Aged; Anticoagulants; Antithrombin III; Blood Coagulation; Blood Viscosity; Convalescence; Erythrocyte Aggregation; Female; Fibrinogen; Follow-Up Studies; Hemorheology; Heparin; Humans; Male; Middle Aged; Peptide Fragments; Peptide Hydrolases; Postoperative Complications; Prothrombin; Thrombophilia; Thrombophlebitis; Wounds and Injuries | 1998 |