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Thrombotic Episode (thrombotic + episode)
Selected AbstractsEtiology of thrombocytopenia in all patients treated with heparin productsEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 2 2005Damian A. Laber Abstract:,Purpose:,To characterize the cause of thrombocytopenia in all patients treated with heparin products, to determine the incidence of heparin-induced thrombocytopenia (HIT) in unselected hospitalized patients, and to have modern data of the magnitude of this problem. Methods:,Retrospective hospital-based cohort study. During a random 2-month period, we reviewed the medical records of all patients treated with heparin agents, screened them for thrombocytopenia, and determined the cause of it. Results:,Out of 674 patients who received heparin products, 110 (16%) had thrombocytopenia. The most common causes included cancer chemotherapy, surgery, sepsis, and medications. Three patients met the clinical criteria for HIT. One had antibodies for heparin-platelet factor-4, and received a direct thrombin inhibitor. The other two individuals had a clinical syndrome that resembled immune HIT, but were not tested for HIT antibodies. One suffered a thrombotic episode that led to the death of her fetus. The other died of a possible thromboembolism. Conclusions:,This study provides evidence-based data for the differential diagnosis of thrombocytopenia after treatment with heparin products. Our findings suggest that increased awareness of the HIT syndrome might reduce morbidity and mortality. Patients exposed to heparin products, who develop thrombocytopenia, should not be overlooked. [source] Human platelet antigens polymorphisms and susceptibility of thrombosis in hemodialysis patientsHEMODIALYSIS INTERNATIONAL, Issue 3 2008Yousr GORGI Abstract To investigate the association between the polymorphisms of human platelet antigen (HPA)-1,2,3,4,5 and susceptibility to develop thrombosis accident in arteriovenous fistula (AVF), genomic DNA of 112 hemodialysis (HD) patients and 100 healthy blood donors were genotyped by PCR-SSP. The patients were classified into 2 groups: G1 included 54 HD patients presented at least one thrombotic episode on the level of the AVF, and G2 included 58 HD patients without any episode of thrombosis. The allelic frequencies of HPA-1, 2, 3, and 5 among patients and controls did not reveal significant differences. However, the HPA-4b allele was significantly more frequent in G1 than in controls or in G2 patients (23.1% vs. 11.5% and 0.9%, respectively), p<0.01 and p<0.001. The genotype distribution of HPA-4 polymorphism reveals that the HPA-4a4b genotype was more frequent in G1 patients (23/54: 42.6%) than in all HD patients (25/112: 22.3%) or in G2 patients (1/58: 1.72%) (p<0.001, odds ratio: 45.6). Among 24 HD patients with HPA-4a4b genotype, 23 (96%) developed at least 1 or more thrombotic episode on the level of their AVF. However, 30 patients (34.5%) among 87 HD patients with HPA-4a4a genotype presented thrombotic episode (p<0.001). These results reveal a significant association between HPA-4a4b and thrombosis, and it is likely that HPA polymorphisms could be useful markers for potential risk of thrombosis in hemodialysis. [source] Leukocytosis is a risk factor for recurrent arterial thrombosis in young patients with polycythemia vera and essential thrombocythemia,AMERICAN JOURNAL OF HEMATOLOGY, Issue 2 2010Valerio De Stefano There is evidence that leukocytosis is associated with an increased risk of first thrombosis in patients with polycythemia vera (PV) and essential thrombocythemia (ET). Whether it is a risk factor for recurrent thrombosis too is currently unknown. In the frame of a multicenter retrospective cohort study, we recruited 253 patients with PV (n = 133) or ET (n = 120), who were selected on the basis of a first arterial (70%) or venous major thrombosis (27.6%) or both (2.4%), and who were not receiving cytoreduction at the time of thrombosis. The probability of recurrent thrombosis associated with the leukocyte count recorded at the time of the first thrombosis was estimated by a receiver operating characteristic analysis and a multivariable Cox proportional hazards regression model. Thrombosis recurred in 78 patients (30.7%); multivariable analysis showed an independent risk of arterial recurrence (hazard ratio [HR] 2.16, 95% CI 1.12,4.18) in patients with a leukocyte count that was >12.4 × 109/L at the time of the first thrombotic episode. The prognostic role for leukocytosis was age-related, as it was only significant in patients that were aged <60 years (HR for arterial recurrence 3.35, 95% CI 1.22,9.19). Am. J. Hematol., 2010. © 2009 Wiley-Liss, Inc. [source] Deep vein thrombosis in patients with multiple myeloma treated with thalidomide and chemotherapy: effects of prophylactic and therapeutic anticoagulationBRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2004Maurizio Zangari Summary A group of 256 newly diagnosed myeloma patients were enrolled in a phase III study that included 4 monthly cycles of induction chemotherapy and tandem transplant. All patients were randomized to either receive or not receive thalidomide. A total of 221 patients (86%) received no prophylactic anticoagulation (cohort I); 35 patients received low dose coumadin (cohort II). The incidence of deep vein thrombosis (DVT) was significantly higher in the thalidomide arm hazard ratio: 4·5; P < 0·0001). As low dose coumadin (1 mg/d) failed to decrease thrombotic complications in 35 patients (cohort II), low molecular weight heparin (LMWH, enoxaparin 40 mg s.c. q.d.) was instituted as DVT prophylaxis in the thalidomide-treated patients (n = 68) of the subsequent cohort (n = 130, cohort III). This intervention eliminated the difference in DVT incidence between the two arms (thalidomide and no thalidomide). Within cohorts I and II, 36 patients, in whom thalidomide was discontinued after experiencing a thrombotic episode during chemotherapy, subsequently resumed the drug on full anticoagulation; with a median follow-up of 22 months, DVT recurred in four patients (11%). After completing induction and tandem transplantation, 55 patients were re-exposed to thalidomide and chemotherapy during consolidation treatment. Thrombotic complications were observed in 4%. Our experience, although not based on a randomized study, suggests that the excess frequency of thrombosis in patients treated with chemotherapy and thalidomide can be safely reduced by the prophylactic use of LMWH. The rate of DVT recurrence observed in our study upon thalidomide resumption was sufficiently low to allow its continuation in patients who may benefit from this therapeutic intervention. [source] Recombinant factor IX (BeneFix®) by adjusted continuous infusion: a study of stability, sterility and clinical experienceHAEMOPHILIA, Issue 2 2001P. Chowdary The safety and efficacy of adjusted continuous infusion (CI) of recombinant factor IX (FIX; BeneFix®) was assessed in vitro and in a clinical study. BeneFix® was reconstituted at 100 IU mL,1 with or without unfractionated heparin (4 U mL,1) and stored at either 4 °C or room temperature. Reconstituted BeneFix® retained at least 90% activity over 14 days if stored at 4 °C but stability was reduced at room temperature. BeneFix® reconstituted in a sterile pharmacy was free of bacterial contamination. Six patients with haemophilia B received seven CIs of BeneFix® to cover routine surgery and severe bleeding episodes. The CIs lasted between 3 and 10 days. In all cases, haemostasis was excellent and the desired therapeutic FIX level was easily maintained. No thrombotic episodes or inhibitor development occurred but two patients developed thrombophlebitis at the infusion site when heparin was not added to the infusion. BeneFix® is not currently licensed for CI and we suggest that studies to enable licensing should be established as soon as possible. [source] Milder clinical presentation of haemophilia A with severe deficiency of factor VIII as measured by one-stage assayHAEMOPHILIA, Issue 1 2001K. Ghosh During the course of investigations we encountered 11 patients with haemophilia A who had severe factor VIII deficiency as measured by one-stage assay but had surprisingly mild clinical presentation. Four of these patients had either a brother, nephew or maternal uncle with severe clinical manifestations. Two patients had low protein S levels, and one was heterozygous for the factor V Leiden mutation. One patient had a combined deficiency of protein C and antithrombin III. Four patients had a two-stage factor VIII assay value that was much higher than the one-stage assay value. Five patients were heterozygous for the MTHFR gene C677T polymorphism, of whom two patients were also deficient for protein S and one had two-stage factor assay values higher than the one-stage assay values. The patient who was both factor VIII deficient and heterozygous for factor V Leiden had mild clinical presentation as compared to his maternal uncle who was only factor-VIII deficient. The maternal cousin of the same patient was heterozygous for factor V Leiden and had suffered two thrombotic episodes. Thus, the present study advocates that the physiological inhibitors of blood coagulation also play an important role in cases of haemophilia A in the final outcome of haemostasis in vivo. [source] Long-term survival of a child with homozygous protein C deficiency successfully treated with living donor liver transplantationPEDIATRIC TRANSPLANTATION, Issue 2 2009Mee Jeong Lee Abstract:, Homozygous protein C deficiency is an autosomal recessive disorder often presenting with purpura fulminans. Fresh frozen plasma and oral anticoagulation have been used in the treatment of this disease. Lately, protein C concentrate has become the treatment of choice. However, protein C concentrate is not yet widely available in many countries. We report a six-month-old girl with homozygous protein C deficiency who had suffered from frequent thrombotic episodes. She was successfully treated with living donor liver transplantation. Eight years after the transplantation, she remains symptom free. As described here, the liver transplantation offers an alternative curative treatment for children with homozygous protein C deficiency. [source] Reduced in vivo oxidative stress following 5-methyltetrahydrofolate supplementation in patients with early-onset thrombosis and 677TT methylenetetrahydrofolate reductase genotypeBRITISH JOURNAL OF HAEMATOLOGY, Issue 1 2005Antonio Coppola Summary The protective role of folate in vascular disease has been related to antioxidant effects. In 45 patients with previous early-onset (at age <50 years) thrombotic episodes and the 677TT methylenetetrahydrofolate reductase genotype, we evaluated the effects of a 28d-course (15 mg/d) of 5-methyltetrahydrofolate (MTHF) on homocysteine metabolism and on in vivo generation of 8-iso-prostaglandin F2, (8-iso-PGF2,), a reliable marker of oxidative stress. At baseline, patients' fasting total homocysteine (tHcy) was 11·5 ,mol/l (geometric mean) and urinary excretion of 8-iso-PGF2, was 304 pg/mg creatinine, with the highest metabolite levels in the lowest quartile of plasma folate distribution (P < 0·05). After 5-MTHF supplementation, plasma folate levels increased approximately 13-fold (P < 0·0001 versus baseline); tHcy levels (6·7 ,mol/l, P < 0·0001) and urinary 8-iso-PGF2, (254 pg/mg creatinine, P < 0·001) were both significantly lowered, their reduction being proportional to baseline values (r = 0·98 and r = 0·77, respectively) and maximal in patients with the lowest pre-supplementation folate levels (P < 0·05). The effects on folate (P < 0·0001) and tHcy (P = 0·0004) persisted for at least up to 2 months after withdrawing 5-MTHF. In parallel with long-lasting tHcy-lowering effects, a short-course 5-MTHF supplementation reduces in vivo formation of 8-iso-PGF2, in this population, supporting the antioxidant protective effects of folate in vascular disease. [source] Thromboembolic events with lenalidomide-based therapy for multiple myelomaCANCER, Issue 7 2008Smitha Patiyil Menon MBBS Abstract BACKGROUND. The purpose was to evaluate the incidence and risk factors of thromboembolism associated with lenalidomide therapy in newly diagnosed myeloma. METHODS. A pooled analysis was performed of patients with previously untreated multiple myeloma enrolled in clinical trials of lenalidomide-based therapy at the Mayo Clinic, Rochester, Minnesota, and the Italian Myeloma Network, Italy. The incidence of thrombosis, the effect of risk factors such as steroid dose and erythropoietin supplementation, and the effect of prophylaxis were examined. RESULTS. In all, 125 patients enrolled in 3 clinical trials were identified. Patients were stratified based on the concomitant corticosteroid dose. Fifty-two patients were in the high-dose group (dexamethasone 40 mg, 12 days a month); 73 patients were in the low-dose group (prednisone at any dose; or dexamethasone 40 mg, 4 days a month). A total of 110 patients were initiated on thromboprophylaxis; of these, 104 patients (95%) received aspirin. Ten patients (8%) developed deep vein thrombosis, including 4 who were not receiving any thromboprophylaxis at the time of the event. The rate of thromboembolic events was not different between patients who received concomitant erythropoietin therapy and those who did not, 4.8% and 8.6%, respectively (P = .54). A higher number of venous thrombotic episodes occurred in the high-dose corticosteroid group compared with the low-dose corticosteroid therapy group (12% vs 6%), but the difference was not statistically significant (P = .3). CONCLUSIONS. The incidence of deep vein thrombosis is lower than previously reported in the literature. There was a trend to a higher incidence of thrombosis in patients receiving high-dose corticosteroid therapy. Cancer 2008. © 2008 American Cancer Society. [source] | ||||||||||