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Journal: Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis

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Patients with iliac deep vein thrombosis (DVT) have a poor prognosis and high incidence of postthrombotic syndrome (PTS). We evaluated the effect of low-molecular-weight heparin (LMWH; tinzaparin) versus usual care (tinzaparin plus warfarin for ≥12 weeks at home) in the development of PTS according to DVT location (iliac/noniliac) by retrospective analysis of the Home-LITE cohort (480 patients with proximal DVT). Patients with iliac DVT had an overall odds ratio of 0.53 (95% confidence interval [CI] 0.33, 0.83; P = .0079) for PTS (including ulcer data) in favor of tinzaparin. Patients with noniliac DVT had a similar odds ratio (0.79 [95% CI 0.67, 0.93], P = .0046) to that reported in the overall Home-LITE population (0.76 [95% CI 0.66, 0.89], P = .0004; including ulcer data), both in favor of tinzaparin. Long-term LMWH may be a suitable alternative for the prevention of PTS in patients with iliac DVT who are unlikely to undergo invasive thrombolysis.

Concepts: Stroke, Thrombosis, Pulmonary embolism, Vein, Low molecular weight heparin, Anticoagulant, Deep vein thrombosis, Deep vein

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Inflammation is a key feature of atherosclerosis and its clinical manifestations. The leukocyte count has emerged as a marker of inflammation that is widely available in clinical practice. Since inflammation plays a key role in atherosclerosis and its end results, discovering new biomarkers of inflammation becomes important in order to help diagnostic accuracy and provide prognostic information about coronary cardiac disease. In acute coronary syndromes and percutaneous coronary intervention, elevated levels of almost all subtypes of white blood cell counts, including eosinophils, monocytes, neutrophils, and lymphocytes, and neutrophil-lymphocyte ratio and eosinophil-leukocyte ratio constitute independent predictors of adverse outcomes. Eosinophil count and eosinophil-leukocyte ratio, in particular, emerge as novel biomarkers for risk stratification in patients with coronary artery disease. Since the presence of eosinophils denotes hypersensitivity inflammation and hypersensitivity associated with Kounis syndrome, this reality is essential for elucidating the etiology of inflammation in order to consider predictive and preventive measures and to apply the appropriate therapeutic methods.

Concepts: Immune system, Inflammation, White blood cell, Monocyte, Blood, Atherosclerosis, Heart, Artery

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Hyperglycemia alone may not explain the increased risk of cardiovascular diseases (CVDs) in patients with type 1 diabetes (T1D) compared with type 2. This study emphases on the evaluation of some platelet activity markers in patients with T1D, with relevance to some metabolic disorders as hyperlipidemia and hyperglycemia. This study was performed on 35 patients with T1D and 20 healthy controls. All participants were subjected to full history taking, clinical examination and assay of glycated hemoglobin (HbA1c), and lipid profile. The expression of CD62P and CD36 on platelets and the frequency of platelet-monocyte, and platelet-neutrophil aggregates were assessed by flow cytometry. Patients showed significantly higher expression of CD62P and CD36 than the control group. Platelets aggregates with monocytes were also higher among patients than the control group. Levels of CD36+ platelets, CD62P+ platelets, and platelet-monocyte aggregates revealed significant correlations with the levels of HbA1c, total cholesterol, low-density lipoprotein, and triglycerides. Hyperlipidemia and hyperglycemia accompanying T1D have a stimulatory effect on platelet activation which probably makes those patients vulnerable to CVD than nondiabetics.

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Complication of disseminated intravascular coagulation (DIC) is a determinant of the prognosis for patients with sepsis. The purpose of this study was to find DIC-related peptides in blood for prediction and early diagnosis of DIC in patients with sepsis. The participants were 20 patients with sepsis (age: 68.9 ± 11.4 years) and they were divided into 2 groups with (n = 8) and without (n = 12) a complication of DIC. Peptides in the serum of the patients were inclusively analyzed by a new method for peptidome analysis using a target plate, BLOTCHIP. By differential analysis of peptides in the blood from patients in the groups with and without DIC, we selected 13 mass spectrometry (MS) peaks as candidate marker peptides for prediction of DIC. By subsequent MS/MS structural analysis, 8 peptides were successfully identified as marker peptides for DIC in patients with sepsis. The peptides were fragments of serum amyloid A-2 protein, α2-HS-glycoprotein, fibrinogen α chain, fibrinogen β chain, serum albumin, collagen α1 (I) chain, collagen α1 (III) chain, and coagulation factor XIII A chain. In receiver-operating characteristic analysis for the relationships between the marker peptides and DIC, the area under the curve for each of these peptides was 0.594 to 0.760. We identified 8 blood marker peptides for prediction of DIC complication in patients with sepsis. Further studies by direct measurements of the serum peptide levels in larger numbers of patients with sepsis-induced DIC are needed to confirm the findings of this study.

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Disseminated intravascular coagulation (DIC) is an acquired clinicobiological syndrome characterized by widespread activation of coagulation leading to fibrin deposition in the vasculature, organ dysfunction, consumption of clotting factors and platelets, and life-threatening hemorrhage. Disseminated intravascular coagulation is provoked by several underlying disorders (sepsis, cancer, trauma, and pregnancy complicated with eclampsia or other calamities). Treatment of the underlying disease and elimination of the trigger mechanism are the cornerstone therapeutic approaches. Therapeutic strategies specific for DIC aim to control activation of blood coagulation and bleeding risk. The clinical trials using DIC as entry criterion are limited. Large randomized, phase III clinical trials have investigated the efficacy of antithrombin (AT), activated protein C (APC), tissue factor pathway inhibitor (TFPI), and thrombomodulin ™ in patients with sepsis, but the diagnosis of DIC was not part of the inclusion criteria. Treatment with APC reduced 28-day mortality of patients with severe sepsis, including patients retrospectively assigned to a subgroup with sepsis-associated DIC. Treatment with APC did not have any positive effects in other patient groups. The APC treatment increased the bleeding risk in patients with sepsis, which led to the withdrawal of this drug from the market. Treatment with AT failed to reduce 28-day mortality in patients with severe sepsis, but a retrospective subgroup analysis suggested possible efficacy in patients with DIC. Clinical studies with recombinant TFPI or TM have been carried out showing promising results. The efficacy and safety of other anticoagulants (ie, unfractionated heparin, low-molecular-weight heparin) or transfusion of platelet concentrates or clotting factor concentrates have not been objectively assessed.

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Severe thrombocytopenia is a serious condition that frequently arises in patients with myelodysplastic syndrome (MDS) and is associated with poor prognosis. Few studies have investigated the prognostic significance of platelet recovery in patients with MDS having thrombocytopenia. We retrospectively analyzed 117 patients with de novo MDS complicated with thrombocytopenia (platelet count [PLT] < 100 × 109/L). Patients received decitabine treatment (schedule A) or decitabine followed by allogeneic hematopoietic stem cell transplantation (allo-HSCT; schedule B). Severe thrombocytopenia (PLT < 20 × 109/L), identified in 31 (26.5%) patients, was associated with poor survival. The PLT increased significantly after decitabine treatment in the 2 groups. Patients with thrombocytopenia treated with schedule B showed a superior prognosis compared to those treated with schedule A. On analysis of overall survival by platelet response in patients with severe thrombocytopenia, a significant survival advantage was observed in patients who achieved a platelet response, who would further benefit from allo-HSCT following decitabine therapy. The results indicate a potentially favorable prognostic impact of platelet response achieved with decitabine. Patients with MDS having severe thrombocytopenia may benefit from the effective recovery of platelets and further allo-HSCT following decitabine therapy.

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The aim of our study was to evaluate GP6 gene in patients with sticky platelet syndrome (SPS) and fetal loss. Platelet aggregability was tested with platelet-rich plasma using PACKS-4 aggregometer (Helena Laboratories). High-resolution melting analysis on LightCycler 480 II (Roche Diagnostics) was used for single-nucleotide polymorphism (SNP) genotyping. We examined 64 patients with SPS and 54 control participants. We found significantly higher occurrence of 5 SNPs in patients with SPS versus controls (rs1671152, rs1654433, rs1613662, rs1654416, and rs2304167). Moreover, the haplotype analysis showed a significantly higher occurrence of 7 haplotypes in patients with SPS compared to controls (acgg and aagg in GP6_5reg haplotype; ccgt in GP6_3reg haplotype; gg and ta in GP6_REG haplotype; SKTH and PEAN in GP6_PEAN haplotype). Our results, especially higher occurrence of 4 nonsynonymous variants within the coding region, support the idea that GP6 polymorphisms are associated with the platelet hyperaggregability accompanied by fetal loss.

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Venous thromboembolism (VTE) is a highly morbid condition with several available oral anticoagulant treatment options. Numerous studies have been published comparing warfarin to direct oral anticoagulants; however, several populations remain underrepresented in these reports. We surveyed members of The Venous ThromboEmbolism Network U.S. working group regarding their oral anticoagulant preferences for the treatment of VTE in different and challenging populations. In individuals with VTE and no other medical comorbidities, respondents preferred either rivaroxaban (48.7%) or apixaban (48.7%). Apixaban (53.3%) was preferred in elderly individuals with an increased risk of bleeding. Warfarin was preferred in individuals with liver or kidney dysfunction (42% and 47%), altered metabolism (>55%), and antiphospholipid antibody syndrome (84.2%). Low-molecular-weight heparin was preferred in individuals with malignancy (56.6%), followed by edoxaban (23.7%). These findings may help guide clinicians when choosing an anticoagulant in these challenging situations and demonstrate the urgent need for additional study in these groups.

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Our aim is to determine the most appropriate laboratory tests, besides anti-factor Xa (anti-FXa) chromogenic assays, to estimate the degree of anticoagulation with apixaban and compare it with that of rivaroxaban in real-world patients. Twenty patients with nonvalvular atrial fibrillation treated with apixaban 5 mg twice daily and 20 patients on rivaroxaban 20 mg once daily were studied. Conventional coagulation tests, thrombin generation assay (TGA), and thromboelastometry (nonactivated TEM [NATEM] assay) were performed in the 40 patients and 20 controls. The anti-FXa chromogenic assays were used to measure apixaban and rivaroxaban plasma levels. The NATEM measurements showed no significant difference between the 2 groups of patients. Concerning TGA, endogenous thrombin potential (ETP) was significantly decreased in patients on rivaroxaban as compared to those treated with apixaban ( P < .003). A statistically significant, strong inverse correlation between apixaban plasma concentrations and ETP ( P < .001) was observed. Apixaban significantly reduces ETP compared to controls, but to a lesser extent than rivaroxaban. Thrombin generation assay might provide additional information on apixaban exposure, which is required in order to individualize treatment especially for patients with a high bleeding risk. Our findings have to be further investigated in studies with larger sample sizes, in the entire range of apixaban exposure, with other direct oral anticoagulants, and in relation to clinical outcomes.

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Anti-beta-2-glycoprotein 1 (anti-β2GP1) antibodies are associated with increased thrombotic risk in patients with autoimmune disease. There is conflicting evidence on the effects of anti-β2GP1 antibodies on platelets, with both enhanced and inhibited aggregation previously reported. However, previous studies did not include isotype antibodies to ensure the observed effects were due to anti-β2GP1 antibodies. The aims of this study were to (1) investigate the effects of anti-β2GP1 antibodies on collagen-induced platelet aggregation in parallel with negative control (buffer normal saline) and isotype control antibodies and (2) determine the lupus anticoagulant (LA) activity of anti-β2GP1 antibodies used. Three animal-derived anti-human-β2GP1 antibodies (1.25, 2.5, and 5 μg/mL) incubated with healthy platelet-rich plasma were activated by collagen (2.5 μg/mL). Each anti-β2GP1 antibody demonstrated the inhibition of aggregation compared to negative control, but not to isotype control. No anti-β2GP1 antibody demonstrated LA activity, suggesting they were probably nonpathological. This study highlights both negative and isotype control markers are important to validate the effects of anti-β2GP1 antibodies. Assays to measure anti-domain I-β2GP1 antibodies are recommended to be used in conjunction with functional measures to further investigate the effects of anti-β2GP1 antibodies.