No abstract available.
Gastrectomy* ; Hyperhomocysteinemia ; Obesity, Morbid* ; Thrombophilia*

No abstract available.
Adenocarcinoma ; Cerebral Infarction ; Pancreatic Neoplasms ; Stroke ; Thrombophilia

Humans ; Myocardial Infarction/complications* ; Thrombophilia/complications*

China ; Humans ; Risk Factors ; Thrombophilia/prevention & control*

In acute myocardial infarction, mural thrombi occur in approximately 20 per cent of patients who do not receive anticoagulant therapy and about 10 percent of thrombi result in systemic embolization. Threrfore, in acute phase of myocardial infarction, heparinization is considered as essential therapeutic regimen which afterwards acute phase, might have no clinical significance. We experienced a patient with recurrent LV apical thrombi inspite of an sufficient anticoagulation. This patient was treated with primary balloon PTCA and optimal duration of anticoa-gulation with IV heparin was maintained. At predischarge follow-up, TTE revealed huge LV apical thrombi and warfarinization was started. Three episodes of appearance and disappearance of thrombi have been noted and we report this patient as thrombophilia associated with acute myocardial infarction.
Follow-Up Studies ; Heparin ; Humans ; Myocardial Infarction* ; Thrombophilia* ; Warfarin

This article summarizes the pathogenesis of hypercoagulability in β thalassemia patients, including platelet activation, alteration of red blood cell membranes, abnormal expression of adhesion molecules on vascular endothelial cells and iron overload. Clinical evidence, clinical manifestations of hypercoagulable state and thrombosis in β thalassemia and the effect of splenectomy on hypercoagulable state were reviewed. Strategies to prevent and treat the thromboembolic events in β-thalassemia intermedia are also discussed, including transfusion therapy to raise hemoglobin levels, avoidance or delay of splenectomy and a number of treatments in the exploration.
Erythrocyte Aggregation ; Humans ; Thrombophilia ; etiology ; prevention & control ; beta-Thalassemia ; complications

Thrombosis of the inferior vena cava (IVC) is a rare condition that can result from various underlying diseases including deep vein thrombosis, major trauma, hypercoagulability disorders, and an obstruction due to tumor involvement and idiopathic causes. Chronic obstruction of the IVC may not be recognized due to the lack of signs and symptoms. Here we report a case of a chronic post-thrombotic obstruction of the inferior vena cava, which was believed to be the cause of a painless gross hematuria.
Hematuria* ; Thrombophilia ; Thrombosis ; Vena Cava, Inferior ; Venous Thrombosis

Hypercoagulability can result from a variety of inherited and, more commonly, acquired conditions. Testing for the underlying cause of thrombosis in a patient is complicated both by the number and variety of clinical conditions that can cause hypercoagulability as well as the many potential assay interferences. Using an algorithmic approach to hypercoagulability testing provides the ability to tailor assay selection to the clinical scenario. It also reduces the number of unnecessary tests performed, saving cost and time, and preventing potential false results. New oral anticoagulants are powerful tools for managing hypercoagulable patients; however, their use introduces new challenges in terms of test interpretation and therapeutic monitoring. The coagulation laboratory plays an essential role in testing for and treating hypercoagulable states. The input of laboratory professionals is necessary to guide appropriate testing and synthesize interpretation of results.
Anticoagulants* ; Antiphospholipid Syndrome ; Humans ; Thrombophilia ; Thrombosis ; Venous Thromboembolism

OBJECTIVE: To assess the changes in the coagulation profiles of patients with chronic kidney disease (CKD) using thromboelastography (TEG) and identify the risk factors of hypercoagulation in CKD patients. METHODS: A total of 128 patients with CKD admitted in Hunan Provincial People's Hospital between August, 2018 and May, 2019 were recruited. The results of conventional coagulation test and TEG were compared between patients with CKD and 21 healthy control adults. The patients with CKD were divided into hypercoagulation group with a maximum amplitude (MA) > 68 mm (=66) and non-hypercoagulation group (MA≤68 mm, =62). The laboratory indicators were compared between the groups, and the factors affecting the hypercoagulable state in patients with CKD were analyzed. RESULTS: The levels of fibrinogen and D-Dimer increased significantly in patients with CKD at different stages as compared with the control subjects ( < 0.05). In the patients with CKD, the reaction time and K time decreased while MA, α-angle and coagulation index increased significantly in patients in stage 3-4 and those in stage 5 either with or without hemodialysis compared with the control group ( < 0.05). The estimated glomerular filtration rate (eGFR), percentage of patients with diabetes mellitus, history of stroke, percentage of neutrophils, neutrophil-lymphocyte ratio, red blood cell count, hemoglobin levels, platelet count, serum creatinine, serum cystatin-C, serum albumin, and lipoprotein (a) all differed significantly between hypercoagulation group and non-hypercoagulation group ( < 0.05). The eGFR, platelet count and hemoglobin levels were identified as independent factors affecting hypercoagulability in patients with CKD ( < 0.05). CONCLUSIONS s The hypercoagulable state of patients with CKD worsens gradually with the disease progression, and eGFR, platelet count and hemoglobin levels are all risk factors for the hypercoagulable state in patients with CKD.
Blood Coagulation ; Humans ; Renal Insufficiency, Chronic ; Risk Factors ; Thrombelastography ; Thrombophilia

Adult ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Phenotype ; Thrombophilia ; genetics ; Thrombosis ; Young Adult