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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombotic complications of heparin-induced thrombocytopenia (HIT) can be devastating if not recognized and treated promptly. We describe an unusual case of rapid-onset HIT resulting in massive-bilateral pulmonary emboli in a 70 year-old man who developed chest pain during elective percutaneous coronary intervention (PCI). The diagnosis was made the following day after persistent chest pain and laboratory work demonstrating a new thrombocytopenia, a mildly elevated troponin, and positive DIC panel led to confirmatory imaging tests. HIT-related thrombosis should be considered in the differential diagnosis of chest pain in patients undergoing PCI.
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PMID:Heparin-induced thrombocytopenia (HIT) causing pulmonary emboli during coronary intervention. 1879 44

Disorders of haemostasis and haemocoagulation are often seen in patients with cancer as a part of paraneoplastic syndrome. Thrombotic and/or haemorrhagic complications are the second most common cause of mortality in patients with cancer. The evaluation of the haemostatic parameters of 67 patients with gastric cancer have indicated tendency to thrombophilia and activation of intravascular coagulation, of which 31.3% showed tendency to hypercoagulation and 47.8% disseminated intravascular coagulation (DIC). Only 7.5% of subjects have yielded normal laboratory findings while 5.9% of patients had DIC with remarkable hypocoagulation. Thrombocytosis, platelet hyperaggregability and elevation of beta-thromboglobulin are the indicators of changes in primary haemostasis and elevation of thrombomodulin indicates vascular wall damage. Lower antithrombin III levels, C-protein and S-protein in plasma have indicated lower antithrombotic potential in patients with gastric cancer. It can be concluded that patients suffering from gastric cancer are at higher risk of thromboembolism as for haemorrhagic diathesis (20.1% thromboembolism, 11.94% fatal thromboembolic events vs 5.9 % haemorrhagic diathesis) (Tab. 5, Ref. 22). Full Text (Free, PDF) www.bmj.sk.
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PMID:General changes in hemostasis in gastric cancer. 2019 67

Disseminated intravascular coagulation (DIC) is the physiologic result of pathologic overstimulation of the coagulation system. Despite multiple triggers, a myriad of laboratory abnormalities, and a clinical presentation ranging from gross hemostatic failure to life-threatening thrombosis, or even both simultaneously, a simplified clinical approach augmented by a few readily available tests allows prompt identification of the process and elucidation of treatment opportunities. Platelet counts in DIC may be low, especially in acute sepsis-associated DIC, yet increased in malignancy-associated chronic DIC. Thrombotic risk is not a function of the platelet count, and thrombocytopenia does not protect the patient from thrombosis. The stratification of both thrombotic risk and hemorrhagic risk will be addressed.
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PMID:Thrombocytopenia and thrombosis in disseminated intravascular coagulation (DIC). 2000 4

Thrombotic thrombocytopenia purpura (TTP) is a severe multisystem disorder characterized by fever, microangiopathic hemolytic anemia, thrombocytopenia, neurologic symptoms, and impaired renal function. Platelet counts are usually diminished, whereas the bone marrow shows a large number of megakaryocytes indicating peripheral destruction and consumption of platelets. Coagulation studies in patients with TTP are normal or slightly elevated, which helps differentiate this entity from disseminated intravascular coagulation. The peripheral smear shows an abundance of schistocytes, reticulocytes, and, at times, nucleated red blood cells. Serum lactate dehydrogenase and indirect bilirubin are elevated as a result of mechanical destruction of red blood cells. Legionella pneumophila has been identified as a relatively common cause of both community-acquired and hospital-acquired pneumonia. An association between Legionella and TTP has only been cited once in the literature. Here we present a case of severe TTP with concurrent Legionella infection. Our patient presented with the classic clinical findings of TTP and an ADAMTS13 level of less than 5% associated with an inhibitor. After a 3-week treatment course with plasma exchange, steroids, and antibiotics, he had complete clinical recovery and his ADAMTS13 level increased to greater than 75%.
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PMID:A case of severe thrombotic thrombocytopenic purpura with concomitant Legionella pneumonia: review of pathogenesis and treatment. 2021 82

Thrombotic microangiopathies (TMAs) are syndromes associated with thrombocytopenia and multiple organ failure. Plasma exchange is a proven therapy for primary TMA such as thrombotic thrombocytopenic purpura (TTP). There is growing evidence that plasma exchange therapy might also facilitate resolution of organ dysfunction and improve outcomes for secondary TMAs such as disseminated intravascular coagulation (DIC) and systemic inflammation-induced TTP. In this review, we survey the current available evidence and practice of plasma exchange therapy for TMAs.
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PMID:Plasma exchange therapy for thrombotic microangiopathies. 2129 77

Neonatal renal vein thrombosis (RVT) is associated with potentially serious morbidities. Almost 80% of cases of RVT present within the first postnatal month. The most common risk factors for RVT are birth asphyxia/ in utero fetal distress, being the infant of a diabetic mother, volume contraction and coagulation abnormalities. Thrombus formation may be initiated by vascular injury, diminished vascular flow, increased blood viscosity, hyperosmolality or underlying thrombophilia. The classic triad of RVT includes gross hematuria, flank mass (unilateral or bilateral enlargement of kidneys) and thrombocytopenia. Laboratory tests may reveal hematuria, proteinuria, polycythemia, hemolytic anemia, thrombocytopenia and possibly acute kidney injury. The etiology for a hypercoagulable state should be investigated. Renal ultrasound with Doppler may show increased size of the affected kidney, increased echogenicity and loss of corticomedullary differentiation. Renal venography remains the gold standard for the diagnosis of RVT. Other causes of renal enlargement must be considered. Supportive treatment includes correction of fluid and electrolyte disturbances and treatment of infection and underlying pathophysiologic abnormalities. Use of unfractionated heparin (UFH) or low molecular weight heparin (LMWH) should be considered if there is evidence of disseminated intravascular coagulation. Conventional anticoagulants may attenuate hypercoagulability and decrease the risk for thrombus progression and embolism. Surgery is rarely indicated unless there is bilateral involvement with involvement of the IVC. RVT carries the risk of hypertension and chronic kidney disease.
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PMID:Renal venous thrombosis in neonates. 2508 63

In severe acute pancreatitis (SAP), systemic inflammation leads to endothelial dysfunction and activation of coagulation. Thrombotic disorders in acute pancreatitis (AP) include disseminated intravascular coagulation (DIC). Recently, angiopoietin-2 and soluble fms-like tyrosine kinase 1 (sFlt-1) were proposed as markers of endothelial dysfunction in acute states. Our aim was to assess the frequency of coagulation abnormalities in the early phase of AP and evaluate the relationships between serum angiopoietin-2 and sFlt-1 and severity of coagulopathy. Sixty-nine adult patients with AP were recruited: five with SAP, 15 with moderately severe AP (MSAP) and 49 with mild AP. Six patients were diagnosed with DIC according to International Society on Thrombosis and Haemostasis (ISTH) score. All patients had at least one abnormal result of routine tests of hemostasis (low platelet count, prolonged clotting times, decreased fibrinogen, and increased D-dimer). The severity of coagulopathy correlated with AP severity according to 2012 Atlanta criteria, bedside index of severity in AP and duration of hospital stay. D-dimers correlated independently with C-reactive protein and studied markers of endothelial dysfunction. Angiopoietin-2, D-dimer, and ISTH score were best predictors of SAP, while sFlt-1 was good predictor of MSAP plus SAP. In clinical practice, routine tests of hemostasis may assist prognosis of AP.
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PMID:Serum Concentrations of Angiopoietin-2 and Soluble fms-Like Tyrosine Kinase 1 (sFlt-1) Are Associated with Coagulopathy among Patients with Acute Pancreatitis. 2836 36

Thrombotic microangiopathies (TMAs) are a heterogeneous group of syndromes presenting with a distinct clinical triad: microangiopathic hemolytic anemia, thrombocytopenia, and organ damage. We currently recognize two major entities with distinct pathophysiology: thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). Beyond them, differential diagnosis also includes TMAs associated with underlying conditions, such as drugs, malignancy, infections, scleroderma-associated renal crisis, systemic lupus erythematosus (SLE), malignant hypertension, transplantation, HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), and disseminated intravascular coagulation (DIC). Since clinical presentation alone is not sufficient to differentiate between these entities, robust pathophysiological features need to be used for early diagnosis and appropriate treatment. Over the last decades, our understanding of the complement system has evolved rapidly leading to the characterization of diseases which are fueled by complement dysregulation. Among TMAs, complement-mediated HUS (CM-HUS) has long served as a disease model, in which mutations of complement-related genes represent the first hit of the disease and complement inhibition is an effective and safe strategy. Based on this knowledge, clinical conditions resembling CM-HUS in terms of phenotype and genotype have been recognized. As a result, the role of complement in TMAs is rapidly expanding in recent years based on genetic and functional studies. Herein we provide an updated overview of key pathophysiological processes underpinning complement activation and dysregulation in TMAs. We also discuss emerging clinical challenges in streamlining diagnostic algorithms and stratifying TMA patients that could benefit more from complement modulation. With the advent of next-generation complement therapeutics and suitable disease models, these translational perspectives could guide a more comprehensive, disease- and target-tailored complement intervention in these disorders.
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PMID:Complement in Thrombotic Microangiopathies: Unraveling Ariadne's Thread Into the Labyrinth of Complement Therapeutics. 3089 Oct 33

Coronavirus disease 2019 (COVID-19) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus strain disease, has recently emerged in China and rapidly spread worldwide. This novel strain is highly transmittable and severe disease has been reported in up to 16% of hospitalized cases. More than 600,000 cases have been confirmed and the number of deaths is constantly increasing. COVID-19 hospitalized patients, especially those suffering from severe respiratory or systemic manifestations, fall under the spectrum of the acutely ill medical population, which is at increased venous thromboembolism risk. Thrombotic complications seem to emerge as an important issue in patients infected with COVID-19. Preliminary reports on COVID-19 patients' clinical and laboratory findings include thrombocytopenia, elevated D-dimer, prolonged prothrombin time, and disseminated intravascular coagulation. As the pandemic is spreading and the whole picture is yet unknown, we highlight the importance of coagulation disorders in COVID-19 infected patients and review relevant data of previous coronavirus epidemics caused by the severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1) and the Middle East Respiratory Syndrome coronavirus (MERS-CoV).
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PMID:Coagulation disorders in coronavirus infected patients: COVID-19, SARS-CoV-1, MERS-CoV and lessons from the past. 3230 83

Thrombotic complications and coagulopathy frequently occur in COVID-19. However, the characteristics of COVID-19-associated coagulopathy (CAC) are distinct from those seen with bacterial sepsis-induced coagulopathy (SIC) and disseminated intravascular coagulation (DIC), with CAC usually showing increased D-dimer and fibrinogen levels but initially minimal abnormalities in prothrombin time and platelet count. Venous thromboembolism and arterial thrombosis are more frequent in CAC compared to SIC/DIC. Clinical and laboratory features of CAC overlap somewhat with a hemophagocytic syndrome, antiphospholipid syndrome, and thrombotic microangiopathy. We summarize the key characteristics of representative coagulopathies, discussing similarities and differences so as to define the unique character of CAC.
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PMID:The unique characteristics of COVID-19 coagulopathy. 3255 65


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