Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three laboratory tests for the measurement of antithrombin III (AT III) were evaluated. The tests measured functional AT III in serum and plasma, and the third measured AT III antigen in plasma. Normal values for each method were obtained by testing samples from 20 normal subjects. Each test was then performed on specimens from 15 patients clinically suspected of having hypercoagulable states. Each determination was run in duplicate. The hypercoagulable states included disseminated intravascular coagulation, pulmonary embolism, and pregnancy. Two-thirds of these patients were found to have antithrombin III levels below the normal range by all three of the methods studied. Patients who had decreased AT III activity in the functional assays also had decreased AT III antigen.
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PMID:An evaluation of antithrombin III laboratory tests. 736 77

We report the case of a 22-year-old obese woman with severe protein S deficiency, probably genetic in nature, associated with recurrent venous thrombosis. Protein S deficiency is a rather rare disease: it may be an inherited, either homozygous (purpura fulminans at neonatal age), heterozygous, or acquired disorder. The thrombophilic state may be manifested as deep vein thrombosis or thrombophlebitis of the superficial veins with a high risk of pulmonary embolism in the young, and it is often exacerbated by pregnancy. In our case, the presenting event, bilateral deep venous (iliac-femoral) thrombosis complicated by disseminated intravascular coagulation, had occurred when the patient was 13 years old. We started long-term therapy with oral coagulants, i.e. warfarin even if the latter may cause skin necrosis ("warfarin dermatitis") in some patients with protein S deficiency. The clinician must consider protein S deficiency in cases of recurrent thrombosis, particularly in young patients: the importance of early implementation of long-term preventive therapy should not be underestimated.
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PMID:[Protein S deficiency and thrombophilia: presentation of a clinical case and review of the literature]. 794 92

Of 1,048 renal transplants performed between 1971 and 1990, transplant nephrectomy was performed in 86 (8.2%). Mean patient age was 33 years (range 3.8 to 66.5). Postoperative complications occurred in 60% of the patients, including wound infection in 20% and major hemorrhage in 4 patients. The external iliac artery was ligated in 4 patients. The incidence and severity of the complications were greater in patients with acute rejection. Four patients died: 1 of ischemic bowel and metastatic carcinoma, 1 of pulmonary embolism, and 2 of sepsis and disseminated intravascular coagulation. The nephrectomy rate increased significantly (p < 0.005) when cyclosporine A was initially introduced. Added care is necessary when new immunosuppressants are used. The majority of our failed transplants were left in situ without compromising overall patient well-being.
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PMID:Transplant nephrectomy over 20 years: factors involved in associated morbidity and mortality. 812 9

This is a case report on a course of gemini-pregnancy complicated by gestosis, recurrent submassive pulmonary embolism and discordant growth of the hypotrophic twins. It is concluded from this report that: 1. the AT-III-deficiency in gestosis can be caused by loss and consumption; 2. due to decrease below a critical AT-III-level the coagulation-fibrinolysis system tends to decompensate, reflected in a disseminated intravascular coagulation and/or a pulmonary embolism. The tendency consists particularly in immobilisation and stasis; 3. the daily determination of AT III, better of TAT-complex and D-dimer, the daily clinical examination regarding signs of thrombosis and in cases of heparinization the measurement of PTT several times daily, are necessary to avoid or recognise disorders, of the coagulation-fibrinolysis-system at an early stage. 4. The increased consumption in coagulation systems can be avoided by AT-III substitution and correct heparinisation. 5. In cases of risk of pulmonary embolisation in pregnancy a cava filter should be temporarily implanted. The filter must be changed every 3 days, if it is required for a longer period. 6. In high-risk pregnancy the check for factors of thrombophilia is a basic diagnostic procedure.
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PMID:[Gestosis, thrombophilia and pulmonary embolism in a primipara with twin pregnancy]. 848 92

The relationship between cancer and abnormalities of blood coagulation has been recognized for well over a century. Deep venous thrombosis of the lower extremities is most common, but pulmonary embolism, upper extremity vein thrombosis, disseminated intravascular coagulation, and other, more unusual, clinical events may occur. Chemotherapy also has been linked to thrombotic episodes. Anticoagulant therapy is appropriate in many patients with venous or arterial thrombosis. Prophylaxis of venous thrombosis is particularly important in hospitalized cancer patients who are at bed rest or undergoing surgery.
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PMID:Thrombosis in patients with cancer. 850 72

A low-D-Dimer concentration has a high negative predictive value for thromboembolic events. Actual and proposed applications include exclusion diagnosis of DIC, DVT and pulmonary embolism (1-7), follow up of cancer therapy (8) and diagnosis of abruptio placentae(9). A variety of tests are commercially available. Unfortunately, due to differences in standardization protocols, the cut-off normal/pathological of one test can usually not be used for another(10). As was shown by Nieuwenhuizen, one way to at least reduce these discrepancies is to use patient material as a reference(11). We have used this approach to standardize the latex test Tinaquant a D-Dimer against the ELISA test Asserachrom D-Dimer.
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PMID:Pooled patient samples as reference material for D-Dimer. 857 41

Although rare, exertional collapse and sudden death are the most serious potential complications of sickle cell trait. Studies suggest that this condition may occur in susceptible persons when poor physical conditioning, dehydration, heat stress or hypoxic states precipitate sickling of the abnormal erythrocytes. Sickling leads to endothelial damage, which can cause vasoconstriction, disseminated intravascular coagulation and local tissue damage. Cardiac effects include acute ischemia and arrhythmias. Muscle damage results in acute compartment syndromes and release of myoglobin into the circulation. Acute renal failure is possible. Diagnosis is based on a high index of suspicion, and characteristic presentation and laboratory findings, including myoglobinuria, hyperkalemia, hypocalcemia, hyperphosphatemia and elevated creatine kinase levels. The differential diagnosis includes pulmonary embolism, acute cardiac events, anaphylaxis and heat stroke. Management is based on stabilization, rehydration, and the treatment and prevention of complications.
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PMID:Exertional collapse and sudden death associated with sickle cell trait. 904 99

Until recently, the confusing clinical profile of HIT and the widespread unavailability of reliable diagnostic assays have conspired to produce under-recognition-if not frank skepticism-of the clinical importance of HIT. However, during the 1990s, HIT has emerged as one of the major-if not the most important-immunohematologic problems in clinical medicine. The clinical and laboratory investigations summarized here have contributed to a greater understanding of the frequency, clinical spectrum, pathogenesis, laboratory diagnosis, and-potentially-the prevention of this important drug allergy. Further, the demonstration of increased platelet procoagulant activity and, thrombin generation in HIT, together with insights into the pathogenesis of a new clinicopathologic syndrome (venous limb gangrene), help explain how a disorder characterized by IgG-mediated platelet activation can lead to such diverse clinical sequelae as venous thrombosis, pulmonary embolism, disseminated intravascular coagulation, and venous limb gangrene. These studies should lead to improved treatment of HIT (new emphasis on suppression of thrombin generation, eg, hirudin and its analogs), future avoidance of HIT (preparation of low-molecular-weight heparins and heparinoids that are less immunogenic), and a greater understanding of the interaction between platelet activation and procoagulant/anticoagulant processes.
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PMID:Heparin-induced thrombocytopenia: IgG-mediated platelet activation, platelet microparticle generation, and altered procoagulant/anticoagulant balance in the pathogenesis of thrombosis and venous limb gangrene complicating heparin-induced thrombocytopenia. 889 54

The incidence and clinical significance of pulmonary embolism (PE) in pulmonary malignancy were analysed among 111 autopsy cases including: 65 primary and 24 metastatic lung cancer, 8 hematological malignancies and 14-malignant pleural mesothelioma. In 34 (31%) cases PE was found, in 4 (12%) patients cancer tissue emboli was documented. In nonsmall cell lung cancer the frequency of PE was 40%, compared to 24% in small cell, 25% in metastatic lung cancer and 14% in mesothelioma. Deep venous thrombosis of lower extremities was the source of thrombotic material in 35% cases. In remaining cases the sources of thrombotic material were different (caval vein inferior, superior, and their main branches, right heart cavities, pulmonary artery). In 8 patients with PE the acute form of DIC was observed. In 15 (44%) patients the clinical ante mortem diagnosis of PE was done. In 26% of all analysed cases PE was the direct cause of death. We concluded that PE is a frequent and dangerous complication of lung neoplasms. Clinical diagnosis can be extremely difficult.
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PMID:[Pulmonary embolism in malignancy of the lung: a retrospective clinical evaluation and pathomorphologic personal material]. 898 39

Intracranial surgery is often complicated by thromboembolic events including the life-threatening pulmonary embolism. After head trauma and in patients with brain tumors disseminated intravascular coagulation (DIC) can occur, characterized by the triggering of the coagulation cascade and the depletion of coagulation factors which ultimately leads to bleeding. The identification of patients at high risk as well as the early diagnosis of hemostatic problems uses routine laboratory parameters such as partial thromboplastin time and prothrombin time reflecting the intrinsic and the extrinsic pathway of the coagulation respectively. Thrombin antithrombin III complexes (TAT) and prothrombin fragment 1 + 2 (F1 + 2) are further indicators of an activation of the coagulation whereas fibrinogen degradation products (FDP) refer to the fibrinolytic system. The basic principles of coagulation and fibrinolysis are summarized as well as the changes of laboratory parameters accompanying DIC, hypercoagulability and hyperfibrinolysis.
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PMID:What the neurosurgeon needs to know about the coagulation system. 898 62


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