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

Thromboembolic (TE) events have been frequently reported in beta-thalassemic patients in association with known risk factors such as diabetes, complex cardiopulmonary abnormalities, hypothyroidism, liver function anomalies, and postsplenectomy thrombocytosis. In a recent survey involving 9 Italian thalassemic centers, we identified 32 patients with TE episodes in a total of 735 subjects, of whom 683 had thalassemia major and 52 thalassemia intermedia, corresponding to 3.95 and 9.61%, respectively. There was a great variation in localization: the main one (16/32) was CNS, with a clinical picture of headache, seizures and hemiparesis. Other localizations were the pulmonary (3 patients), mesenteric (1 patient) and portal (2 patients) sites. There were 6 cases of deep venous thrombosis (2 in the upper limbs, 4 in the lower ones). Intracardiac thrombosis was found in 2 subjects and clinical and laboratory signs of DIC were observed in 2 others during pregnancy. Since our patients with TE events present a statistically significantly higher incidence of associated dysfunction (cardiomyopathy, diabetes, liver function anomalies, hypothyroidism) than those without TE events (50 vs. 13.8%), we suggest close monitoring of those patients who are at higher risk of developing TE events because of the presence of one or more of these predisposing factors.
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PMID:Thromboembolic events in beta thalassemia major: an Italian multicenter study. 985 99

Alistair Reid was an outstanding clinician, epidemiologist and scientist. At the Penang General Hospital, Malaya, his careful observation of sea snake poisoning revealed that sea snake venoms were myotoxic in man leading to generalized rhabdomyolysis, and were not neurotoxic as observed in animals. In 1961, Reid founded and became the first Honorary Director of the Penang Institute of Snake and Venom Research. Effective treatment of sea snake poisoning required specific antivenom which was produced at the Commonwealth Serum Laboratories in Melbourne from Enhydrina schistosa venom supplied by the Institute. From the low frequency of envenoming following bites, Reid concluded that snakes on the defensive when biting man seldom injected much venom. He provided clinical guidelines to assess the degree of envenoming, and the correct dose of specific antivenom to be used in the treatment of snake bite in Malaya. Reid demonstrated that the non-clotting blood of patients bitten by the pit viper, Calloselasma rhodostoma [Ancistrodon rhodostoma] was due to venom-induced defibrination. From his clinical experience of these patients, Reid suggested that a defibrinating derivative of C. rhodostoma venom might have a useful role in the treatment of deep vein thrombosis. This led to Arvin (ancrod) being used clinically from 1968. After leaving Malaya in 1964, Alistair Reid joined the staff of the Liverpool School of Tropical Medicine, as Senior Lecturer. Enzyme-linked immunosorbent assay (ELISA) for detecting and quantifying snake venom and venom-antibody was developed at the Liverpool Venom Research Unit: this proved useful in the diagnosis of snake bite, in epidemiological studies of envenoming patterns, and in screening of antivenom potency. In 1977, Dr H. Alistair Reid became Head of the WHO Collaborative Centre for the Control of Antivenoms based at Liverpool.
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PMID:Hugh Alistair Reid OBE MD: investigation and treatment of snake bite. 963 63

It is clear that patients with malignancy, particularly adenocarcinomas, have an increased propensity to thrombosis. It also appears that patients with malignancy and thrombosis are relatively refractory to warfarin therapy and some may not respond ideally to heparin preparations. Occult malignancy in patients with unexplained thrombosis is of concern; however, the incidence varies with the age of the patient approaching 10% in those over 50 years of age. The extent of the evaluation for an underlying occult malignancy should be dictated by clinical judgment. Recurrent unexplained DVT, resistance to warfarin, and thrombosis of unusual sites are the major clues to significantly enhance the suspicion of an occult malignancy. In general, patients with thrombosis and malignancy need not be evaluated for hereditary or acquired hemostasis defects; finding one of these defects is both unlikely and will probably not alter antithrombotic therapy. Hemorrhage in cancer patients is usually due to thrombocytopenia related to chemotherapy (particularly solid tumors) or bone marrow failure (usually leukemias), or disseminated intravascular coagulation (DIC). DIC is usually seen in M-3 and M-4 leukemia or in septic patients with solid tumors. Finally, catheter thrombosis is a common problem in patients with cancer and can be significantly decreased with the routine use of low-dose warfarin therapy.
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PMID:Issues of thrombosis and hemorrhagic events in patients with cancer. 989 Dec 25

Many studies have demonstrated increased coagulation activation in cancer patients and have shown evidence of chronic, low-grade disseminated intravascular coagulation, although most patients remained asymptomatic. In general, patients have not been screened for deep venous thrombosis (DVT). We screened 98 patients with advanced malignancy for DVT using light reflection rheography. Coagulation profiles of DVT and non-DVT groups were studied. We found a high prevalence of DVT (50%) on screening. Overall, the patients had raised levels of fibrinogen (66% patients), factor VIII:C (43%), fragment 1 + 2 (71%) and TAT levels (89%). Patients with DVT had a significantly lower level of fibrinogen than those without (4.0 g/dl, SD 1.4, compared with 4.7 g/dl SD 1.6, P = 0.04). There was no significant difference in other coagulation or liver function tests between the DVT and non-DVT groups. The wide variation of results makes their interpretation difficult and unlikely to be of predictive value in estimating individual thrombotic risk.
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PMID:Abnormal coagulation and deep venous thrombosis in patients with advanced cancer. 1019 64

The HELLP syndrome (HS) belongs to the list of obstetric complications believed to be associated with coagulation disorders. It was formerly thought that chronic intravascular clotting (DIC) in the placental vessels was the main cause. A hypercoagulable state has been reported in cases of severe HS associated with microvascular abnormalities that may involve cerebral, placental, hepatic and renal vessels. A case of acute pancreatitis and DVT of inferior cava in a pregnant woman, presenting with HS at 29 weeks, who was found to have a R506Q mutation, is reported. Preeclampsia-associated pancreatitis and DVT have rarely been reported. It is hypothesized that APC-R and Factor V Leiden mutation may prove to be new and more important markers capable of predicting a more significant maternal morbidity associated with HS. Thrombosis prophylaxis may be considered during pregnancy in order to reduce hazardous multiorgan failure (MOF) in women who are heterozygous for Factor V Leiden mutation.
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PMID:Acute pancreatitis and deep vein thrombosis associated with HELLP syndrome. 1023 Feb 42

Hemostatic disorders are frequently observed in patients with malignancy with a significant proportion developing thrombotic and/or hemorrhagic complications including disseminated intravascular coagulation (DIC), deep venous thrombosis (DVT), and thrombocytopenia. Together, these abnormalities are the second most common cause of mortality in cancer patients, which has led many investigators to try to unravel the pathogenesis of thromboembolic disease, in the eventuality that this will lead to novel therapeutic treatments. The plasminogen activation system is one pathway that has been consistently implicated in cancer. Its relevance to cancer extends from being responsible for many of the hemorrhagic episodes that occur in cancer patients to being fundamental to many, if not all of the molecular mechanisms that define tumor progression. Recent developments of clinical significance shall be reviewed with respect to the role of the plasminogen activation system in tumor growth and metastasis dissemination and in the thrombophilic state in the cancer patient.
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PMID:The role of the plasminogen activation system in cancer. 1035 86

Rocky Mountain spotted fever and Mediterranean spotted fever are rickettsial infections primarily of endothelial cells that normally have a potent anticoagulant function. As a result of endothelial cell infection and injury, the hemostatic system is perturbed and shows changes that vary widely from a minor reduction in the platelet count (frequently) to severe coagulopathies, such as deep venous thrombosis and disseminated intravascular coagulation (rarely). Changes favoring a hypercoagulable state include endothelial injury and release of procoagulant components, activation of the coagulation cascade with thrombin generation, platelet activation, increased antifibrinolytic factors, consumption of natural anticoagulants, and possibly high levels of coagulation-promoting cytokines. Yet, most studies have been performed on endothelial cell cultures that provide nonphysiologic, reductionistic, experimental conditions. The lack of flow, platelets, and WBCs makes these experiments far from simulating the response of endothelial cells in the human body. Coagulopathies and thrombotic events should be considered as potential complications of severe Rocky Mountain spotted fever and Mediterranean spotted fever.
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PMID:Hemostatic changes in Rocky Mountain spotted fever and Mediterranean spotted fever. 1043 95

Budd-Chiari syndrome is a rare disease, but there are many known causes. Recent studies showed that it can be an acquired lesion resulting from thrombosis in some elderly patients. We report a 74-year-old man with Budd-Chiari syndrome attributed to chronic deep venous thrombosis and alcoholic liver cirrhosis. When he was aged 45 years, stasis ulcers of the lower extremities appeared. Cerebral infarction and left hemiparesis occurred at age 71. Ultrasonography, venacavography, and three-dimensional-magnetic resonance imaging on admission demonstrated total obstruction of the inferior vena cava with several massive thrombi and developed collateral vessels. Although the etiology of the thrombosis remained obscure, we made some speculative assumptions that chronic disseminated intravascular coagulation (which is frequently observed in cirrhosis) or hereditary coagulopathy could be involved, from his familial history of thrombotic phenomena and a severe deficiency of clotting inhibitors. Despite the high mortality of untreated Budd-Chiari syndrome reported in previous studies, this patient had been alive for about 30 years from the suspected onset.
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PMID:Aged Budd-Chiari syndrome attributed to chronic deep venous thrombosis with alcoholic liver cirrhosis. 1053 95

This article addresses the issue of thromboembolic disorders associated with the prothrombin G20210A gene mutation, with heparin cofactor II (HC-II) defects and with primary (essential) thrombocythemia. The prothrombin gene mutation is of recent discovery, is inherited as an autosomal dominant disorder, and seems to be highly prevalent in the general white population. The incidence is almost as high as that known for factor V Leiden. Both venous and arterial thromboses are noted, especially deep venous thrombosis, including cerebral venous events and myocardial infarction. As with other congenital thrombophilic states, additional risk factors or multiple defects seem to precipitate the events. Although initially elevated plasma prothrombin levels were described in these patients, this is no longer valid for all patients. At this time there is no easy screening test to detect this defect, but, because of the high prevalence, prothrombin G20210A gene mutation should routinely be assayed for in thrombophilic patients. The association between HC-II defects and thromboembolism is more controversial, and reports both confirming and denying this association have been described. The congenital form of HC-II defect is autosomal dominant. HC-II can be determined by its activity and immunologically. HC-II defects very likely play a role in conjunction with other congenital or acquired defects. Acquired HC-II defects are found in association with systemic disseminated intravascular coagulation (DIC) but not with local activation of the hemostasis system. HC-II levels are also decreased in preeclamptic women, and newborns have physiologically low levels. HC-II defects in thrombophilic patients should be considered after the more common disorders have been ruled out. Primary (essential) thrombocythemia can be associated with both thromboembolic events and bleeding. Typical thrombotic manifestations are erythromelalgia and microvascular thrombosis. Also, pregnant females suffer high rates of complications, such as spontaneous abortion. A number of treatment modalities are at present available to not only decrease platelet counts but also manage thromboembolic events.
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PMID:Prothrombin G20210A gene mutation, heparin cofactor II defects, primary (essential) thrombocythemia, and thrombohemorrhagic manifestations. 1054 71

Thrombosis of the caudal vena cava in a dog secondary to metastatic neoplasia is described. The dog had a palpable abdominal mass and persistent thrombocytopenia due to a thrombosed caudal vena cava that was surgically removed. A few days after its removal, the dog died and neoplastic cells of neural crest origin were identified at the edge of the thrombus. Massive thrombosis can be an unusual cause of platelet consumption, leading to thrombocytopenia and disseminated intravascular coagulation. Deep vein thrombosis of the vena cava can occur in dogs and may mimic an abdominal mass. Multiple mechanisms may be involved in the development of venous thrombosis, including endothelial damage by neoplastic cells and the presence of a hypercoagulable state secondary to neoplasia. Extensive collateral circulation may allow removal of diseased vena cava.
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PMID:Thrombosis of the caudal vena cava presenting as an unusual cause of an abdominal mass and thrombocytopenia in a dog. 1073 Jun 25


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