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)

A 67-year-old woman with a history of thrombophlebitis had been taking warfarin sodium for 1 1/2 years when she developed multiple skin lesions resembling warfarin-induced skin necrosis or purpura fulminans. Despite discontinuing the warfarin and administering prednisone, the lesions increased in size. Disseminated intravascular coagulation (DIC) was found and resolved with heparin sodium therapy, and her skin lesions healed. This patient was believed to have an atypical form of purpura fulminans rather than warfarin-induced skin necrosis because of the duration of warfarin therapy and the dramatic resolution with heparin. A monoclonal (IgG) gammopathy was found, which stabilized as the skin lesions resolved, and fulfilled the criteria for a benign (asymptomatic) monoclonal gammopathy.
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PMID:Atypical purpura fulminans with benign monoclonal gammopathy. 64 71

Purpura Fulminans and DIC were the main clinical manifestations of the antiphospholipid syndrome observed in a 62-year-old man. The patient was well until 44 years of age when he began to suffer from recurrent thrombophlebitis, without other symptoms suggestive of immune disease. At the time of hospital admission the pt. appeared acutely ill, showing high fever, severe anemia, massive urinary blood loss, multiple purpuric patches evolving to hemorrhagic bullae and gangrene rapidly spreading over about 30% of the total body area. No signs of neurological involvement or of visceral thrombotic occlusions were present. Clotting tests were consistent with a diagnosis of DIC, further confirmed by skin biopsy showing the presence of thrombi in dermal arterioles. The autoantibody research was positive as follows: Waaler-Rose 1:40, Anti-DNA 1:80; ANF 1:640, aCA IgG 100 GPL. LA was diagnosed according to standard criteria: prolonged KCT and RVVT not corrected by a mixture of normal plasma and abnormal TTI. Plasma exchange in association with heparin and prednisone was effective in arresting the progression of the skin lesion; nevertheless the patient died ten days after hospital admission for sepsi and acute renal failure.
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PMID:Purpura fulminans as clinical manifestation of atypical SLE with antiphospholipid antibodies: a case report. 180 49

Blood assay in patients with DIC-syndrome and thrombosis has shown different changes in red blood cell acid resistance: it is increased in acute noninfectious DIC-syndrome, and significantly decreased in the presence of sepsis, in patients with chronic DIC-syndrome and acute thrombophlebitis it is less lowered, while it is significantly elevated in the development of thromboembolism of the pulmonary artery. At the same time red blood cells damaged due to DIC-syndrome are characterized by increased acid resistance and high coagulation potential. This combination has proved the pathogenetic role of damaged red blood cells and the process of fragmentation in the development of intravascular blood coagulation.
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PMID:[Coagulative activity and acid resistance of damaged and intact erythrocytes in various types of intravascular blood coagulation]. 206 59

A cerebral infarct due to a thrombosis of the left pericallosal artery was the first manifestation of an ovarian adenocarcinoma in a 42-year-old woman. A paraneoplastic origin was suggested by the observation that this patient had chronic intravenous coagulation and subsequently developed migratory thrombophlebitis (Trousseau's syndrome) despite high dose vitamin K antagonists therapy. This was supported by the fact that all manifestations of the hypercoagulable state disappeared following surgical cure of the cancer. Because cerebral infarction can be the first manifestation of a potentially curable cancer, patients with a cerebral infarct of an unknown etiology should be investigated for a malignant process, if there is laboratory or clinical evidence od disseminated intravascular coagulation.
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PMID:Ischemic stroke as the presenting manifestation of localized systemic cancer. 245 36

Experience gained with the use of plasmapheresis in 336 children with different diseases is described. In patients with bacterial and inflammatory processes, the effect was attained after the first plasmapheresis session. Acuity of the immunomediated processes decreased after exfusion of 2-3.5 volumes of the circulating plasma. The replacement of the exfused plasma by protein blood preparations was made only in patients with hepatodystrophy, bacterial and inflammatory diseases, and immune complex diseases combined with the signs of consumption coagulopathy. After a course of plasmapheresis there was a significant lowering of total protein, albumin and immunoglobulin G. The reduction of the content of hemoglobin and red blood cells was related to hemodilution Iron homeostasis remained unchanged. The use of plasmapheresis in atopic dermatitis without preventive administration of an antibiotic is associated with the risk of the development of post-catheterization thrombophlebitis.
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PMID:[Intensive plasmapheresis (programs, laboratory monitoring, complications)]. 258 44

Antithrombin III (AT III) determinations were done in healthy and sick horses using the chromogenic substrate Chromozym TH. Reference values for adult horses at 25 degrees C were 18-25 IU AT III per ml plasma and 84-118% AT III activity of normal horse plasma, respectively. Precision and accuracy were good (intra assay coefficient of variation less than 2%, accuracy 10%). Surgical operations on healthy horses led to a biphasic decrease in AT III activity touching the lower border of the reference values on the second postoperative day. Other reasons for acquired AT III deficiencies included disseminated intravascular coagulation (DIC), liver disease and glomerulonephritis. Using follow-up studies, differences in the dynamics of acquired AT III deficiency and coagulation promoting factors were demonstrated. 12 of 35 horses with decreased AT III values suffered from phlebothrombosis of the jugular veins. It was presumed that acquired AT III deficiencies promote development and progression of phlebothrombosis/thrombophlebitis in horses.
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PMID:[Antithrombin III determination in horses. Reference values and acquired antithrombin III deficiency]. 359 Jan 68

Four patterns of tissue involvement can be distinguished in sepsis due to gram-negative enteric bacilli. When intense local inflammation predominates, cellulitis or thrombophlebitis results, often with venous or arterial obstruction. Bacteria are present in the affected tissues, but not in sufficient numbers to be seen microscopically. When bacterial proliferation is unchecked by an appropriate leukocyte response, ecthyma gangrenosum, erythema multiforme, or diffuse bullous lesions may occur with minimal clinical or histologic signs of inflammation. In symmetric peripheral gangrene associated with disseminated intravascular coagulation, bland fibrinous deposits are seen in small vessels but neither inflammatory cells nor bacteria are present. The fourth kind of lesion is that seen in bacterial endocarditis. In all four patterns a vascular component is prominent clinically and histologically. The pathogenesis of these lesions is multifactorial; in each individual case the interaction between bacterial and host factors probably determines which clinical picture will result. The appearance of symmetric soft tissue lesions of the extremities in the absence of predisposing local conditions suggests the possibility of sepsis due to gram-negative bacilli, especially if other clinical features indicate that sepsis might be present.
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PMID:Cutaneous and soft-tissue manifestations of sepsis due to gram-negative enteric bacilli. 701 88

Of 13,913 patients examined at autopsy between 1939 and 1980, the diagnosis of nonbacterial thrombotic endocarditis (NBTE) was made in 99 instances. There were 53 males and 46 females ranging in age from 4 to 89 years. Vegetations were found on the aortic valve in 39; the mitral in 37; the tricuspid in nine; and the mitral in 37; the tricuspid in nine; and the pulmonic in two. Two-valve involvement was present in 12 cases. Malignant neoplasms were found in 42 autopsies. Embolism to the brain was found in 33 cases and to other organs in 62. Coagulation abnormalities were documented in 22 cases, and a distinct picture of disseminated intravascular coagulation of thrombophlebitis elsewhere in the body should arouse suspicion of NBTE. The high incidence of multiple emboli and its association with malignant neoplasms and with a variety of cardiovascular, pulmonary, renal, and gastrointestinal disorders should provide clues for recognition of this serious disorder.
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PMID:Nonbacterial thrombotic endocarditis. A neurologic perspective of clinicopathologic correlations of 99 patients. 705 7

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

Disseminated intravascular coagulation (DIC) may result in hemorrhagic and thrombotic complications and is rarely associated with stable abdominal aortic aneurysms. In a retrospective review of our experience over the past 5 years, we identified only two instances of DIC-associated abdominal aortic aneurysms among a total of 67 patients who were operated on for asymptomatic aneurysms. In the first patient with DIC induced by abdominal aortic aneurysm, consumptive coagulopathy and a bleeding diathesis developed. The second patient's course was complicated by consumptive coagulopathy and migrating thrombophlebitis. In both instances coagulopathy resolved after surgical intervention. In this report we briefly discuss the pathogenesis and laboratory diagnosis of aneurysm-associated DIC and review current management strategies.
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PMID:Aortic aneurysm-induced disseminated intravascular coagulation. 887 98


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