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)

The appearance of lesional edema in the region of the alveolar wall constitues the initial phenomenon of involvement of the pulmonary parenchyma during shock lung, fat embolism, DIC and post perfusion lung syndrome. The alveolar septum reacts in a monomorphous manner to these various agressions, although the responsible physiopathological factors are numerous and varied. The lung in E.C.C. represents a vertiable experimental post-agressive lung. It has been studied in man from the clinical, radiological, hemodynamic and anatomopathological standpoints. The modifications found enable one to better understand the etiological factors intervening in the other post-agressive lungs.
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PMID:[Pulmonary edema due to shock, fat embolism, disseminated intravascular coagulation and post extracorporeal circulation]. 0 70

Previous studies have demonstrated that new antigenic specificities, not detectable on parental cells, can be induced by in vivo treatment of murine leukemic cells with anti-neoplastic agents. The immunologic properties of leukemic cells altered by treatment with 5-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide (DIC) were investigated further. Immunologic cross-reactivity between two DIC-treated leukemic sublines has been demonstrated by cell-mediated immunity in vitro and by active or adoptive immunity in vivo. Rabbit antiserum to DIC-treated sublines absorbed with the parental cells showed residual activity against the DIC-sublines that was specifically inhibited by further absorption with DIC-cells.
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PMID:Immunologic cross-reactivity of antigen(s) induced by drug treatment in two leukemic sublines. 5 28

Sixteen patients with Hodgkin's (10) and non-Hodgkin's (6) lymphoma were treated by the "ABCD scheme", which is a combination of adriamycin (25-30 mg/m2 day 1), bleomycin (15 mg day 1-5), CCNU (60 mg/m2 day 1) and DIC (90-100 mg/m2 day 1-5). 15 results are evaluable and included 5 complete remissions, 5 partial remissions, 2 stabilizations, 2 progressions and 1 early death (remission rate: 66%). 45 ABCD courses were given. 8 patients received more than one course (maximum 7 courses). Toxicity was tolerable and consisted mainly of myelodepression, nausea, vomiting and muco-cutaneous alterations. Two patients died following toxicity, one from myelosuppression and the other from interstitial pulmonary fibrosis. The results suggest that this combination can be useful where the usual chemotherapy combination fails.
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PMID:[Simultaneous combination of adriamycin, bleomycin, cyclohexyl-chloroethyl nitrosourea with dimethyl-triazeno imidazole carboxamide in the treatment of Hodgkin's lymphoma]. 6 45

DIC may complicate prostatic disease either in its acute type during resection of the prostate causing excessive intra- or postoperative bleeding, or in its chronic type in cases with adenocarcinoma of the prostate with haematogenous metastases. Pathogenesis, diagnosis, clinical course, differentiation of the condition against consumption of clotting factors by primary fibrinolysis, and treatment are discussed. The course in four characteristic cases is demonstrated.
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PMID:Disseminated intravascular coagulation in prostatic disease. 6 93

In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates. During the DIC reaction increasing inhibition of aggregability of circulating platelets against collagen and ADP is observed. Furthermore, ASA prevents the increase in the plasma haemoglobin level caused by DIC.
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PMID:[Effect of ASS on platelet function in experimental DIC]. 9 74

DIC is a hemorrhagic syndrome frequently encountered as a complication in severe gram-negative bacterial sepsis. An animal model for sepsis-associated DIC was developed in order to permit study of the appearance and development of this syndrome in relation to the entire disease process. Rhesus monkeys (4 to 6 kg) were infected by intravenous injection of 10(9) Salmonella typhimurium organisms and studied for a period of 7 to 10 days following infection. Ten of 23 infected monkeys developed petechial rash characteristic of DIC, which appeared on days 1 to 2 infection and lasted 4 to 5 days. In the group of monkeys developing rash, activation of coagulation was suggested by an 80% decrease in platelet count and 20% to 30% increases in PT and APTT. Fibrinolytic system activation was indicated by the appearance of FDP. Kinin system activation was evidenced by decreases in both prekallikrein nad kininogen. Changes in laboratory tests suggestive of subclinical DIC were also noted in infected monkeys which did not develop a rash. Pathologic evidence of DIC was obtained through observation of numerous fibrin thrombi in the kidneys of the only monkey which died in the course of infection. Occurrence of DIC in association with this experimental infection in rhesus monkeys was established on the basis of clinical, laboratory, and pathologic criteria. Expression of the syndrome on days 1 to 2 following infection correlated with the period of increasing bacteremia.
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PMID:Model for disseminated intravascular coagulation: bacterial sepsis in rhesus monkeys. 9 3

Dyspnea, back pain, edema, and cyanosis developed suddenly in a 23-year-old woman during the last trimester of her first pregnancy. Although she had been noticed to have the enlarged heart and exertional shortness of breath to a slight degree, she had been apparently in good condition without any significant heart murmurs. Clinically, recurrent episodes of disseminated intravascular coagulation, including pulmonary thrombosis, were thought to be superimposed to Eisenmenger syndrome associated with toxemia of pregnancy. Anticoagulant and fibrinolytic treatments were tried, but their effectiveness was limited by hemorrhagic diathesis. She died of respiratory and circulatory failure after delivery of a moribund baby. Autopsy revealed Eisenmenger complex (a defect in the membranous portion of the interventricular septum and pulmonary vascular disease) and many fresh hemmorrhages in both lungs with a lot of new and organized thrombi. Fresh thrombi were also seen in the heart, the pancreas and the kidneys. The high peripartal mortality in Eisenmenger syndrome could be attributed to pulmonary thrombosis, which may be related to DIC, as well as to peripartal changes in circulatory function.
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PMID:An autopsied case of Eisenmenger syndrome complicated by recurrent thromboembolic phenomena in postpartal period. 13 43

Both deep venous thrombosis and DIC are intermediate mechanisms of disease--both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.
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PMID:The intravascular generation of fibrinogen derivatives and the blood vessel wall in venous thrombosis and disseminated intravascular coagulation. 14 74

In states of plasmic hypercoagulability and consumption coagulopathy ethanol favours the non-enzymatic polymerization of circulating soluble fibrinogen fibrin monomer complexes (FFMC) in vitro. The ethanol-gelation test of Godal and Abildgaard makes use of this phenomenon, called paracoagulation. The present studies show that it is also possible to visualize soluble FFMC by means of ethanol-gelation. In the electron microscope, FFMC, polymerized non-enzymatically by ethanol in the spleen, are characterized by plump or slender mycelioid fibrillar precipitates that show a uniform rhythmic transverse striation, a period-coincidental filamentary arrangement and an average periodicity of 23 nm. The ultrastructure demonstrates these ethanol-induced filaments to be in vitro-polymerized fibrin monomer derivatives. Paracoagulation with ethanol allows the identification of soluble FFMC in the tissue prior to the formation of highly polymerized fibrin-rich microthrombi, the established equivalents of the DIC-syndrome. The electron microscope studies also show the existence of a second type of fibrillary structure in the tissue polymerized by ethanol. This second type lacks the characteristic periodicity of fibrin and the period-coincidental arrangement of the filamentary structures, but is characterized by closely packed or chain-like aligned, irregularly sized spherical bodies. There is some evidence that these spherical bodies in vitro represent non-enzymatically polymerized complexes of fibrin monomers and fibrin degradation products (FDP), the equivalent of a limited local or generalized fibrinolysis in vivo.
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PMID:Identification of soluble fibrinogen fibrin monomer complexes by non-enzymatic polymerisation in the tissue. 14 78

Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
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PMID:Changes of prekallikrein in the cases with disseminated intravascular coagulation syndrome. 16 Jan 91


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