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

Disseminated intravascular coagulation (DIC) was produced by an infusion of a prothrombin activator (Echis carinatus venom; 30 minutes; 0.5 NIH thrombin equivalent U/kg) in mongrel dogs (Echis group, n = 7). Fibrinogen declined to below measurable levels (less than 25 mg/dl), and fibrin-fibrinogen degradation products appeared (53 +/- 8 micrograms/ml) at end venom infusion in the Echis group. These alterations were not seen when an irreversible thrombin inhibitor, D-phenylalanyl-L-prolyl-L-arginine-L-chloromethyl ketone (PPACK) (57 nmol/kg/min for 120 minutes), was given alone (PPACK group, n = 5) or in association with venom (Echis + PPACK group, n = 5). Factor II activity (1% +/- 1%) in the Echis and Echis + PPACK groups was significantly below the PPACK (55% +/- 9%) and the control (79% +/- 2%) levels at 120 minutes. In contrast, factor VIII coagulant (factor VIII:C) activity in the Echis group (1% +/- 1%) remained significantly below that in the Echis + PPACK (68% +/- 8%), PPACK (78% +/- 10%), and control (91% +/- 9%) groups at this interval. No change in factors X (91% +/- 7% to 81% +/- 7%, P not significant) and VII (64% +/- 10% to 48% +/- 11%, P not significant) activities were observed. Hemolysis was observed only in the Echis group, whereas thrombocytopenia and leukopenia were noted in both the Echis and the Echis + PPACK groups. These data show that large amounts of E. carinatus venom produce rapid DIC in vivo, because of the activation of prothrombin. In contrast, the decline in factor VIII:C activity appeared to be the result of the liberated thrombin. PPACK antagonized all of the venom-released thrombin without any major deleterious clotting abnormalities. This inhibitor appears to prevent thrombin-mediated DIC in vivo. In contrast, heparin was found to be an unreliable antagonist of the venom-released thrombin in vitro. PPACK also inhibited the marked hemolysis usually observed after venom. In addition, we found that the esterolytic (N-benzoyl-L-prolyl-L-phenylalanyl-L-arginine-p-nitroanilide HCL) activity of E. carinatus venom degrades fibrinogen in vitro.
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PMID:Disseminated intravascular coagulation following Echis carinatus venom in dogs: effects of a synthetic thrombin inhibitor. 308 70

The toxicity of hemoglobin solutions was studied in the context of their ability to activate serum complement (C). Three bovine polymerized hemoglobin solutions (BPHSs) with different degrees of purity were used for experiments in vitro and in vivo. BPHS-1 contained bacterial endotoxins (E) (5 EU/ml) and stromal phospholipids (PLs) (1.2 mg/dl), BPHS-2 contained only PLs (2.0 mg/dl), while BPHS-3 was completely free of both contaminants. C-activation was studied by the direct measurement of C3a, C4a, and C5a des Arg fragments, using commercially available RIA kits. During 1 hour of incubation with fresh monkey plasma, BPHS-1 and -2 activated both pathways of C, while BPHS-3 caused no activation of any factor. In vivo, Hb solutions were used to replace one-third of blood volume in three groups of six Coebus monkeys each, while fresh homologous plasma was used in a control group of four animals. Impure solutions activated the alternative pathway of C and caused significant reactions of the circulating blood (thrombocytopenia, leukopenia, and disseminated intravascular coagulation) associated with multiorgan dysfunction (cardiac arrhythmias, hypoxemia, reduction of renal clearance of endogenous creatinine, and elevation of liver enzyme SGPT). The pure solution neither activated C nor caused any reaction in the circulating blood. However, it caused a moderate degree of direct tissue injury, evidenced by transient reduction of creatinine clearance and elevation of SGPT. These observations suggest that impure and pure Hb solutions carry separate mechanisms of toxicity. Complement, activated by toxic impurities, plays an active role in the toxicity of impure solutions. C-activation in vitro could be used as a screening test of biocompatibility.
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PMID:Complement activation and the toxicity of stroma-free hemoglobin solutions in primates. 316 73

Four solutions of bovine polymerized hemoglobin (BPHS) and rabbit plasma were used to replace one-third of the blood volume in five groups of rabbits. The first three solutions were "impure" because of the presence of stromal phosphatidyl-ethanolamine and phosphatidyl-serine in BPHS-1, environmental endotoxins in BPHS-2, and a large amount of higher molecular weight hemoglobin-glutaraldehyde polymers in BPHS-3. These solutions caused a 33 per cent mortality rate and significant morbidity which was characterized by hemodynamic instability, respiratory and renal insufficiency, elevation of hepatic enzyme levels, thrombocytopenia, leukopenia, disseminated intravascular coagulation (DIC) and activation of the alternate pathway of complement. Histopathologic changes found in the heart, lungs, liver, spleen and kidney were characterized by a combination of ischemic and inflammatory lesions. Fibrin thrombi were visible by immunofluorescence in the microcirculation. In contrast, the fourth solution (BPHS-4) was free of the aforementioned impurities; caused no deaths and minimal morbidity, which was limited to elevated levels of serum glutamic pyruvic transaminase and reduction of creatinine clearance; no DIC or complement activation, and mild histopathologic changes which were exclusively ischemic in nature. The results of this study indicated that the toxicity of polymerized hemoglobin solutions is due principally to the presence of impurities. Pure hemoglobin does exhibit mild toxicity when compared with a control solution which is most likely due to a vasoconstrictor effect of oxyhemoglobin.
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PMID:Toxicity of polymerized hemoglobin solutions. 334 50

Antiserum raised to a rough mutant Escherichia coli, termed J5 (anti-J5 RS), protected against lethal gram-negative bacterial sepsis in a guinea pig model when animals were pretreated with both antiserum and heparin. This same model was used to examine and compare the effects of pretreatment with anti-J5 RS, normal rabbit serum (NRS), or saline, each +/- heparin on physiologic and metabolic parameters during a septic insult. Results demonstrated that leukopenia and thrombocytopenia occurred to a similar degree in all pretreatment groups; no significant leuko- or thrombostasis was noted on examination of histologic specimens; complement activation was maximal in those animals receiving anti-J5 RS alone without heparin; the most abnormal amino acid profile was present in the NRS + heparin group; and only the anti-J5 RS + heparin group did not develop glomerular lesions indicative of disseminated intravascular coagulation. A complement-mediated cell aggregation-type injury does not appear to occur in this model. It is hypothesized that both excessive complement and coagulation system activation occur after bacterial challenge when antibody directed against the bacteria is present (anti-J5 RS) leading to antigen-antibody complex formation and complement and coagulation cascade activation. Heparin may block either or both these cascade systems allowing enhanced, antibody-mediated opsonization and clearance of blood-borne bacteria, thus preventing end-organ alterations and organ failure during sepsis when combined with anti-J5 RS.
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PMID:Metabolic effects of pretreatment with Escherichia coli J5 antiserum on guinea pig gram-negative bacterial sepsis. 388 2

Three antimicrobial agents were evaluated as to their ability to neutralize the toxic effects of endotoxin in rabbits. These consisted of two cyclic polypeptides, polymyxin B sulfate and colymycin M (sodium colistimethate), and an aminoglycoside, gentamicin sulfate. Polymyxin B regularly prevented endotoxin-induced leukopenia, thrombocytopenia, and disseminated intravascular coagulation. Colymycin M had similar activity but was not as effective as polymyxin B. Gentamicin demonstrated no neutralizing ability in this study.
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PMID:Comparison between the polymyxins and gentamicin in preventing endotoxin-induced intravascular coagulation and leukopenia. 434 9

Hematologic alterations unrelated to neoplastic bone marrow involvement include polycythemia, anemia, leukocytosis, leukopenia, thrombocytosis, thrombocytopenia and coagulopathies. Serum globulin levels may be increased or decreased, depending on the type of neoplasm. Plasma fibrinogen and fibrin degradation product concentrations are usually elevated in cancer patients, whereas cancer patients with DIC have low plasma fibrinogen concentrations. Hypercalcemia can be a sequel of osseous metastases. Neoplasia may cause the nephrotic syndrome in some patients. Effusions should be examined microscopically for signs of malignancy. Elevated serum enzyme levels are not specific in neoplastic disease.
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PMID:Laboratory aspects of cancer. 650 15

This report describes fatal colchicine toxicity occurring after a total dose of 9.3 mg. The reaction was characterized by leukopenia, thrombocytopenia, hypotension. disseminated intravascular coagulation and metabolic acidosis. Autopsy findings included a markedly hypocellular bone marrow, epithelial atypia of the trachea and esophagus, mid-zonal hepatic necrosis, sepsis and small vessel occlusion by fibrin thrombi. Possible mechanisms of colchicine toxicity are discussed.
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PMID:Fatal colchicine toxicity: report of a case. 653 21

With our present day highly mobile population, the diagnosis of kala-azar must be considered in any patient presenting with fever, enlarged liver and spleen, anemia and leukopenia who has visited a region where this disease is endemic, particularly since the incubation period may be as long as a year. We report a case in which disseminated intravascular coagulation was an unusual complication.
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PMID:Kala-azar as a cause of disseminated intravascular coagulation. 735 Nov 5

Human ehrlichiosis is a newly recognized tick-borne disease. Since 1935 Ehrlichia canis has been known as a cause of illness in dogs and other canine species, and for a few years it was related with human disease. In 1990, Ehrlichia chaffeensis was isolated from a man suspected of having ehrlichiosis. Partial sequencing of the rRNAS from the human isolate and E. canis, indicated that they are 98.7% related. More recently (May 1994) an "human granulocytic ehrlichiosis" have been reported in USA. PCR amplification and sequence of 16S rDNA, showed that the human isolate was virtually identical to those reported for E. phagocytophila y E. equi, organisms that cause ehrlichiosis in rumiant and in horses. Most patients shows fever, headache, malaise, nausea or vomiting, anorexia and in a minority of cases rash is present. Some of them have complications such as pulmonary infiltrates, gastrointestinal problems, renal dysfunction or failure, hepatoesplenomegaly, neurologic abnormalities, DIC and some times death. Leucopenia, thrombocytopenia and elevated liver enzyme values have been common findings. Tetracycline and cloramphenicol have been using in adults and children as especific theraphy.
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PMID:[Human ehrlichiosis. Review]. 773 23

Since acute disseminated intravascular coagulation (DIC) often contributes to a fatal outcome in patients with systemic lupus erythematosus (SLE), prediction of its development is important to prevent the occurrence of such an event. To analyze the risk factor(s) contributing to the development of acute DIC in SLE, we carried out a retrospective study of a series of 129 SLE patients, eight of whom developed DIC during the course of this disease, to assess which of the easily assessable parameters, present at the time of first medical examination, were of predictive significance. The important individual variables, determined by univariate analysis, were male sex, leukopenia, and infection. These factors were placed in a multivariate logistic regression model, and only one factor, infection at first medical examination, was found to have predictive significance for the development of acute DIC in SLE patients. The prevention and control of infection in SLE patients might have implications for preventing the development of acute DIC.
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PMID:Risk factors for the development of acute disseminated intravascular coagulation in patients with systemic lupus erythematosus. 778 59


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