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)

Liver changes and associated host responses were evaluated in four groups of male rats, weighing 300 +/- 20 gm., which received intravenous injection of 2.2 times 10(9) live Escherichia coli. This bolus was given either without additional treatment (group A) or prior to the following regimens: intramuscular injection of gentamicin sulfate, 5 mg. per kg. (group B); intravenous injection of methylprednisolone sodium succinate, 40 mg. per kg. (group C); and intramuscular injection of gentamicin immediately after methylprednisolone sodium succinate treatment (group D). Rats given injections of saline or methylprednisolone sodium succinate served as controls. Survival rates at 10 and 20 hours were 25 per cent and 4 per cent for group A; 44 per cent and 28 per cent for group B; 94 per cent and 70 per cent for group C; 98 per cent and 98 per cent for group D, respectively. In rats of groups A and B, killed at 1, 2, 4, and 6 hours, progressive liver changes included intravascular sequestration of rapidly degranulating leukocytes, fibrinous deposits, and platelet aggregates in sinusoids as well as in spaces of Disse adjacent to subendothelial collagen, and extensive Kupffer cell disruption in association with severe midzonal necrosis. These alterations were accompanied by progressive hypoglycemia and elevations of serum enzymes, glutamic pyruvic transaminase, lactate dehydrogenase, and glutamic oxaloacetic transaminase. Hematologic studies revealed that E. coli bacteremia results in rapid leukopenia and disseminated intravascular coagulation primarily due to activation of the intrinsic coagulation pathway. All above reactions were delayed and markedly reduced in rats treated with methylprednisolone sodium succinate. The results indicate that antibiotic treatment of lethal, Gram-negative bacteremia is effective only in conjunction with early steroid treatment. The protective effects of glucocorticoids on the liver microcirculation and polymorphonuclear leukocytes appear to play a basic role in preventing the early development of disseminated intravascular coagulation, hepatocellular necrosis, and associated major host responses, thereby attenuating lethality of gram-negative septic shock.
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PMID:Glucocorticoid and antibiotic effects on hepatic microcirculation and associated host responses in lethal gram-negative bacteremia. 36 36

Venom from newborn Bothrops asper snakes has higher lethal, hemorrhagic, edema-forming, proteolytic and defibrinating activities than venom from adult B. asper specimens. Electrophoretic analysis confirmed the variation between these venoms. Intramuscular injection of 100 micrograms of venom from newborn specimens in mice induced defibrination, together with moderate increments of serum levels of lactate dehydrogenase, creatine kinase, hemoglobin and total proteins. A conspicuous hemorrhage developed in injected muscle rapidly after envenomation, probably due to a drastic alteration in capillaries and larger blood vessels. Other histological alterations included moderate myonecrosis, lung collapse and prominent renal damage, characterized by tubular necrosis and hyalinization. Polyvalent antivenom effectively neutralized lethal, hemorrhagic and indirect hemolytic activities of newborn B. asper venom, although requiring higher antivenom doses than neutralization of venom from adult B. asper.
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PMID:Pathological and biochemical changes induced in mice after intramuscular injection of venom from newborn specimens of the snake Bothrops asper (Terciopelo). 144 Jun 47

Micro-angiopathic haemolytic anaemia is an unusual but well-recognized complication of metastatic adenocarcinoma. A young black man presented with red cell fragmentation, compensated disseminated intravascular coagulation and leuco-erythroblastosis. Metastatic adenocarcinoma of the stomach was suspected but only demonstrated at autopsy. An unusual finding was the elevation of the slow-moving lactate dehydrogenase iso-enzyme (LDH5) level in the plasma which was shown to be produced by metastatic tumour cells recovered from the bone marrow.
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PMID:Micro-angiopathic haemolytic anaemia and an unusual lactate dehydrogenase iso-enzyme pattern in metastatic adenocarcinoma. A case report. 404 83

A rare isozyme of serum creatine kinase (CK) migrating cathodic to CK-MM on electrophoresis was found in a 30-year-old male with stomach cancer complicated by disseminated intravascular coagulation leading to massive upper gastrointestinal bleeding and marked anemia. Serum CK activity rose to a maximum of 374 U/l without detectable CK-MB isoenzyme. The patient was also characterized by a marked increase in serum lactate dehydrogenase (all isozymes elevated) and by preferential leakage of mitochondrial aspartate aminotransferase and glutamate dehydrogenase, indicating the presence of extensive tissue damage involving mitochondria. Skeletal muscle mitochondria were considered the most likely source of the additional CK isozyme.
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PMID:Cathodic isozyme of serum creatine kinase in a case of stomach cancer complicated by disseminated intravascular coagulation. 744 49

An 8-month-old male infant with severe anemia and thrombocytopenia was brought to our hospital due to fever and pallor. The physical examination on admission showed pale conjunctivae, skin rash, lymphadenopathy and hepatosplenomegaly. Subsequent laboratory studies showed pancytopenia, impaired liver function, elevated lactate dehydrogenase level but without evidence of disseminated intravascular coagulation. Bone marrow aspiration demonstrated increased macrophages and prominent hemophagocytosis. The serological studies revealed a recent infection of human herpesvirus-6 which was confirmed by blood mononuclear cell culture and polymerase chain reaction. This infant was also found to have beta-thalassemia which was confirmed by hemoglobin electrophoresis performed before first transfusion. After treatment with intravenous immunoglobulin and other supportive therapies, the bone marrow abnormalities has completely recovered after 5 days, and the hemogram improved. This report demonstrates the human herpesvirus-6 as the etiology of hemophagocytic syndrome.
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PMID:Human herpesvirus-6 associated hemophagocytic syndrome in beta-thalassemia: report of one case. 860 65

1. The effects of the selective and potent novel platelet-activating factor (PAF) antagonist, UR-12633 (1-(3,3-diphenylpropionyl)-4-(3-pyridylcyanomethyl)piperidin e) on several markers of endotoxic shock syndrome were evaluated in rats and mice. 2. UR-12633, administered 60 min after E. coli lipopolysaccharide (LPS), reversed the LPS-induced sustained hypotension in rats at doses of 0.01 to 1 mg kg-1, i.v. The reference compound WEB-2086 (1 mg kg-1) also reversed the LPS-induced hypotension. UR-12633 (1 mg kg-1), administered 10 min before LPS, almost fully inhibited sustained hypotension. The immediate hypotension (within 1 min) caused by LPS was not prevented by either UR-12633 or WEB-2086. 3. Pretreatment with 10 mg kg-1, i.v. of either UR-12633 or WEB-2086 inhibited the increase in disseminated intravascular coagulation markers, such as activated partial thromboplastin time (55 and 74% inhibition, respectively), and prothrombin time (22 and 72% inhibition) and prevented the decrease in plasma fibrinogen content (100 and 29% inhibition). 4. Increases in acid phosphatase (ACP) plasma activity, a marker of lysosomal activation, and in lactate dehydrogenase (LDH), a marker of tissue damage, were inhibited by pretreatment with 10 mg kg-1, i.v. of either UR-12633 or WEB-2086 (100% and 69% inhibition, ACP; 62 and 48% inhibition, LDH). Hyperglycaemia (71 and 46%) and hyperlactacidaemia (92 and 56%) were also inhibited. 5. UR-12633, but not WEB-2086, inhibited the LPS-induced increase in vascular permeability in rats, as shown by prevention of haemoconcentration and, to a lesser degree, the increase in Evans blue dye extravasation. 6. In a series of nine reference compounds and UR-12633, we found a high correlation (P < 0.001) between PAF antagonist activity, measured as the inhibition of PAF-induced rabbit platelet aggregation or PAF-induced mortality in mice and the inhibition of LPS-induced mortality. 7. In spite of the multifactorial nature of endotoxic shock, in which many mediators may be involved, the new potent PAF antagonist, UR-12633, proved effective in protecting against changes in most shock markers. These data strongly suggest a key role for PAF in the pathogenesis of endotoxic shock in rodents.
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PMID:Effects of UR-12633, a new antagonist of platelet-activating factor, in rodent models of endotoxic shock. 881 47

In a first experiment, 28 specific pathogen-free chickens aged 3 weeks showed clinical signs 1 to 5 days after intramuscular inoculation with Erysipelothrix rhusiopathiae. Twelve of 28 birds died 2 to 4 days after inoculation. Macroscopically, the liver, spleen and kidneys were seen to be enlarged and congested. Histologically, fibrinous thrombus formation, seen in the hepatic sinusoids, renal glomerular capillaries and small pulmonary blood vessels, was a characteristic feature. In addition, the liver showed marked congestion, increase of mononuclear cells and heterophils in the sinusoids, hyperplasia of sinusoidal lining cells, and vacuolar changes in hepatic cells. The spleen showed fibrinous exudation of the lymphoid follicles and ellipsoids with lymphocytic depletion, and hyperplasia of ellipsoidal reticular cells. There was oedema, congestion and cellular infiltration in the interstitium of the kidney. The bursa of Fabricius and thymus showed marked lymphocytic depletion. In a second experiment, the blood chemical values (uric acid, glutamic-oxalacetic transaminase, lactate dehydrogenase and gamma-glutamyl transpeptidase) of birds inoculated intramuscularly with E. rhusiopathiae were significantly higher than those of uninfected controls. The blood prothrombin times and activated partial thromboplastin times of the inoculated group were significantly greater than those of the control group. The pathological and haematological findings demonstrated that E. rhusiopathiae induced disseminated intravascular coagulation in the chickens.
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PMID:Disseminated intravascular coagulation in chickens inoculated with Erysipelothrix rhusiopathiae. 935 39

UR-12670 is a novel and potent PAF antagonist, eg., it displaces [3H]WEB-2086 from PAF receptors in rabbit platelet membranes (Ki = 0.6 nM) and inhibits PAF-induced increase in vascular permeability in rat trachea (100%), thymus (44%), seminal vesicles (100%) and stomach (54%) at a dose of 0.01 mg/kg i.v. Since PAF is thought to be an important mediator in endotoxic shock, the effect of pretreatment with UR-12670 on changes in vascular permeability, disseminated intravascular coagulation (DIC) and plasma biochemical parameters were determined in a rat model of acute endotoxemia. UR-12670 and the reference PAF antagonist, lexipafant (10 mg/kg i.v.), strongly inhibited lipopolysaccharide (LPS, 25 mg/kg i.v.)-induced plasma leakage in the trachea (49 and 100%, respectively) and seminal vesicles (81 and 100%), as assessed by the Evans blue extravasation method. Only lexipafant inhibited the increase in vascular permeability in the thymus (36%). Neither PAF antagonist was effective in the stomach. Both UR-12670 and lexipafant at 10 mg/kg i.v. attenuated the LPS-induced variation of some DIC markers, such as activated partial thromboplastin time increase (56 and 58%, respectively) and the fibrinogen concentration decrease (53 and 31%), whereas the increase in prothrombin time was not affected. Increased plasma acid phosphatase (ACP, a lysosomal activation marker) and lactate dehydrogenase (LDH, a tissue damage marker) activity elicited by LPS was attenuated by pretreatment with 10 mg/kg i.v. of either UR-12670 or lexipafant (ACP: 55 and 48%; LDH: 50 and 33%). LPS-induced hyperglycemia (46 and 37%) and hyperlactacidemia (100% both) were also inhibited. UR-12670 protected against several shock symptoms, confirming the role of PAF in the pathogenesis of rodent endotoxemia.
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PMID:Effects of a new platelet-activating factor antagonist, UR-12670, on several endotoxic shock markers in rats. 951 29

A high frequency of disseminated intravascular coagulation (DIC) in adult acute lymphoblastic leukemia (ALL) has been reported; however, its clinical relevance and characteristics have not been fully determined. We studied 67 adults with newly diagnosed ALL between 1982 and 1996 to clarify these questions. DIC was diagnosed in ten of 64 patients (16%) who underwent coagulation study at presentation and in 14 of 40 patients (35%) screened for DIC within 7 days after starting remission induction therapy. Overall, 24 of 67 patients (36%) had DIC during this period. Hemorrhagic symptoms were generally mild, while two patients required red blood cell transfusions. Patients who developed DIC had higher white blood cell counts and more frequently a palpable spleen than those who did not. There was no difference in age, French-American-British subtype, karyotype, immunophenotype, lactate dehydrogenase level, percentage of blasts in bone marrow, or frequency of lymphadenopathy or hepatomegaly between patients who had DIC and those who did not. Fibrinolysis tended to be milder in DIC complicating ALL than in that complicating acute promyelocytic leukemia; however, there was no difference in other coagulation parameters between these two subtypes. An etiological link between CD34 expression in common ALL patients and DIC was suggested.
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PMID:Disseminated intravascular coagulation in acute lymphoblastic leukemia at presentation and in early phase of remission induction therapy. 969 14

Cisplatin is a known cause of hemolytic uremic syndrome (HUS). The acute, fulminant form of cisplatin-induced HUS is almost always fatal. We present a 67-year-old Hispanic woman who was treated with cisplatin for squamous cell carcinoma of the tongue. Three days after receiving the treatment, she presented with increasing fatigue, decreased urine output, and confusion. Physical examination was remarkable for tachycardia of 130 beats/min, peripheral edema, and mental obtundation. Laboratory investigations showed a white cell count of 5,500/microL, hemoglobin level of 9.6 g/dL, hematocrit of 29.6%, and platelet count of 13,000/microL. Schistocytes were present on peripheral smear. Screening for disseminated intravascular coagulation was negative. Serum chemistry values included blood urea nitrogen 111 mg/dL, creatinine 3.8 mg/dL, and lactate dehydrogenase (LDH) 927 IU. The patient underwent hemodialysis and therapeutic plasma exchange (TPE), using fresh frozen plasma (FFP). Dialysis was no longer required after the fifth day. TPE was performed daily until the platelet count normalized on the 13th day, after which intertreatment intervals were extended until normalization of LDH levels on the 50th day. We conclude that the normally fatal, fulminant form of cisplatin-induced HUS can be successfully treated with standard TPE, using FFP replacement.
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PMID:Successful treatment of cisplatin-induced hemolytic uremic syndrome with therapeutic plasma exchange. 970 19


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