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)

Sixty-five cases of nonbacterial thrombotic endocarditis (NBTE) were discovered at autopsy during a 10 year period--an incidence of 1.6 per cent in the adult autopsy population. In 51 cases, one or more malignant neoplasms were associated; adenocarcinoma represented the most frequent histologic type of related neoplasm. Coagulation abnormalities suggestive of disseminated intravascular coagulation (DIC) were present in 18.5 per cent of the cases. It is possible that both the valvular and peripheral intravascular thromboses in at least some cases of NBTE represent the abnormal coagulation of DIC. Arterial thrombosis with infarction occurred in many peripheral organs. Splenic and renal were most frequent, but cerebral and cardiac consequences were the most significant.
Am Heart J 1976 Dec
PMID:Non-bacterial thrombotic endocarditis: clinicopathologic correlations. 99 78

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
Blood 1976 Dec
PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

New Zealand white rabbits were given 30 ml of goat serum intravenously. This procedure resulted in an immediate decrease in platelet count, fibrinogen, and levels of coagulation factors II, V, VII, and X, due to consumption coagulopathy. These factors returned toward baseline levels approximately 12 hr after the injection. Plasma from rabbits who had received goat serum 48 hr previously (donor rabbits) was injected into recipient rabbits. This procedure resulted in a slight rise in the level of coagulation factor II (range, 20%-30%) and a significant rise in factors V (35%-75%), VII (35%-235%), and X (35%-75%) in the recipients. When plasma from control donor rabbits who had not received goat serum was injected into recipients, there was no change in these coagulation factors. It is postulated that the reduction in coagulation factor levels in donor rabbits induces a "coagulopoietin" for each factor or one "coagulopoietin" for all factors which stimulates increased synthesis and/or release of these factors in recipient rabbits.
Blood 1976 Dec
PMID:Evidence suggesting the regulation of a coagulation factor levels in rabbits by a transferable plasma agent. 100 86

Alaria americana is a trematode, the adult of which is found in mammalian carnivores. The first case of disseminated human infection by the mesocercarial stage of this worm occurred in a 24-year-old man. The infection possibly was acquired by the eating of inadequately cooked frogs, which are intermediate hosts of the worm. The diagnosis was made during life by lung biopsy and confirmed at autopsy. The mesocercariae were present in the stomach wall, lymph nodes, liver, myocardium, pancreas and surrounding adipose tissue, spleen, kidney, lungs, brain and spinal cord. There was no host reaction to the parasites. Granulomas were present in the stomach wall, lymph nodes and liver, but the worms were not identified in them. Hypersensitivity vasculitis and a bleeding diathesis due to disseminated intravascular coagulation and a circulating anticoagulant caused his death 8 days after the onset of his illness.
Can Med Assoc J 1976 Dec 04
PMID:Systemic infection with Alaria americana (Trematoda). 100 Apr 45

A newborn infant with a large hepatic hemangioma developed congestive heart failure, consumption coagulopathy, microangiopathic hemolytic anemia, and obstructive jaundice. The patient was mildly heparinized (250 units per kg and day) and underwent successful resection of the tumor without lobectomy at the age of 3 days. Blood volume increased from 93.9 ml/kg at the age of 5 h to 124.2 ml/kg prior to surgery. Red-cell mass simultaneously decreased from 53.8 to 39.4 ml/kg. The increase of blood volume is explained by congestive heart failure, the decrease of red-cell mass by intravascular coagulation within the tumor resulting in formation of thrombi and microangiopathic hemolytic anemia. A review of the literature on infants with symptoms caused by an intrahepatic hemangioma during the first month of life confirms that surgical intervention is the treatment of choice for infants with giant solitary hemangioma of the liver.
Eur J Pediatr 1976 Dec 09
PMID:Solitary hepatic hemangioma in a newborn infant complicated by cardiac failure, consumption coagulopathy, microangiopathic hemolytic anemia, and obstructive jaundice. Case report and review of the literature. 100 25

The possible predisposing causes of difibrination in the pregnant woman are discussed. Coagulation profiles and qualitative and quantitative assessment of fibrinolytic activity during labor, delivery and the early puerperium in normal pregnancies are presented. These factors were also studied in patients with abruptio placentae and prolonged intrauterine fetal death and in women whose pregnancies were terminated with intraamniotic infusion of hypertonic saline or prostaglandin F2alpha. The findings suggest that a minor degree of physiologic defibrination develops during normal labor that is qualitatively similar to, but of much lesser magnitude than, the pathologic defibrination syndrome commonly associated with abruptio placentae or prolonged intrauterine fetal death. Some degree of defibrination occurs in women undergoing saline abortion, similar to that of women during normal parturition, but does not usually reach clinically significant levels. The coagulation changes seen during prostaglandin abortion suggest that a minor degree of defibrination occurs that is substantially less than that seen during saline abortion. The findings presented form a basis for the rational management of defibrination in the pregnant woman.
J Reprod Med 1976 Dec
PMID:Current concepts of defibrination in the pregnant woman. 100 95

Intravascular coagulation was induced by two appropriately spaced doses of endotoxin and by infusion of thromboplastin. The resulting fibrin deposition was measured by a previously described quantitative technique. Evidence of thrombin elaboration was obtained indirectly by measurement of fibrin monomer (FM) and by the detection and isolation of a thrombin-induced anticlotting activity. Venous segments were isolated at intervals and examined for thrombus formation following 40 minutes of stasis. Endotoxin triggered thrombin elaboration was not detectable in the circulation for at least one hour and was not accompanied by any thrombosis in isolated venous segments. No thrombin elaboration was found in leukopenic rabbits given endotoxin. In the thromboplastin infused animals, the quantity of fibrin deposited in the organs was comparable to that found after endotoxin. However, thrombin was found in the blood immediately and was associated with thrombosis in the isolatet venous segments. Less thrombin-induced anticoagulant activity was found after thromboplastin than after endotoxin. The findings suggest that endotoxin-induced intravascular coagulation is probably not caused by a mechanism of systemic hypercoagulability due to the release of thromboplastic material into the blood stream. A focal process of thrombin elaboration involving leukocytes is postulated. The study is believed relevant to patients with disseminated intravascular coagulation in whom venous thromboembolism is rarely found despite evidence of extensive microvascular fibrin deposition.
Thromb Haemost 1976 Dec 31
PMID:Thrombin elaboration in endotoxin-induced intravascular fibrin deposition. A leukocyte dependent process distinct from systemic hypercoagulability. 103 55

Analysis of Factor-VIII-related antigen (vWAg) in normal plasma by crossed immunoelectrophoresis reveals an asymmetric pattern indicative of molecular heterogeneity. This asymmetric pattern apparently results from the presence of multiple molecular forms of VWAg with distinct, though partially overlapping, mobilities on crossed immunoelectrophoresis. Evidence for this conclusion has been obtained by separating these forms, one from another, utilizing cryoprecipitation, agarose gel chromatography, and ion-exchange chromatography. Variation in the relative destribution of VWAg forms in liver disease and disseminated intravascular coagulation suggests that the processes which govern generation and/or breakdown of these forms can be altered by disease.
Proc Natl Acad Sci U S A 1975 Dec
PMID:Factor-VIII-related antigen: multiple molecular forms in human plasma. 108 39

Acute renal failure of obstetric origin is common among North Indian patients and comprised 72 (22.1%) of 325 patients undergoing dialysis over an 11-year period. Of these, 46 gravidas had developed renal failure following abortion, and 29 cases were due to complications of late pregnancy. The most striking feature of this study was a high incidence of irreversible renal lesions of bilateral diffuse cortical necrosis in early (18.6%) as well as late pregnancy (37.8%). Overall incidence of diffuse cortical necrosis was 25%. In the remainder, acute tubular necrosis was seen in 52 (72.2%), patchy cortical necrosis in 1 (1.4%), and tubular necrosis along with glomerular involvement in 1 patient (1.4%). Pathogenetic factors which contributed to the development of renal failure, either singly or in combination, were loss of blood failure, either singly or in combination, were loss of blood (79.1%), septicemia (31.9%), hypotension due th hemorrhagic and septicemic shock (51.4%), eclamptic toxemia (11.1%), and disseminated intravascular coagulation in 12.5% patients. Infrequent occurrence of disseminated intravascular coagulation in the septic anc eclamptic patients who developed diffuse cortical necrosis was an interesting finding, as was the fact that coagulopathy was more frequently observed in acute tubular necrosis. Late referral, frequent sepsis, and high incidence of bilateral diffuse cortical necrosis contributed significantly to a high mortality (55.3%).
Obstet Gynecol 1976 Dec
PMID:Acute renal failure of obstetric origin. 108 92

We have studied the role of complement in lipopolysaccharide (LPS)-induced hypotension and disseminated intravascular coagulation (DIC) by comparing the effects of injection of three preparations of LPS from E. Coli 0111:B4, S. minnesota Re595, and S. marcescens. Injections of nonlethal doses of these LPS preparations into normal rabbits produced decreases in mean arterial blood pressure during a 5-h period. When rabbits treated with cobra venom factor (CoF) to deplete C3 were injected with the various LPS preparations, mean arterial pressures fell at a rate and extent essentially identical to that observed in normal rabbits. Rabbits genetically deficient in C6 also demonstrated LPS-induced hypotensive changes. Only minimal, or no changes in plasma C3 levels or serum CH50 values were detected in normal rabbits after LPS injection. Hypotensive changes were also induced in rabbits when complement was rapidly activated by intravenous injection of CoF. In contrast to the hypotension induced by LPS, the fall in arterial pressure associated with the consumption of complement was short lived and required the rapid consumption of considerable amounts of C3. The occurrence of DIC noted in normal rabbits injected with each preparation of LPS was not inhibited in either rabbits treated with cobra factor or in C6-deficient rabbits. The DIC was most pronounced after injection of Re595 and S. marcescens LPS. Injection of the various LPS preparations produced a rapid disappearance of circulating neutrophils and mononuclear cells, which occurred with the same kinetics and to the same extent in normal, CoF-treated, and C6-deficient rabbits. Injection of either Re595 LPS or S. marcescens LPS produced a biphasic disappearance of circulating 51Cr-platelets. In contrast, injection of 0111:B4 LPS affected only slightly the rate of disappearance of 51Cr-platelets. Depletion of C3 by cobra factor treatment had no effect on the disappearance of platelets in animals injected with 0111:B4. In marked contrast cobra factor treatment greatly reduced the initial rapid disappearance of platelets in rabbits injected with either Re595 or S. marcescens LPS, but had no effect in the secondary disappearance phase.
J Exp Med 1975 Dec 01
PMID:Mediation systems in bacterial lipopolysaccharide-induced hypotension and disseminated intravascular coagulation. I. The role of complement. 110 50


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