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 previously healthy 37-year-old woman had a 5-week febrile disease starting 10 days after delivery, which was complicated by disseminated intravascular coagulation and treated with fresh blood transfusions. She developed severe encephalitis with coma. She also had signs of perimyocarditis and enlargement of liver and lymph nodes. The encephalitis was completely reversible. There was a 16-fold rise in complement-fixing antibodies against cytomegalovirus.
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PMID:Cytomegalovirus infection associated with severe encephalitis. 19 92

Two cases of fatal heat stroke, concerning a 20 year-old soldier and a 44 year-old psychiatric patient, treated with neuroleptics, are reported. The clinical picture, starting suddenly with coma and hyperthermia, was quite identical for both. Secondarily, while hyperthermia decreases and the conscience improved partially, an hemorrhagic syndrome similar to a consumption coagulopathy, acute renal insufficiency and acute hepatic failure appear. Death occurred after aggravated neurological disorders and respiratory distress. The anatomical lesions spread on all the viscera include tubular nephritis, and hepatic centro-lobular necrosis and an interstitial and alveolar oedema with hemorrhages and hyaline membranes in the lungs.
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PMID:[Heat stroke and disseminated intravascular coagulation. Apropos of 2 cases]. 21 8

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

A coagulation screen consisting of measurement of the prothrombin time, thrombin time, kaolin caphalin clotting time, platelet count, plasma fibrinogen level, fibrin degradation products and ethanol gelation test was performed on 24 patients with impairment of consciousness due to acute diabetic metabolic decompensation at the start of treatment and 24 hours later. 22 out of 24 patients showed at least one coagulation abnormality on admission of which the commonest were a prolonged prothrombin time, shortened kaolin cephalin clotting.time and raised plasma fibrinogen level. After 24 hours of treatment these values were more normal but 20 out of 22 patients still displayed some abnormality. 15 patients had two or more coagulation abnormalities on admission including 3 patients with haematological abnormalities suggestive of disseminated intravascular coagulation. This group was older and had higher blood ureas than those with fewer abnormalities, but plasma glucose, sodium, potassium and bicarbonate levels were similar in both groups of patients. All 5 patients with hyperosmolar non-ketotic coma and all 3 patients who died without recovering consciousness had two or more coagulation abnormalities on admission.
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PMID:Coagulation abnormalities in diabetic coma before and 24 hours after treatment. 53 72

Severe hypertonic dehydration with hyperglycemia developed in a 7-week-old infant girl after she was fed an overconcentrated milk formula for five days. Renal failure,disseminated intravascular coagulation, gangrene of the legs, and coma were added complications. Intravenous rehydration, peritoneal dialysis, and heparin administration corrected the metabolic and coagulation derangements, and renal function returned to normal. Bilateral below-the-knee amputations were performed and the child subsequently learned to walk with artificial limbs. The dangers of overconcentrated formulas in infant feeding should be widely publicized through warnings printed on all commercial milk preparations.
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PMID:Hazards of overconcentrated milk formula. Hyperosmolality, disseminated intravascular coagulation and gangrene. 117 15

Two patients in a family of exertion-induced heat stroke were reported. Case 1: A 23-year-old male, paternal cousin of case 2, was admitted to our hospital because of loss of consciousness during running under a burning sun. On physical and neurological examinations, he was deeply comatose with high fever, tachycardia, and increased deep tendon reflexes. Laboratory findings disclosed rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, liver injury, and brain edema. He recovered after intensive cooling, some antibiotics, glycerol and sodium dantrolene administration. Case 2: A 19-year-old male experienced loss of consciousness and high fever during playing soccer at 15 years of age, and was admitted to a hospital. On admission, he had high fever of 38.7 degrees C, and increased serum CK level. He recovered two weeks after admission. He was readmitted to our hospital to evaluate the predisposition for malignant hyperthermia. His physical and neurological examinations showed no abnormalities. Routine laboratory findings were within normal limits. Muscle biopsy findings of cases 1 and 2 were mildly increased number of fibers with centrally placed nuclei. Caffeine test on skinned muscle fibers from the biopsies showed normal response in both type 1 and 2 fibers. The present patients were diagnosed as having exertion-induced heat stroke, but with no increased muscle fiber sensitivity to caffeine, suggesting that the pathomechanism differs from that of malignant hyperthermia induced by malfunction of sarcoplasmic reticulum.
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PMID:[Two familial cases with exertion-induced heat stroke--relationship to malignant hyperthermia]. 139 27

Serial EEGs have been carried out during the acute phase of haemorrhagic shock and encephalopathy syndrome (HS&E) in 22 infants and children aged 3 months to 14 years. Most patients presented with fits and coma and all had shock with bleeding and disseminated intravascular coagulation (DIC). The initial EEG showed prolonged runs of often rhythmic discharges which fluctuated in amount and amplitude with varying distribution and morphology ("electrical storms"). Over a period of days the "electrical storms" gradually decreased leaving only low amplitude EEG activities or evolving to electrocerebral silence (7 cases). Fifteen patients died and all five children with multifocal "electrical storms" who survived showed gross neurological handicap. The rather distinctive EEG pattern is unusual in the context of an acute encephalopathy outside the neonatal period although similar "electrical storms" may be seen in a less extreme form in infants and children with other conditions associated with DIC. This EEG pattern presumably reflects changes in the cerebral microcirculation which in HS&E are usually relentlessly progressive and associated with devastating cortical damage.
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PMID:EEG features and their evolution in the acute phase of haemorrhagic shock and encephalopathy syndrome. 177 15

The analysis of 88 lethal outcomes of hemorrhagic fever with renal syndrome (HERS) showed the occurrence of adenohypophyseal hemorrhage and necrotic foci in 75.5% of cases as well as combined involvement of adenohypophysis and adrenals in 18.4%. Pathogenetically, adenohypophyseal affection is related to anatomical-physiological features of the vessels, microcirculatory disorders, acute venous congestion. Contributing factors may be acute DIC syndrome, relapsing and prolonged collapses, hyperhydration leading to brain edema and hemostasis. Uncontrollable vomiting recorded in all the deceased patients seemed to promote destruction of adenohypophysis. Clinically, this gross pathomorphology ++ was equivalent to severe form of the disease--hypopituitary coma. Proper prophylaxis of the above complications is one of the conditions entailing reduction of mortality in HFRS.
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PMID:[Analysis of fatal outcome in hemorrhagic fever with renal syndrome]. 198 56

After an accidental or intentional ingestion of lindane, clinical manifestations of poisoning may include rapid onset of nausea and vomiting, coma, seizures, respiratory failure, and death. While rhabdomyolysis, secondary renal failure, and aplastic anemia have also been reported, coagulopathies have not been observed following poisoning with this pesticide. In this case report we describe a 43-year-old female who intentionally ingested 8 oz of a 20% lindane solution. Her serum lindane concentration reached 1.3 mcg/ml and her clinical manifestations included seizures, coma, rhabdomyolysis, secondary renal failure, and disseminated intravascular coagulation. The coagulopathy presented early in her clinical course and resolved when serum lindane levels fell. The patient died 11 days after the ingestion.
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PMID:Disseminated intravascular coagulation in a case of fatal lindane poisoning. 245 26

1. The concentration in plasma of fibrinogen derivatives fibrinopeptide A (FPA) and B beta 1-42 and the platelet release products beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) have been determined in patients with acute and chronic liver disease. 2. In 21 patients with fulmiant hepatic failure on admission in grade III or IV coma the plasma FPA, B beta 1-42, beta TG and PF4 levels were significantly increased compared with those in normal control subjects. On heparinization before haemoperfusion the FPA levels returned to the normal range and during resin and charcoal haemoperfusion there were no significant changes in the coagulation or platelet factors, except for a small increase in FPA with charcoal haemoperfusion. 3. In ten patients with compensated chronic liver disease there was a significant increase in B beta 1-42 and beta TG levels but not FPA and PF4 as compared with normal controls. 4. Interpretation of the results is complicated by the possible reduced clearance of these proteins as a result of renal failure in some of the patients with fulminant hepatic failure and also by the damaged liver itself. However, these results have confirmed that disseminated intravascular coagulation can occur in both acute and chronic liver disease.
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PMID:Fibrinogen derivatives and platelet activation products in acute and chronic liver disease. 248 73


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