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)

Seven children (aged 8--17 years) presented with a high fever, headache, confusion, conjunctival hyperaemia, a scarlatiniform rash, subcutaneous oedema, vomiting, watery diarrhoea, oliguria, and a propensity to acute renal failure, hepatic abnormalities, disseminated intravascular coagulation, and severe prolonged shock. One patient died, one had gangrene of the toes, and all have had fine desquamation of affected skin and peeling of palms and soles during convalescence. Five patients were studied prospectively. Staphylococcus aureus related to phage-group I was isolated from mucosal (nasopharyngeal, vaginal, tracheal), or sequestered (empyema, abscess) sites, but not from blood. This organism produces an exotoxin which causes a positive Nikolsky sign in the newborn mouse and which is biochemically, pathologically, and immunologically distinct from phage-group-II stapphylococcal exfoliatin.
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PMID:Toxic-shock syndrome associated with phage-group-I Staphylococci. 8 81

Coagulation studies were done on 78 consecutive cases of obstructive jaundice with or without biliary tract infection. Among 26 cases with biliary tract infection 20 cases showed no bleeding tendency but remarkable hypercoagulability with decreased fibrinolytic activity. Other six cases developed diffuse bleeding tendency in addition to the signs of hypotension and multiorgan dysfunction such as oliguria, respiratory distress and mental confusion. Most showed marked coagulation defects characterized by thrombocytopenia, decreased fibrinogen, antithrombin III and plasminogen levels and narrowing of maximal amplitude in thrombelastogram as well as the increase of fibrin degradation products and positive soluble fibrin monomer complexes. All except one died and three cases were autopsied. In two cases postmortem examination revealed multiple fibrin thrombi in lungs and other organs. A cause of the development of bleeding tendency in obstructive jaundice presently observed may likely to be due to the occurrence of disseminated intravascular coagulation (DIC), i.e. hypercoagulability caused by the biliary tract infection is responsible.
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PMID:Occurrence of disseminated intravascular coagulation (DIC) in obstructive jaundice and its relation to biliary tract infection. 32 28

Twenty-three cases of delayed hemolytic transfusion reaction (DHTR) occurring at the Mayo Clinic from 1964 through 1973 are reviewed. Nineteen patients had clinical manifestations of hemolysis, of which fever was the most frequent presenting symptom. The degree of hemolysis served as an index of morbidity. In four cases, there was oliguria, two of these patients experiencing renal shutdown. In one case, hemolysis led to a disseminated intravascular coagulation syndrome. Death occurred subsequent of DHTR in three patients. The direct antiglobulin test was positive in all but one case; this finding coincided with elevated unconjugated bilirubin in 14 cases and decreased haptoglobin levels in 15 cases. Anti-Jka antibody accounted for somewhat more than one-third of reactions and, along with anti-E, c, D, Fya, and K antibodies accounted for 91 per cent of cases.
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PMID:Transfusion reaction. An immunologic hazard of blood transfusion. 41 92

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

Shock continues to be associated with a high mortality rate primarily because of delays in diagnosis and therapy. To diagnose shock early, and thereby increase the chances of reversal before there is extensive deterioration of vital organs, one should look for any decrease in pulse pressure, urine output, urine sodium concentration, alertness or any increase in urine osmolarity, tachypnea or tachycardia. Systolic hypotension, oliguria, metabolic acidosis and a cold clammy skin are late signs of shock. The pathophysiology of early hypovolemic shock includes hyperventilation, vasoconstriction, cardiac stimulation, fluid shifts into the vascular system and platelet aggregation. Late shock is characterized by lysosomal breakdown, subsequent release of kinins (especially bradykinin), impaired cell metabolism and organ function, fluid shifts out of the vascular system because of capillary endothelial damage and intravascular coagulation. The primary cause of shock should not be neglected in favor of treating signs, symptoms, and laboratory data. The resuscitation from the shock process itself involves correction of pathophysiologic changes, based on objective trends and responses rather than isolated measurements. A suggested outline of therapies in order of their use includes: 1) correction of the primary problem; 2) ventilation and oxygen; 3) fluid-loading: 4) inotropic agents; 5) correction of acid-based and electrolyte abnormalities; 6) steroids ("physiologic" or "pharmacologic" doses); 7) vasopressors (especially in elderly, severely hypotensive patients); 8) vasodilators (if excess vasoconstriction); 9) diuretics (if oliguric in spite of the above), and 10) heparin (if DIC). The most common errors are 1) late diagnosis; 2) inadequate control of the primary problems; 3) inadequate fluid loading; 4) delayed ventilator assistance, and 5) excessive reliance on and use if vasopressors and diuretics.
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PMID:Shock in the emergency department. 79 60

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

Under the proper experimental conditions, disseminated intravascular coagulation,"an intermediary mechanism of disease," results in the classic endotoxin-induced generalized Shwartzman reaction. Other substances, such as liquoid, a highly negatively charged anticoagulant, trigger a generalized Shwartzman reaction-like phenomenon in rabbits. We studied the effects of a single high intravenous dose of liquoid (12.5 mg.) upon the rat's coagulation and complement systems and their correlation with the kidney morphology by light, fluorescence, and electron microscopy. Thrombin time was prolonged; fibrinogen, plasminogen, and factors VIII and XII concentrations were markedly decreased, whereas fibrin degradation products were increased in the experimental animals when compared with the saline-injected controls (p greater than 0.001). Total hemolytic complement, hemolytic activity of terminal components (C3 to C9), and C3 protein concentration were significantly reduced (p greater than 0.001). The liquoid-injected rats developed cortical necrosis and manifested oliguria and anuria, with elevated blood urea nitrogen levels, when survival was longer than 3 hours. Histologically, thrombi of fibrin-like material filled the glomerular capillaries. Deposits of fibrin, and also of immunoglobulin G and C3, were readily identifiable by specific immunofluorescence, Linear or granular fluorescent deposits (or both) along the glomerular basement membranes and in the mesangium were observed. Electron microscopy demonstrated necrosis of glomeruli and abundant thrombi of fluffy, compact granular, or fibrillar electron-dense material. No typical fibrin periodicity was detected. These experiments support the concept of activation of the coagulation and the complement systems. We postulate that liquoid produced not only a consumptive coagulopathy in the rat but also a direct or perhaps anindirect activation of complement. Whether this latter has occurred through the classic or an alternate pathway remains to be elucidated.
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PMID:Disseminated intravascular coagulation induced by liquoid in the rat. I. Correlation of hematologic and complement abnormalities with renal lesions studied by light, fluorescence, and electron microscopy. 112 10

Nephropathia epidemica (NE) in Scandinavia is a zoonosis caused by Puumala virus. The main animal reservoir is the bank vole. NE predominantly affects men. Its annual incidence varies in a cyclic fashion, with peaks occurring every third to fourth year. The clinical picture of NE in Scandinavia is similar to that of hemorrhagic fever with renal syndrome in other parts of the world, although NE generally has a milder course. The case-fatality rate is approximately 0.2%. The most common clinical findings in NE are an acute onset of symptoms, fever (greater than or equal to 38 degrees C), oliguria, headache, back pain, and polyuria. Hemorrhagic manifestations are seen in about one-third of cases, and up to 5% of patients have gastrointestinal bleeding or disseminated intravascular coagulation. Thrombocytopenia occurs in a majority of patients. In the acute phase, the glomerular filtration rate is markedly decreased and tubular dysfunction is evident. Most patients with NE recover within 6 months.
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PMID:Nephropathia epidemica (hemorrhagic fever with renal syndrome) in Scandinavia. 168 81

We observed 73 patients with the hemolytic uremic syndrome (HUS) in 9 years (1980-1988), comprising 34% of patients with acute renal failure treated over the same period. There were 53 boys and 20 girls; 59% were below the age of 2 years and 33% between 2 and 5 years. Acute, usually severe dysentery, responding poorly to various antibiotics, was the prodromal illness in 80%, whereas 12% had watery diarrhea. Most patients had severe renal involvement with anuria in 56% and oliguria in 30%. A polymorphonuclear leukocytosis was present in 85% of cases, but had no correlation with the highest levels of blood urea. Coagulation abnormalities suggesting consumption coagulopathy were found in 24 of 30 cases. The results of stool culture showed Shigella species in 7 cases and nontyphoidal Salmonella in 9. Escherichia coli were isolated in 11 cases, but were not further characterized. Renal biopsy showed total or patchy cortical necrosis in 20 of 50 cases. The patients were managed with supportive care, including transfusion of fresh blood or plasma and dialysis as required. The mortality was 60%, being chiefly related to the duration of renal failure and presence of renal cortical necrosis, whereas persistent dysentery and infections were complicating factors. The presence of convulsions and coagulation defects had no relation to the outcome. Our observations indicate that HUS in children in northern India is mostly related to dysentery, likely to be shigellosis, and is usually associated with severe renal damage and a high death rate.
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PMID:Hemolytic uremic syndrome in children in northern India. 186 81

The retrospective study of acute renal failure (ARF) in patients with hematologic neoplasms was carried out. ARF occurred in 32 (6.1%) of 526 patients with hematologic neoplasms. Twenty-one (66%) patients recovered from ARF, but only 7 (22%) survived and were discharged from the hospital and 25 (78%) died of ARF or other complications. In 17 patients with leukemia or malignant histiocytosis, sepsis and/or disseminated intravascular coagulation were the most common causes of ARF, and all 17 patients died. In 11 patients with multiple myeloma, ARF was always attributable to the underlying disease, and the clinical course improved with the initiation of blood purification therapy (hemodialysis, plasma exchange) and chemotherapy. Five patients in blast crisis of chronic myelogenous leukemia or non-Hodgkin's lymphoma developed ARF as a result of tumor lysis syndrome. In this group, renal function improved with hemodialysis but only 2 patients survived. Patients with oliguria had worse outcomes than those without oliguria. Survival appeared to depend not on renal function but on the underlying disease, the cause of ARF, and other complications. These findings suggest that, in patients with hematologic neoplasms complicated by ARF, early initiation of blood purification therapy will improve the prognosis.
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PMID:[Acute renal failure in patients with hematologic neoplasms]. 238 Oct 56


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