Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight cases of ecstasy related acute liver damage referred to a specialised liver unit are described. Two patients presented after collapse within six hours of ecstasy ingestion with hyperthermia, hypotension, fitting, and subsequently disseminated intravascular coagulation with rhabdomyolysis together with biochemical evidence of severe hepatic damage. One patient recovered and the other with evidence of hyperacute liver failure was transplanted but subsequently died, histological examination showing widespread microvesicular fatty change. Four patients presented with acute liver failure without hyperthermia. All four fulfilled criteria for transplantation, one died before a donor organ became available, and two died within one month post-transplantation of overwhelming sepsis. Histological examination showed submassive lobular collapse. Two patients presented with abdominal pain and jaundice and recovered over a period of three weeks; histological examination showed a lobular hepatitis with cholestasis. Patients developing jaundice or with evidence of hepatic failure particularly encephalopathy and prolongation of the international normalised ratio, or both, whether or not preceded by hyperthermia, should be referred to a specialised liver unit as liver transplantation probably provides the only chance of recovery.
 ...
PMID:Acute liver damage and ecstasy ingestion. 867 2

Reported is a case of hemorrhagic shock and encephalopathy syndrome (HSE) with extensive white matter involvement. A three year old, previously healthy boy was presented with an acute onset of fever, loss of consciousness and convulsions. He had disseminated intravascular coagulation, metabolic acidosis, non-ketotic hypoglycemia and hepatorenal dysfunction. The computed tomography (CT) scan of his head on the second day of illness demonstrated symmetric, extensive low-density areas in the cerebral and cerebellar white matter. The child died on the 13th hospital day. A post-mortem histopathological examination of the liver revealed centrilobular necrosis and infiltration of fatty acid droplets. The concentrations of serum 2',5'-oligoadenylate synthetase and urinary neopterin were markedly elevated, indicating excessively activated cell-mediated immunity. This overproduction of inflammatory cytokines might play an important role in the pathogenesis of the brain lesion as well as in other clinical and laboratory manifestations. The patient had a decreased serum level of alpha l-antitrypsin, which may have been associated with the development of uncontrolled inflammation and coagulation disorder.
 ...
PMID:Extensive white matter involvement in hemorrhagic shock and encephalopathy syndrome. 874 21

The objective of this pilot controlled study was to evaluate the extracorporeal liver assist device (ELAD) in patients with acute liver failure who were judged to still have a significant chance of survival (approximately 50%) and in those who had already fulfilled criteria for transplantation. Twenty-four patients were divided into two groups, 17 with a potentially recoverable lesion (group I) and 7 listed for transplantation (group II), and then randomly allocated to ELAD haemoperfusion or control. The median period of ELAD haemoperfusion was 72 hours (range 3-168 h). Biocompatibility of the device was good, with no acceleration in platelet consumption, and haemodynamic stability was maintained. Two patients were withdrawn from the study because of worsening of preexisting disseminated intravascular coagulation in one case and a hypersensitivity reaction in the other. Deterioration with respect to encephalopathy grade was more frequent in the control patients, 7 of 12 (58%), than in the ELAD-treated patients, 3 of 12 (25%). In group I where survival for the ELAD cases was 7 of 9 (78%), there was a higher than expected survival in the controls, 6 of 8 (75%). For group II cases, survival was 1 of 3 (33%) for the ELAD-treated patients, and 1 of 4 (25%) for the controls. Both of the survivors underwent transplantation. Assessment of additive function for the device revealed an improvement in galactose elimination capacity after 6 hours of haemoperfusion. Based on the results of this pilot-controlled trial, better indices of prognosis will be required, in addition to those used to select for transplantation, if patients at an earlier stage of clinical deterioration are to be included in future studies.
 ...
PMID:Pilot-controlled trial of the extracorporeal liver assist device in acute liver failure. 893 79

Hemorrhagic shock and encephalopathy syndrome (HSES) is a sudden-onset symptom complex occurring in previously healthy infants and children. It was first described in 1983 in the United Kingdom in 10 infants. Subsequently, > 140 cases have been reported worldwide, although no cases have been previously reported in the forensic literature. Typically the child presents with fever, shock, encephalopathy with coma and seizures, evidence of hemorrhage, and diarrhea. Laboratory investigation reveals falling hemoglobin and platelet counts, renal impairment, evidence of disseminated intravascular coagulation, metabolic acidosis, and raised serum transaminases. Microbiological cultures are uniformly negative. The condition has a high mortality and morbidity. The etiology is unknown and may be multifactorial. However, hyperpyrexia appears to play a central role in pathogenesis. The diagnosis of HSES in the deceased child is one of exclusion and requires a careful antemortem history as well as a thorough autopsy with toxicological and microbiological investigations. A case of HSES is reported and the literature reviewed.
 ...
PMID:Hemorrhagic shock and encephalopathy syndrome. An unusual cause of sudden death in children. 909 7

We describe a male infant with early myoclonic encephalopathy (EME) associated with the congenital nephrotic syndrome, microcephaly, multiple minor anomalies, and cerebellar hypoplasia. He had erratic and massive myoclonus, and partial seizures from the neonatal period. Electroencephalography showed the so-called suppression-burst pattern. He died of disseminated intravascular coagulation caused by the congenital nephrotic syndrome at the age of two months. Our patients is the first reported case with EME associated with the congenital nephrotic syndrome.
 ...
PMID:A case of early myoclonic encephalopathy with the congenital nephrotic syndrome. 910 63

A 4-year-old boy was admitted with disturbed consciousness following a convulsion. He developed bilateral pyramidal tract signs and showed a decerebrate posture. Laboratory findings revealed severe liver dysfunction and disseminated intravascular coagulation. On the eighth day eight in hospital he developed parkinsonism. However, 5 months from onset he had recovered almost completely. Brain CT on admission showed low density areas in the basal ganglia, thalamus, midbrain and pons. A T2-weighted scan in magnetic resonance imaging (MRI) showed almost symmetrical high signal intensities in both basal ganglia (including putamen, caudate nucleus, globus pallidus), external capsule, internal capsule thalamus, midbrain, pons and white matter of the peribasal ganglia; but a T1-weighted scan showed low signal intensities in the same regions during all phases. Therefore hemorrhagic lesions or the presence of thalamic methemoglobin were excluded. It was considered that the pathogenesis may be cytotoxic cellular edema due to cytotoxic agents or acute metabolic factors. Clinical presentation, laboratory findings and radiological findings were most suggestive of acute necrotizing encephalopathy. As differential diagnoses, acute disseminated encephalomyelitis and brainstem encephalitis were considered.
 ...
PMID:Suspected acute encephalopathy with symmetrical abnormal signal areas in the basal ganglia, thalamus, midbrain and pons diagnosed by magnetic resonance imaging. 931 91

We report 81 of 107 cases of hemolytic uremic syndrome (HUS), admitted between July 1994 and February 1996, following an outbreak of Shigella dysenteriae type 1 dysentery in Kwazulu/Natal. All patients, excluding 1, were black with a mean age of 38 months (range 1-121); 50 (61.7%) were males. The mean duration of dysentery was 11.3 days (range 1-41) and HUS 15 days (range 1-91). Most patients had acute oliguric renal failure (90.1%), 42 (51.6%) required peritoneal dialysis. Complications included encephalopathy 30 (37.0%), convulsions 12 (14.8%) and hemiplegia 2 (2.3%), gastrointestinal perforation 8 (9.9%), protein losing enteropathy 26 (32.1%), toxic megacolon 4 (4.9%), rectal prolapse 5 (6.2%), hepatitis 11 (13.6%), myocarditis 5 (6.2%), congestive cardiac failure 3 (3.7%), cardiomyopathy 3 (3.7%), infective endocarditis 1 (1.2%), septicemia 15 (18.5%), disseminated intravascular coagulation 17 (21%). Leukemoid reactions were found in 74 (91.3%) patients, hyponatremia in 56 (69.1%), and hypoalbuminemia in 67 (82.7%). Stool culture for Shigella dysenteriae type I was positive in only 7 (8.6%) patients; Shiga toxin assays were not performed. Outcome was as follows: recovery 32 (39.5%), impaired renal function 8 (9.9%), chronic renal failure 26 (32.1%), end-stage renal disease 1 (1.2%), and death 14 (17.3%) patients.
 ...
PMID:Post-dysenteric hemolytic uremic syndrome in children during an epidemic of Shigella dysentery in Kwazulu/Natal. 932 80

Haemorrhagic shock and encephalopathy syndrome (HSES) is a devastating disorder affecting infants. So far no cases have been reported in Switzerland. It is characterised by the abrupt onset of hyperpyrexia, shock, encephalopathy, diarrhoea, disseminated intravascular coagulation (DIC) and renal and hepatic failure in previously healthy infants. Severe hypoglycaemia has been repeatedly reported in association with HSES. However, the pathophysiology of the hypoglycaemia is not clear. We report on two infants (2 and 7 months old) with typical HSES, both of whom were presented with nonketotic hypoglycaemia. In the first case, plasma insulin was 23 pmol/l at the time of hypoglycaemia (0.1 mmol/l). In the second case, increased values for interleukin-6 (IL-6) (319 pg/ml) and IL-8 (1382 pg/ml) were found 24 hours after admission, whereas IL-1 and tumour necrosis factor-alpha (TNF-alpha) were not measurable. Alpha-1-antitrypsin was decreased (0.6 g/l). In hyperpyrexic, unconscious and shocked infants, HSES should be considered and hypoglycaemia should be specifically looked for. Hypoglycaemia is not caused by hyperinsulinism but may be secondary to the release of cytokines.
 ...
PMID:Haemorrhagic shock and encephalopathy syndrome: report of two cases with special reference to hypoglycaemia. 1070 Dec 32

CT/MRI findings, laboratory examinations and prognoses of 42 patients with acute encephalopathy (AE) (Japan Coma Scale > or = 200) were reported. 1. Findings on CT/MRI were divided into the following 7 categories: Group 1 (normal), Group 2 (CT/MRI looked normal in acute phase, but brain atrophy developed and progressed slowly by weeks or months), Group 3 (CT/MRI looked normal within a few days after the onset of AE, but cortical laminar necrosis developed at 4-5 days after the onset), Group 4 (marked brain edema developed within 2 days after the onset of AE), Group 5 (AE with symmetric thalamic lesions), Group 6 (symmetric pallidum, lesions on MRI which appeared after brain edema disappeared), and Group 7 (the brain shrinked during acute phase, which normalized on the follow up CT/MRI). 2. Serum AST elevated in approximately 50% of the patients with AE. Sixty percent of them exhibited DIC, whose prognoses were poor. Cerebrospinal fluids (CSF) neopterin (NP) and/or interleukin (IL)-6 were elevated in all the 8 patients examined. In the two cases whose serum NP and IL-6 were measured at the same time, their values in the CSF were higher than those in the serum in one case, and almost the same in the other. In a patient with a condition mimicking hemorrhagic shock and encephalopathy, serum IL-6 concentration was very high (94,000 pg/ml). 3. Mild hypothermia (around 34 degrees C) combined with methylprednisolone pulse therapy was excellently effective on AE. A 6-year-old boy exhibited tonsillar herniation at admission recovered well to be able to run. 4. Differentiation between Reye syndrome and HSE, and the pathogenesis of AE were also discussed.
 ...
PMID:[Infection-related acute encephalopathy: CT scan/MRI finding, laboratory examination and prognosis]. 1072 91

Data on 1112 tuberculosis patients with various neurological complications who were treated at Moscow Tuberculosis Clinical Hospital No. 7 during 1997-1999 are analyzed. A working classification of neurological complications in tuberculosis, which may be recommended to therapeutists, phthisiologists, and neurologists, is proposed. The leading neurological complications in nonspecific tuberculosis are described. The acute toxic encephalopathy syndrome that is characterized by a combination of impaired consciousness, meningeal syndrome without spinal fluid changes, epileptic seizures, disseminated neurological symptoms, disseminated intravascular coagulation syndrome, and high death rates holds the lead. Mono- and polyneuropathies of predominantly the lower extremities are frequently detectable in tuberculosis. Concomitant alcoholism, diabetes mellitus, and isoniazid treatment make their course poorer. Vascular abnormalities of the nervous system in patients with tuberculosis run much more favourably that in those without it. Mild forms of parkinsonism were observed in 3% of patients with tuberculosis, vascular dementia is detectable rarely (0.2%), strokes run without severe overall cerebral symptoms. The high incidence of neurological diseases in patients with tuberculosis requires that specialized departments of neurology should be set up at the institutes of tuberculosis and at multidisciplinary related hospitals. The tuberculosis curricula for students and postgraduate physicians should envisage additional sections to study diseases of the nervous system in tuberculosis.
 ...
PMID:[Clinical aspects, diagnosis and treatment of neurological complications of tuberculosis]. 1150 28


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>