Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study included 13 infants under one year complaining of acute gastroenteritis and dehydration who were still in oliguria or anuria 6 hours after rehydration was initiated. They were given a single dose of furosemide at the rate of 1 mg/kg and indices of U/P of urea and osmolarity, ratio urea/plasmatic creatinine, urinary volume, natriuresis and evolution of urea plasmatic figures and of creatinine were determined. Four patients showed no response to the diuretic; all of them died and through clinical and histopathologic evaluation they were classified as having acute renal insufficiency (IRA). The nine patients showing response to the drug with an increase of 5 to 30 times the control figure for urine and natriuresis showed an index U/P of urea of 5.52 +/- 3.82, U/P of osmolarity of 1.32 +/- 09, ratio urea/plasmatic creatinine of 58.7 +/- 19.8 and the figures for urea and creatinine in blood turned normal within 2 to 4 days. This was classed as prerenal azotemia (APR). It is thus concluded that furosemide appears to be a good parameter to make an early differentiation of cases with IRA, but that this measure, the same as the rest of the indices cannot show an absolute value since there are important variations in each individual.
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PMID:[Furosemide in the early diagnosis of acute renal insufficiency in the newborn infant]. 58 41

The clinical features and X-ray manifestations of 50 cases of legionnaires disease were analysed. 8 cases might be due to nosocomial infection through breathing in flying particles of the saliva or phlegm. According to the main clinical features, this disease could be divided into common pneumonia type; acute gastroenteritis type; encephalopathy type; shock type; acute renal insufficiency type. The differential diagnosis of legionnaires disease with mycoplasmal pneumonia, pneumococcal pneumonia and infiltrative pulmonary tuberculosis was also discussed. The first choice for treatment is erythromycin or erythromycin with rifampicin.
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PMID:[A clinical study of 50 cases of Legionnaires disease]. 130 5

In the fall of 1981 the San Francisco Bay Area Regional Poison Control Center received more than 100 calls regarding wild mushroom ingestion. Ten cases, including three fatalities, had all the features of Amanita phalloides poisoning. Encephalopathy, coma and renal insufficiency occurred in all three patients who died, but did not occur in those who survived. Two of the three patients who died arrived at the hospital late in the course of their illness, and severe gastroenteritis with accompanying dehydration probably contributed to their deaths. The poison control center promoted public awareness of the mushroom hazard through newspaper and television stories and by notifying local health departments. It also has devised a simple form to improve the quality of data collection and to assist in later verification of suspected A phalloides poisoning.
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PMID:Amanita phalloides-type mushroom poisoning. 717 45

Every year in France, about 100 children, most of them less than 3 years old, have typical diarrhea-associated HUS (D + HUS). Evidence of exposure to verotoxin producing E. coli (VTEC), mostly the O157: H7 serotype, is demonstrated in about 85% of cases. A prodromal illness of acute gastroenteritis with diarrhea, often bloody, precedes the HUS by 1 to 15 days. HUS onset is sudden, with the typical association of hemolytic anemia with fragmented red blood cells, thrombocytopenia and acute renal insufficiency. Involvement of other organs than the kidneys may occur, such as severe hemorrhagic colitis with rectal prolapse, bowel wall necrosis or secondary stenosis, acute pancreatitis, central nervous system involvement which determines the vital outcome. Early accurate supportive treatment allows a current mortality rate below 5%, with most deaths due to central nervous system involvement. Five to 10% of children develop end stage renal disease, rarely directly, more often after having recovered some renal function with chronic renal insufficiency during a few years. After 15 or more years follow-up, at least one third of patients have some degree of proteinuria and/or hypertension, and eventually chronic or end stage renal failure. Predictive features of poor renal outcome at the acute phase are severe gastrointestinal involvement, severe CNS involvement, polyncleosis over 20,000/mm3, and duration of initial anuria longer than one week. The role of VTEC in D + HUS makes the disease a public health problem. Preventive measures are essential.
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PMID:[Post-diarrhea hemolytic-uremic syndrome: clinical aspects]. 1158 27

This article describes the birth of the Canadian Pediatric Kidney Disease Research Centre (CPKDRC) in 1985 and the activities that have transpired as a result of collaborative research at paediatric centres across Canada. These include the National Retrospective Study of Childhood Hemolytic Uremic Syndrome (HUS), National Prospective Study of Risk Factors for Developing Escherichia coli O157:H7 Infection, and Intervention Studies for the Prevention of HUS. A look to the future describes possible studies to determine potential factors (surrogate markers) to identify children who are at risk for developing HUS following verotoxin-producing E coli gastroenteritis, other intervention studies and a more accurate understanding of permanent renal insufficiency in children who have had HUS.
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PMID:Hemolytic uremic syndrome: Events of the past decade. 2004 65

Risk assessment of the amnesic shellfish poison, domoic acid, a potent neurotoxin, is evaluated based on its current knowledge and its harmful effects, and is presented under four headings, viz., (1) hazard identification, (2) dose response assessment, (3) exposure assessment and (4) risk characterization. Domoic acid binds the glutamate receptor site of the central nervous system (CNS) of humans and causes depolarization of neurons and an increase in cellularcalcium. In nature, domoic acid is produced by the algae, Pseudonitzschia spp. and they enter into the body of shellfish through their consumption. This toxin is reported to cause gastroenteritis, renal insufficiency confusion and memory loss in humans, since it affects the hippocampus of the brain. In rats, intraperitonial and oral administration of domoic acid result in scratching, tremor and convulsions, and in monkeys, the toxic symptoms like mastication, salivation, projectile vomiting, weakness, teeth grinding and lethargy are apparent. The no-observed-adverse-effect-level (NOAEL) in animals reveals that pure toxin is more effective than those isolated from shellfish. Based on LD50 values, it is found that intraperitonial administration of this toxin in animals is 31 fold more effective than oral administration. Low levels of domoic acid (0.20-0.75 ppm) show no toxic symptoms in non-human primates, but clinical effects are apparent in them and in humans, at a concentration of 1.0 ppm. The tolerable daily intake (TDI) of domoic acid for humans is calculated as 0.075 ppm, whereas for razor clams and crabs, the TDI are 19.4 and 31.5 ppm respectively. The hazard quotient (HQ) is found to be 2. Being an irreversible neurotoxin, domoic acid has severe public health implications. Death occurs in those above 68 years old. In order to ensure adequate protection to public health, the concentration of domoic acid in shellfish and shellfish parts at point of sale shall not exceed the current permissible limit of 20 microg g(-1) tissue. While processing shellfish, it maybe advisable to pay attention to factors such as environmental conditions, inter-organ variability in concentrations of domoic acid and cross contaminations.
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PMID:Risk assessment of the amnesic shellfish poison, domoic acid, on animals and humans. 2012 Apr 52

An investigation into the health of green turtles was undertaken near Gladstone, Queensland, in response to a dramatic increase in stranding numbers in the first half of 2011. A total of 56 live turtles were subject to clinical examination and blood sampling for routine blood profiles, and 12 deceased turtles underwent a thorough necropsy examination. This population of green turtles was found to be in poor body condition and a range of infectious and non-infectious conditions were identified in the unhealthy turtles, including hepato-renal insufficiency (up to 81%, 27/33 based on clinical pathology), cachexia (92%, 11/12), parasitism (75%, 9/12), cardiopulmonary anomalies (42%, 5/12), gastroenteritis (25%, 3/12), masses (25%, 3/12) and mechanical impediments (17%, 2/12 based on necropsy). Overall, there was no evidence to indicate a unifying disease as a primary cause of the mass mortality. Recent adverse weather events, historic regional contamination and nearby industrial activities are discussed as potential causative factors.
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PMID:Clinical and Pathological Findings in Green Turtles (Chelonia mydas) from Gladstone, Queensland: Investigations of a Stranding Epidemic. 2525 11