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)

A 31 year-old man ingested 10 mL of a photographic toning solution containing 600 mg of potassium chloroplatinite in a suicide attempt. Subsequent toxic effects included acute oliguric renal failure, metabolic acidosis, fever, muscle cramps, gastroenteritis and rhabdomyolysis. Laboratory abnormalities included mildly elevated liver enzymes and elevated peripheral blood neutrophil and eosinophil counts. All symptoms and signs of toxicity resolved over a six day hospital stay with supportive medical management only; thereafter he was lost to medical follow-up. A spot serum platinum concentration was 245 mcg/dL and a spot urine platinum concentration was 4200 mcg/L.
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PMID:Toxicity after self-poisoning by ingestion of potassium chloroplatinite. 174 52

The diuretic effect of high doses of furosemide alone and furosemide plus mannitol was analysed retrospectively in 30 children with acute renal failure. In 10 children (Group 1) renal failure developed mainly during glomerulonephritis, and in 20 children (Group 2) the cause was gastroenteritis. The diuretic effects of furosemide and furosemide plus mannitol were evaluated measuring the 24-hour urine volume at the time of anuria, oliguria or normal diuresis. The highest mean single intravenous doses of furosemide were 6.5 and 14 mg/kg in Groups 1 and 2, respectively; the highest average daily doses were 10.1 and 25.5 mg/kg, respectively. A broad relationship was observed between single i.v. dose and diuretic response following administration of furosemide (1.2 to 30.8 mg/kg). In both groups of patients a statistically significant negative linear correlation was found between the daily intravenous dose of furosemide and the 24-hour urine volume. Calculations based on the obtained regression equations showed that the expected 24-hour urine volumes corresponding to daily diuresis normal for age could be obtained after administration of daily 2.8 to 1.4 mg/kg furosemide in Group 1 and 9.3 to 2.3 in Group 2. It is therefore suggested that the total daily dose of furosemide should not exceed 100 mg in children with acute renal failure. Administration of furosemide plus mannitol did not result in higher daily diuresis as compared to 24-hour urine volume obtained when furosemide was given alone. Furosemide was well tolerated. Electrolyte disturbances, especially in Group 2, were the most frequent side effects due to high doses of furosemide.
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PMID:High doses of furosemide in children with acute renal failure. A preliminary retrospective study. 193 35

Nine fatal cases of systemic mucormycosis observed in association with renal failure are described. Four patients were hospitalized for chronic renal failure as a consequence of chronic glomerulonephritis, myeloma kidney, chronic pyelonephritis, and polycystic kidney disease, respectively; and five patients presented with acute renal failure. The underlying causes in three of these five patients were gentamycin nephrotoxicity, acute gastroenteritis, and allograft rejection, respectively, and in the remaining two, acute renal failure was the result of extensive renal vascular and parenchymal invasion by mucor hyphae. Tissue invasion with mucormycosis was documented during life in two patients and at autopsy in seven patients. The infection was disseminated in five patients, and isolated pulmonary and rhinocerebral involvement occurred in two patients each. Our observations have shown that patients with renal failure are prone to develop mucormycosis, which carries a grave prognosis if therapy is not instituted in time.
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PMID:Mucormycosis in patients with renal failure. 248 82

Clinical and epidemiological data on 16 patients with HFRS admitted to the University Hospital of Infectious Diseases in Zagreb during the past 10 years (1977-1986) are reported. In 13 of them, the diagnosis was confirmed serologically by indirect fluorescent method. All but two were men between 20 and 45 years of age (80% of patients). The disease appeared sporadically only. According to the domicile, way of living and working all the patients but three mentioned the contact with rodents in the fields or in other places (mill, storehouse). Three patients live in Zagreb and there was no possibility to get infected out of the town. The disease had moderate course, more rarely severe course when shock and acute renal failure developed. General symptoms with fever and algias dominated (febrile stage). Some of the patients had ophthalmic disturbances. Patients with a pronounced gastroenteritis developed shock the most frequently. In some of the patients back and abdominal pains followed by obstipation appeared. HFRS was incriminated disease because of febrile stage followed by the acute renal failure, oliguria, azotemia, polyuria and low urine osmolity. One female patient with active rheumatoid arthritis died after two-week staying in hospital due to irreversible shock followed by cardiopulmonary and renal failure.
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PMID:[Clinical and epidemiologic characteristics of hemorrhagic fever with renal syndrome]. 256 68

Clinical details and present day problems encountered in 425 cases of falciparum malaria (PF) are reported. 10.11% had taken chloroquine prior to reporting to us. Parasitic count done in 23.05% cases lacked correlation with severity of disease. Pattern of fever varied markedly but 5.4% were afebrile throughout and presented only with bodyache and malaise. Apyrexial spell was noted in 5.64%. 28.70% had typical facial looks of anaemia and sallow complexion. Cerebral symptoms were noted in 3.05%. Other symptoms were severe headache 33.4%, pain abdomen 3.29%, gastroenteritis 5.64%, jaundice 2.58% and bronchitis in 7.50%. We encountered subconjunctival haemorrhages with purpura and/or urticaria in four cases, symptoms suggestive of shock lung in 3, pulmonary oedema in 2, severe anaemia (HB less than 4 g%) in seven pregnant ladies, extrapyramidal symptoms in follow up period in 5 and congenital malaria in 2 cases. 83.25% were cured with chloroquine and oxytetracycline. 8.47% (who deteriorated despite the above treatment) were treated with quinine for 6 days. 5.17% (with severe disease) were also given quinine as first line drug. 2.82% (unresponsive to chloroquine and oxytetracycline but with mild disease) were treated with pyrimethamine-sulphamezathine combination for 5 days. One case who did not respond to quinine was treated with quinidine. Recrudescence was seen in 3.67% of patients treated with chloroquine and oxytetracycline. There was no case with renal failure, haemolysis due to G6PD deficiency and black water fever. There was only one death (0.23%) in our series. Self-medication, haphazard therapy and the slogan "Fever may be malaria-take chloroquine" can lead to problems in falciparum malaria.
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PMID:Falciparum malaria--present day problems. An experience with 425 cases. 269 36

In the second part of this review of mushroom poisonings, the syndromes with intermediate and long lag-times are discussed. They include the coprinus-, phalloides-, gyromitrin- and the orellanus syndrome. The coprinus syndrome occurs whenever alcohol is consumed after a meal containing coprine. The lag-time varies according to the amount and time of alcohol intake. It is very similar to the disulfiram syndrome which is known from the adverse therapy of alcoholism. The lag-time of the phalloides syndrome varies between 7 and 24 hours. It starts with massive gastroenteritis followed by hepatopathia which can lead to hepatic coma and kidney failure. The phalloides syndrome is caused by the amatoxins of the death caps, which inhibit the RNA Polymerase B in the nucleus of the liver cell. The gyromitrin syndrome exhibits also a delayed onset. The hepatotoxicity and the nephrotoxicity are less severe than in the phalloides syndrome. The first metabolite of gyromitrin monomethylhydrazin is responsible for CNS-symptoms such as delirium and convulsions. In contrast to the phalloides syndrome vomiting can be the only leading symptom in gyromitrin poisoning. The orellanus syndrome has the most delayed onset of all mushroom poisonings with 1-3 weeks. It should be thought of in all cases of kidney insufficiency of unknown origin. The orellanines damage the kidney and induce all degrees of kidney insufficiency according to the amount of ingested poison. Terminal kidney failure which requires hemodialysis treatment can occur in severe cases.
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PMID:[Diagnosis and therapy of mushroom poisoning (II)]. 361 14

At least 150 cases of mushroom poisoning occur in Canada each year, 75% in the Province of Ontario. Eighty per cent of the total are in children under the age of 9, and most do not require hospitalization. Amanita virosa poisoning is a potentially fatal medical emergency which presents as an acute gastroenteritis, progressing to hepatorenal failure. Treatment consists of elimination of undigested mushrooms, rapid rehydration, management of acute liver and renal failure, and prevention of infection during the recovery phase.
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PMID:Mushroom poisoning in Canada: report of a fatal case. 544 50

Plasma VIII:von Willebrand factor antigen (VIII:vWF) levels were elevated approximately two- to eightfold in seven patients (three adults and four children) during acute episodes of thrombocytopenia, renal failure, and hemolytic anemia (the hemolytic-uremic syndrome, HUS). In all seven patients, there was an alteration in plasma VIII:vWF patterns during these acute HUS episodes, so that the largest VIII:vWF forms were relatively decreased. Plasma VIII:vWF multimer patterns returned to normal, or nearly to normal, as platelet counts returned to preexisting levels, even in the patients whose recovery of renal function was incomplete and whose plasma VIII:vWF antigen level remained above normal. The sister of one of the HUS patients had a similar clinical prodrome (gastroenteritis) that was not followed by thrombocytopenia or renal failure and was not accompanied by an elevated level or abnormal forms of plasma VIII:vWF. These results suggest that an alteration in VIII:vWF metabolism, distribution, or interaction with platelets is associated with acute HUS episodes. In contrast to patients with chronic relapsing thrombotic thrombocytopenic purpura, none of the HUS patients (either during or after the acute HUS episodes) had a defect in the conversion of unusually large VIII:vWF multimers derived from endothelial cells to the VIII:vWF forms found in normal plasma.
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PMID:Abnormal VIII: von Willebrand factor patterns in the plasma of patients with the hemolytic-uremic syndrome. 643 74

Seventy-two patients with neoplastic disease in a variety of anatomic sites were treated with sequential methotrexate (MTX) and 5-fluorouracil (5-FU) followed by leucovorin (LV) rescue. Treatment consisted of MTX, 160 mg/m2 as a 10-min infusion; 5-FU, 600 mg/m2 as a bolus 90 min later; and LV, a minimum of 25 mg/m2 or 15 mg/m2 p.o. q.6h. X 4, repeated at 1- or 2-wk intervals. Responses of any type included 4 of 24 colon cancers, 3 of 12 stomach cancers, 0 of 6 pancreas cancers, 1 of 2 gallbladder cancers, 4 of 6 breast cancers, 1 of 1 uterus cancer, 2 of 2 selected lung cancers, 1 of 1 parotid cancer, 1 of 2 sarcomas, and 0 of 6 ovary cancers. Response appeared to increase survival. The best-quality responses were observed in patients with stomach, breast, and parotid tumors. Toxicities included anemia requiring transfusion (20%), anorexia during treatment with LV (16%), moderate thrombocytopenia (12%), grade 3 stomatitis (12%), moderate granulocytopenia (10%), severe conjunctivitis (6%), severe gastroenteritis (6%), vomiting (6%), anamnestic reactions (6%), possible renal failure (4%), and possible pulmonary failure (2%). One patient had life-threatening gastroenteritis and reappearance of a grade 1 to 2 skin reaction of the entire treatment field more than 5 yr after radiotherapy. Patients with prior cis-platin therapy had a 50% risk of life-threatening pancytopenia. The results encourage controlled primary trials testing intensification of the sequential combinations with parallel investigations of MTX alone with and without diminished doses of LV.
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PMID:MTX/5-FU trials in gastrointestinal and other cancers. 660 24

A review of the causes of death in 276 patients with sickle-cell disease showed that although the greatest mortality occurred in the first five years of life, roughly one-quarter were aged over 30. Commonest causes of death in the first ten years included acute splenic sequestration, septicaemia, meningitis, aplastic crises, and gastroenteritis. In older patients cerebrovascular accidents and renal failure became common. The acute chest syndrome affected all age groups about equally but appeared to result predominantly from infection in the young and embolism or thrombosis in the old.
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PMID:Causes of death in sickle-cell disease in Jamaica. 681 42


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