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)

Treatment of severe iron overdose in two children is described, and the pathophysiology of iron toxicity and management of acute iron poisonings are reviewed. An 11-month-old boy was comatose and in shock several hours after ingesting approximately 50 ferrous sulfate tablets (elemental iron 390 mg/kg). He had hyperglycemia and leukocytosis. Lavage was performed with a solution containing deferoxamine and sodium bicarbonate, and deferoxamine was given by continuous i.v. infusion for 48 hours. The initial serum iron (SI) concentration of 14,250 micrograms/dL decreased to 657 micrograms/dL nine hours after i.v. deferoxamine therapy was initiated. A roentgenogram showed tablets in the stomach and small bowel. Packed red blood cells were administered to treat apparent necrotizing gastroenteritis. SI concentration returned to normal by day three [corrected], and the child recovered. A 2.5-year-old boy was examined 1.25 hr after ingesting an estimated 55 tablets of ferrous gluconate 325 mg (elemental iron 130 mg/kg). Initial SI concentration was 134 micrograms/dL, and total iron-binding capacity (TIBC) was 219 micrograms/dL. A roentgenogram indicated iron concretion in the stomach and iron tablets in the small bowel. He underwent lavage with solution containing sodium bicarbonate. An i.m. dose of deferoxamine was administered, followed by i.v. deferoxamine therapy. SI concentration eight hours after the ingestion was 290 micrograms/dL, and whole-bowel irrigation was begun with polyethylene glycol-electrolyte solution. The irrigation and deferoxamine therapy were discontinued 20 hours after the ingestion, when SI concentration was 73 micrograms/dL, and the child recovered. Acute iron ingestions of more than 60 mg/kg are potentially serious. Patient 1 had severe iron intoxication, while aggressive treatment prevented severe toxicity in patient 2. Acute iron toxicity includes effects on the GI tract and the cardiovascular, metabolic, hepatic, and central nervous systems. Guidelines for assessing the severity of an overdose and selecting the most appropriate therapy are provided. The indications for chelation therapy with deferoxamine, gastric decontamination procedures including use of lavage solutions and whole-bowel irrigation, and adjunctive measures are described. Management of acute iron overdose includes supportive care, GI decontamination, and chelation therapy.
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PMID:Management of acute iron overdose. 266 31

The prevalence and pathogenesis of hyperglycaemia were investigated in a consecutive series of 27 black infants admitted to hospital with gastroenteritis over a period of three months. Hyperglycaemia (plasma glucose concentration greater than 10 mmol/l) occurred in 15 (55%) of these patients. The pathogenesis was not clear but possible contributory factors included raised concentrations of the stress hormones pancreatic glucagon, growth hormone, and cortisol; hypokalaemia; and peripheral insulin resistance. Intravenous rehydration, without insulin, corrected the plasma glucose concentrations and restored the hormonal profile towards normal within 36 to 48 hours.
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PMID:Hyperglycaemia in infantile gastroenteritis. 638 26

Hyperglycemia and glucosuria are frequently seen during the acute phase of dehydration secondary to gastroenteritis. In this paper, 33 patients in hypovolemic shock due to diarrhea were studied. Serum glucose resulted above 140 mg/100 ml. in 14 patients (41%); it was below 27 mg/100 ml. in 2 more patients (5.8%). Despite high glucose concentration, only 4 out of the 14 hyperglycemic patients had serum insulin concentration above that observed in normal fasting children. Plasma cortisol was significantly higher in the group with hyperglycemia (54 +/- 24 micrograms/100 ml.) in comparison with the group with normal glucose levels (15 +/- 6.4 micrograms/100). No correlation was found between serum glucose and the concentrations of sodium, potassium, bicarbonate, growth hormone nor with plasma osmolarity. All disturbances observed turned normal after rehydration. Hyperglicemia is explained as a response to stress and is probably due to the gluconeogenic action of cortisol and the inhibitory effect of catecholamines upon insulin secretion.
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PMID:[Hyperglycemia of the dehydrated infant]. 699 Sep 40

There are only 6 published reports of pancreatitis associated with oral contraception (OC). This article presents 1 additional case. A 28 year old white woman was hospitalized for severe abdominal pains; gastroenteritis was diagnosed and the patient treated with Compazine and Maalox. Because of the increasing severity of pains the patient was rehospitalized and pancreatitis secondary to hyperlipoproteinemia was diagnosed. OC treatment was suspended, and the patient was successfully treated with Cimetidine, antacids, and insulin for elevated glucose. Pancreatitis caused by OC is probably due to alterations in lipid metabolism, and related to the estrogen content of the preparation used. A major study done recently with 2 types of synthetic estrogens combined with 3 types of progestogens confirmed that hypertriglyceridemia induced by OC was estrogen dosage-related. It seems apparent that OC use in patients with intrinsic lipid abnormalities may be contraindicated; other risk patients are those who are obese, diabetic, or with family antecedents of diabetes or hyperlipidemia.
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PMID:Birth control pills and pancreatitis. 707 Jan 28

The nonketotic hyperglycemic syndrome is rare during childhood and may occur as the initial manifestation of insulin-dependent diabetes mellitus or during an episode of gastroenteritis. In this article, we report an unusual case of this syndrome in a female infant who had atypically severe hyperglycemia in association with gastroenteritis. In addition, we provide a review of the literature and summarize the pathophysiologic mechanisms of the nonketotic hyperglycemic syndrome.
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PMID:An unusual case of the nonketotic hyperglycemic syndrome during childhood. 780 54

A 66-year old female was admitted to our ICU in septic shock with accompanying signs of gastroenteritis and diabetic-related hyperglycemia. Computer tomography of the abdomen revealed the rare diagnosis of emphysematous pyelonephritis. Immediate nephrectomy led to a favourable outcome in this dramatic case. Although abscess drainage and broad-based antibiotic therapy are generally the first-line therapy today, emergency surgery would seem to be indicated in selected cases.
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PMID:[Emphysematous pyelonephritis--a rare cause of sepsis]. 982 59

Rotavirus is a ubiquitous double-stranded RNA virus responsible for most cases of infantile gastroenteritis. It infects pancreatic islets in vitro and is implicated as a trigger of autoimmune destruction of islet beta cells leading to type 1 diabetes, but pancreatic pathology secondary to rotavirus infection in vivo has not been documented. To address this issue, we inoculated 3 week-old C57Bl/6 mice at weaning with rhesus rotavirus, which is closely related to human rotaviruses and known to infect mouse islets in vitro. Virus was quantified in tissues by culture-isolation and enzyme-linked immunosorbent assay. A requirement for viral double stranded RNA was investigated in toll-like receptor 3 (TLR3)-deficient mice. Cell proliferation and apoptosis, and insulin expression, were analyzed by immunohistochemistry. Following rotavirus inoculation by gavage, two phases of mild, transient hyperglycemia were observed beginning after 2 and 8 days. In the first phase, widespread apoptosis of pancreatic cells was associated with a decrease in pancreas mass and insulin production, without detectable virus in the pancreas. These effects were mimicked by injection of the double-stranded RNA mimic, polyinosinic-polycytidylic acid, and were TLR3-dependent. By the second phase, the pancreas had regenerated but islets were smaller than normal and viral antigen was then detected in the pancreas for several days. These findings directly demonstrate pathogenic effects of rotavirus infection on the pancreas in vivo, mediated initially by the interaction of rotavirus double-stranded RNA with TLR3.
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PMID:Rotavirus infection induces transient pancreatic involution and hyperglycemia in weanling mice. 2518 16