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)

During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty-five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. Diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua.
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PMID:Hypoglycemia: causes, neurological manifestations, and outcome. 400 66

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

The levels of beta-endorphin, insulin, cortisol, GH, glucagon, prolactin and TSH were measured in serum samples of 9 hyperglycaemic patients (3 female, 6 male) with a mean age of 4.1 years admitted to the pediatric emergency unit. All patients were in acute stress due to severe diseases (acute gastroenteritis, bronchopneumonia, septicaemia, etc.). Initial and repeat blood samples for hormone determination were taken at admission and in the recovery phase (after 4-6 weeks of treatment). OGTT was also performed in the recovery phase. The hyperglycaemia, monitored hourly following the initial determination, returned to normal in all patients in 1-5 h without specific treatment. Mean serum glucose values at admission and in the recovery phase were 287.0 and 84.1 mg/dl. Concomitant to the hyperglycaemia encountered in these patients in the acute phase of stress, an increase was noted in all hormone levels excluding glucagon and cortisol. All elevated hormone levels fell to normal in 4-6 weeks with significant differences from initial levels for beta-endorphin (P < 0.05) and insulin (P < 0.01). OGTT gave a normal curve. These results indicate that stress hyperglycaemia, despite high insulin levels, is associated with an increase in beta-endorphin levels. The results also show that hyperglycaemia in acute disease does not alter OGTT in short-term follow up.
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PMID:beta-Endorphin and some hormonal levels in children with acute stress hyperglycaemia. 795 15

Pancreatic islet autoimmunity leading to type 1 diabetes could be triggered by viruses in genetically susceptible individuals. Rotavirus (RV), the most common cause of childhood gastroenteritis, contains peptide sequences highly similar to T-cell epitopes in the islet autoantigens GAD and tyrosine phosphatase IA-2 (IA-2), suggesting T-cells to RV could trigger islet autoimmunity by molecular mimicry. We therefore sought an association between RV infection and islet autoantibody markers in children at risk for diabetes who were followed from birth. There was a specific and highly significant association between RV seroconversion and increases in any of these antibodies: 86% of antibodies to IA-2, 62% to insulin, and 50% to GAD first appeared or increased with increases in RV IgG or IgA. RV infection may therefore trigger or exacerbate islet autoimmunity in genetically susceptible children.
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PMID:Association between rotavirus infection and pancreatic islet autoimmunity in children at risk of developing type 1 diabetes. 1092 32

Noroviruses (NoVs) are a leading cause of gastroenteritis worldwide and are recognized as the foremost cause of foodborne illness. Despite numerous efforts, routine cell cultures have failed to yield replicating NoV. This paper describes methods used to try to grow NoV in vitro in two laboratories. Cells (A549, AGS, Caco-2, CCD-18, CRFK, CR-PEC, Detroit 551, Detroit 562, FRhK-4, HCT-8, HeLa, HEC, HEp-2, Ht-29, HuTu-80, I-407, IEC-6, IEC-18, Kato-3, L20B, MA104, MDBK, MDCK, RD, TMK, Vero and 293) were cultured on solid or permeable surfaces. Differentiation was induced using cell culture supplements such as insulin, DMSO and butyric acid. In some cases, the cells and the NoV-containing stool samples were treated with bioactive digestive additives. Variables evaluated in cultivation experiments included the method of preparation of the virus inoculum, the genotype of the virus, conditions for maintenance of cell monolayers, additives in the maintenance medium and the method of inoculation of the cells. Serial blind passage studies were performed routinely. In addition to evaluation for CPE, evidence of virus replication was sought using immunofluorescent assays to detect newly produced viral capsid antigen and RT-PCR assays to detect the viral genome. Although some infected cultures remained NoV positive by RT-PCR for up to five passages and an occasional cell in a monolayer showed evidence of specific immunofluorescence, no reproducible NoV-induced CPE was observed and all RT-PCR results that were positive initially were negative following continued passaging. Thus, attempts to develop a method for the cultivation of NoV were unsuccessful.
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PMID:Laboratory efforts to cultivate noroviruses. 1471 22

In this study, we aimed to compare bone calcium system changes from children with diabetic ketoacidosis or acute metabolic acidosis due to dehydration to find out the relative contribution of metabolic acidosis and diabetes-related factors on expected negative calcium balance. We studied a set of non-invasive parameters of bone remodeling in 16 children with diabetic ketoacidosis due to new onset type 1 diabetes and 25 children with acute metabolic acidosis due to dehydration complicating acute gastroenteritis before and after the correction of acidosis. The two groups of subjects were matched for age, sex, pubertal status, and degree of metabolic acidosis and dehydration. A group of 18 age and sex-matched healthy children served as the control group. Plasma ionized calcium levels were increased in both groups, significantly more so in diabetic ketoacidosis. While osteoblastic markers, osteocalcin and alkaline phosphatase, were depressed to a comparable degree in both groups, urinary calcium/creatinine ratio and hydroxyproline excretion were significantly greater in diabetic ketoacidosis. No significant changes in calcitrophic hormone (intact PTH, calcitonin, 25-hydroxy vitamin D3) levels were observed. All study parameters except for serum phosphate levels behaved in parallel in both clinical conditions, and abnormalities disappeared with the correction of acidosis except for IGF-1, which remained low in diabetic subjects. In conclusion, our results suggest that, in diabetic ketoacidosis, the observed severe negative calcium balance occurred through diminished bone formation mediated by metabolic acidosis per se and increased bone mineral dissolution and bone resorption because of severe insulin deficiency and secondarily via metabolic acidosis. Observed changes appear to be independent of calcitrophic hormones.
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PMID:Bone calcium changes during diabetic ketoacidosis: a comparison with lactic acidosis due to volume depletion. 1586 25

We provide a global assessment, with detailed multi-scale data, of the ecological and toxicological effects generated by inorganic nitrogen pollution in aquatic ecosystems. Our synthesis of the published scientific literature shows three major environmental problems: (1) it can increase the concentration of hydrogen ions in freshwater ecosystems without much acid-neutralizing capacity, resulting in acidification of those systems; (2) it can stimulate or enhance the development, maintenance and proliferation of primary producers, resulting in eutrophication of aquatic ecosystems; (3) it can reach toxic levels that impair the ability of aquatic animals to survive, grow and reproduce. Inorganic nitrogen pollution of ground and surface waters can also induce adverse effects on human health and economy. Because reductions in SO2 emissions have reduced the atmospheric deposition of H2SO4 across large portions of North America and Europe, while emissions of NOx have gone unchecked, HNO3 is now playing an increasing role in the acidification of freshwater ecosystems. This acidification process has caused several adverse effects on primary and secondary producers, with significant biotic impoverishments, particularly concerning invertebrates and fishes, in many atmospherically acidified lakes and streams. The cultural eutrophication of freshwater, estuarine, and coastal marine ecosystems can cause ecological and toxicological effects that are either directly or indirectly related to the proliferation of primary producers. Extensive kills of both invertebrates and fishes are probably the most dramatic manifestation of hypoxia (or anoxia) in eutrophic and hypereutrophic aquatic ecosystems with low water turnover rates. The decline in dissolved oxygen concentrations can also promote the formation of reduced compounds, such as hydrogen sulphide, resulting in higher adverse (toxic) effects on aquatic animals. Additionally, the occurrence of toxic algae can significantly contribute to the extensive kills of aquatic animals. Cyanobacteria, dinoflagellates and diatoms appear to be major responsible that may be stimulated by inorganic nitrogen pollution. Among the different inorganic nitrogenous compounds (NH4+, NH3, NO2-, HNO2NO3-) that aquatic animals can take up directly from the ambient water, unionized ammonia is the most toxic, while ammonium and nitrate ions are the least toxic. In general, seawater animals seem to be more tolerant to the toxicity of inorganic nitrogenous compounds than freshwater animals, probably because of the ameliorating effect of water salinity (sodium, chloride, calcium and other ions) on the tolerance of aquatic animals. Ingested nitrites and nitrates from polluted drinking waters can induce methemoglobinemia in humans, particularly in young infants, by blocking the oxygen-carrying capacity of hemoglobin. Ingested nitrites and nitrates also have a potential role in developing cancers of the digestive tract through their contribution to the formation of nitrosamines. In addition, some scientific evidences suggest that ingested nitrites and nitrates might result in mutagenicity, teratogenicity and birth defects, contribute to the risks of non-Hodgkin's lymphoma and bladder and ovarian cancers, play a role in the etiology of insulin-dependent diabetes mellitus and in the development of thyroid hypertrophy, or cause spontaneous abortions and respiratory tract infections. Indirect health hazards can occur as a consequence of algal toxins, causing nausea, vomiting, diarrhoea, pneumonia, gastroenteritis, hepatoenteritis, muscular cramps, and several poisoning syndromes (paralytic shellfish poisoning, neurotoxic shellfish poisoning, amnesic shellfish poisoning). Other indirect health hazards can also come from the potential relationship between inorganic nitrogen pollution and human infectious diseases (malaria, cholera). Human sickness and death, extensive kills of aquatic animals, and other negative effects, can have elevated costs on human economy, with the recreation and tourism industry suffering the most important economic impacts, at least locally. It is concluded that levels of total nitrogen lower than 0.5-1.0 mg TN/L could prevent aquatic ecosystems (excluding those ecosystems with naturally high N levels) from developing acidification and eutrophication, at least by inorganic nitrogen pollution. Those relatively low TN levels could also protect aquatic animals against the toxicity of inorganic nitrogenous compounds since, in the absence of eutrophication, surface waters usually present relatively high concentrations of dissolved oxygen, most inorganic reactive nitrogen being in the form of nitrate. Additionally, human health and economy would be safer from the adverse effects of inorganic nitrogen pollution.
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PMID:Ecological and toxicological effects of inorganic nitrogen pollution in aquatic ecosystems: A global assessment. 1678 74


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