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 concentration of nitrate (the stable oxidation product of nitric oxide) in plasma and its excretion in urine was measured in 20 patients with a diagnosis of gastroenteritis. On day 1 of the illness plasma nitrate concentration was significantly elevated compared with a healthy control population (92.7 +/- 17.0 mumol/l vs. 33.1 +/- 1.6 mumol/l; P < 0.001) and continued to be elevated on days 2 and 3. Urinary nitrate excretion was also elevated. The plasma nitrate concentration correlated with disease severity as assessed by stool frequency and plasma urea concentration. Plasma nitrate concentration may be a sensitive and clinically useful indicator of severity of gastroenteritis.
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PMID:Plasma nitrate concentration and urinary nitrate excretion in patients with gastroenteritis. 852 41

Nitric oxide (NO) production is increased in several inflammatory disorders, although the role of this gas is not clear. The purpose of this study was to determine whether luminal NO in the intestine is increased in infective gastroenteritis. Rectal gas was sampled in 17 patients with gastroenteritis and 10 healthy volunteers, with balloon catheters made of 100% silicone and analyzed for NO by chemiluminescence. Plasma nitrate and nitrite levels were determined by capillary electrophoresis. Rectal NO was (mean+/-SEM) 9441+/-3126 parts per billion (ppb) in the patients and 74+/-13 ppb in controls (P<.0001). There was no individual overlap. Plasma nitrite but not nitrate was significantly increased in patients compared with controls. These data indicate that luminal NO is greatly increased in gastroenteritis. The high levels of NO are easily measurable by rectal sampling, and measurement of luminal NO seems to be useful for evaluating local NO production in the gut in health and disease.
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PMID:Increased nitric oxide in infective gastroenteritis. 1039 79

In humans, the role of nitric oxide (NO) in host defence is controversial. We prospectively studied plasma levels of nitrate, the stable end-product of NO formation, during acute infection in 43 patients controlled with regard to dietary nitrate/nitrite. During acute gastroenteritis the mean plasma nitrate level was significantly increased compared with at recovery 4-5 weeks later (118 vs. 32.5 micromol/l; p < 0.001), in contrast with the findings in patients with acute pneumonia (PN; 34.6 vs. 42.8 micromol/l) or febrile urinary tract infection (UTI; 27.7 vs. 31.3 micromol/l). In a second group of 20 retrospectively studied patients with severe PN or UTI, of whom 70% were bacteraemic, no significantly increased nitrate levels could be demonstrated during the acute stage of infection. These findings indicate that increased NO production, as measured by plasma nitrate, is not a general finding in patients with acute infectious diseases, but may rather be associated with certain pathogens or sites of infection.
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PMID:Plasma nitrate as an index of nitric oxide formation in patients with acute infectious diseases. 1052 82

Formula-fed babies contract gastroenteritis more than breast-fed babies, which is of concern to mothers who cannot breastfeed or, as with HIV-infected mothers, are discouraged from breastfeeding. The ability of endogenous breastmilk xanthine oxidase to generate the antimicrobial radical nitric oxide has been measured and its influence on the growth of Escherichia coli and Salmonella enteritides examined. Breastmilk, but not formula feed, generated nitric oxide. Xanthine oxidase activity substantially inhibited the growth of both bacteria. An important natural antibiotic system is missing in formula feeds; the addition of xanthine oxidase may improve formula for use when breastfeeding is not a safe option.
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PMID:Antibacterial properties of xanthine oxidase in human milk. 1102 33

Over the last years the important role of nitric oxide (NO) as endogenous modulator of numerous physiological functions has been shown. NO is involved in the regulation of blood flow, maintenance of vascular tone, control of platelet aggregation, and modulation of the activity of the mastocytes. It also plays a key role as neurotransmitter in the central and peripheric nervous system (non adrenergic non colinergic, NANC, neurons), in the nervous control of the cerebral blood flow and in the neuroendocrine regulation or synaptic plasticity. However, NO shows a dual behavior: at physiological concentrations, released through the constitutive synthase (cNOS), it regulates house-keeping functions, whereas its overproduction by the inducible isoenzyme (iNOS) exhibits cytotoxic activity because interacting with reactive species producing peroxinitrites (ONOO) and other compounds, which are highly damaging for the tissues. In the gastrointestinal tract (GIT) NO participates in the modulation of the smooth musculature tone, such as the regulation of intestinal peristaltism, gastric emptying and antral motor activity. It also regulates acid and gastric mucus secretion, alkaline production, and is involved in the maintenance of mucosal blood flow. In physiological conditions, NO acts as an endogenous mediator modulating both, the repairing and integrity of the tissues, and exhibits gastroprotective properties against different types of aggressive agents. However, high concentrations of NO are related to numerous pathological processes of GIT including peptic ulcer, chronic gastritis, gastrointestinal cancer, bacterial gastroenteritis, celiac or chronic inflammatory bowel diseases. Recently, this hypothesis that cNOS is always beneficial and iNOS is always deleterious, has been questioned, since that a series of data suggest that the increase of cNOS activity could be responsible for the derived pathological changes and, by contrast, NO liberated by the inducible isoenzyme might play a repairing effect in certain pathological disorders. The pharmaceutical industry is really interested in proving the clinical benefits of the mediator. Numerous NO-donor drugs, nitrate derivatives, have been frequently used in the cardiovascular diseases due to their vasodilating properties, which allow an enhancement of coronary blood flow. More recently, the protective effect of NO against non steroidal antiinflammatory drugs (NSAID)-gastroenteropathy has been shown, because its vasodilating and antioxidant properties render it a potentially useful agent. Different NSAID, including acetyl salicylic acid, diclofenac or naproxen, have been formulated by attaching a NO releasing-moiety. These NO-NSAID, antiinflammatories combined with precursors of the mediator, or with inhibitors of the inducible synthase, are currently being evaluated. However, although the pharmacotherapeutical possibilities of NO are considerable, it is necessary to elucidate the exact mechanisms derived from stimulation/inhibition of the isoenzymes in order to determine the clinical utility of NO-donors.
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PMID:New issues about nitric oxide and its effects on the gastrointestinal tract. 1147 46

Australian Aboriginal children hospitalized with diarrhoeal disease have severe manifestations with acidosis, hypokalaemia, osmotic diarrhoea and abnormal small bowel permeability. Nitric oxide (NO) production is increased in diarrhoeal disease, but its relationship to mucosal function and diarrhoeal complications is not known. We examined the relationship between NO production and complications of acute diarrhoea in Aboriginal and non-Aboriginal children between February 1998 and February 2000. We enrolled 318 children admitted to Royal Darwin Hospital into one of three groups: acute diarrhoea, non-diarrhoeal controls with no inflammatory illness, and non-diarrhoeal controls with inflammatory illness. Nitric oxide production was measured by urine nitrate-creatinine (NOx/Cr) excretion on a low nitrate diet. Small bowel intestinal permeability was measured by the lactulose-rhamnose (L/R) ratio on a timed blood specimen. The NOx/Cr ratios were markedly elevated in Aboriginal diarrhoeal cases (geometric mean [GM] = 1.23, 95% confidence interval [95% CI] 1.07-1.44), lowest in non-Aboriginal non-inflammatory controls (GM = 0.13, 95% CI 0.10-0.16) and intermediate in all other groups (GM = 0.35, 95% CI 0.28-0.43). Convalescent levels (day 5) in the Aboriginal diarrhoeal group (GM = 1.02, 95% CI 0.82-1.28) were slower to fall than L/R ratios. Multivariate analysis in the diarrhoeal group indicated that high NO production was associated with abnormal permeability, hypokalaemia and malnutrition, but not with the severity of diarrhoea, acidosis or osmotic diarrhoea. We concluded that increased NO production may contribute to impaired mucosal barrier function and hypokalaemia in acute gastroenteritis, which may be the cost of the known gut-protective and antimicrobial effects mediated by NO in acute intestinal inflammation.
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PMID:Increased nitric oxide production in acute diarrhoea is associated with abnormal gut permeability, hypokalaemia and malnutrition in tropical Australian aboriginal children. 1288 17

Nitric oxide (NO) is a highly reactive free radical that is involved in a variety of different biological process. In recent reports, the putative role of NO in the neuropathogenesis of brain inflammation has been demonstrated. And then the relation between neuronal NO and convulsive seizures induced by virus has been suggested. However, there are few reports about NO in vivo under viral neurological infections. In order to evaluate the relation between NO production and neurological disorders induced by viral infection, sixty-six cases including 11 patients with rotavirus gastroenteritis admitted for convulsions were examined in this study. NO metabolites (NOx) levels in both serum and cerebrospinal fluid obtained from rotavirus gastroenteritis patients with convulsion were much higher than in those of patients with purulent meningitis, encephalitis, febrile convulsion or in the control group. There was a relative correlation between IL-6 and NOx in some cases. These results indicated that NO may have a pathophysiological role in convulsions associated by rotavirus infection either through indirect or direct effects of NO. Consequently, NOx inhibitors might be helpful for the treatment of rotavirus encephalopathy.
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PMID:Serum and cerebrospinal fluid nitrite/nitrate levels in patients with rotavirus gastroenteritis induced convulsion. 1470 70

Nitric oxide (NO) is known to be an important inflammatory mediator with a potential role in gastrointestinal diseases. We prospectively studied the luminal NO levels in 51 patients with infectious gastroenteritis, 35 patients with nonenteric bacterial infections, and 11 healthy control subjects. The levels of proinflammatory cytokines were simultaneously measured in the stools of patients with gastroenteritis. Rectal gas was sampled with balloon catheters made of silicone and was analyzed for NO levels by chemiluminescence. The median rectal NO level was 2,450 ppb in the acute phase of gastroenteritis and gradually decreased to 225 ppb after 3 to 8 weeks, whereas the median NO values were 150 ppb in patients with nonenteric bacterial infections and 100 ppb in healthy control subjects. Patients with Salmonella, Shigella, and Campylobacter infections generally had more severe symptoms and a higher median NO level (17,250 ppb) than patients with Clostridium difficile-associated diarrhea (median NO value, 275 ppb). Interleukin-1 beta levels were elevated in 82% of the patients at disease onset and decreased during the convalescent phase. In contrast, gamma interferon was detected in only 16% of the patients and was predominantly collected in stool samples collected during the subacute and convalescent stages. Our data point to the possibility of using this easy, minimally invasive method for luminal NO measurement as a diagnostic tool, among others, to evaluate the degree of intestinal inflammation in patients with infectious gastroenteritis.
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PMID:Rectal nitric oxide gas and stool cytokine levels during the course of infectious gastroenteritis. 1501 71

Irritable bowel syndrome (IBS) is one of the most common disorders and a heterogeneous condition in view of symptoms and underlying mechanisms. Though underlying causes of pathophysiologic changes remain unclear, low grade mucosal inflammation and abnormal intestinal motility are accepted mechanisms which alter gut function and generate symptoms of IBS. First, before 1980s, abnormal colonic and rectal motor functions were regarded as the main pathophysiology of IBS, but only 25-75% of IBS patients have apparent motor abnormalities which differ from the motor functions in normal controls. So, various gastrointestinal motility tests were not indicated for the diagnosis of IBS. The high-amplitude propagating contractions of colon in IBS patients may be related to the visceral pain perception. Second, the low grade mucosal inflammation may be involved in the pathophysiology of visceral hypersensitivity. Post infectious IBS (PI-IBS) occupied 6-17% of the total IBS and some previous prospective studies reported that 7-33% of acute bacterial enteritis patients developed IBS after 6-12 months of infection. The relative risk of IBS in the gastroenteritis cohort was 11.9 and the strongest risk factor is the duration of diarrhea. After enteritis event, the increased number of immunocytes, mast cells and large amount of lymphocytes infiltration were revealed in mucosa and enteric nervous system of the gut. Beside the inflammatory cells, enterochromaffin cells, cytokines and inducible nitric oxide may be related to the pathophysiologic mechanism of PI-IBS. Lastly, the abnormalities in the gastrointestinal autonomic nervous system can induce constipation or motor disorders, but further research should elucidate it.
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PMID:[The pathophysiology of irritable bowel syndrome: inflammation and motor disorder]. 1649 75

There is now substantial evidence that reduced expression of neuronal nitric oxide synthase (nNOS) is implicated in the pathogenesis of infantile hypertrophic pyloric stenosis (IHPS). This study aimed to investigate the role of plasma nitric oxide (NO) in patients with IHPS. Blood and pylorous biopsies of 13 IHPS patients were examined. The control group consisted of 19 age-matched healthy infants and 22 age-matched acute gastroenteritis patients. Plasma nitrite (NO(2-)) and nitrate (NO(3-)) levels were detected with an NO analyzer. Pylorus biopsies of 13 IHPS patients were examined for nitric oxide synthase isoform expression. Plasma nitrite levels in the 13 IHPS patients were significantly lower than in the age-matched healthy controls (0.97 +/- 0.19 vs. 3.53 +/- 0.79 microM; P < 0.001) and the acute gastroenteritis controls (0.97 +/- 0.19 vs.1.39 +/- 0.45 microM; P = 0.006). Decreased expression of nNOS in the nerve fibers of the pylorus circular muscle was found in the 13 IHPS patients. The decreased plasma nitrite levels rose to the normal range (3.27 +/- 0.77 M) after pyloromyotomy. There was no significant correlation between plasma nitrite levels and muscle wall thickness in IHPS patients. We conclude that NO is implicated in the occurrence of IHPS and the plasma nitrite level is valuable for the diagnosis of IHPS.
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PMID:Low plasma nitrite in infantile hypertrophic pyloric stenosis patients. 1675 11


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