Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hp now appears to be more than a simple commensal organism in patients with gastritis or peptic ulcer disease. Microbiologic, serologic, and epidemiologic studies all confirm that Hp has an important role in children with abdominal pain. Hp is found in the gastric mucosa of children with histologically proven gastritis or peptic ulcer. The organism can be transmitted from human to human with evidence of colonization, appearance of gastritis, and serum antibody response. Antimicrobial therapy directed at Hp eradicates colonization and resolves symptoms. Hp antibodies appear more frequently in familial clusters and the frequency of antibody positivity increases with age. Children are more likely to have symptomatic disease associated with elevated antibody titers. Recurrence of disease is associated with reappearance of the organism. At the present time, colonization can be detected only by gastric biopsy; however, it may be possible eventually to diagnose or follow infections by obtaining serum antibody titers or urea breath-testing. The natural history of Hp infection is unclear. Although it can cause an acute gastritis, it generally is found in association with chronic gastritis. The increase in seropositivity with age may mean that slow changes evolve over decades or that age cohorts have been infected differentially. How does antral colonization with Hp cause duodenal ulceration? The organism is not found in the duodenum and most patients with gastritis do not develop ulcers. This may be related to changes in acid production and mucosal protection associated with Hp colonization, but few studies have been done. What factors initiate Hp infection? Both volunteers who became colonized first suppressed acid secretion with H2-antagonists. Hypochlorhydria also seems to follow Hp infection in these same studies. The role of diet and drugs, or other environmental and genetic factors, in initiating infection is largely unexplored. An effective means of therapy needs to be developed. Although Hp appears sensitive in vitro to many compounds, it is difficult to eradicate in vivo, especially with monotherapy. Single-drug therapy suppresses the organism, but recurrence rates are high. It is difficult to deliver effective doses of drugs to the mucous niche the organism has selected and concerns about long-term therapy and its side effects persist. Current data suggest no ready solution to the initial case presentation. A child with primary gastritis or duodenal ulcer should be treated first with standard antacid and H2-receptor antagonist therapy. If endoscopy is performed, biopsies of normal-appearing areas of gastric antrum should be stained for Hp and a biopsy urease test should be performed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Helicobacter pylori, gastritis, and ulcers in pediatrics. 144 15

The authors studied the role of Helicobacter pylori at recurrent abdominal pain in childhood. Helicobacter pylori infection hasn't been found at the 42 examined children. The endoscopy showed esophagitis in 34 cases. The quick urease test, the histological examination, and the bacterial culture are proposed to carry out in ulcus duodeni, gastritis typ. B ulcus ventriculi and not necessary to carry out if the endoscopy shows only esophagitis--emphasize the authors.
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PMID:[Studying the role of Helicobacter pylori infection in recurrent abdominal pain in children]. 160 7

Helicobacter (Campylobacter) pylori has been cultured from the antral biopsies of 85-90% of patients of gastritis, gastric ulcer and duodenal ulcer at different centres. Studies conducted all over the world have firmly implicated this organism in the aetiology of active superficial gastritis and recurrences of duodenal ulcer. Two hundred patients with upper abdominal pain, distension, vomiting and/or haemetemesis were subjected to OGD scopy. In 163 of these patients there was endoscopic evidence of gastritis; in 24 there was DU; in 3, GU and in 10 it was normal. Diagnosis of H pylori infection was made by the rapid biopsy urease test which is nearly 100% specific and 98% sensitive. 170 out of 200 patients were positive for H pylori. Among these were 138 patients of gastritis (84.6%); 22 cases of DU (91.6%); 2 cases of GU (66.6%) and 8 in whom endoscopy was normal. Histological examination of the antral biopsy specimens showed mild to severe infiltration of mucosa with lymphocytes and plasma cells. None of the 170 H pylori positive cases showed polymorphonuclear infiltration which has been stressed repeatedly by most Western authors to be characteristic of "active" superficial gastritis associated with H pylori infection. Even in those with a history of dyspepsia of barely 4 weeks duration or less there was no PMN infiltration in the mucosa. Thus the local response to infection by H pylori of the gastric mucosa is different in Indian patients.
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PMID:Unusual features of Helicobacter (Campylobacter) pylori--associated gastritis in India. A study of 200 cases. 209 22

We evaluated the diagnostic accuracy of endoscopic finding of nodular antritis and rapid urease test (RUT) in order to simplify the approach to the diagnosis of Helicobacter pylori (H. pylori) infection. Forty-four consecutive patients (mean age 7.9 yr, range 6-13 yr) referred because of recurrent abdominal pain as the main symptom, were prospectively investigated for the presence of H. pylori. H. pylori positivity or negativity was defined as the concordance of two of the following tests: RUT, microbiologic culture, and histologic examination on bioptic samples. RUT sensitivity was 100%, whereas specificity was 87.5%. The presence of nodular antritis had a sensitivity of 96.4% and specificity of 87.5% in H. pylori infection diagnosis. The predictivity value of combined RUT and nodular antritis, whether positive or negative, was 100%. Only in case of discordance do we suggest the utilization of other expensive tools for diagnosis of H. pylori infection.
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PMID:Helicobacter pylori infection: a simplified diagnostic approach. 188 14

Urease of Helicobacter pylori (formerly Campylobacter pylori) is believed to represent a critical virulence determinant for this species. Ammonia generated by hydrolysis of urea may protect the acid-sensitive bacterium as it colonizes human gastric mucosa. An H. pylori strain, cultured from a gastric biopsy of a patient with complaints of abdominal pain and a history of peptic ulcer disease, was isolated on selective medium and cultured in Mueller-Hinton broth supplemented with 4% fetal calf serum. Whole cells were ruptured by French pressure cell lysis, and soluble protein was chromatographed on DEAE-Sepharose, phenyl-Sepharose, Mono-Q, and Superose 6 resins. Purified urease represented 6% of the soluble protein of crude extract, was estimated to have a native molecular size of 550 kilodaltons (kDa), and was composed of two distinct subunits of apparent molecular sizes of 66 and 29.5 kDa. On the basis of subunit size, a 1:1 subunit ratio as measured by scanning densitometry of Coomassie blue-stained sodium dodecyl sulfate-polyacrylamide gels, and estimated native molecular size, the data are consistent with a stoichiometry of (29.5 kDa-66 kDa)6 for the structure of the native enzyme. Km for urea was estimated at 0.2 mM. By N-terminal analysis, the 29.5-kDa subunit of H. pylori urease was found to share significant amino acid sequence similarity with the smallest of three subunits of the Proteus mirabilis and Morganella morganii ureases, as well as to the amino terminus of the unique jack bean subunit. The 66-kDa subunit also shared up to 80% similarity with the largest of three subunits of P. mirabilis, M. morganii, and Klebsiella aerogenes ureases and to internal sequences (amino acids 271 to 285) of the jack bean urease subunit. Thus, the amino acid sequence is conserved among ureases with one, two, and three distinct subunits, suggesting a common ancestral urease gene. Also, urease subunits of M. morganii and jack bean were specifically recognized by antisera raised against the 66-kDa subunit of H. pylori urease, demonstrating that at least some antigenic determinants were conserved among ureases from different species.
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PMID:Purification and N-terminal analysis of urease from Helicobacter pylori. 231 39

To evaluate the accuracy of IgG and IgA serological tests in establishing a diagnosis of Helicobacter (Campylobacter) pylori gastric infection, 60 children presenting with chronic abdominal pain were prospectively studied. Endoscopic antral biopsies were obtained and analyzed for the presence of H. pylori using three standard methods: culture and identification of bacterial isolates, microscopic examination for morphologically characteristic bacteria, and urease production by the biopsy specimen. Concomitantly obtained serum samples were analyzed for the presence of IgG and IgA antibodies against H. pylori surface antigens using enzyme-linked immunosorbent assay (ELISA). Thirty-four of 60 (56.6%) had histological evidence of chronic active gastritis, eight of whom (13.3%) also had evidence of H. pylori infection by at least one criteria. Six of the eight infected patients had H. pylori demonstrated by all three methods. Of the eight infected patients, seven had IgG antibodies against H. pylori (sensitivity of 87%) and six had IgA antibodies (sensitivity of 75%). Among the six patients who had H. pylori infection confirmed by all three methods, all had IgG antibodies (sensitivity of 100%). In the patients without evidence of H. pylori infection, the IgG ELISA had a specificity of 96% (50/52), and the IgA ELISA had a specificity of 100% (52/52). Our data suggest that serological testing for the presence of antibodies against H. pylori may be a useful diagnostic tool in screening children with chronic abdominal pain for the presence of gastric infection with H. pylori.
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PMID:Helicobacter pylori-related gastroduodenal disease in children. Diagnostic utility of enzyme-linked immunosorbent assay. 238 45

Numerous reports have established the association of Helicobacter pylori and peptic ulcer disease in adults. Recently, this association has also been demonstrated in children. We investigated 14 children and adolescents with recurrent abdominal pain. In six patients, endoscopy revealed gastritis and Helicobacter pylori was identified. Giemsa stain was more sensitive than culture or urease testing in identifying the bacteria. In four of the six, a nodular appearance of the antral mucosa was observed. The histological examination suggests lymphoid hyperplasia as the cause of the nodularity. All of the patients became symptomless after combined treatment with amoxicillin and bismuth subsalicylate. We conclude that nodular gastritis is a peculiar type of gastritis in children. It is frequently found in association with Helicobacter pylori infection.
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PMID:Nodular gastritis and Helicobacter pylori. 205 Dec 85

A consecutive series of 51 children (mean age 11 years) who presented with recurrent abdominal pain were investigated by upper gastrointestinal endoscopy including three antral biopsies for microscopy, culture and urease testing. Serum IgG, IgA, and IgM antibodies to Campylobacter pylori (C pylori) were measured by the ELISA technique. Serum pepsinogen I was also measured. Thirty two children showed histological evidence of gastritis. All had C pylori on microscopy and or culture. Nineteen children showed no histological gastritis nor evidence of C pylori on microscopy, culture and/or urease testing. The IgG and IgA antibody levels to C pylori were significantly higher in C pylori positive children than in the negative group (p less than 0.001). Serum pepsinogen I concentrations were also significantly higher in C pylori positive children than in negative (p less than 0.001). Measurement of IgG antibody levels, combined with serum pepsinogen I estimation, predict the presence of C pylori associated gastritis in children with a sensitivity and specificity of up to 95%. It may be used therefore to predict gastritis and even peptic ulceration in children presenting with non-specific upper abdominal pain.
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PMID:Serum pepsinogen I and IgG antibody to Campylobacter pylori in non-specific abdominal pain in childhood. 275 88

Campylobacter pylori, a suspected agent of gastritis and peptic ulceration, rapidly hydrolyzes urea. Because urease serves as the basis of detection of the organism in gastric biopsies and may represent an important virulence factor, biochemical characteristics of the enzyme were determined. C. pylori was isolated from antral biopsies from 10 patients with complaints of abdominal pain or history of peptic ulcer disease. All isolates were urease positive, with an average rate of hydrolysis by cell lysates being 36 +/- 28 mumol of NH3 per min per mg of protein, more than twice that of Proteus mirabilis and 10 times that of other urinary tract isolates. The enzyme had an apparent molecular weight of 625,000 +/- 15,000 by column chromatography, an isoelectric point of 5.9, a Km of 0.8 +/- 0.1 mM urea, an optimal temperature of 45 degrees C, and an optimal pH of 8.2. Ten isolates tested produced ureases with identical electrophoretic mobilities on nondenaturing 5% polyacrylamide activity gels. Acetohydroxamic acid (100 micrograms/ml), hydroxyurea (85 micrograms/ml), flurofamide (0.05 micrograms/ml), and EDTA (8 mM) inhibited enzyme activity by 50%. Cell lysates retained 50% of initial urease activity after 6 days and 40% activity after 18 days when stored at 4 degrees C in 20 mM sodium phosphate, pH 6.8. At -70 degrees C for 18 days, 1 mM EDTA or 15% glycerol preserved 40 or 34%, respectively, of initial activity. The urease of C. pylori appears to be biochemically unique from the enzymes of other common urease-producing species.
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PMID:Characterization of urease from Campylobacter pylori. 338 8

Campylobacter pyloridis infection of the stomach has been associated with gastric ulcer, duodenal ulcer, nonulcer dyspepsia, and gastritis. The etiological role of C. pyloridis in most of those conditions remains unclear. We reviewed what is known about C. pyloridis infections in man. Considerable clinical data on C. pyloridis infections was available in older literature concerning gastritis and gastric urease. C. pyloridis causes a form of type B gastritis. In some individuals the acute infection is associated with abdominal pain and transient hypochlorhydria. C. pyloridis infection is difficult to eradicate with current therapies. The mechanisms by which C. pyloridis infection may lead to development of peptic ulcers, nonulcer dyspepsia, or atrophic gastritis are discussed. Recent technological advances, such as the 13C-urea breath test, provide rapid noninvasive methods of identifying active C. pyloridis infection. These methods will permit the rapid execution of definitive investigations of the epidemiology, transmission patterns, and possible reservoirs of C. pyloridis infection and will delineate the spectrum of C. pyloridis-associated disorders.
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PMID:Campylobacter pyloridis gastritis: the past, the present, and speculations about the future. 355 84


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