Transient protein losing enteropathy associated with acute gastritis and campylobacter pylori.

Hill, Ivor D.; Sinclair-Smith, C; Lastovica, Albert J.; Bowie, M. D.; Emms, M.

doi:10.1136/adc.62.12.1215

Cited by 58 publications

(34 citation statements)

References 6 publications

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“…Moreover, these mechanisms are controversial, and there are other potential mechanisms by which H pylori could lead to gastroenteritis-like illness. H pylori infection has been linked to proteinlosing enteropathy 62 and to food allergies, 63 which can cause diarrhea. Application of the H pylori cytotoxin VacA to the surface of human intestine-derived cell monolayers promotes apical Cl Ϫ and water secretion.…”

Section: Figmentioning

confidence: 99%

Acute Helicobacter pylori Infection Is Followed by an Increase in Diarrheal Disease Among Peruvian Children

et al. 2001

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ABSTRACT. Background. Cohort and case-crossover studies were conducted to evaluate whether new Helicobacter pylori infections are followed by increased diarrhea.Methods. Participants were 6-month-old to 12-yearold shantytown residents living near Lima, Peru. Baseline data were collected from community households. Health interviews were completed daily, and sera, drawn every 4 months, were tested for H pylori immunoglobulin G. Diarrhea rates among newly H pylori-infected (seroconverting) children were compared with rates among persistently uninfected and infected children using cohort and case-crossover analyses.Results. Sera were obtained from 345 children from January 1, 1995, through September 1, 1997. H pylori incidence was 12% per year (36 H pylori infections in 109 866 seronegative days). In adjusted cohort analyses, seroconverters had more diarrhea days (rate ratio: 2.0; 95% confidence interval: 1.6 -2.4), episodes, and sick days in the year after infection than did uninfected children; and more diarrhea days and sick days than did persistently infected children. This effect was strongest in the first 2 months. Case-crossover analyses supported these findings.Conclusion. Preventing H pylori infection may help reduce pediatric diarrheal disease. Pediatrics 2001;108(5). URL: http://www.pediatrics.org/cgi/content/full/108/5/ e87; Helicobacter pylori, diarrheal disease, cohort study, case-crossover study, Poisson regression, childhood, achlorhydria, incidence, serology.ABBREVIATIONS. IgG, Immunoglobulin G; EIA, enzyme-linked immunosorbent assay; OD, optical density; PAR, population-attributable risk; 95% CI, confidence interval; RR, rate ratio.H elicobacter pylori infection is extremely common, infecting 20% to 60% of adults in developed countries and nearly all adults in developing countries. 1-8 Chronic infection with H pyloriwhich is typically acquired in childhood and persists throughout life-causes a variety of chronic diseases: duodenal 9,10 and gastric 11 ulcers, gastric cancer, 12,13 and gastric lymphoma. 14,15 The health effects of acute H pylori infection, however, are unknown. Reports in adults suggest that newly established infection is accompanied by mild gastrointestinal symptoms, although no controlled studies have been performed. 16 -20 Childhood infection has been linked to chronic diarrhea and growth retardation. Whether H pylori causes these problems or is simply a marker for other factors is unclear. [21][22][23] Acute H pylori infections often cause transient hypochlorhydria beginning as soon as 2 weeks after infection. 18,20,24 -26 In a cluster of probable H pylori infections transmitted by nasogastric instrumentation, hypochlorhydria lasted for a median of 4 months after infection among 14 of the 17 adults who recovered normal gastric acidity; 3 adults remained hypochlorhydric during throughout the year-long study period. 17,19 Hypochlorhydria has also been demonstrated in newly H pylori-infected Gambian infants. 23 Although there are several potential mechanisms by which H pylori coul...

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Section: Figmentioning

confidence: 99%

Acute Helicobacter pylori Infection Is Followed by an Increase in Diarrheal Disease Among Peruvian Children

et al. 2001

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“…In addition, recent studies indicate that this organism may be associated with primary antral gastritis, antral lymphoid hyperplasia, and protein-losing enteropathy in children (4,5).…”

Section: B L Wetherall* a M Johnsonmentioning

confidence: 97%

Haemolytic activity ofCampylobacter pylori

Wetherall

Johnson

1989

Eur. J. Clin. Microbiol. Infect. Dis.

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The haemolytic activity of several clinical and reference strains of Campylobacter pylori was determined using cell-free preparations of broth-grown organisms and human, horse, guinea pig, rabbit and sheep erythrocytes. Significant levels of haemolysis were produced only when the cell-free preparations were concentrated tenfold. However, three of 14 strains still gave haemolysis values of less than 50% when tested with guinea pig erythrocytes. Significant haemolytic activity could not be demonstrated with preparations derived from bacteria cultured on solid medium. Irrespective of the strain examined or the type of preparation, strong urease activity was demonstrable. Purified urease had no effect on erythrocytes, and thiourea failed to inhibit the haemolytic activity of Campylobacter pylori cell-free preparations. It was concluded that ureolytic activity was not implicated in the lysis of erythrocytes, either by direct action or via the generation of ammonia. Furthermore, the haemolytic activity produced by Campylobacter pylori was found to be due to a secreted factor, possibly a haemolysin.

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“…The patients had circulating antibody to the bacterium, and treatment eradicated the organism and resulted in resolution of inflammation and symptoms. Hill et al (50) reported three children with protein-losing enteropathy associated with acute gastritis and infection with C. pylori. Two of the patients were treated with erythromycin and the third was treated with antacids.…”

Section: Gastritismentioning

confidence: 99%

“…One of the problems with assessing these data is that there is an age-related increase in the prevalence of the organism (43,50,92), and, thus, C. pylori is found in about 50% of asymptomatic individuals 50 to 60 years old. Graham and Klein (41) have argued that, because many of the individuals with NUD are in this age group, the statistical relationship with NUD may be a coincidence.…”

Section: Nudmentioning

confidence: 99%

“…83:202, 1988), but highly sensitive methods, such as DNA probes, have not yet been used to address this question. The age-related increase in prevalence suggests that the organism is acquired as people become older, although the actual prevalence may depend on ethnic or geographic differences (109 (35), and the organism seems to congregate especially at intercellular junctions (35,49,65) and cause disruption of the junctions (13,50). A cytotoxin has been described that causes nonlethal effects on various mammalian cells (67).…”

Section: Mode Of Transmissionmentioning

confidence: 99%

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Campylobacter pylori and gastroduodenal disease

Buck

1990

Clin Microbiol Rev

139

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Campylobacter pylori is a newly described, spiral-shaped, gram-negative bacillus that is oxidase positive, catalase positive, and urease positive and grows slowly in culture. Although observed in human tissue at the beginning of the century, it was not cultured until 1982. Because there are significant morphological and genetic differences between this organism and other species of Campylobacter, it will probably be reclassified in a new genus. Current information indicates that the organism primarily resides in the stomach tissue of humans and nonhuman primates and may occasionally spread to the esophagus or other parts of the alimentary tract under appropriate conditions. Significant evidence has accumulated in the last several years to show that it causes gastritis, and there is mounting evidence that it may participate in the development of duodenal ulcers. It may also be associated with gastric ulcers and nonulcer dyspepsia. It can be detected in patients by culture of biopsy specimens or histological staining of biopsy tissue. Indirect evidence for the presence of the organism can be obtained by detection of urease in a tissue biopsy specimen, by urea breath tests, or by detection of specific antibody. It may not be necessary to implement these procedures for routine use, however, until the role of the organism can be defined better. Ultimately, the discovery of this organism may lead to radical changes in the diagnosis and treatment of gastric disease.

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Transient protein losing enteropathy associated with acute gastritis and campylobacter pylori.

Cited by 58 publications

References 6 publications

Acute Helicobacter pylori Infection Is Followed by an Increase in Diarrheal Disease Among Peruvian Children

Acute Helicobacter pylori Infection Is Followed by an Increase in Diarrheal Disease Among Peruvian Children

Haemolytic activity ofCampylobacter pylori

Campylobacter pylori and gastroduodenal disease

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