A GRAM-NEGATIVE, microaerophilic curved bacillus found in gastric-biopsy specimens from patients with histologie gastritis was successfully cultured in Perth, Australia, in 1982 and was soon named Campylobacter pylori 1 (a name later changed to Helicobacterpylori). Little attention had been paid to previous descriptions of spiral organisms in biopsy specimens of human gastric mucosa,2 , 3 but it now appears that at the least the organism is responsible for most cases of gastritis not associated with another known primary cause (e.g., autoimmune gastritis or eosinophilic gastritis) and that it may also be a major factor in the pathogenesis of peptic ulcer disease. The . . .

Helicobacter pylori and Peptic Ulcer Disease

https://www.gastrojournal.org/article/S0016-5085(98)70364-6/pdf

The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease

/pdf/parasitism-by-the-slow-bacterium-helicobacter-pylori-leads-4rksqohdk1.pdf

Parasitism by the "slow" bacterium Helicobacter pylori leads to altered gastric homeostasis and neoplasia.

Helicobacter pylori is now accepted as the major cause of chronic gastritis in humans. The histologic pattern of H . pylori gastritis is typically one of patchy acute on chronic inflammation, most severe in the antrum. The association of chronic gastritis with the environmental or epidemic type of gastric carcinoma prompted a number of investigations of the epidemiology of gastritis, and the results of those studies could be reasonably transferred to H . pylori to provide H . pylori investigators with a head start in the study of the epidemiology of a new disease, H . pylori gastritis. This data transfer allowed early definition of important questions designed to confirm previous associations with gastritis and extend them to H . pylori. Factors known to be associated with gastritis include low socioeconomic class, large family size, crowding, and ethnic group.lV2 Factors found to be unimportant in the pathogenesis of chronic gastritis included use of drugs such as ethanol, nicotine, or nonsteroidal anti-inflammatory drugs (Table l).' The prevalence of gastritis increases with age. For many years it was thought that the gastric mucosa of geriatric patients was normally atrophic, a 'wear-and-tear' phenomenon. Although it is difficult to distinguish changes in the gastrointestinal tract due to ageing from those resulting from environmental effects acting over long periods of time, most now believe that chronic gastritis in the elderly is generally the end result of H . pylori infection.a-6 The acquisition of H . pylori infection continues throughout life but, once acquired, the duration of the infection appears to be very long, possibly for life.7 The rate of acquisition of H . pylori infection varies remarkably between and within populations. The age-specific prevalence of H. pylori infections (usually measured as presence of anti-Hi. pylori IgG) is higher in developing countries than developed countries (Fig. 1). Within a specific country there are further stratifications; the age-specific rate of acquisition of H . pylori infection is higher in those of lower socio-economic status whether assessed by income, housing, educational level, ethnic or religious group. One factor that appears to unify the disparate epidemiology results is differences in sanitation and hygiene practices.8 The mode(s) of transmission is unknown but the geographic and social patterns of H. pylori infection are consistent with faecal-oral transmission as one major pathway. This is also consistent with recent data Peru, demonstrating a direct association bet valence of H. pylori infection and source of drinking water (Fig. 2).9 One particularly striking recent finding is that motile spiral forms of H. pylori can survive for at least a week in river water.I0 Coccoid forms of H. pylori can also survive in river water for a year or more, but the clinical relevance of that observation remains unclear.tX\"rin my opinion, coccoid forms from nature are unlikely to be infectious for %mans. Coccoid forms have also been found in the stomach. Although coccoid forms are unlikely to survive long in the stomach becsuse the rapid turnover of the gastric epithelium probably precludc; prolonged residence, they may be responsible for some instances of relapse after antimicrobial therapy. H . pylon' has not yet been isolated from the environment but the technology now available (e.g. cDNA probes) can address this question. Iatrogenic transmission of H. pylori infection has been documented12*13 and the high prevalence of H. pylori infection in endoscopists who did not always use gloves suggests s p r e e o m instruments contaminated with gastric secretions (gastric secretion!oral spread).'j Finally, H. pylori has been recovered from dental plaque15 and, although this appears to be a rare phenomenon, it emphasizes that there may be many potential pathways for transmission. In developed countries, H . pylori infection is infrequent in children and increases at 1-270 per year (Fig. 3), approximately the same rate as previously described for gastritis or for the onset of new cases of dyspepsia.16-z1 The rate of acquisition of H . pylori infection appears to be similar in the United States, Australia and the United Kingdom. Even within developed countries, there are ethnic and racial differences in the prevalence of H . pylm' For example, in the United States, the rate of acquisition of H. pylori infection is higher in blacks than whites and preliminary studies have shown high ageadjusted rates in Chinese, East Indians and Mexicans studying in, or recently emigrating to, the United States.7.23.24 In most instances the difference in prevalence Between ethnic group or race represents a surrogate xrwb~ for differences in exposure(s), such as differences in standards of living or sanitation practices. Importantly, the differences in age-adjusted frequency of H. pylon' between whites and blacks in the United State8 remains when

I. Helicobacter pylori: Its epidemiology and its role in duodenal ulcer disease

Background: In the Western world, the incidence of oesophageal adenocarcinoma has increased over the last 30 years coinciding with a decrease in the prevalence of Helicobacter pylori . Trends of increasing oesophageal adenocarcinoma can be linked causally to increasing gastro-oesophageal reflux disease (GORD) which can be linked to an increasingly obese population. However, there is no plausible biological mechanism of association between H pylori , obesity, and GORD. Ghrelin, a peptide produced in the stomach, which regulates appetite, food intake, and body composition, was studied in H pylori positive asymptomatic subjects. Methods: Plasma ghrelin, leptin, and gastrin were measured for six hours after an overnight fast, before and after cure of H pylori in 10 subjects. Twenty four hour intragastric acidity was also assessed. Results: After cure, median (95% confidence intervals) integrated plasma ghrelin increased from 1160.5 (765.5–1451) pg/ml×h to 1910.4 (1675.6–2395.6) pg/ml×h (p=0.002, Wilcoxon’s rank sum test), a 75% increase. This was associated with a 14% increase in 24 hour intragastric acidity (p=0.006) and non-significant changes in leptin and gastrin. There was a significant positive correlation between plasma ghrelin and intragastric acidity ( r s 0.44, p=0.05, Spearman’s rank correlation) Conclusions: After H pylori cure, plasma ghrelin increased profoundly in asymptomatic subjects. This could lead to increased appetite and weight gain, and contribute to the increasing obesity seen in Western populations where H pylori prevalence is low. This plausible biological mechanism links H pylori , through increasing obesity and GORD, to the increase in oesophageal adenocarcinoma observed in the West.

/pdf/plasma-ghrelin-following-cure-of-helicobacter-pylori-3cxfro8fog.pdf

Plasma ghrelin following cure of Helicobacter pylori

An ELISA test determined serologically that eight of 95 apparently healthy men (aged 19-26 years) had an asymptomatic infection with Helicobacter pylori at the time of simultaneous measurement of 24 hour intragastric acidity and 24 hour plasma gastrin concentration. There was no significant difference in the median integrated 24 hour intragastric acidity between the H. pylori positive and H. pylori negative subjects (688 and 842 mmol/h/l; p = 0.271, respectively), whereas the median integrated 24 hour plasma gastrin concentration was significantly higher in the H pylori positive than in the H pylori negative subjects (389 and 198 pmol/h/l; p less than 0.001). Longterm hypergastrinaemia, associated with persistent H pylori infection, could be a cause of the increased parietal cell mass that is considered characteristic of duodenal ulcer patients.

https://gut.bmj.com/content/gutjnl/31/5/522.full.pdf

D. G. Evans

Papers

Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected with Helicobacter pylori.