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

A study of the relationship between serum group I pepsinogen levels and gastric acid secretion.

The histamine-infusion test

In a preliminary communication on the immunological relationship between pernicious anemia and thyroid disease it was reported that the sera of 75 per cent of 41 patients with Addisonian pernicious anemia contained complement-fixing antibody specific for gastric body mucosa and tha t 37 per cent of these sera contained complement-fixing antibody specific for thyroid. Conversely, while the sera of 70 per cent of 121 patients with either Hashimoto thyroiditis or spontaneous hypothyroidism contained complement fixing antibody to thyroid, 25 per cent were found to contain complement-fixing antibody specific for gastric body mucosa.' These laboratory tests, which have since been confirmed by Taylor et a1.' and by Doniach et al.,,' are in accord with the known clinical association between pernicious anemia and thyroid d i ~ e a s e . ~ In our previous study 6 of 14 patients with untreated spontaneous hypothyroidism had a histamine-fast achlorhydria with normal serum vitamin BI2 levels; five of these six had a positive complement fixation test with gastric extract in contrast to none of the other eight patients. This observation, together with the fact tha t the antigen was only to be found in the gastric body mucosa and not in the pyloric antrum or elsewhere in the alimentary tract, suggested that gastric complement-fixing antibody might be specific for parietal cells; this specificity has now been established by the fluorescent antibody technique.' '-' I t has also been demonstrated that the antibody will react with the patient's own parietal cells and is therefore a true autoantibody.\" The purpose of this paper is to assess the clinical and pathological significance of gastric parietal cell antibody; that is, what the ptesence of the antibody in the patient's serum means in terms of gastric histology and function.

The clinical and pathological significance of gastric parietal cell antibody

https://www.gastrojournal.org/article/S0016-5085(99)70025-9/pdf

The gastric transitional zones: Neglected links between gastroduodenal pathology and Helicobacter ecology

The relationship between the acid output of the stomach following "maximal" histamine stimulation and the parietal cell mass.

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The relationship between the acid output of the stomach following "maximal" histamine stimulation and the parietal cell mass.