Helicobacter pylori (H. pylori) infection is etiologically associated with gastric cancer and peptic ulcer diseases which are both important public health burdens which could be largely eliminated by H. pylori eradication. However, some investigators urge caution based on the hypothesis that eradication of H. pylori may result in an increase in the incidence of gastroesophageal reflux disease, esophageal adenocarcinoma, and childhood asthma. The ethnic Malays of northeastern Peninsular Malaysia have long had a low prevalence of H. pylori infection and, as expected, the incidence of gastric cancer and its precursor lesions is exceptionally low. The availability of a population with a low H. pylori prevalence and generally poor sanitation allows separation of H. pylori from the hygiene hypothesis and direct testing of whether absence of H. pylori is associated with untoward consequence. Contrary to predictions, in Malays, erosive esophagitis, Barrett’s esophagus, distal esophageal cancers, and childhood asthma are all of low incidence. This suggests that H. pylori is not protective rather the presence of H. pylori infection is likely a surrogate for poor hygiene and not an important source of antigens involved in the hygiene hypothesis. Helicobacter pylori in Malays is related to transmission from H. pylori-infected non-Malay immigrants. The factors responsible for low H. pylori acquisition, transmission, and burden of H. pylori infection in Malays remain unclear and likely involves a combination of environmental, host (gene polymorphisms), and strain virulence factors. Based on evidence from this population, absence of H. pylori infection is more likely to be boon than a bane.

Under the assumption that sanitary, sociocultural, and dietary habits have not changed over the years, we can conclude that an increased risk of H. pylori was associated with unsanitary practices whereas protection was associated with consumption of tea and locally produced foods, "pegaga" and "budu." These dietary factors are candidates for future study on the effects on H. pylori transmission.

The prevalence of Helicobacter pylori infection was determined in peptic ulcer patients, in non-ulcer dyspepsia (NUD) patients, and in the general adult population. The H. pylori infection rate ascertained by microbiologic examination of multiple gastric antral biopsy specimens was 50% (17 of 34) in duodenal ulcer (DU), 5% (1 of 22) in gastric ulcer, and 9% (15 of 159) in NUD patients. A seroepidemiologic survey showed a prevalence of only 4.2% among 496 blood donors and 4.8% among 921 subjects who attended health screening clinics. H. pylori infection is relatively uncommon and does not appear to be the predominant factor in the pathogenesis of peptic ulcer disease in the area. The incidence of peptic ulcer perforations in the area in 1991-92 was 1.5 per 100,000 person-years, reflecting a relatively low frequency of peptic ulcers, which might be due to the low prevalence of H. pylori infection in the population.

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The Helicobacter pylori infection rate was determined in 124 consecutive patients with duodenal ulcers (DU), gastric ulcers (GU), duodenal erosions or gastric erosions diagnosed by endoscopy at a single institution in north-eastern peninsular Malaysia in 1996-97. Biopsies of the gastric antrum and body were subjected to the urease test, Gram staining of impression smears, culture and histopathological examination. Serology was undertaken on all patients using a locally validated commercial kit. Infection was defined as a positive result in at least one test. The infection rates were 20% (10/50), 21.2% (7/33), 16.7% (1/6) and 17.1% (6/35) in DU, GU, duodenal erosion and gastric erosion patients, respectively. The infection rate among Malays [7.0%, (6/86)] was lower than in non-Malays [47.4% (18/38)] (P < 0.001). There was a higher infection rate among males, who constituted 62.1% (77/124) of the sample. Seventy-eight patients (62.9%) were receiving non-steroidal anti-inflammatory drugs (NSAIDs) and 33 patients (26.6%) were neither receiving NSAIDs nor were infected with H. pylori. The H. pylori infection rate among peptic ulcer patients in this predominantly Malay rural population appears to be the lowest reported in the world thus far. Empirical H. pylori eradication therapy in peptic ulcer patients is clearly not indicated in this community. The possible reasons for the low prevalence of H. pylori infection are discussed.

Whether the exceptionally low prevalence of Helicobacter pylori (HP) infection reported among Malays is also present among aborigines (the Orang Asli) living in northeastern Peninsular Malaysia is unknown. We studied asymptomatic Orang Asli from settlements situated 210 km from the city of Kota Bharu. The HP infection status was confirmed by a validated serology test. Nineteen percent of 480 Orang Asli tested positive for HP infection. The prevalence was 40.6% in the birth cohort of the 1940s and declined steadily in later cohorts to under 10% among 12-30 year olds. This may be related to the phases of relocation from the jungles into resettlement camps and ultimately into designated villages near rivers. The low prevalence pattern after the 1970s was probably partly a result of improvement in sanitation and hygiene practice in these villages but other unidentified factors may also be operating.

The low rates of adenocarcinoma and squamous cell carcinoma of the esophagus in the study area, despite the fact that H. pylori infection is virtually absent, does not support the hypothesis that the absence of H. pylori infection is a pivotal factor in the pathogenesis of these cancers.

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