Many tests are available for the diagnosis of H. pylori infection. Broadly they can be divided into invasive- endoscopy biopsy based tests and non-invasive tests. Of the endoscopy biopsy based tests the rapid urease tests (RUT) have been found to be the most convenient, accurate and inexpensive tests and they have therefore been recommended by several consensus panels and working parties as the test of choice during endoscopy. Several RUTS are available; some are commercial: CLO test, Pyloritek, Helicobacter urease test, H. yylori test and others- "homemade". We strongly recommend the "homemade" 1 min rapid urease test using an unbuffered solution as originally described by Arvind et al. This test has been shown to be easy to prepare, inexpensive and accurate on field-testing. Several factors affect the accuracy of the RUT. The larger the size of biopsy samples, the quicker is the postive reaction time. With the CLO test, warming the tests to 37'C has also been shown to hasten the reaction time. The effect of blood on the RUT poses an important problem in testing. It is vitally important to determine the H. yylori status in patients with bleeding peptic ulcers as the recurrence of bleeding has been shown to be markedly reduced or virtually abolished with H. yylori eradication. While the results of studies have not been entirely consistent, it is likely that presence of blood does reduce the sensitivity of the RUT. It is therefore sensible that in patients with bleeding ulcers, the RUT should not be the sole endoscopy biopsy test used and that samples should also be taken for histological examination.
The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction
To determine the prevalence of Helicobacter pylori antigen carriage in stool in the Penan ethnic minority in Malaysian Borneo, we studied 295 Penans 0.6-89.0 years of age from 1) the remote Limbang Division, 2) Mulu regional center, and 3) Belaga village. Overall, 37.7% of the subjects tested positive. Peak prevalence was reached by 10 years of age. There were no differences in age, sex, body mass index, and socioeconomic/domestic variables between antigen-positive and antigen-negative subjects. In a logistic regression analysis, subjects from Limbang were least likely to be antigen-positive (odds ratio [OR] = 0.23, 95% confidence interval [CI] = 0.12-0.44 versus other sites, P < 0.001). Availability of a flushing toilet was protective against H. pylori carriage (OR = 0.51, 95% CI = 0.27-0.95, P = 0.031). Infection with H. pylori among the Penan was less than reported in other low socioeconomic groups. The lowest prevalence in the most remote setting suggests that the infection has been a recent arrival in previously isolated communities.
Helicobacter pylori-associated gastric carcinoma is generally more common in the antrum/body and is of the intestinal type. The aim of this study was to determine the pattern of gastric carcinoma in an area known to have a low prevalence of H. pylori. Pathology records of gastric carcinoma diagnosed at Hospital University Sains Malaysia between 1995 and 1999 were retrieved and studied. There were a total of 23 cases. The median age was 60 years. Eighteen patients were Malay and 5 were Chinese. The most common location of the tumour was the cardia/gastrooesophageal junction (61%, 14/23 patients). The majority was of the intestinal type (69.6%, 16/23). The frequency of gastric carcinoma appears to be exceptionally low in the area of study. The Chinese population was over-represented. The higher frequency of tumour in the cardia/gastro-oesophageal junction as compared to the antrum and body is in sharp contrast to most other studies. This reaffirms the notion that Helicobacter pylori infection is a causative agent for non-cardia gastric carcinomas.
Helicobacter pylori (H. pylori) is a major gastric pathogen that has been associated with humans for more than 60,000 years. H. pylori causes different gastric diseases including dyspepsia, ulcers and gastric cancers. Disease development depends on several factors including the infecting H. pylori strain, environmental and host factors. Another factor that might influence H. pylori colonization and diseases is the gastric microbiota that was overlooked for long because of the belief that human stomach was a hostile environment that cannot support microbial life. Once established, H. pylori mainly resides in the gastric mucosa and interacts with the resident bacteria. How these interactions impact on H. pylori-caused diseases has been poorly studied in human. In this study, we analyzed the interactions between H. pylori and two bacteria, Streptococcus mitis and Lactobacillus fermentum that are present in the stomach of both healthy and gastric disease human patients. We have found that S. mitis produced and released one or more diffusible factors that induce growth inhibition and coccoid conversion of H. pylori cells. In contrast, both H. pylori and L. fermentum secreted factors that promote survival of S. mitis during the stationary phase of growth. Using a metabolomics approach, we identified compounds that might be responsible for the conversion of H. pylori from spiral to coccoid cells. This study provide evidences that gastric bacteria influences H. pylori physiology and therefore possibly the diseases this bacterium causes.
Helicobacter pylori strains secrete a vacuolating cytotoxin (VacA), plays an important role for the development of peptic ulcer disease and gastro-duodenal diseases. vacA gene is responsible to regulate the activity of the vacuolating cytotoxin. The objective of this study was molecular detection of vacA gene and observes the vacuolating activity on human gastric adenocarcinoma (AGS) cells.
Using genome-wide case-control association approach, the current study aimed to determine whether genetic polymorphism(s) is/are associated with H. pylori infection among ethnic Malays from the north-eastern region of Peninsular Malaysia, a region with an exceptionally low prevalence for H. pylori infection and gastric cancer.
The prevalence of Helicobacter pylori infection is exceptionally low among the Malays in the north-eastern region of Peninsular Malaysia. The reasons are unknown. Our aim was to compare environmental factors that differed in relation to H. pylori prevalence among Malays born and residing in Kelantan.
The prevalence of antibiotic resistance varies in geographic areas. The information on the antibiotic susceptibility patterns of Helicobacter pylori (H. pylori) in our local setting is therefore relevant as a guide for the treatment options.
As in developed societies, the prevalence of Helicobacter pylori has declined rapidly in Asia. This has been shown in both seroprevalence-based and endoscopy-based studies. While the decline in the incidence of gastric cancer has now been observed, a decrease in peptic ulcer disease has not been so clearly evident. This apparent paradox can be explained by an increase in non-H. pylori associated ulcers - such as those related to non-steroidal anti-inflammatory drugs or idiopathic ulcers. The increase of gastroesophageal reflux disease in Asia has been widely observed and commented on and its relationship to the decline in H. pylori speculated upon. However there have been few conclusive studies from Asia on this subject. While the improved diagnosis and elimination of H. pylori has contributed to its decline, a more basic change involving large segments of the Asian population must be responsible. An improvement in hygiene and living conditions that results from more affluent Asian societies is thought to be a possible cause.
Helicobacter pylori is one of the few remaining major pathogens that accompanied humans on their travels from Africa. A recently published study reports the unexpected finding of a low H. pylori prevalence among pregnant women in Zanzibar (Farag, T.H., Stolzfus, R.J., Khalfan, S.S., Tielsch, J.M., 2007. Unexpectedly low prevalence of Helicobacter pylori infection among pregnant women on Pemba Island, Zanzibar. Trans. R. Soc. Trop. Med. Hyg. 101). The apparent epidemiology of higher prevalence with higher socioeconomic status and decrease with age are unprecedented. As with many 'unexpected' events, a search of the literature reveals evidence of low prevalence populations in Java and Malaysia, with clues dating back to the mid-twentieth century. Why some populations apparently lost H. pylori infection remains an open question. However, the tools needed to resolve the dilemma are readily available and we hope investigators will soon rise to the challenge.
Sir, Delirium is defined as a clinical state characterised by an acute fluctuating change in mental status with inattention and altered levels of consciousness. Delirium in the older person is a common manifestation of sepsis,• electrolyte imbalance, intracranial pathology, urinary retention, fecal impaction, myocardial pathology or drug related. In this letter, we would like to share a report of an acute episode of delirium in a 94 year old man most likely induced by Clarithromycin which is a component of triple therapy for Helicobacter pylori (H. plyoriJ eradication.
A retrospective study on demographics of gastric carcinoma was conducted in Hospital Pulau Pinang (HPP) with the aim of comparing it to a previous study done in Hospital Universiti Sains Malaysia (HUSM), Kelantan. The incidence of gastric carcinoma was much higher in Penang compared to Kelantan. It was commonest in males and Chinese. The incidence and site of gastric carcinoma closely parallels Helicobacter pylori infection rates. This was evidenced by the higher incidence and non-cardia location of gastric carcinomas in an area with higher H. pylori infection rates (HPP) compared to a much lower incidence and preponderance of cardia tumours in HUSM where the H. pylori infection rate is exceptionally low.
Helicobacter pylori have been shown to influence physiological regulation of metabolic hormones involved in food intake, energy expenditure and body mass. It has been proposed that inducing H. pylori-induced gastric atrophy damages hormone-producing endocrine cells localized in gastric mucosal layers and therefore alter their concentrations. In a recent study, we provided additional proof in mice under controlled conditions that H. pylori and gut microbiota indeed affects circulating metabolic gut hormones and energy homeostasis. In this addendum, we presented data from follow-up investigations that demonstrated H. pylori and gut microbiota-associated modulation of metabolic gut hormones was independent and precedes H. pylori-induced histopathological changes in the gut of H. pylori-infected mice. Thus, H. pylori-associated argumentation of energy homeostasis is not caused by injury to endocrine cells in gastric mucosa.
Helicobacter pylori colonizes almost half of the human population worldwide. H. pylori strains are genetically diverse, and the specific genotypes are associated with various clinical manifestations including gastric adenocarcinoma, peptic ulcer disease (PUD), and nonulcer dyspepsia (NUD). However, our current knowledge of the H. pylori metabolism is limited. To understand the metabolic differences among H. pylori strains, we investigated four Malaysian H. pylori clinical strains, which had been previously sequenced, and a standard strain, H. pylori J99, at the phenotypic level.
Helicobacter pylori infection has many different clinical outcomes. Not all infected persons need to be treated. Therefore, indications for treatment have to be clear, and several consensus guidelines have been formulated to aid the medical practitioner in this decision-making process. Triple therapy with a proton pump inhibitor (PPI), in combination with amoxicillin and clarithromycin is the established treatment of choice. For patients with penicillin hypersensitivity, metronidazole can be substituted for amoxicillin. Bacterial resistance to antibiotics is a major factor adversely affecting treatment success. Resistance to metronidazole has been reported in up to 80%, and resistance to clarithromycin in 2-10% of strains cultured. Resistance to either one of the antibiotics has been reported to result in a drop in efficacy of up to 50%. Emergence of resistance to both metronidazole and clarithromycin following failed therapy is a cause for concern; this underlines the need to use the best available first-line therapy. To avoid the emergence of resistance to both key antibiotics, the combination of metronidazole and clarithromycin should be avoided where possible. For failed treatment, several strategies can be employed. These include ensuring better compliance with repeat therapy, and maximizing the efficacy of repeat treatment by increasing dosage and duration of treatment, as well as altering the choice of drugs. Quadruple therapy incorporating a bismuth compound with a PPI, tetracycline and metronidazole has been a popular choice as a "rescue" therapy. Ranitidine bismuth citrate has been shown to be able to overcome metronidazole and clarithromycin resistance; it may be a useful compound drug to use in place of a PPI in "rescue" therapies. In the case of persistent treatment failures, it is useful to consider repeating gastroscopy and obtaining tissue for culture, and then prescribe antibiotics according to bacterial susceptibility patterns. It is also important in refractory cases to review the original indication for treatment and determine the importance of the indication.