Displaying publications 61 - 80 of 242 in total

Abstract:
Sort:
  1. Vale FF, Vadivelu J, Oleastro M, Breurec S, Engstrand L, Perets TT, et al.
    Sci Rep, 2015;5:14333.
    PMID: 26387443 DOI: 10.1038/srep14333
    Prophages of Helicobacter pylori, a bacterium known to co-evolve in the stomach of its human host, were recently identified. However, their role in the diversity of H. pylori strains is unknown. We demonstrate here and for the first time that the diversity of the prophage genes offers the ability to distinguish between European populations, and that H. pylori prophages and their host bacteria share a complex evolutionary history. By comparing the phylogenetic trees of two prophage genes (integrase and holin) and the multilocus sequence typing (MLST)-based data obtained for seven housekeeping genes, we observed that the majority of the strains belong to the same phylogeographic group in both trees. Furthermore, we found that the Bayesian analysis of the population structure of the prophage genes identified two H. pylori European populations, hpNEurope and hpSWEurope, while the MLST sequences identified one European population, hpEurope. The population structure analysis of H. pylori prophages was even more discriminative than the traditional MLST-based method for the European population. Prophages are new players to be considered not only to show the diversity of H. pylori strains but also to more sharply define human populations.
    Matched MeSH terms: Helicobacter pylori; Helicobacter Infections
  2. Hanafiah A, Lopes BS
    Infect Genet Evol, 2020 Mar;78:104135.
    PMID: 31837482 DOI: 10.1016/j.meegid.2019.104135
    Helicobacter pylori is the most predominant bacterium in almost 50% of the world's population and colonization causes a persistent inflammatory response leading to chronic gastritis. It shows high genetic diversity and individuals generally harbour a distinct bacterial population. With the advancement of whole-genome sequencing technology, new H. pylori subpopulations have been identified that show admixture between various H. pylori strains. Genotypic variation of H. pylori may be related to the presence of virulence factors among strains and is associated with different outcomes of infection in different individuals. This review summarizes the genetic diversity in H. pylori strain populations and its virulence characteristics responsible for variable outcomes in different ethnic groups.
    Matched MeSH terms: Helicobacter pylori; Helicobacter Infections
  3. Chua EG, Debowski AW, Webberley KM, Peters F, Lamichhane B, Loke MF, et al.
    Gastroenterol Rep (Oxf), 2019 Feb;7(1):42-49.
    PMID: 30792865 DOI: 10.1093/gastro/goy048
    Background: Metronidazole is one of the first-line drugs of choice in the standard triple therapy used to eradicate Helicobacter pylori infection. Hence, the global emergence of metronidazole resistance in Hp poses a major challenge to health professionals. Inactivation of RdxA is known to be a major mechanism of conferring metronidazole resistance in H. pylori. However, metronidazole resistance can also arise in H. pylori strains expressing functional RdxA protein, suggesting that there are other mechanisms that may confer resistance to this drug.

    Methods: We performed whole-genome sequencing on 121 H. pylori clinical strains, among which 73 were metronidazole-resistant. Sequence-alignment analysis of core protein clusters derived from clinical strains containing full-length RdxA was performed. Variable sites in each alignment were statistically compared between the resistant and susceptible groups to determine candidate genes along with their respective amino-acid changes that may account for the development of metronidazole resistance in H. pylori.

    Results: Resistance due to RdxA truncation was identified in 34% of metronidazole-resistant strains. Analysis of core protein clusters derived from the remaining 48 metronidazole-resistant strains and 48 metronidazole-susceptible identified four variable sites significantly associated with metronidazole resistance. These sites included R16H/C in RdxA, D85N in the inner-membrane protein RclC (HP0565), V265I in a biotin carboxylase protein (HP0370) and A51V/T in a putative threonylcarbamoyl-AMP synthase (HP0918).

    Conclusions: Our approach identified new potential mechanisms for metronidazole resistance in H. pylori that merit further investigation.

    Matched MeSH terms: Helicobacter pylori; Helicobacter Infections
  4. Rosaida MS, Goh KL
    JUMMEC, 2000;5:11-16.
    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.
    Matched MeSH terms: Helicobacter pylori; Helicobacter Infections
  5. Simadibrata DM, Syam AF, Lee YY
    J Gastroenterol Hepatol, 2022 Dec;37(12):2217-2228.
    PMID: 36181401 DOI: 10.1111/jgh.16017
    BACKGROUND AND AIM: Potassium-competitive acid blocker (PCAB) is a recent alternative to proton pump inhibitor (PPI) for potent acid suppression. The current systematic review and meta-analysis aimed to compare the efficacy and safety of PCAB versus PPI in treating gastric acid-related diseases.

    METHODS: We searched up to June 5, 2022, for randomized controlled trials of gastric acid-related diseases that included erosive esophagitis, symptomatic gastroesophageal reflux disease (GERD), peptic ulcers, and Helicobacter pylori infection. The pooled risk ratio (RR) was evaluated for the efficacy outcome and treatment-emergent adverse events (TEAEs) as the safety outcome. Sensitivity analyses were performed to test the robustness of the study findings.

    RESULTS: Of the 710 screened studies, 19 studies including 7023 participants were analyzed. The RRs for the healing of erosive esophagitis with Vonoprazan versus PPI were 1.09 (95% confidence interval [CI] 1.03-1.14), 1.03 (95% CI 1.00-1.07), and 1.02 (95% CI 1.00-1.05) in Weeks 2, 4, and 8, respectively. There were no differences in the improvement of GERD symptoms and healing of gastric and duodenal ulcers between PCAB and PPI. The pooled eradication rates of H. pylori were significantly higher in Vonoprazan versus PPI first-line treatment (RR 1.13; 95% CI 1.04-1.22). The overall RR of TEAEs with Vonoprazan versus PPI was 1.08 (95% CI 0.89-1.31). Overall, the risk of bias was low to some concerns. Furthermore, sensitivity analyses confirmed the robustness of the study's conclusion.

    CONCLUSION: Vonoprazan is superior to PPI in first-line H. pylori eradication and erosive esophagitis but non-inferior in other gastric acid-related diseases. Likewise, short-term safety is comparable in both treatment groups.

    Matched MeSH terms: Helicobacter pylori*
  6. Khosravi Y, Dieye Y, Loke MF, Goh KL, Vadivelu J
    PLoS One, 2014;9(11):e112214.
    PMID: 25386948 DOI: 10.1371/journal.pone.0112214
    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.
    Matched MeSH terms: Helicobacter pylori/physiology*; Helicobacter Infections/microbiology*
  7. Alfizah H, Noraziah MZ, Chao MY, Rahman MM, Ramelah M
    Clin Ter, 2013;164(4):301-5.
    PMID: 24045512 DOI: 10.7417/CT.2013.1577
    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.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter Infections/complications*
  8. Goh KL, Chan WK
    Aliment Pharmacol Ther, 2012 Aug;36(3):291-2; discussion 292-3.
    PMID: 22747451 DOI: 10.1111/j.1365-2036.2012.05164.x
    Matched MeSH terms: Helicobacter pylori/isolation & purification*; Helicobacter Infections/epidemiology*
  9. Maran S, Lee YY, Xu S, Rajab NS, Hasan N, Mustaffa N, et al.
    Hepatogastroenterology, 2013 Jan-Feb;60(121):124-8.
    PMID: 22829558
    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.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/genetics*
  10. Raj SM, Lee YY, Choo KE, Noorizan AM, Zulkifli A, Radzi M, et al.
    Trans R Soc Trop Med Hyg, 2008 Nov;102(11):1163-4.
    PMID: 18678380 DOI: 10.1016/j.trstmh.2008.06.015
    Matched MeSH terms: Helicobacter pylori/isolation & purification*; Helicobacter Infections/epidemiology*
  11. Tan HJ, Goh KL
    J Dig Dis, 2008 Nov;9(4):186-9.
    PMID: 18959588 DOI: 10.1111/j.1751-2980.2008.00344.x
    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.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/epidemiology*
  12. Graham DY, Yamaoka Y, Malaty HM
    Trans R Soc Trop Med Hyg, 2007 Sep;101(9):849-51.
    PMID: 17658569
    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.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/epidemiology*
  13. Gurjeet K, Subathra S, Bhupinder S
    Med J Malaysia, 2004 Oct;59(4):560-1.
    PMID: 15779598 MyJurnal
    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.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/epidemiology*
  14. Khosravi Y, Bunte RM, Chiow KH, Tan TL, Wong WY, Poh QH, et al.
    Gut Microbes, 2016;7(1):48-53.
    PMID: 26939851 DOI: 10.1080/19490976.2015.1119990
    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.
    Matched MeSH terms: Helicobacter pylori/metabolism*; Helicobacter Infections/microbiology
  15. Goh KL
    J Gastroenterol Hepatol, 2002 Apr;17(4):482-7.
    PMID: 11982731
    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.
    Matched MeSH terms: Helicobacter pylori/physiology*; Helicobacter Infections/drug therapy*
  16. Goh KL, Peh SC, Wong NW, Parasakthi N, Puthucheary SD
    J Gastroenterol Hepatol, 1990 5 1;5(3):277-80.
    PMID: 2103410
    Over a 15-month period, 399 patients with dyspepsia were investigated for the presence of Campylobacter pylori infection. Half of the patients (50.6%) had Campylobacter organisms in the antrum of the stomach. C. pylori was found in 96.1% of patients with histological changes of chronic active gastritis in the antrum. Of patients with duodenal and gastric ulcers, 87.8% and 87.5%, respectively, had Campylobacter organisms, as did 39.3% of patients with non-ulcer dyspepsia. C. pylori infection was most commonly found in Chinese and Indians. Although the prevalence of infection appeared to increase with age, there was an equal distribution amongst the sexes.
    Matched MeSH terms: Helicobacter pylori/isolation & purification*; Helicobacter Infections/epidemiology*
  17. Wong EH, Ng CG, Chua EG, Tay AC, Peters F, Marshall BJ, et al.
    PLoS One, 2016;11(11):e0166835.
    PMID: 27870886 DOI: 10.1371/journal.pone.0166835
    BACKGROUND: Biofilm formation by Helicobacter pylori may be one of the factors influencing eradication outcome. However, genetic differences between good and poor biofilm forming strains have not been studied.

    MATERIALS AND METHODS: Biofilm yield of 32 Helicobacter pylori strains (standard strain and 31 clinical strains) were determined by crystal-violet assay and grouped into poor, moderate and good biofilm forming groups. Whole genome sequencing of these 32 clinical strains was performed on the Illumina MiSeq platform. Annotation and comparison of the differences between the genomic sequences were carried out using RAST (Rapid Annotation using Subsystem Technology) and SEED viewer. Genes identified were confirmed using PCR.

    RESULTS: Genes identified to be associated with biofilm formation in H. pylori includes alpha (1,3)-fucosyltransferase, flagellar protein, 3 hypothetical proteins, outer membrane protein and a cag pathogenicity island protein. These genes play a role in bacterial motility, lipopolysaccharide (LPS) synthesis, Lewis antigen synthesis, adhesion and/or the type-IV secretion system (T4SS). Deletion of cagA and cagPAI confirmed that CagA and T4SS were involved in H. pylori biofilm formation.

    CONCLUSIONS: Results from this study suggest that biofilm formation in H. pylori might be genetically determined and might be influenced by multiple genes. Good, moderate and poor biofilm forming strain might differ during the initiation of biofilm formation.

    Matched MeSH terms: Helicobacter pylori/classification; Helicobacter pylori/genetics; Helicobacter pylori/physiology*
  18. Parasakthi N, Goh KL
    Am J Gastroenterol, 1995 Mar;90(3):519.
    PMID: 7872306
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter Infections/drug therapy
  19. Sukri A, Hanafiah A, Kosai NR, Taher MM, Mohamed Rose I
    Malays J Pathol, 2017 Dec;39(3):235-242.
    PMID: 29279585 MyJurnal
    The multiracial population in Malaysia has lived together for almost a century, however, the risk of gastric cancer among them varies. This study aimed to determine the distribution of different gastric adenocarcinoma subtypes and Helicobacter pylori infection status among gastric adenocarcinoma patients. Patients with gastric adenocarcinoma were enrolled from November 2013 to June 2015. Blood samples were collected for detection of H. pylori using ELISA method. Gastric adenocarcinoma cases were more prevalent in the Chinese (52.8%), followed by the Malays (41.7%) and least prevalent in the Indians (5.6%). Gastric adenocarcinoma located in the cardia was significantly more prevalent in the Malays (66.7%) compared to the Chinese (26.3%), whereas non-cardia cancer was diagnosed more in the Chinese (73.7%) compared to the Malays (33.3%) [P = 0.019; OR = 5.6, 95 CI: 1.27 to 24.64]. The Malays also had significantly higher prevalence of gastric tumour located at the cardia or fundus than other gastric sites compared to the Chinese (P = 0.002; OR: 11.2, 95% CI: 2.2 to 56.9). Among the cardia gastric cancer patients, 55.6% of the Malays showed intestinal histological subtype, whereas all the Chinese had the diffuse subtype. More than half of the patients (55.3%) with gastric adenocarcinoma were positive for H. pylori infection and among them, 66.7% were Chinese patients. The risk of gastric adenocarcinoma in our population is different among ethnicities. Further studies on host factors are needed as it might play an important role in gastric cancer susceptibility in our population.
    Matched MeSH terms: Helicobacter pylori; Helicobacter Infections/complications; Helicobacter Infections/epidemiology
  20. Said RM, Cheah PL, Chin SC, Goh KL
    Eur J Gastroenterol Hepatol, 2004 Feb;16(2):195-9.
    PMID: 15075994
    BACKGROUND: The gastric biopsy urease test is the most frequently used test for the diagnosis of Helicobacter pylori infection in routine gastrointestinal endoscopy practice. In Malaysia up to recently, only one commercial biopsy urease test was available: the CLO test (Ballard Medical Products, Draper, Utah, USA). Large endoscopy units use their own 'homemade' unbuffered ultra rapid urease test for diagnosis of H. pylori infection.

    OBJECTIVE: To compare the accuracy and reaction time of a new biopsy urease test, Pronto Dry (Medical Instruments Corporation, Solothurn, Switzerland) and the CLO test in the diagnosis of H. pylori infection.

    METHODS: Consecutive patients presenting with dyspepsia to the endoscopy unit, University of Malaya Medical Centre were recruited for the study. Patients who were previously treated for H. pylori infection or who had received antibiotics, proton pump inhibitors or bismuth compounds in the preceding 4 weeks were excluded. H. pylori diagnosis was made based on the ultra rapid urease test and histological examination of gastric biopsies. Four antral and four corpus biopsies were taken for this purpose from all patients. A diagnosis of H. pylori infection was made when both the ultra rapid urease test and histology were positive in either the antral or corpus biopsies. A negative diagnosis of H. pylori was made when both tests from antral and corpus biopsies were all negative. Another four antral and four corpus biopsies (two each) were taken for the Pronto Dry and CLO tests. The Pronto Dry and CLO tests were stored and performed according to the manufacturer's instruction.

    RESULTS: Two hundred and eight patients were recruited in the study. Eighty-six of the patients were males and 122 were females. The mean age was 46.3 years with a range of 15-82 years. The results for both the Pronto Dry and the CLO tests were completely concordant with sensitivity, specificity, positive predictive value, negative predictive value and diagnostic accuracy of 98.1%, 100%, 100%, 98.1% and 99%, respectively. The Pronto Dry test showed a faster reaction time to positive compared with the CLO test, with 96.2% positive reaction by 30 min versus 70.8% and 100% positive reaction time by 55 min versus 83%. The colorimetric change was also more distinct with the Pronto Dry test compared with the CLO test.

    CONCLUSIONS: Both the Pronto Dry and the CLO tests were highly accurate for the diagnosis of H. pylori infection. The Pronto Dry test showed a quicker positive reaction time and the positive colour change was more distinct.

    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/diagnosis*
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links