Displaying publications 101 - 120 of 222 in total

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  1. Butt J, Jenab M, Pawlita M, Tjønneland A, Kyrø C, Boutron-Ruault MC, et al.
    Cancer Epidemiol Biomarkers Prev, 2020 Jul;29(7):1475-1481.
    PMID: 32332031 DOI: 10.1158/1055-9965.EPI-19-1545
    BACKGROUND: While Helicobacter pylori (H. pylori) is the major cause of gastric cancer, it has also been suggested to be involved in colorectal cancer development. However, prospective studies addressing H. pylori and colorectal cancer are sparse and inconclusive. We assessed the association of antibody responses to H. pylori proteins with colorectal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.

    METHODS: We applied H. pylori multiplex serology to measure antibody responses to 13 H. pylori proteins in prediagnostic serum samples from 485 colorectal cancer cases and 485 matched controls nested within the EPIC study. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable conditional logistic regression to estimate the association of H. pylori overall and protein-specific seropositivity with odds of developing colorectal cancer.

    RESULTS: Fifty-one percent of colorectal cancer cases were H. pylori seropositive compared with 44% of controls, resulting in an OR of 1.36 (95% CI, 1.00-1.85). Among the 13 individual H. pylori proteins, the association was driven mostly by seropositivity to Helicobacter cysteine-rich protein C (HcpC; OR: 1.66; 95% CI, 1.19-2.30) and Vacuolating cytotoxin A (VacA) (OR: 1.34; 95% CI, 0.99-1.82), the latter being nonstatistically significant only in the fully adjusted model.

    CONCLUSIONS: In this prospective multicenter European study, antibody responses to H. pylori proteins, specifically HcpC and VacA, were associated with an increased risk of developing colorectal cancer.

    IMPACT: Biological mechanisms for a potential causal role of H. pylori in colorectal carcinogenesis need to be elucidated, and subsequently whether H. pylori eradication may decrease colorectal cancer incidence.

    Matched MeSH terms: Helicobacter pylori/pathogenicity*
  2. Lee WC, Anton BP, Wang S, Baybayan P, Singh S, Ashby M, et al.
    BMC Genomics, 2015;16:424.
    PMID: 26031894 DOI: 10.1186/s12864-015-1585-2
    The genome of the human gastric pathogen Helicobacter pylori encodes a large number of DNA methyltransferases (MTases), some of which are shared among many strains, and others of which are unique to a given strain. The MTases have potential roles in the survival of the bacterium. In this study, we sequenced a Malaysian H. pylori clinical strain, designated UM032, by using a combination of PacBio Single Molecule, Real-Time (SMRT) and Illumina MiSeq next generation sequencing platforms, and used the SMRT data to characterize the set of methylated bases (the methylome).
    Matched MeSH terms: Helicobacter pylori/genetics*
  3. Bujanda L, Nyssen OP, Ramos J, Bordin DS, Tepes B, Perez-Aisa A, et al.
    Am J Gastroenterol, 2024 Apr 01;119(4):646-654.
    PMID: 37983769 DOI: 10.14309/ajg.0000000000002600
    INTRODUCTION: Antibiotic resistance is one of the main factors that determine the efficacy of treatments to eradicate Helicobacter pylori infection. Our aim was to evaluate the effectiveness of first-line and rescue treatments against H. pylori in Europe according to antibiotics resistance.

    METHODS: Prospective, multicenter, international registry on the management of H. pylori (European Registry on H. pylori Management). All infected and culture-diagnosed adult patients registered in the Spanish Association of Gastroenterology-Research Electronic Data Capture from 2013 to 2021 were included.

    RESULTS: A total of 2,852 naive patients with culture results were analyzed. Resistance to clarithromycin, metronidazole, and quinolones was 22%, 27%, and 18%, respectively. The most effective treatment, regardless of resistance, were the 3-in-1 single capsule with bismuth, metronidazole, and tetracycline (91%) and the quadruple with bismuth, offering optimal cure rates even in the presence of bacterial resistance to clarithromycin or metronidazole. The concomitant regimen with tinidazole achieved an eradication rate of 99% (90/91) vs 84% (90/107) with metronidazole. Triple schedules, sequential, or concomitant regimen with metronidazole did not achieve optimal results. A total of 1,118 non-naive patients were analyzed. Resistance to clarithromycin, metronidazole, and quinolones was 49%, 41%, and 24%, respectively. The 3-in-1 single capsule (87%) and the triple therapy with levofloxacin (85%) were the only ones that provided encouraging results.

    DISCUSSION: In regions where the antibiotic resistance rate of H. pylori is high, eradication treatment with the 3-in-1 single capsule, the quadruple with bismuth, and concomitant with tinidazole are the best options in naive patients. In non-naive patients, the 3-in-1 single capsule and the triple therapy with levofloxacin provided encouraging results.

    Matched MeSH terms: Helicobacter pylori*
  4. Alfizah H, Ramelah M, Rizal AM, Anwar AS, Isa MR
    Helicobacter, 2012 Oct;17(5):340-9.
    PMID: 22967117 DOI: 10.1111/j.1523-5378.2012.00956.x
    Polymorphisms of Helicobacter pylori cagA and vacA genes do exist and may contribute to differences in H. pylori infection and gastroduodenal diseases among races in the Malaysian population. This study was conducted to characterize the polymorphisms in H. pylori cagA and vacA in Malaysian population.
    Matched MeSH terms: Helicobacter pylori/classification; Helicobacter pylori/genetics*; Helicobacter pylori/isolation & purification; Helicobacter pylori/pathogenicity*
  5. Teh X, Khosravi Y, Lee WC, Leow AH, Loke MF, Vadivelu J, et al.
    PLoS One, 2014;9(7):e101481.
    PMID: 25003707 DOI: 10.1371/journal.pone.0101481
    Helicobacter pylori is the etiological agent for diseases ranging from chronic gastritis and peptic ulcer disease to gastric adenocarcinoma and primary gastric B-cell lymphoma. Emergence of resistance to antibiotics possesses a challenge to the effort to eradicate H. pylori using conventional antibiotic-based therapies. The molecular mechanisms that contribute to the resistance of these strains have yet to be identified and are important for understanding the evolutional pattern and selective pressure imposed by the environment.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter pylori/genetics*
  6. Bhewa Y, Hilmi I, Cheah PL, Navaratnam P, Goh KL
    J Dig Dis, 2007 Nov;8(4):207-10.
    PMID: 17970878
    Although well established in the West, stool antigen tests (SAT) are not widely used in Asia. Data on the accuracy of this test in Asia is sparse and, to date, there have been no studies looking at the more refined monoclonal SAT. The aim of this study is to validate the diagnostic accuracy of a stool antigen test, Hp STAR, for the detection of Helicobacter pylori.
    Matched MeSH terms: Helicobacter pylori/immunology; Helicobacter pylori/isolation & purification*
  7. Rajendra S, Ackroyd R, Robertson IK, Ho JJ, Karim N, Kutty KM
    Helicobacter, 2007 Apr;12(2):177-83.
    PMID: 17309756
    Ethnic differences in gastroesophageal reflux disease (GERD) and its complications as well as racial variations in the prevalence of Helicobacter pylori infection are well documented. Nevertheless, the association between reflux disease, H. pylori, and race has not been adequately explored.
    Matched MeSH terms: Helicobacter pylori/genetics; Helicobacter pylori/pathogenicity
  8. Tan HJ, Rizal AM, Rosmadi MY, Goh KL
    J Gastroenterol Hepatol, 2006 Jan;21(1 Pt 1):110-5.
    PMID: 16706821
    The role of Helicobacter pylori (HP) in non-ulcer dyspepsia is debatable. Eradicating HP will help a small group of non-ulcer dyspeptic patients. However, it is unclear which subgroup of patients will benefit from eradication therapy. The aim of the present study was to compare the cagA and cagE status, as well as vacA genotypes, of HP in non-ulcer dyspeptic patients who responded successfully to eradication therapy compared with those patients who did not.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/pathogenicity
  9. Tan HJ, Rizal AM, Rosmadi MY, Goh KL
    J Gastroenterol Hepatol, 2005 Apr;20(4):589-94.
    PMID: 15836708
    There is a geographic variation in Helicobacter pylori (HP) genotypes and virulence factors. Cytotoxin associated genes A (cagA) and E (cagE), and certain vacuolating cytotoxin (vacA) genotypes are associated with peptic ulcer disease (PUD). There is also a different prevalence of PUD among different ethnic groups in Malaysia. The present study compared the distribution of vacA alleles and cagA and cagE status in three ethnic groups residing in Kuala Lumpur, Malaysia, and their association with clinical outcome.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/pathogenicity
  10. Ramelah M, Aminuddin A, Alfizah H, Isa MR, Jasmi AY, Tan HJ, et al.
    FEMS Immunol. Med. Microbiol., 2005 May 1;44(2):239-42.
    PMID: 15866222
    Helicobacter pylori infection of a distinct subtype of cagA may lead to different pathological manifestation. The aim of this study is to determine the presence of cagA gene and its variants in H. pylori infection among different ethnic groups and its effect on gastroduodenal diseases. Overall detection of cagA among the 205 clinical isolates of H. pylori was 94%. Variations in size of the 3' region of cagA gene were examined among 192 Malaysian H. pylori cagA-positive strains. Results showed that three cagA variants differing in fragment length of PCR products were detected and designated as type A (621-651bp), type B (732-735bp) and type C (525 bp). Although there was no association between any of the cagA subtypes with peptic ulcer disease (p>0.05), an association between cagA subtypes with a specific ethnic group was observed. Specific-cagA subtype A strains were predominantly isolated from Chinese compared to Malays and Indians (p<0.0005), and cagA subtype B strains were predominantly isolated from Malays and Indians compared to Chinese (p<0.05). The cagA type A strains of H. pylori is commonly found in the Chinese patients who have a higher risk of peptic ulcer disease, thus indicating that it could be used as an important clinical biomarker for a more severe infection.
    Matched MeSH terms: Helicobacter pylori/classification*; Helicobacter pylori/genetics
  11. Alfizah H, Norazah A, Hamizah R, Ramelah M
    J Med Microbiol, 2014 May;63(Pt 5):703-709.
    PMID: 24757218 DOI: 10.1099/jmm.0.069781-0
    Antibiotic resistance is increasing worldwide, and it has been regarded as the main factor reducing the efficacy of Helicobacter pylori therapy. The aim of this study was to determine the phenotype and genotype of antibiotic-resistant strains of H. pylori in the Malaysian population and to evaluate the impact of antibiotic resistance to eradication outcome. One hundred and sixty-one H. pylori isolates were analysed in this study. Metronidazole, clarithromycin, fluoroquinolone, amoxicillin and tetracycline susceptibilities were determined by Etest. PCR followed by DNA sequencing was carried out to determine mutations. The medical records of the patients infected with resistant strains were reviewed to determine the eradication outcome. Metronidazole resistance was encountered in 36.6 % of H. pylori isolates, whereas clarithromycin and fluoroquinolone resistance was observed in 1.2  and 1.9 % of isolates, respectively. All strains tested were susceptible to amoxicillin and tetracycline. Frameshift and nonsense mutations in rdxA and frxA genes resulting in stop codons contributed to metronidazole resistance, which leads to reduced eradication efficacy. A2142G and A2143G mutations of 23S rRNA were identified as causing failure of the eradication therapy. Mutation at either codon 87 or 91 of the gyrA gene was identified in fluoroquinolone-resistant strains. However, the effect of resistance could not be assessed. This study showed that frameshift and nonsense mutations in rdxA or frxA genes and point mutations in the 23S rRNA affected the efficacy of H. pylori eradication therapy.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter pylori/isolation & purification
  12. Al-Maleki AR, Loke MF, Lui SY, Ramli NSK, Khosravi Y, Ng CG, et al.
    Cell. Microbiol., 2017 12;19(12).
    PMID: 28776327 DOI: 10.1111/cmi.12771
    Outer inflammatory protein A (OipA) is an important virulence factor associated with gastric cancer and ulcer development; however, the results have not been well established and turned out to be controversial. This study aims to elucidate the role of OipA in Helicobacter pylori infection using clinical strains harbouring oipA "on" and "off" motifs. Proteomics analysis was performed on AGS cell pre-infection and postinfection with H. pylori oipA "on" and "off" strains, using liquid chromatography/mass spectrometry. AGS apoptosis and cell cycle assays were performed. Moreover, expression of vacuolating cytotoxin A (VacA) was screened using Western blotting. AGS proteins that have been suggested previously to play a role or associated with gastric disease were down-regulated postinfection with oipA "off" strains comparing to oipA "on" strains. Furthermore, oipA "off" and ΔoipA cause higher level of AGS cells apoptosis and G0/G1 cell-cycle arrest than oipA "on" strains. Interestingly, deletion of oipA increased bacterial VacA production. The capability of H. pylori to induce apoptosis and suppress expression of proteins having roles in human disease in the absence of oipA suggests that strains not expressing OipA may be less virulent or may even be protective against carcinogenesis compared those expressing OipA. This potentially explains the higher incidence of gastric cancer in East Asia where oipA "on" strains predominates.
    Matched MeSH terms: Helicobacter pylori/metabolism*; Helicobacter pylori/chemistry
  13. Huang J, Zagai U, Hallmans G, Nyrén O, Engstrand L, Stolzenberg-Solomon R, et al.
    Int J Cancer, 2017 Apr 15;140(8):1727-1735.
    PMID: 28032715 DOI: 10.1002/ijc.30590
    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 pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.
    Matched MeSH terms: Helicobacter pylori/isolation & purification*; Helicobacter pylori/pathogenicity
  14. Qin H, Tang G, Yi P, Pan X, Huang H, Chang R, et al.
    Saudi Pharm J, 2016 May;24(3):265-72.
    PMID: 27275113 DOI: 10.1016/j.jsps.2016.04.015
    The present study aimed to establish a genus-specific PCR-based assay to detect helicobacters using 16S rRNA gene as the target template. We designed the hemi-nested primers based on sequences of 16S rRNA gene of 34 types of Helicobacter species. The inclusivity, sensitivity, and specificity of the PCR assay using these primers were examined in three different models, comprising feces simulated samples, BLAB/c mice infection model and clinic patients samples. The detection sensitivity of Helicobacter pylori, Helicobacter hepaticus and Helicobacter bilis strains from feces simulated samples was all 102 CFU/ml. We successfully detected H. hepaticus and H. bilis in the liver, cecum and feces of experimentally infected mice. H. pylori was successfully detected in the feces samples from 3 patients infected with H. pylori while not in the feces samples from 3 healthy human. However, the C97/C05-C97/C98 PCR assay detected H. pylori in the 2 positive samples. Due to the PCR assay's excellent inclusivity, high sensitivity and specificity it may be used to detect the presence of Helicobacters.
    Matched MeSH terms: Helicobacter pylori
  15. Khalilpour A, Osman S, Yunus MH, Santhanam A, Vellasamy N, Noordin R
    BMC Res Notes, 2014;7:809.
    PMID: 25406411 DOI: 10.1186/1756-0500-7-809
    Helicobacter pylori is a human pathogen and during the process of infection, antigens from the bacterium elicit strong host humoral immune responses. In our previous report, native H. pylori UreG protein showed good reactivity with sera from H. pylori patients. This study was aimed at producing the recombinant form of the protein (rUreG) and determining its seroreactivities.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/immunology*; Helicobacter pylori/metabolism
  16. Rehvathy V, Tan MH, Gunaletchumy SP, Teh X, Wang S, Baybayan P, et al.
    Genome Announc, 2013;1(5).
    PMID: 24051312 DOI: 10.1128/genomeA.00687-13
    Helicobacter pylori causes human gastroduodenal diseases, including chronic gastritis and peptic ulcer disease. It is also a major microbial risk factor for the development of gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. Twenty-one strains with different ethnicity, disease, and antimicrobial susceptibility backgrounds were sequenced by use of Illumina HiSeq and PacBio RS platforms.
    Matched MeSH terms: Helicobacter pylori
  17. Norazah A, Rasinah WZ, Zaili Z, Aminuddin A, Ramelah M
    Malays J Pathol, 2009 Jun;31(1):29-34.
    PMID: 19694311 MyJurnal
    This study was conducted to determine whether there was any genetic heterogeneity among Helicobacter pylori strains isolated from the antrum and corpus of the same individual in a Malaysian population and to determine the presence of heterogeneous susceptibility of the isolates by comparing PCR-RAPD and antibiotic profiles. Forty-four H. pylori isolates cultured from the antrum and corpus of 22 patients were analyzed. Antibiotic susceptibility testing was carried out by minimum inhibitory concentration determination, using E-Test method strips. PCR-RAPD was carried out on all the strains and the profiles generated were analysed for cluster analysis. Twenty-nine different PCR-RAPD profiles were observed in the 44 isolates. Fifteen pairs of the isolates from the same patients had the same PCR-RAPD patterns while in 7 pairs, the profiles were different. The strains were clustered into 2 separate clusters at a low coefficient of similarity, where most of the strains were in cluster 1. The degree of similarity was very low among most of the isolates. Most of the patients (16 of 22) were infected with strains that have the same antibiotic susceptibility profiles. Out of these, only 10 pairs shared the same PCR-RAPD and antibiotic profiles. Five pairs of isolates with similar PCR-RAPD profiles differed in their antibiotic profiles due to metronidazole resistance in one of the sites. A large degree of genetic heterogeneity was observed among H. pylori strains circulating among Malaysian patients. An individual patient can be infected with multiple strains and the strains can be antibiotic resistant.
    Matched MeSH terms: Helicobacter pylori/drug effects; Helicobacter pylori/genetics; Helicobacter pylori/isolation & purification*
  18. Goh KL
    J Dig Dis, 2007 Nov;8(4):179-85.
    PMID: 17970873
    The new millennium has seen distinct changes in the pattern of gastrointestinal disease in the Asia-Pacific region. These changes are important as more than half of the world's population come from the region and therefore impact significantly on the global disease burden. The highest incidence of gastric cancer (GCA) has been reported from Asia and GCA remains a very important cancer. However time-trend studies have shown a decrease in GCA incidence in several countries in Asia. A rise in cardio-esophageal cancers as seen in the West has not been reported. On the other hand, colorectal cancer has been steadily increasing in Asia with age-standardized incidence rates of some countries approaching that of the West. The pattern of acid-related diseases has also changed. Gastroesophageal reflux disease is a fast emerging disease with an increasing prevalence of reflux esophagitis and reflux symptoms. The prevalence of peptic ulcer disease has at the same time declined in step with a decrease in H. pylori infection. Many of the changes taking place mirror the Western experience of several decades ago. Astute observation of the epidemiology of emerging diseases combined with good scientific work will allow a clearer understanding of the key processes underlying these changes. With rapid modernization, lifestyle changes have been blamed for an increase in several diseases including gastroesophageal reflux disease, nonalcoholic fatty liver disease and colorectal cancer. A worrying trend has been the increase in obesity among Asians, which has been associated with an increase in metabolic diseases and various gastrointestinal cancers. Conversely, an improvement in living conditions has been closely linked to the decrease in GCA and H. pylori prevalence.
    Matched MeSH terms: Helicobacter pylori
  19. Wan Najmi WD, Noorfizura A, Wan Anna MA
    Med J Malaysia, 2016 02;71(1):35-6.
    PMID: 27130744
    We report a middle age man who presented with intermittent vomiting and loss of weight. Oesophagogastroduodenoscopy showed numerous antral hyperplastic polyps with inaccessible duodenum. Contrast enhanced computed topography demonstrated a classical target sign of intussusception. This finding was later confirmed at laparotomy. This rare presentation and management strategy is discussed.
    Matched MeSH terms: Helicobacter pylori
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