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Fulltext Elucidation of the Metabolic Network of Helicobacter pylori J99 and Malaysian Clinical Strains by Phenotype Microarray

Lee WC, Goh KL, Loke MF, Vadivelu J

Helicobacter, 2017 Feb;22(1).
PMID: 27258354 DOI: 10.1111/hel.12321

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.

Matched MeSH terms: Helicobacter Infections/microbiology
Other Helicobacters, gastric and gut microbiota

Péré-Védrenne C, Flahou B, Loke MF, Ménard A, Vadivelu J

Helicobacter, 2017 Sep;22 Suppl 1.
PMID: 28891140 DOI: 10.1111/hel.12407

The current article is a review of the most important and relevant literature published in 2016 and early 2017 on non-Helicobacter pylori Helicobacter infections in humans and animals, as well as interactions between H. pylori and the microbiota of the stomach and other organs. Some putative new Helicobacter species were identified in sea otters, wild boars, dogs, and mice. Many cases of Helicobacter fennelliae and Helicobacter cinaedi infection have been reported in humans, mostly in immunocompromised patients. Mouse models have been used frequently as a model to investigate human Helicobacter infection, although some studies have investigated the pathogenesis of Helicobacters in their natural host, as was the case for Helicobacter suis infection in pigs. Our understanding of both the gastric and gut microbiome has made progress and, in addition, interactions between H. pylori and the microbiome were demonstrated to go beyond the stomach. Some new approaches of preventing Helicobacter infection or its related pathologies were investigated and, in this respect, the probiotic properties of Saccharomyces, Lactobacillus and Bifidobacterium spp. were confirmed.

Matched MeSH terms: Helicobacter Infections/microbiology*
Genetic polymorphisms in the Toll-like receptor signalling pathway in Helicobacter pylori infection and related gastric cancer

Castaño-Rodríguez N, Kaakoush NO, Pardo AL, Goh KL, Fock KM, Mitchell HM

Hum Immunol, 2014 Aug;75(8):808-15.
PMID: 24929142 DOI: 10.1016/j.humimm.2014.06.001

Gastric cancer (GC) is a progressive process initiated by Helicobacter pylori-induced inflammation. Initial recognition of H. pylori involves Toll-like receptors (TLRs), central molecules in the host inflammatory response. Here, we investigated the association between novel polymorphisms in genes involved in the TLR signalling pathway, including TLR2, TLR4, LBP, MD-2, CD14 and TIRAP, and risk of H. pylori infection and related GC.

Matched MeSH terms: Helicobacter Infections/microbiology
Chronic atrophic antral gastritis and risk of metaplasia and dysplasia in an area with low prevalence of Helicobacter pylori

Yeh LY, Raj M, Hassan S, Aziz SA, Othman NH, Mutum SS, et al.

Indian J Gastroenterol, 2009 08 21;28(2):49-52.
PMID: 19696988 DOI: 10.1007/s12664-009-0017-0

INTRODUCTION: The Northeastern region of Peninsular Malaysia is an area with exceptionally low prevalence for Helicobacter pylori infection. The risk of intestinal metaplasia and dysplasia in patients with chronic atrophic gastritis (CAG) and its association with Helicobacter pylori is unknown in this region.
METHODS: This was a cross-sectional study on gastric biopsies from 234 consecutive patients (mean age 53.5 [14.8] years) who underwent upper gastrointestinal endoscopy between January 2006 and December 2006.
RESULTS: There were 137 (59%) men and 185 (79%) Malay patients. Among 234 biopsies, CAG was found in 99 and non-atrophic gastritis in 135. Intestinal metaplasia and dysplasia were detected in 8 and 6 atrophic gastritis biopsies, respectively, and in 10 and 3 of non-atrophic gastritis biopsies, respectively. H. pylori were detected in 16 (9 Malays, 7 non- Malays) biopsies (p=0.024); intestinal metaplasia was detected in 4 biopsies (p=0.3) and dysplasia in 5 biopsies (p=0.3). Of the 218 biopsies negative for H. pylori, intestinal metaplasia was found in 14 and dysplasia in 4. The risk of intestinal metaplasia as well as dysplasia was associated with presence of H. pylori infection (p=0.029 and p<0.001 respectively).
CONCLUSION: Even in a setting of low prevalence of H. pylori, intestinal metaplasia and dysplasia were significantly associated with H. pylori infection. The frequency of intestinal metaplasia and dysplasia was similar different between biopsies with atrophic gastritis and non-atrophic gastritis.

Matched MeSH terms: Helicobacter Infections/microbiology
Fulltext Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case-control study

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

Matched MeSH terms: Helicobacter Infections/microbiology*
Fulltext Helicobacter pylori Virulence Factor Cytotoxin-Associated Gene A (CagA)-Mediated Gastric Pathogenicity

Ansari S, Yamaoka Y

Int J Mol Sci, 2020 Oct 08;21(19).
PMID: 33050101 DOI: 10.3390/ijms21197430

Helicobacter pylori causes persistent infection in the gastric epithelium of more than half of the world's population, leading to the development of severe complications such as peptic ulcer diseases, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Several virulence factors, including cytotoxin-associated gene A (CagA), which is translocated into the gastric epithelium via the type 4 secretory system (T4SS), have been indicated to play a vital role in disease development. Although infection with strains harboring the East Asian type of CagA possessing the EPIYA-A, -B, and -D sequences has been found to potentiate cell proliferation and disease pathogenicity, the exact mechanism of CagA involvement in disease severity still remains to be elucidated. Therefore, we discuss the possible role of CagA in gastric pathogenicity.

Matched MeSH terms: Helicobacter Infections/microbiology
Fulltext Green synthesis of silver nanoparticles through reduction with Solanum xanthocarpum L. berry extract: characterization, antimicrobial and urease inhibitory activities against Helicobacter pylori

Amin M, Anwar F, Janjua MRSA, Iqbal MA, Rashid U

Int J Mol Sci, 2012;13(8):9923-9941.
PMID: 22949839 DOI: 10.3390/ijms13089923

A green synthesis route for the production of silver nanoparticles using methanol extract from Solanum xanthocarpum berry (SXE) is reported in the present investigation. Silver nanoparticles (AgNps), having a surface plasmon resonance (SPR) band centered at 406 nm, were synthesized by reacting SXE (as capping as well as reducing agent) with AgNO(3) during a 25 min process at 45 °C. The synthesized AgNps were characterized using UV-Visible spectrophotometry, powdered X-ray diffraction, and transmission electron microscopy (TEM). The results showed that the time of reaction, temperature and volume ratio of SXE to AgNO(3) could accelerate the reduction rate of Ag(+) and affect the AgNps size and shape. The nanoparticles were found to be about 10 nm in size, mono-dispersed in nature, and spherical in shape. In vitro anti-Helicobacter pylori activity of synthesized AgNps was tested against 34 clinical isolates and two reference strains of Helicobacter pylori by the agar dilution method and compared with AgNO(3) and four standard drugs, namely amoxicillin (AMX), clarithromycin (CLA), metronidazole (MNZ) and tetracycline (TET), being used in anti-H. pylori therapy. Typical AgNps sample (S1) effectively inhibited the growth of H. pylori, indicating a stronger anti-H. pylori activity than that of AgNO(3) or MNZ, being almost equally potent to TET and less potent than AMX and CLA. AgNps under study were found to be equally efficient against the antibiotic-resistant and antibiotic-susceptible strains of H. pylori. Besides, in the H. pylori urease inhibitory assay, S1 also exhibited a significant inhibition. Lineweaver-Burk plots revealed that the mechanism of inhibition was noncompetitive.

Matched MeSH terms: Helicobacter Infections/microbiology
Draft genome sequences of Helicobacter pylori isolates from Malaysia, cultured from patients with functional dyspepsia and gastric cancer

Gunaletchumy SP, Teh X, Khosravi Y, Ramli NS, Chua EG, Kavitha T, et al.

J Bacteriol, 2012 Oct;194(20):5695-6.
PMID: 23012278

Helicobacter pylori is the main bacterial causative agent of gastroduodenal disorders and a risk factor for gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. The draft genomes of 10 closely related H. pylori isolates from the multiracial Malaysian population will provide an insight into the genetic diversity of isolates in Southeast Asia. These isolates were cultured from gastric biopsy samples from patients with functional dyspepsia and gastric cancer. The availability of this genomic information will provide an opportunity for examining the evolution and population structure of H. pylori isolates from Southeast Asia, where the East meets the West.

Matched MeSH terms: Helicobacter Infections/microbiology
Fulltext Helicobacter pylori vacA as marker for gastric cancer and gastroduodenal diseases: one but not the only factor

Abadi AT, Lee YY

J Clin Microbiol, 2014 Dec;52(12):4451.
PMID: 25399000 DOI: 10.1128/JCM.02640-14
Matched MeSH terms: Helicobacter Infections/microbiology*
Clarithromycin resistance and point mutations in the 23S rRNA gene in Helicobacter pylori isolates from Malaysia

Ho SL, Tan EL, Sam CK, Goh KL

J Dig Dis, 2010 Apr;11(2):101-5.
PMID: 20402836 DOI: 10.1111/j.1751-2980.2010.00423.x

To determine the prevalence of primary clarithromycin resistance amongst Helicobacter pylori (H. pylori) strains in Malaysian patients with gastroduodenal diseases, by using restriction fragment length polymorphism (RFLP) in domain V of 23S rRNA.

Matched MeSH terms: Helicobacter Infections/microbiology*
Efficacy of 1-week proton pump inhibitor triple therapy as first-line Helicobacter pylori eradication regime in Asian patients: is it still effective 10 years on?

Qua CS, Manikam J, Goh KL

J Dig Dis, 2010 Aug;11(4):244-8.
PMID: 20649738 DOI: 10.1111/j.1751-2980.2010.00445.x

OBJECTIVE:
To re-examine the efficacy and tolerability of 1-week proton pump inhibitor triple therapy as a first-line Helicobacter pylori (H. pylori) eradication therapy.

METHODS:
Consecutive participants with a positive rapid urease test during an outpatient upper endoscopy were included. All participants were given pantoprazole 40 mg b.i.d., amoxycillin 1 g b.i.d. and clarithromycin 500 mg b.i.d. for 1 week. They were asked to return after 1 week to report any side effects related to the medications and to check for compliance. Successful eradication was defined by negative (13)C-urea breath test at least 4 weeks after the completion of therapy.

RESULTS:
A total of 191 patients were recruited into the study, of whom 81 were male (42.4%) and 110 female (57.6%), with a mean age of 55.6 (range 21-88) years. Overall 26 patients (13.6%) defaulted follow up and five patients were not compliant (taking less than 85%) with the medications. Per-protocol and intention-to-treat eradication rates were 84.4% (95% CI: 78.6-89.9%) and 71.2% (95% CI: 64.5-77.6%), respectively. Overall 68 participants (42.5%) reported no side effects, followed by 58 (36.3%) with a taste disturbance, 16 (10.0%) with epigastric pain, 15 (9.4%) with diarrhea, 13 (8.1%) with nausea or vomiting, 12 (7.5%) with loss of appetite, nine (5.6%) with dizziness and two (1.3%) with an allergic skin rash, none of which was severe.

CONCLUSION:
The current regime using pantoprazole, amoxycillin and clarithromycin is highly tolerable and effective and should continue to be recommended as a first-line therapy for H. pylori eradication in our setting.

Matched MeSH terms: Helicobacter Infections/microbiology
Role of Helicobacter pylori virulence factor and genotypes in non-ulcer dyspepsia

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 Infections/microbiology
Distribution of Helicobacter pylori cagA, cagE and vacA in different ethnic groups in Kuala Lumpur, Malaysia

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 Infections/microbiology*
Resistotype of Helicobacter pylori isolates: the impact on eradication outcome

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 Infections/microbiology*
Seroprevalence of Helicobacter pylori infection in Malaysian children: evidence for ethnic differences in childhood

Boey CC, Goh KL, Lee WS, Parasakthi N

J Paediatr Child Health, 1999 Apr;35(2):151-2.
PMID: 10365351

OBJECTIVES: To determine the prevalence of Helicobacter pylori (H. pylori) in healthy Malaysian children and to discover whether differences exist among children of different races.
METHODS: Serum samples from asymptomatic children tested for H. pylori seropositivity using an ELISA test.
RESULTS: Five hundred and fourteen healthy urban Malaysian children aged 0.5 to 17 (mean 5.9) years from three different racial groups had their blood tested for H. pylori antibodies. The overall prevalence was 10.3%. There was no significant difference in the prevalence of infection between boys and girls, but a significant rise was noted with increasing age (P = 0.009). Seropositivity was most common in the Indians and lowest in the Malays (P = 0.001). Father's level of education did not affect the child's rate of H. pylori seropositivity.
CONCLUSION: The prevalence of H. pylori seropositivity among asymptomatic urban Malaysian children is lowest in Malays. Intermediate in Chinese and highest in Indians. The racial differences found in children are consistent with those found in Malaysian adults.

Matched MeSH terms: Helicobacter Infections/microbiology*
Fulltext Comparative efficacy sensitivity and specificity of the tests used for the diagnosis of Helicobacter pylori

Suhaila N, Hussin S, Rahman MM

Pak J Biol Sci, 2010 Nov 01;13(21):1057-61.
PMID: 21313878

Abstract: A total number of 157 samples were examined by 4 different tests-In-house rapid urease (iRUT), Culture, Histopathology and Immunochromatography (Immuno CardSTAT) for the detection of Helicobacter pylori from the patients reported to Hospital Kuala Lumpur, Malaysia during 2007 to 2008. Out of the samples examined 47 (29.9%) were positive for H. pylori by the tests used in the laboratory. Efficacy of detection of the bacteria by the tests- In-house rapid urease, Culture, Histopathology and Immuno CardSTAT were 31.8, 13.9, 30.3 and 32.8%, respectively. However, sensitivity and specificity of the iRUT were 91.5 and 93.6%, respectively and the Positive Predictive Value (PPV) was 86% and the Negative Predictive Value (NPV) was 96.3%. The sensitivity for Immuno CardSTAT rapid test was 100% and the specificity was 79.3%. The PPV was 50% and the NPV was 100%. Convenient methods to the authors were 'In house rapid urease test and Immunochromatography though variability of specificities were observed.

Matched MeSH terms: Helicobacter Infections/microbiology
Fulltext Streptococcus mitis induces conversion of Helicobacter pylori to coccoid cells during co-culture in vitro

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 Infections/microbiology*
Fulltext Functional and molecular surveillance of Helicobacter pylori antibiotic resistance in Kuala Lumpur

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 Infections/microbiology*
Fulltext Changes in Metabolic Hormones in Malaysian Young Adults following Helicobacter pylori Eradication

Yap TW, Leow AH, Azmi AN, Francois F, Perez-Perez GI, Blaser MJ, et al.

PLoS One, 2015;10(8):e0135771.
PMID: 26291794 DOI: 10.1371/journal.pone.0135771

More than half of the world's adults carry Helicobacter pylori. The eradication of H. pylori may affect the regulation of human metabolic hormones. The aim of this study was to evaluate the effect of H. pylori eradication on meal-associated changes in appetite-controlled insulinotropic and digestive hormones, and to assess post-eradication changes in body mass index as part of a currently on-going multicentre ESSAY (Eradication Study in Stable Adults/Youths) study.

Matched MeSH terms: Helicobacter Infections/microbiology
Fulltext Polymorphisms at Locus 4p14 of Toll-Like Receptors TLR-1 and TLR-10 Confer Susceptibility to Gastric Carcinoma in Helicobacter pylori Infection

Ravishankar Ram M, Goh KL, Leow AH, Poh BH, Loke MF, Harrison R, et al.

PLoS One, 2015;10(11):e0141865.
PMID: 26559190 DOI: 10.1371/journal.pone.0141865

Helicobacter pylori (H. pylori) -induced gastric inflammation impacts the functions of leptin- and ghrelin-producing cells in the gastroduodenum. Inflammation resulting from H. pylori sensing via Toll-like receptors (TLRs) and the associated downstream signaling largely remain ambiguous. Here, we investigated the role of gut hormones, pro-inflammatory cytokines and single nucleotide polymorphisms (SNPs) associated with TLR 4p14 in H. pylori disease in 30 subjects with non-ulcer dyspepsia (NUD), 40 with peptic ulcer disease (PUD) and 15 with gastric cancer (GC) subjects positive and negative for H. pylori infection. The level of pro-inflammatory cytokines was directly proportional to the severity of gastritis, and disease status influenced the levels of gut hormones and pro-inflammatory cytokines. TLR-1 SNPs rs4833095 and TLR-10 SNPs rs10004195 and were directly associated with H. pylori disease, and were up-regulated in the presence of H. pylori in a genotype-independent manner. We concluded that TLR-1 rs4833095 and TLR10 rs10004195 confer susceptibility to development of gastroduodenal disease, especially GC in H.pylori disease.

Matched MeSH terms: Helicobacter Infections/microbiology

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