Displaying publications 101 - 120 of 242 in total

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  1. Ethnicity and H. pylori as risk factors for gastric cancer in Malaysia: A prospective case control study
    Goh KL, Cheah PL, Md N, Quek KF, Parasakthi N
    Am J Gastroenterol, 2007 Jan;102(1):40-5.
    PMID: 17100981
    To determine the risk factors for gastric cancer (GCA), with particular emphasis on ethnicity in our multiracial population.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/complications*; Helicobacter Infections/epidemiology
  2. Fulltext Prolonged treatment with omeprazole does not improve the eradication rate of Helicobacter pylori infection--a short report [corrected]
    Goh KL, Parasakthi N, Peh SC, Anderson PE, Tan KK
    Singapore Med J, 1995 Dec;36(6):619-20.
    PMID: 8781634
    Omeprazole has been shown to have a suppressive effect on Helicobacter pylori. The aim of this study was to determine if prolonged treatment with omeprazole would result in a higher eradication rate than short course treatment. Twenty patients with endoscopy proven duodenal ulcers and unequivocal evidence of Helicobacter pylori (HP) infection based on culture, histology, urease test and Gram's stain of a fresh tissue smear were treated with omeprazole 40 mg om for 2-4 weeks. Following ulcer healing, patients received either maintenance omeprazole 20 mg om or placebo for up to one year. All 20 patients had healed ulcers following a 2-4 week course of omeprazole 40 mg om.. All were negative for HP at the end of treatment. Thirteen patients received short course therapy with omeprazole only, followed by placebo. On follow-up endoscopy at 3 months, only one of 13 (7.7%) had eradicated the bacteria. Seven patients received maintenance treatment with omeprazole 20mg om for one year. Following completion of treatment, patients were followed up at 1, 3 and 6 months. Only one of 7 (14.3%) patients had eradicated the infection on long term follow-up. The eradication rates of HP with both short and long course omeprazole monotherapy were low.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter Infections/drug therapy*; Helicobacter Infections/microbiology
  3. Fulltext The rapid urease test in the diagnosis of Helicobacter pylori infection
    Goh KL, Parasakthi N, Peh SC, Puthucheary SD, Wong NW
    Singapore Med J, 1994 Apr;35(2):161-2.
    PMID: 7939811
    With the increasing recognition of the importance of H. pylori in gastrointestinal disease, there is a need for a reliable, efficient and yet inexpensive diagnostic test. The performance of the rapid urease test (RUT) as an endoscopy suite diagnostic test was compared to the established methods of culture, histology and Gram stain of tissue smear, in 274 gastric biopsy samples. Histology had the highest sensitivity of 99.3% followed by the RUT (96.6%). Culture and Gram stain of tissue smear had 100% specificity, while the rapid urease test had 99.2% specificity. The RUT had a positive predictive value of 99.3% and a negative predictive value of 96.2%. The RUT is an inexpensive, rapid and reliable diagnostic test of H. pylori infection.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/diagnosis*; Helicobacter Infections/pathology
  4. 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 pylori/genetics*; Helicobacter pylori/isolation & purification; Helicobacter Infections/microbiology
  5. Fulltext Helicobacter pylori recombinant UreG protein: cloning, expression, and assessment of its seroreactivity
    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; Helicobacter Infections/blood; Helicobacter Infections/diagnosis; Helicobacter Infections/immunology*; Helicobacter Infections/microbiology*
  6. 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 pylori/drug effects*; Helicobacter pylori/genetics*; Helicobacter Infections/microbiology*; Helicobacter Infections/epidemiology*
  7. Fulltext The NOD-like receptor signalling pathway in Helicobacter pylori infection and related gastric cancer: a case-control study and gene expression analyses
    Castaño-Rodríguez N, Kaakoush NO, Goh KL, Fock KM, Mitchell HM
    PLoS One, 2014;9(6):e98899.
    PMID: 24901306 DOI: 10.1371/journal.pone.0098899
    Currently, it is well established that cancer arises in chronically inflamed tissue. A number of NOD-like receptors (NLRs) form inflammasomes, intracellular multiprotein complexes critical for generating mature pro-inflammatory cytokines (IL-1β and IL-18). As chronic inflammation of the gastric mucosa is a consequence of Helicobacter pylori infection, we investigated the role of genetic polymorphisms and expression of genes involved in the NLR signalling pathway in H. pylori infection and related gastric cancer (GC).
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/complications; Helicobacter Infections/genetics*; Helicobacter Infections/metabolism*
  8. 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 pylori/genetics*; Helicobacter Infections/drug therapy*; Helicobacter Infections/microbiology*; Helicobacter Infections/epidemiology
  9. The cag PAI is intact and functional but HP0521 varies significantly in Helicobacter pylori isolates from Malaysia and Singapore
    Schmidt HM, Andres S, Nilsson C, Kovach Z, Kaakoush NO, Engstrand L, et al.
    Eur J Clin Microbiol Infect Dis, 2010 Apr;29(4):439-51.
    PMID: 20157752 DOI: 10.1007/s10096-010-0881-7
    Helicobacter pylori-related disease is at least partially attributable to the genotype of the infecting strain, particularly the presence of specific virulence factors. We investigated the prevalence of a novel combination of H. pylori virulence factors, including the cag pathogenicity island (PAI), and their association with severe disease in isolates from the three major ethnicities in Malaysia and Singapore, and evaluated whether the cag PAI was intact and functional in vitro. Polymerase chain reaction (PCR) was used to detect dupA, cagA, cagE, cagT, cagL and babA, and to type vacA, the EPIYA motifs, HP0521 alleles and oipA ON status in 159 H. pylori clinical isolates. Twenty-two strains were investigated for IL-8 induction and CagA translocation in vitro. The prevalence of cagA, cagE, cagL, cagT, babA, oipA ON and vacA s1 and i1 was >85%, irrespective of the disease state or ethnicity. The prevalence of dupA and the predominant HP0521 allele and EPIYA motif varied significantly with ethnicity (p < 0.05). A high prevalence of an intact cag PAI was found in all ethnic groups; however, no association was observed between any virulence factor and disease state. The novel association between the HP0521 alleles, EPIYA motifs and host ethnicity indicates that further studies to determine the function of this gene are important.
    Matched MeSH terms: Helicobacter pylori/classification; Helicobacter pylori/genetics*; Helicobacter pylori/isolation & purification*; Helicobacter Infections/microbiology*
  10. Evaluation of the monoclonal stool antigen test for Helicobacter pylori in an Asian population with dyspepsia
    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*; Helicobacter Infections/complications; Helicobacter Infections/diagnosis*
  11. Helicobacter pylori, ethnicity, and the gastroesophageal reflux disease spectrum: a study from the East
    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; Helicobacter Infections/ethnology*; Helicobacter Infections/epidemiology
  12. 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 pylori/genetics*; Helicobacter pylori/pathogenicity; Helicobacter Infections/drug therapy*; Helicobacter Infections/microbiology
  13. Prevalence of and risk factors for Helicobacter pylori infection in a multi-racial dyspeptic Malaysian population undergoing endoscopy
    Goh KL
    J Gastroenterol Hepatol, 1997 Jun;12(6):S29-35.
    PMID: 9195409
    The aim of the present study was to determine the risk factors for Helicobacter pylori in a dyspeptic Malaysian population. A cross-sectional survey of 1060 consecutive patients presenting with dyspepsia at the Endoscopic Unit, University Hospital, Kuala Lumpur, Malaysia from January 1994 to July 1995 was undertaken. All patients answered a detailed questionnaire and underwent endoscopy, with two antral biopsies taken for diagnosis of H. pylori using a rapid urease test. An overall H. pylori prevalence of 49.0% was recorded. Helicobacter pylori prevalence in relation to the major endoscopic diagnoses were as follows: non-ulcer dyspepsia (NUD) 31.2%; duodenal ulcer (DU) 91.4%; and gastric ulcer (GU) 74.1%. The prevalence among the races were as follows: Malay 16.4%; Chinese 48.5%; and Indians 61.8%. Multiple logistic regression analysis identified the following as independent risk factors: > 45 years old 1.5 (1.1,2.0); male gender 1.6 (1.2,2.1); ethnic group: Chinese 2.5 (1.7,3.7); Indians 4.9 (3.2,7.5); level of education: low 2.3 (1.5,3.5); middle 1.7 (1.1,2.6); and smoking 1.6 (1.2,2.3). Analysis was also performed on DU, GU and non-UD patients separately; in both DU and GU patients, H. pylori prevalence was high regardless of age, sex, race or level of education. However, in DU patients, Indian race had an independent risk factor (Odds ratio = 7.8 (1.2,48.4)). The findings in the NUD group reflected the findings in the ¿all patients' group; > 45 years old, male gender, Indian and Chinese race, and low level of education were also significant, independent risk factors. The overall differences in H. pylori prevalence between the different subgroups were mainly due to differences in the NUD group. The increased risk of H. pylori infection in Chinese and Indians points to either an inherent ethnic genetic predisposition or to socio-cultural practices peculiar to the particular race which may be responsible for transmission of the infection.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/complications; Helicobacter Infections/ethnology; Helicobacter Infections/epidemiology*
  14. Does Helicobacter pylori infection affect gastric emptying in patients with functional dyspepsia?
    Goh KL, Paramsothy M, Azian M, Parasakthi N, Peh SC, Bux S, et al.
    J Gastroenterol Hepatol, 1997 Dec;12(12):790-4.
    PMID: 9504887
    The objectives of the study were first, to determine if gastric emptying was altered in patients with functional dyspepsia with and without Helicobacter pylori infection compared with normal healthy volunteers; and second, to determine if there were further alterations in gastric emptying when the infection was eradicated. Gastric emptying was measured using a 99mtechnetium radiolabelled solid meal and gastric emptying time was measured as t1/2, viz. time taken for half the radiolabelled meal to be emptied from the stomach. The mean gastric emptying time for H. pylori-positive patients (n=20) was 56.4+/-24.8 min; H. pylori-negative patients (n=19) 67.8+/-31.8 min; and normal controls (n=20) 58.8+/-18.8min. No significant difference was obtained between the groups (ANOVA; P=0.348). Thirteen of 18 H. pylori-positive patients successfully eradicated the infection following treatment with omeprazole 40 mg o.m. and amoxycillin 500 mg t.d.s. for 2 weeks. The mean difference in the gastric emptying time before and after H. pylori eradication was 23.9+/-13.2 min (P= 0.556). There was no significant difference in the frequency of specific dyspeptic symptoms as well as the overall mean symptom score between the H. pylori-positive and -negative patients. Gastric emptying was not different between patients with functional dyspepsia and normal controls. Helicobacter pylori infection does not appear to affect gastric emptying in patients with functional dyspepsia.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/complications*; Helicobacter Infections/drug therapy; Helicobacter Infections/physiopathology*
  15. Capsaicin and gastric ulcers
    Satyanarayana MN
    Crit Rev Food Sci Nutr, 2006;46(4):275-328.
    PMID: 16621751
    In recent years, infection of the stomach with the organism Helicobacter Pylori has been found to be the main cause of gastric ulcers, one of the common ailments afflicting humans. Excessive acid secretion in the stomach, reduction in gastric mucosal blood flow, constant intake of non-steroid anti-inflammatory drugs (NSAIDS), ethanol, smoking, stress etc. are also considered responsible for ulcer formation. The prevalent notion among sections of population in this country and perhaps in others is that "red pepper" popularly known as "Chilli," a common spice consumed in excessive amounts leads to "gastric ulcers" in view of its irritant and likely acid secreting nature. Persons with ulcers are advised either to limit or avoid its use. However, investigations carried out in recent years have revealed that chilli or its active principle "capsaicin" is not the cause for ulcer formation but a "benefactor." Capsaicin does not stimulate but inhibits acid secretion, stimulates alkali, mucus secretions and particularly gastric mucosal blood flow which help in prevention and healing of ulcers. Capsaicin acts by stimulating afferent neurons in the stomach and signals for protection against injury causing agents. Epidemiologic surveys in Singapore have shown that gastric ulcers are three times more common in the "Chinese" than among Malaysians and Indians who are in the habit of consuming more chillis. Ulcers are common among people who are in the habit of taking NSAIDS and are infected with the organism "Helicobacter Pylori," responsible for excessive acid secretion and erosion of the mucosal layer. Eradication of the bacteria by antibiotic treatment and avoiding the NSAIDS eliminates ulcers and restores normal acid secretion.
    Matched MeSH terms: Helicobacter pylori/isolation & purification; Helicobacter Infections/complications; Helicobacter Infections/microbiology; Helicobacter Infections/epidemiology
  16. Fulltext Biofilm Formation and Antibiotic Resistance Phenotype of Helicobacter pylori Clinical Isolates
    Fauzia KA, Miftahussurur M, Syam AF, Waskito LA, Doohan D, Rezkitha YAA, et al.
    Toxins (Basel), 2020 07 24;12(8).
    PMID: 32722296 DOI: 10.3390/toxins12080473
    We evaluated biofilm formation of clinical Helicobacter pylori isolates from Indonesia and its relation to antibiotic resistance. We determined the minimum inhibition concentration (MIC) of amoxicillin, clarithromycin, levofloxacin, metronidazole and tetracycline by the Etest to measure the planktonic susceptibility of 101 H. pylori strains. Biofilms were quantified by the crystal violet method. The minimum biofilm eradication concentration (MBEC) was obtained by measuring the survival of bacteria in a biofilm after exposure to antibiotics. The majority of the strains formed a biofilm (93.1% (94/101)), including weak (75.5%) and strong (24.5%) biofilm-formers. Planktonic resistant and sensitive strains produced relatively equal amounts of biofilms. The resistance proportion, shown by the MBEC measurement, was higher in the strong biofilm group for all antibiotics compared to the weak biofilm group, especially for clarithromycin (p = 0.002). Several cases showed sensitivity by the MIC measurement, but resistance according to the MBEC measurements (amoxicillin, 47.6%; tetracycline, 57.1%; clarithromycin, 19.0%; levofloxacin, 38.1%; and metronidazole 38.1%). Thus, biofilm formation may increase the survival of H. pylori and its resistance to antibiotics. Biofilm-related antibiotic resistance should be evaluated with antibiotic susceptibility.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter pylori/isolation & purification; Helicobacter pylori/physiology; Helicobacter Infections/microbiology
  17. 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 pylori/drug effects*; Helicobacter pylori/isolation & purification; Helicobacter Infections/drug therapy*; Helicobacter Infections/microbiology*
  18. Polymorphisms in the host CYP2C19 gene and antibiotic-resistance attributes of Helicobacter pylori isolates influence the outcome of triple therapy
    Ram M R, Teh X, Rajakumar T, Goh KL, Leow AHR, Poh BH, et al.
    J Antimicrob Chemother, 2019 01 01;74(1):11-16.
    PMID: 30403784 DOI: 10.1093/jac/dky401
    Objectives: Eradication of Helicobacter pylori is influenced by susceptibility to antimicrobial agents, elevated bacterial load and degree of acid inhibition, which can be affected by genotypes of drug-metabolizing enzymes [cytochrome P450 (CYP) 2C19 polymorphism]. Theoretically, the choice and dose of proton pump inhibitor may also influence the suppression of H. pylori infection. The CYP2C19 genotype has recently been found to have an impact on peptic ulcer healing, H. pylori eradication and therapeutic efficacy of proton pump inhibitors.

    Methods: Here, we investigated the impact of the CYP2C19 genotype polymorphism and the success of triple therapy (fluoroquinolones/metronidazole/clarithromycin) on antibiotic-resistant strains in eradicating H. pylori in human subjects with non-ulcer dyspepsia (NUD), in human subjects with peptic ulcer disease (PUD) and in asymptomatic human subjects (positive and negative for H. pylori infection).

    Results: Based on the CYP2C19 genotypes, determined by Droplet Digital PCR (ddPCR) analysis, we found 11.2%, 62.5% and 26.3% corresponding to rapid metabolizers, intermediate metabolizers and poor metabolizers, respectively. However, we did not find any significant effect for homozygous ABCB1 or CYP2C19*2 and CYP2C19*3 alleles. We detected several participants heterozygous for both ABCB1 and CYP2C19*2, CYP2C19*3 and CYP2C19*17 loci. The participants heterozygous for both ABCB1 and CYP2C19*2 and *3 loci should be defined as intermediate and poor metabolizers according to the haplotype analysis in the NUD, PUD and asymptomatic subjects.

    Conclusions: Consequently, fluoroquinolones/metronidazole/clarithromycin-based triple therapies can be used to eradicate H. pylori infection, if one does not know the CYP2C19 genotype of the patient.

    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter Infections/drug therapy*; Helicobacter Infections/genetics; Helicobacter Infections/microbiology
  19. Prevalence and predictors of Helicobacter pylori infection in children and adults from the Penan ethnic minority of Malaysian Borneo
    Huang SS, Hassan AK, Choo KE, Ibrahim MI, Davis TM
    Am J Trop Med Hyg, 2004 Oct;71(4):444-50.
    PMID: 15516641
    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.
    Matched MeSH terms: Helicobacter pylori/isolation & purification*; Helicobacter Infections/ethnology*; Helicobacter Infections/microbiology; Helicobacter Infections/epidemiology*
  20. Fulltext Commentary: rabeprazole improves symptoms in patients with functional dyspepsia in Japan
    Yap PR, Mahadeva S, Goh KL
    Aliment Pharmacol Ther, 2013 Nov;38(10):1321-2.
    PMID: 24134501 DOI: 10.1111/apt.12497
    Matched MeSH terms: Helicobacter Infections/drug therapy*
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