Displaying publications 141 - 160 of 242 in total

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  1. Uyub AM, Anuar AK
    PMID: 11485102
    A study was carried out on 49 H. pylori-positive and 11 H. pylori-negative patients to determine the reactivity of peripheral blood lymphocytes (PBL) to phytohemagglutinin (PHA) and acid glycine extract (AGE) of H. pylori, and to identify cells responsible for imunosuppression. Based on response to PHA stimulation, cell-mediated immunity of all patients were competent. In some patients, however, response to AGE of H. pylori was suppressed by plastic adherent cells. This study provided evidence of the presence of plastic adherent suppressor cells which suppressed PBL response to AGE of H. pylori but not to PHA suggesting that immunosuppression is antigen specific. There is also an indication that immunosuppression may be species-specific as PBL devoid of plastic adherent cells only responded to stimulation by AGE of H. pylori but not that to AGE of C. jejuni.
    Matched MeSH terms: Helicobacter pylori/immunology; Helicobacter pylori/isolation & purification; Helicobacter pylori/physiology*
  2. Rahim AA, Lee YY, Majid NA, Choo KE, Raj SM, Derakhshan MH, et al.
    Am J Trop Med Hyg, 2010 Nov;83(5):1119-22.
    PMID: 21036849 DOI: 10.4269/ajtmh.2010.10-0226
    Whether the exceptionally low prevalence of Helicobacter pylori (HP) infection reported among Malays is also present among aborigines (the Orang Asli) living in northeastern Peninsular Malaysia is unknown. We studied asymptomatic Orang Asli from settlements situated 210 km from the city of Kota Bharu. The HP infection status was confirmed by a validated serology test. Nineteen percent of 480 Orang Asli tested positive for HP infection. The prevalence was 40.6% in the birth cohort of the 1940s and declined steadily in later cohorts to under 10% among 12-30 year olds. This may be related to the phases of relocation from the jungles into resettlement camps and ultimately into designated villages near rivers. The low prevalence pattern after the 1970s was probably partly a result of improvement in sanitation and hygiene practice in these villages but other unidentified factors may also be operating.
    Matched MeSH terms: Helicobacter pylori/isolation & purification*; Helicobacter Infections/epidemiology*
  3. Lee YY, Ismail AW, Mustaffa N, Musa KI, Majid NA, Choo KE, et al.
    Helicobacter, 2012 Feb;17(1):54-61.
    PMID: 22221617 DOI: 10.1111/j.1523-5378.2011.00917.x
    The prevalence of Helicobacter pylori infection is exceptionally low among the Malays in the north-eastern region of Peninsular Malaysia. The reasons are unknown. Our aim was to compare environmental factors that differed in relation to H. pylori prevalence among Malays born and residing in Kelantan.
    Matched MeSH terms: Helicobacter pylori; Helicobacter Infections/epidemiology*
  4. Sasidharan S, Uyub AM, Azlan AA
    Trans R Soc Trop Med Hyg, 2008 Dec;102(12):1226-32.
    PMID: 18586289 DOI: 10.1016/j.trstmh.2008.05.006
    HeIicobacter pylori infection rate was determined in 697 consecutive patients with ulcer, gastritis, duodenitis and non-ulcer dyspepsia by endoscopy at a Malaysian hospital in 1999-2002. Biopsies of the gastric antrum and body were subjected to the urease test, Gram staining of impression smears and culture examination. Infection was defined as a positive result in at least one test. The infection rates were 32.1, 10.4, 20.0 and 16.2% in ulcer, gastritis, duodenitis and non-ulcer dyspepsia patients, respectively. Overall, the prevalence of H. pylori infection was 14.6%, with the rate among the Indian (21.7%), Chinese (19.2%) and Bangladeshi foreign worker (23.1%) groups significantly higher (P<0.05) than that of the Malays (5.8%). Generally, the prevalence rate among males (18.9%) was significantly higher (P<0.001) than that among females (9.0%), but for a particular ethnic group, such trend and significant differences (P<0.05) were observed only among the Malays. In terms of gender, the prevalence rates of Malay males and females were also significantly lower (P<0.05) than those of Chinese and Indians. In conclusion, there is a significant difference in H. pylori infection prevalence rates among ethnic groups (highest in Indians, then Chinese and unusually low in Malays) and gender groups (highest in males) in Malaysia.
    Matched MeSH terms: Helicobacter Infections/ethnology; Helicobacter Infections/epidemiology*
  5. Boey CC, Goh KL
    Dig Liver Dis, 2001 4 17;33(1):83-4.
    PMID: 11303982
    Matched MeSH terms: Helicobacter pylori; Helicobacter Infections/diagnosis
  6. Chua EG, Wise MJ, Khosravi Y, Seow SW, Amoyo AA, Pettersson S, et al.
    DNA Res, 2017 Feb 01;24(1):37-49.
    PMID: 27803027 DOI: 10.1093/dnares/dsw046
    Helicobacter pylori is a highly successful gastric pathogen. High genomic plasticity allows its adaptation to changing host environments. Complete genomes of H. pylori clinical isolate UM032 and its mice-adapted serial derivatives 298 and 299, generated using both PacBio RS and Illumina MiSeq sequencing technologies, were compared to identify novel elements responsible for host-adaptation. The acquisition of a jhp0562-like allele, which encodes for a galactosyltransferase, was identified in the mice-adapted strains. Our analysis implies a new β-1,4-galactosyltransferase role for this enzyme, essential for Ley antigen expression. Intragenomic recombination between babA and babB genes was also observed. Further, we expanded on the list of candidate genes whose expression patterns have been mediated by upstream homopolymer-length alterations to facilitate host adaption. Importantly, greater than four-fold reduction of mRNA levels was demonstrated in five genes. Among the down-regulated genes, three encode for outer membrane proteins, including BabA, BabB and HopD. As expected, a substantial reduction in BabA protein abundance was detected in mice-adapted strains 298 and 299 via Western analysis. Our results suggest that the expression of Ley antigen and reduced outer membrane protein expressions may facilitate H. pylori colonisation of mouse gastric epithelium.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/physiology
  7. Amjad N, Osman HA, Razak NA, Kassian J, Din J, bin Abdullah N
    World J Gastroenterol, 2010 Sep 21;16(35):4443-7.
    PMID: 20845512
    AIM: To study the presence of Helicobacter pylori (H. pylori) virulence factors and clinical outcome in H. pylori infected patients.

    METHODS: A prospective analysis of ninety nine H. pylori-positive patients who underwent endoscopy in our Endoscopy suite were included in this study. DNA was isolated from antral biopsy samples and the presence of cagA, iceA, and iceA2 genotypes were determined by polymerase chain reaction and a reverse hybridization technique. Screening for H. pylori infection was performed in all patients using the rapid urease test (CLO-Test).

    RESULTS: From a total of 326 patients who underwent endoscopy for upper gastrointestinal symptoms, 99 patients were determined to be H. pylori-positive. Peptic ulceration was seen in 33 patients (33%). The main virulence strain observed in this cohort was the cagA gene isolated in 43 patients. cagA was associated with peptic ulcer pathology in 39.5% (17/43) and in 28% (16/56) of non-ulcer patients. IceA1 was present in 29 patients (29%) and iceA2 in 15 patients (15%). Ulcer pathology was seen in 39% (11/29) of patients with iceA1, while 31% (22/70) had normal findings. The corresponding values for iceA2 were 33% (5/15) and 33% (28/84), respectively.

    CONCLUSION: Virulence factors were not common in our cohort. The incidence of factors cagA, iceA1 and iceA2 were very low although variations were noted in different ethnic groups.

    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/pathogenicity
  8. Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ
    Lancet, 2020 11 21;396(10263):1689-1702.
    PMID: 33049222 DOI: 10.1016/S0140-6736(20)30469-4
    Dyspepsia is a complex of symptoms referable to the gastroduodenal region of the gastrointestinal tract and includes epigastric pain or burning, postprandial fullness, or early satiety. Approximately 80% of individuals with dyspepsia have no structural explanation for their symptoms and have functional dyspepsia. Functional dyspepsia affects up to 16% of otherwise healthy individuals in the general population. Risk factors include psychological comorbidity, acute gastroenteritis, female sex, smoking, use of non-steroidal anti-inflammatory drugs, and Helicobacter pylori infection. The pathophysiology remains incompletely understood, but it is probably related to disordered communication between the gut and the brain, leading to motility disturbances, visceral hypersensitivity, and alterations in gastrointestinal microbiota, mucosal and immune function, and CNS processing. Although technically a normal endoscopy is required to diagnose functional dyspepsia, the utility of endoscopy in all patients with typical symptoms is minimal; its use should be restricted to people aged 55 years and older, or to those with concerning features, such as weight loss or vomiting. As a result of our incomplete understanding of its pathophysiology, functional dyspepsia is difficult to treat and, in most patients, the condition is chronic and the natural history is one of fluctuating symptoms. Eradication therapy should be offered to patients with functional dyspepsia who test positive for Helicobacter pylori. Other therapies with evidence of effectiveness include proton pump inhibitors, histamine-2 receptor antagonists, prokinetics, and central neuromodulators. The role of psychological therapies is uncertain. As our understanding of the pathophysiology of functional dyspepsia increases, it is probable that the next decade will see the emergence of truly disease-modifying therapies for the first time.
    Matched MeSH terms: Helicobacter pylori/isolation & purification; Helicobacter Infections
  9. Wong EHJ, Ng CG, Goh KL, Vadivelu J, Ho B, Loke MF
    Sci Rep, 2018 01 23;8(1):1409.
    PMID: 29362474 DOI: 10.1038/s41598-018-19697-0
    The biofilm-forming-capability of Helicobacter pylori has been suggested to be among factors influencing treatment outcome. However, H. pylori exhibit strain-to-strain differences in biofilm-forming-capability. Metabolomics enables the inference of spatial and temporal changes of metabolic activities during biofilm formation. Our study seeks to examine the differences in metabolome of low and high biofilm-formers using the metabolomic approach. Eight H. pylori clinical strains with different biofilm-forming-capability were chosen for metabolomic analysis. Bacterial metabolites were extracted using Bligh and Dyer method and analyzed by Liquid Chromatography/Quadrupole Time-of-Flight mass spectrometry. The data was processed and analyzed using the MassHunter Qualitative Analysis and the Mass Profiler Professional programs. Based on global metabolomic profiles, low and high biofilm-formers presented as two distinctly different groups. Interestingly, low-biofilm-formers produced more metabolites than high-biofilm-formers. Further analysis was performed to identify metabolites that differed significantly (p-value 
    Matched MeSH terms: Helicobacter pylori/metabolism; Helicobacter pylori/physiology*
  10. Ansari S, Yamaoka Y
    Toxins (Basel), 2019 Nov 19;11(11).
    PMID: 31752394 DOI: 10.3390/toxins11110677
    Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world's population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism.
    Matched MeSH terms: Helicobacter pylori/growth & development; Helicobacter pylori/pathogenicity*
  11. Khosravi Y, Seow SW, Amoyo AA, Chiow KH, Tan TL, Wong WY, et al.
    Sci Rep, 2015;5:8731.
    PMID: 25736205 DOI: 10.1038/srep08731
    Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.
    Matched MeSH terms: Helicobacter pylori/physiology; Helicobacter Infections/metabolism*; Helicobacter Infections/microbiology
  12. Osman HA, Hasan H, Suppian R, Bahar N, Hussin NS, Rahim AA, et al.
    Asian Pac J Cancer Prev, 2014;15(13):5245-7.
    PMID: 25040982
    BACKGROUND: Helicobacter pylori (H. pylori) is one of the most important causes of dyspepsia and gastric cancer and diagnosis can be made by invasive or non-invasive methods. The Atlas Helicobacter pylori antigen test is a new rapid non-invasive method which is simple to conduct. The aim of this study was to determine its sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy.

    MATERIALS AND METHODS: This prospective study was conducted between July 2012 and December 2013. Stool samples of 59 dyspeptic patients who underwent upper endoscopy were evaluated for H. pylori stool antigen.

    RESULTS: From the 59 patients who participated in this study, there were 36 (61%) males and 23 (39%) females. H. pylori was diagnosed in 24 (40.7%) gastric biopsies, 22 (91.7 %) of these being positive for the Atlas H. pylori antigen test. The sensitivity, specificity, PPV, NPV and accuracy were 91.7%, 100%, 100%, 94.6% and 96.6% respectively.

    CONCLUSIONS: The Atlas H. pylori antigen test is a new non-invasive method which is simple to perform and avails reliable results in a few minutes. Thus it can be the best option for the diagnosis of H. pylori infection due to its high sensitivity and specificity.

    Matched MeSH terms: Helicobacter pylori/immunology*; Helicobacter Infections/diagnosis*; Helicobacter Infections/immunology*
  13. Maran S, Lee YY, Xu SH, Raj MS, Abdul Majid N, Choo KE, et al.
    J Dig Dis, 2013 Apr;14(4):196-202.
    PMID: 23241512 DOI: 10.1111/1751-2980.12023
    To identify gene polymorphisms that differ between Malays, Han Chinese and South Indians, and to identify candidate genes for the investigation of their role in protecting Malays from Helicobacter pylori (H. pylori) infection.
    Matched MeSH terms: Helicobacter pylori/isolation & purification*; Helicobacter Infections/ethnology*; Helicobacter Infections/genetics*
  14. Yap PR, Goh KL
    Curr Pharm Des, 2015;21(35):5073-81.
    PMID: 26369685
    Non-steroidal anti-inflammatory drugs (NSAIDs) are the most prescribed group of drugs in the world. They are used primarily for pain relief in chronic inflammatory joint disease and act by inhibiting enzymes COX1 and COX2 and ultimately preventing the production of active prostanoids which are required for the innate inflammatory pathway. The use of NSAIDs have been associated with the development of gastrointestinal (GI) symptoms ranging from simple dyspepsia to life threatening GI bleeds and perforations. The definition of dyspepsia has evolved over the years and this has hampered accurate studies on the prevalence of dyspepsia as different studies used varying criteria to define dyspepsia. It is now known that NSAIDs significantly increase the risk of dyspepsia.The risk of developing peptic ulcer disease vary with specific NSAIDs and dosages but there is no correlation between the symptoms of dyspepsia and underlying peptic ulcers. The pathogenesis of dyspepsia with NSAIDs is not completely understood. Peptic ulceration alone is not able to account for the majority of dyspepsia symptoms encountered by NSAIDs users. Erosive oesophagitis secondary to NSAIDs may be contributing factor to the prevalence of dyspepsia in NSAIDs users. Altered gut permeability and changes in gastric mechanosensory function due to NSAIDs may also be a contributory factor. Management of NSAID induced dyspepsia is involves a multipronged approach. Drug avoidance if possible would be ideal. Other options include using the lowest effective dose, changing to an NSAIDs with a safer GI risk profile, avoiding concurrent use with other NSAIDs or if the patient has a previous history of peptic ulcer disease, and co-prescribing with anti-secretory medications such as proton pump inhibitors. Eradication of Helicobacter pylori has a protective role against developing peptic ulcers and may also improve symptoms of NSAIDs induced dyspepsia.
    Matched MeSH terms: Helicobacter pylori/isolation & purification; Helicobacter Infections/complications; Helicobacter Infections/drug therapy
  15. Loke MF, Ng CG, Vilashni Y, Lim J, Ho B
    Sci Rep, 2016 05 25;6:26784.
    PMID: 27222005 DOI: 10.1038/srep26784
    Helicobacter pylori may reside in the human stomach as two morphological forms: the culturable spiral form and the viable but non-culturable (VBNC) coccoid form. This bacterium transforms from spiral to coccoid under in vitro suboptimal conditions. However, both spiral and coccoid have demonstrated its infectivity in laboratory animals, suggesting that coccoid may potentially be involved in the transmission of H. pylori. To determine the relevance of the coccoid form in viability and infectivity, we compared the protein profiles of H. pylori coccoids obtained from prolonged (3-month-old) culture with that of 3-day-old spirals of two H. pylori standard strains using SWATH (Sequential Window Acquisition of all Theoretical mass spectra)-based approach. The protein profiles reveal that the coccoids retained basal level of metabolic proteins and also high level of proteins that participate in DNA replication, cell division and biosynthesis demonstrating that coccoids are viable. Most interestingly, these data also indicate that the H. pylori coccoids possess higher level of proteins that are involved in virulence and carcinogenesis than their spiral counterparts. Taken together, these findings have important implications in the understanding on the pathogenesis of H. pylori-induced gastroduodenal diseases, as well as the probable transmission mode of this bacterium.
    Matched MeSH terms: Helicobacter pylori/drug effects; Helicobacter pylori/genetics; Helicobacter pylori/physiology*; Helicobacter pylori/ultrastructure
  16. Kaushik SP, Vu C
    Aust N Z J Med, 2000 Apr;30(2):231-5.
    PMID: 10833116
    BACKGROUND: From European and North American data, it is recommended in the Asia Pacific consensus statement, that one week therapy with a proton pump inhibitor, amoxycillin and clarithromycin be used for Helicobacter pylori eradication, in areas of high metronidazole resistance. The efficacy of this regimen is unknown in Singapore.

    AIM: To assess the efficacy, safety and compliance of an H. pylori eradication regimen and examine clinical factors that potentially determine eradication.

    METHODS: Consecutive outpatients from a multicultural, south east Asian, population with H. pylori infection, with or without peptic ulcer, were treated with lansoprazole 30 mg, amoxycillin 1 gm, clarithromycin 500 mg, twice a day for seven days. Eradication was assessed by either rapid urease, histology or urea breath test. Compliance and side effects were recorded. The eradication rate and effect of ethnicity, age, sex, usage of alcohol, smoking and non-steroidal anti-inflammatory drugs, history of ulcer and endoscopic diagnosis on eradication were examined by univariate and multivariate analysis.

    RESULTS: Of 113 patients, the eradication rate by intention to treat was 98/113 (87%) (95% confidence interval [CI] 80-93%) and per protocol was 98/106 (92%) (95% CI 87-97%). Using Fisher's exact test, eradication was more successful in Chinese (intention to treat and per protocol respectively p=0.02 and p<0.001) compared to non-Chinese. By logistic regression analysis ethnicity was an independent factor associated with eradication success (p=0.0025). Side effects occurred in five (4.4%), resulting in cessation of treatment.

    CONCLUSIONS: This one week eradication regimen is safe and effective in south east Asians. Chinese ethnicity may be associated with a higher likelihood of eradication success.

    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/drug therapy*; Helicobacter Infections/ethnology
  17. 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 pylori/pathogenicity*; Helicobacter Infections/genetics*; Helicobacter Infections/microbiology
  18. Goh KL, Peh SC, Parasakthi N, Wong NW, Tan KK, Lo YL
    Am J Gastroenterol, 1994 Oct;89(10):1789-92.
    PMID: 7942668
    OBJECTIVES: Our objectives were to determine the effect of dual therapy with omeprazole and amoxicillin and of triple therapy with omeprazole, amoxicillin, and metronidazole in the eradication of Helicobacter pylori (HP) and to study the long-term results of eradication in these patients.
    METHODS: A prospective, randomized, controlled trial was performed. Patients who were recruited had unequivocal evidence of HP infection based on culture, histology, rapid urease test, and Gram's stain of a tissue smear. Eradication was defined as the absence of bacteria in all tests performed on both corpus and antral biopsies.
    RESULTS: The infection was eradicated in 15 of 19 (78.9%) patients randomized to receive dual therapy and in 19 of 22 (86.4%) patients who received triple therapy. We followed the course of 30 patients in whom HP had been eradicated for a prolonged term (up to 12 months). All remained clear of HP. Twenty-five of 28 patients (89.3%) with duodenal ulcers in whom HP was successfully eradicated remained healed at 12 months. Fewer side effects were reported among patients who received the dual therapy.
    CONCLUSIONS: Combination therapy with omeprazole and amoxicillin with or without metronidazole is effective in the eradication of HP. In particular, the dual therapy regimen with amoxicillin is not only effective but is also well tolerated by patients.
    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/complications; Helicobacter Infections/drug therapy*
  19. Goh KL, Navaratnam P, Peh SC
    Eur J Gastroenterol Hepatol, 1996 Dec;8(12):1157-60.
    PMID: 8980932
    OBJECTIVES: To determine the reinfection rate of Helicobacter pylori and duodenal ulcer relapse rate in a group of patients followed up long term.

    DESIGN: Prospective study.

    PATIENTS AND METHODS: Patients were followed up endoscopically at 3, 6, 12 and 24 months after successful H. pylori eradication and duodenal ulcer healing. H. pylori status was determined by culture, rapid urease test, Gram's stain of a fresh tissue smear and histological examination of antral biopsies and rapid urease test and histological examination of corpus biopsies.

    MAIN OUTCOME MEASURES: Duodenal ulcer healing, H. pylori reinfection.

    RESULTS: Thirty-eight patients with duodenal ulcer disease (35 active, 3 healed) had successfully eradicated H. pylori following treatment with omeprazole/amoxycillin (n = 11), omeprazole/amoxycillin/metronidazole (n = 16) and colloidal bismuth subcitrate/ amoxycillin/metronidazole (n = 11). All patients with active duodenal ulcer had healed ulcers at the end of therapy. Thirty-five of 38 patients were seen according to schedule up to 2 years; two patients were seen up to 12 months and one up to 6 months only. Reinfection with H. pylori was not recorded in any of our patients. Shallow duodenal ulcers were noted in three patients at 1-year follow-up, two of whom admitted to taking non-steroidal anti-inflammatory drugs (NSAIDs); H. pylori status was negative in all three. Subsequent follow-up revealed spontaneous healing of the ulcers in all three patients. At 2 years, one patient whose H. pylori status was negative had recurrence of duodenal ulcer. All of the three patients who defaulted subsequent to follow-up were negative for H. pylori and had healed ulcers on follow-up endoscopy at 6 and 12 months.

    CONCLUSION: Reinfection rate with H. pylori was zero in a group of South-East Asian patients who had successfully eradicated the infection. Duodenal ulcer relapse was also low (2.9%) in this group of patients at 2 years.

    Matched MeSH terms: Helicobacter pylori*; Helicobacter Infections/drug therapy; Helicobacter Infections/epidemiology*
  20. 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 pylori/drug effects; Helicobacter Infections/drug therapy*; Helicobacter Infections/microbiology
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