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Journal articles on the topic 'Helicobacter pylori'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Haesebrouck, Freddy, Frank Pasmans, Bram Flahou, Koen Chiers, Margo Baele, Tom Meyns, Annemie Decostere, and Richard Ducatelle. "Gastric Helicobacters in Domestic Animals and Nonhuman Primates and Their Significance for Human Health." Clinical Microbiology Reviews 22, no. 2 (April 2009): 202–23. http://dx.doi.org/10.1128/cmr.00041-08.

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SUMMARY Helicobacters other than Helicobacter pylori have been associated with gastritis, gastric ulcers, and gastric mucosa-associated lymphoid tissue lymphoma in humans. These very fastidious microorganisms with a typical large spiral-shaped morphology were provisionally designated “H. heilmannii,” but in fact they comprise at least five different Helicobacter species, all of which are known to colonize the gastric mucosa of animals. H. suis, which has been isolated from the stomachs of pigs, is the most prevalent gastric non-H. pylori Helicobacter species in humans. Other gastric non-H. pylori helicobacters colonizing the human stomach are H. felis, H. salomonis, H. bizzozeronii, and the still-uncultivable “Candidatus Helicobacter heilmannii.” These microorganisms are often detected in the stomachs of dogs and cats. “Candidatus Helicobacter bovis” is highly prevalent in the abomasums of cattle but has only occasionally been detected in the stomachs of humans. There are clear indications that gastric non-H. pylori Helicobacter infections in humans originate from animals, and it is likely that transmission to humans occurs through direct contact. Little is known about the virulence factors of these microorganisms. The recent successes with in vitro isolation of non-H. pylori helicobacters from domestic animals open new perspectives for studying these microorganisms and their interactions with the host.

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2

Lecoindre, P., M. Chevallier, S. Peyrol, M. Boude, R. L. Ferrero, and A. Labigne. "Gastric Helicobacters in Cats." Journal of Feline Medicine and Surgery 2, no. 1 (March 2000): 19–27. http://dx.doi.org/10.1053/jfms.2000.0063.

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The types of helicobacter which are found in the stomachs of carnivorous pets, especially cats, have been traditionally referred to as ‘gastric helicobacter-like organisms’ (GHLOs). These are microaerophilic, Gram-negative, spiral bacteria with multiple terminal flagellae and are endowed with high-level urease activity which allows them to survive in an acidic environment. Certain species have one or more periplasmic fibrils. The two GHLOs most commonly found in cats are Helicobacter felis and a species related to H heilmannii which was recently cultured from dogs. All phenotypic and genotypic (16S RNA gene sequences) evidence suggests that both of these bacteria belong in the genus Helicobacter. Whether or not helicobacters can be transmitted to humans from carnivorous pets is controversial but the recent discovery of H pylori-infected cats may be evidence of an animal reservoir for this pathogen. Although the role of H pylori in inducing antral gastritis and perpetuating pyloric ulcers in humans is well established, whether or not Helicobacter spp are causally involved in any feline gastric inflammatory conditions is unknown.

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3

Chiba, N., A. Matisko, P. Sinclair, and ABR Thomson. "Helicobacter pylori: From Bench to Bedside." Canadian Journal of Gastroenterology 11, no. 7 (1997): 589–96. http://dx.doi.org/10.1155/1997/975469.

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With the exponential increase in research in the field ofHelicobacter pyloria paradigm shift has occurred. It is now recognized thatH pyloriis a chronic infection of the stomach causing inflammation. Some patients remain asymptomatic, while others may develop dyspepsia, duodenal or gastric ulcer, gastric cancer or a mucosa-associated lymphoid tissue lymphoma. However, the role ofH pyloriin contributing to nonulcer dyspepsia or nonsteroidal anti-inflammatory drug gastropathy remains controversial. An effective vaccine againstH pyloriis years away. Major interest has focused on the questions "who should be investigated and therefore treated" and "what is the latest gold standard for eradication ofH pylori"? In Europe, guidelines have been developed to help the practitioner answer these important questions. Canadian guidelines will soon be available. For persons with known peptic ulcer disease there should be unequivocal acceptance that the good clinical practice of eradicatingH pyloriwill result in substantial savings in health care expenses. The original 'classical triple therapy' (bismuth, metronidazole and tetracycline [BMT]) has now been surpassed by the combination of a proton pump inhibitor (PPI) plus two antibiotics (metronidazole plus clarithromycin; amoxicillin plus clarithromycin; or amoxicillin plus metronidazole), each given twice a day for one week. In Canada, the regimen of omeprazole plus one antibiotic (amoxicillin or clarithromycin) was approved recently but gives an eradication rate that is lower than the current target of 90%. According to the European (Mäastricht) recommendations, if a single treatment attempt with PPI plus two antibiotics fails, PPI plus BMT is recommended.

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4

Jurnalis, Yusri Dianne, Yorva Sayoet, and Sari Dewi. "HELICOBACTER PYLORI INFECTION IN CHILDREN." Majalah Kedokteran Andalas 35, no. 1 (May 1, 2011): 43. http://dx.doi.org/10.22338/mka.v35.i1.p43-49.2011.

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AbstrakFaktor risiko infeksi Helicobacter pylori adalah tinggal di negara berkembang, kondisi sosial ekonomi yang rendah, jumlah anggota keluarga yang banyak, etnik dan genetik. Tatalaksana dan diagnosis Helicobacter pylori belum memuaskan karena adanya resistensi antibiotik pada pasien Helicobacter pylori. Kami melaporkan seorang pasien perempuan usia 8 tahun 6 bulan yang terinfeksi Helicobacter pylori. Diagnosis ditegakkan berdasarkan anamnesis, pemeriksaan fisik, dan hasil laboratorium. Pasien diduga terinfeksi Helicobacter pylori karena mengalami nyeri perut berulang. Dari laboratorium didapatkan serologi IgG Helicobacter pylori positif. Pada hasil endoskopi biopsi ditemukan kuman Helicobacter pylori. Pasien mendapat therapi eradikasi lini pertama untuk infeksi Helicobacter pylori yaitu amoksisilin, klaritromisin dan omeprazol selama dua minggu. Setelah dua minggu pengobatan keluhan pasien tidak ada.Kata kunci: Helicobacter pylori, anak, nyeri perut berulangAbstractRisk factors for acquiring Helicobacter pylori infection include residency of developing country, poor socioeconomic conditions, crowded family, and possibly an ethnic or genetic as predispositions. The diagnosis and management Helicobacter pylori has not been satisfied yet, however, there is problem of increasing resistancy antibiotic due to Helicobacter pylori. Objective: We report a 8 year and 6 month old girl who suffered from Helicobacter pylori. The diagnosis was based on history, clinical finding, and laboratory work-up. Suspicion on the presence of Helicobacter pylori was started when the girl had recurrent abdominal pain. Serology IgG Helicobacter pylori was positive and we had done endoscopic examination and biopsy. Therapy this patient was first line eradication Helicobacter pylori which give amoxicillin, clarithromycin and omeprazole for two weeks. There are no sympthoms after two weeks therapyKey word: Helicobacter pylori, children, recurrent abdominal painLAPORAN KASUS

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5

Garcés-Duran, R., S. Kindt, K. Kotilea, S. François, G. Rasschaert, A. Smet, B. Hauser, et al. "Belgian consensus for Helicobacter pylori management 2023." Acta Gastro Enterologica Belgica 86, no. 1 (March 2023): 74–91. http://dx.doi.org/10.51821/86.1.11327.

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Helicobacter pylori (H. pylori) infection causes chronic gastritis, peptic ulcers and gastric cancer. Although H. pylori prevalence is decreasing worldwide, regional variations exist in Europe, with the lowest infection prevalence in Northern Europe, and the highest in Eastern and Southern Europe (1). Changes in the treatment recommendations and the increasing available evidence have justified the implementation of new recommendations since last Belgian consensus in 1998 (2). Several non-H. pylori Helicobacter species (NH.PYLORI-H), colonizing the stomach of domestic animals, also have the ability to cause gastric disease in humans, although to a lesser extent. These zoonotic NH. PYLORIH are not the subject of the current recommendations.

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Della Bella, Chiara, Sofia D’Elios, Sara Coletta, Marisa Benagiano, Annalisa Azzurri, Fabio Cianchi, Marina de Bernard, and Mario Milco D’Elios. "Increased IL-17A Serum Levels and Gastric Th17 Cells in Helicobacter pylori-Infected Patients with Gastric Premalignant Lesions." Cancers 15, no. 6 (March 8, 2023): 1662. http://dx.doi.org/10.3390/cancers15061662.

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Background: Helicobacter pylori infection is characterized by an inflammatory infiltrate that might be an important antecedent of gastric cancer. The purpose of this study was to evaluate whether interleukin (IL)-17 inflammation is elicited by gastric T cells in Helicobacter pylori patients with gastric intestinal metaplasia and dysplasia (IM/DYS). We also investigated the serum IL-17A levels in Helicobacter pylori patients with gastric intestinal metaplasia and dysplasia, and patients with Helicobacter pylori non-atrophic gastritis (NAG). Methods: the IL-17 cytokine profile of gastric T cells was investigated in six patients with IM/DYS and Helicobacter pylori infection. Serum IL-17A levels were measured in 45 Helicobacter pylori-infected IM/DYS patients, 45 Helicobacter pylori-infected patients without IM/DYS and in 45 healthy controls (HC). Results: gastric T cells from all IM/DYS patients with Helicobacter pylori were able to proliferate in response to Helicobacter pylori and to produce IL-17A. The Luminex analysis revealed that IL-17A levels were significantly increased in Helicobacter pylori IM/DYS patients compared to healthy controls and to Helicobacter pylori gastritis patients without IM/DYS (452.34 ± 369.13 pg/mL, 246.82 ± 156.06 pg/mL, 169.26 ± 73.82 pg/mL, respectively; p < 0.01, p < 0.05). Conclusions: the results obtained indicate that Helicobacter pylori is able to drive gastric IL-17 inflammation in IM/DYS Helicobacter pylori-infected patients, and that IL-17A serum levels are significantly increased in Helicobacter pylori-infected patients with IM/DYS.

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7

KHADEMI, BIJAN, Negar Azar Pira, Mohammad Javad Ashraf, and Abdul Hameed Chohedri. "HELICOBACTER PYLORI IN NASAL POLYPOSIS." Professional Medical Journal 19, no. 04 (August 7, 2012): 455–61. http://dx.doi.org/10.29309/tpmj/2012.19.04.2256.

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Background: Nasal polyposis is an inflammatory condition of unknown etiology. Recently concern regarding GER orHelicobacter pylori as a possible pathologic cause of nasal polyps has been increasing. The present study was planned to investigate thepresence of Helicobacter Pylor in Nassal polyps by PCR , rapid Urease test and serology. Design: Case control study. Setting: ENT ward ofShiraz, Khalilli Hospital, Iran. Period: April 2006 to March 2008. Materials and Methods: 37 patients with nasal polyps who had undergonenasal endoscopic sinus surgery and 38 control subjects who had undergone septoplasty and turbinectomy. Biopsy specimens of nasal polypsand inferior turbinates were assessed by PCR and Rapid Urease test. Blood sample of both study and control subjects were evaluated for antiH.pylori Ig G by ELISA. HP status was regarded as positive, if 2 tests were positive. Results: Seropositivity was more common in the patientswith nasal polyps (72.97%) than in the control patients (31.57%) (P-value= 0.000) RUT was positive in 9 (24.3%) of 37 patients with nasalpolyps, but was not positive in control group (P-value= 0.001). only 3 of (8.1%) of 37 patients with nasal polyps were positive for both RUT andELISA (P-value =0.115). PCR was negative in all patients and controls. Conclusions: Polypoid tissue can be colonized by some other agentscontaining a urease enzyme other than Helicobacer Pylori. So, result of RUT can be false positive, and addition test may be performed. In theour study by using PCR , we were not able to confirm presence of Helicobacter pylori in the nasal polyps. However, further epidemiologic studiesusing different and specific diagnostic tests with control of documented GER is recommended.

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FAISAL, NABIHA, MUHAMMAD MANSOOR UL HAQ, HAFEEZULLAH SHAIKH, Pervez Ashraf, and Jamila H. Esmail. "HELICOBACTER PYLORI INFECTION;." Professional Medical Journal 19, no. 02 (February 22, 2012): 202–7. http://dx.doi.org/10.29309/tpmj/2012.19.02.2011.

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Objective: To determine the frequency of H. pylori infection in dyspeptic patients undergoing endoscopy at a tertiary care centerin Karachi. Data source: Patients undergoing endoscopy at Liaquat National Hospital, Karachi. Design of study: Cross sectional descriptivestudy. Setting: Department of Gastroenterology, Liaquat National Hospital, Karachi. Period: May 2008–October 2008. Material andmethods: All adult patients with symptoms of dyspepsia for more than 1 month duration were included. Patients with upper gastrointestinalbleed, anemia or weight loss were excluded. Upper gastrointestinal endoscopy was performed in all patients and biopsy specimens two eachfrom antrum and body and one from fundus were taken for histology. Results: A total of 123 dyspeptic patients were included in the study. 76(61.8%) patients were males and 47 (38.2%) were females. H pylori was detected in mucosa of 49 (39.8%) patients. The mean age of thepatients was 41.41 ± 13.15 Years (95%CI; 39.06 to 43.75). Rate of H.pylori infection was not found statistical significant with age, gender,duration of symptoms and BMI. Conclusions: The prevalence of H pylori infection in dyspeptic patients was lower than reported in previousstudies from other centers in Pakistan. Other environmental factors should be evaluated in every patient especially who is negative for H. pyloriin our setup.

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Ferrero, Richard L., Patrick Avé, Delphine Ndiaye, Jean-Christophe Bambou, Michel R. Huerre, Dana J. Philpott, and Sylvie Mémet. "NF-κB Activation during Acute Helicobacter pylori Infection in Mice." Infection and Immunity 76, no. 2 (December 10, 2007): 551–61. http://dx.doi.org/10.1128/iai.01107-07.

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ABSTRACT Nuclear factor κB (NF-κB) plays a key regulatory role in host cell responses to Helicobacter pylori infection in humans. Although mice are routinely used as a model to study H. pylori pathogenesis, the role of NF-κB in murine cell responses to helicobacters has not been studied in detail. We thus investigated the abilities of different Helicobacter isolates to induce NF-κB-dependent responses in murine gastric epithelial cells (GECs) and in transgenic mice harboring an NF-κB-responsive lacZ reporter gene. H. pylori and Helicobacter felis strains up-regulated the synthesis in mouse GECs of the NF-κB-dependent chemokines KC (CXCL1) and MIP-2 (CXCL2). These responses were cag pathogenicity island (cagPAI) independent and could be abolished by pretreatment with a pharmacological inhibitor of NF-κB. Consistent with the in vitro data, experimental Helicobacter infection of transgenic mice resulted in increased numbers of GECs with nuclear β-galactosidase activity, which is indicative of specific NF-κB activation. The numbers of β-galactosidase-positive cells in mice were significantly increased at day 1 postinoculation with wild-type H. pylori strains harboring or not harboring a functional cagPAI, compared to naive animals (P = 0.007 and P = 0.04, respectively). Strikingly, however, no differences were observed in the levels of gastric NF-κB activation at day 1 postinoculation with H. felis or at day 30 or 135 postinoculation with H. pylori. This work demonstrates for the first time the induction of NF-κB activation within gastric mucosal cells during acute H. pylori infection. Furthermore, the data suggest that helicobacters may be able to regulate NF-κB signaling during chronic infection.

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Dunn, B. E., H. Cohen, and M. J. Blaser. "Helicobacter pylori." Clinical Microbiology Reviews 10, no. 4 (October 1997): 720–41. http://dx.doi.org/10.1128/cmr.10.4.720.

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Helicobacter pylori is a gram-negative bacterium which causes chronic gastritis and plays important roles in peptic ulcer disease, gastric carcinoma, and gastric lymphoma. H. pylori has been found in the stomachs of humans in all parts of the world. In developing countries, 70 to 90% of the population carries H. pylori. In developed countries, the prevalence of infection is lower. There appears to be no substantial reservoir of H. pylori aside from the human stomach. Transmission can occur by iatrogenic, fecal-oral, and oral-oral routes. H. pylori is able to colonize and persist in a unique biological niche within the gastric lumen. All fresh isolates of H. pylori express significant urease activity, which appears essential to the survival and pathogenesis of the bacterium. A variety of tests to diagnose H. pylori infection are now available. Histological examination of gastric tissue, culture, rapid urease testing, DNA probes, and PCR analysis, when used to test gastric tissue, all require endoscopy. In contrast, breath tests, serology, gastric juice PCR, and urinary excretion of [15N]ammonia are noninvasive tests that do not require endoscopy. In this review, we highlight advances in the detection of the presence of the organism and methods of differentiating among types of H. pylori, and we provide a background for appropriate chemotherapy of the infection.

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Manyakina, O. M., I. S. Akkuratova-Maksimova, T. G. Pukhova, and A. S. Shitova. "Role of genetic structure of Helicobacter Pylori in formation of chronic inflammatory process in gastric mucosa." Perm Medical Journal 38, no. 1 (April 22, 2021): 87–99. http://dx.doi.org/10.17816/pmj38187-99.

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The literature review highlights the questions of the interaction of Helicobacter pylori and the human body. Modern data on the structure of the pathogenicity island in the Helicobacter pylori genome are presented. There is given a detailed description of both well-known virulence and pathogenicity factors of the infection (genes encoding the formation of urease subunits, in particular urel, cytotoxin associated gene A, vacuolating cytotoxin gen A, blood group associated binding adhesion, induced by contact with epithelium) and less studied ones (sialic acid-binding adhesion, adhesion-associated lipoprotein A and B, adhesin gene of Helicobacter pylori, Hp outer membrane protein). The significance of individual genes and proteins encoded by them in the development of chronic inflammatory process in diseases of the upper digestive tract, as well as in ulcer and carcinogenesis is analyzed. Mechanisms of interaction of bacteria with epithelial cells of the gastric mucosa, adhesive and cytotoxic effects of Helicobacter pylori, factors of biofilm formation are described. The influence of the genetic structure of Infect on cytological composition of the gastric glands in the form of reduction of specialized glandular cells chief and parietal cells of pyloric glands and the increase of endocrine cells in the pool is assessed. It is shown that colonization of the gastric mucosa by highly pathogenic strains of Helicobacter pylori contributes to the development of widespread pronounced and active inflammation in it, the appearance of morphological signs of atrophy. The role of the genetic characteristics of the infection in the failure of anti-helicobacter therapy is emphasized. Separately, the question of the effect of combined infection of the gastric mucosa with highly pathogenic strains of Helicobacter pylori and Epstein-Barr virus is highlighted.

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Chen, Jiaqin, Junning Zhang, Xiaolu Ma, Yuehan Ren, Yi Tang, Zhongmian Zhang, Wangyu Ye, et al. "Causal relationship between Helicobacter pylori antibodies and gastroesophageal reflux disease (GERD): A mendelian study." PLOS ONE 18, no. 12 (December 11, 2023): e0294771. http://dx.doi.org/10.1371/journal.pone.0294771.

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Background Observational studies have indicated that both Helicobacter pylori infection and the presence of Helicobacter pylori antibodies may increase the risk of gastroesophageal reflux disease (GERD). However, the exact association between Helicobacter pylori antibodies and the occurrence of GERD remains largely unresolved. Therefore, this two-sample Mendelian randomization (MR) study aims to investigate the causal relationship between Helicobacter pylori infection and GERD. Methods This study encompassed seven different specific protein antibodies targeting Helicobacter pylori and utilized a genome-wide association study (GWAS) on GERD. MR analysis was conducted to assess the causal relationship between Helicobacter pylori antibodies and the development of GERD. Results Genetically predicted serum levels of Helicobacter pylori IgG antibodies were positively associated with an increased risk of GERD (odds ratio [OR] = 1.001, 95% CI 1.000–1.003, P = 0.043). No causal relationship was found between other Helicobacter pylori antibodies and gastroesophageal reflux disease. Conclusion The outcomes derived from our two-sample Mendelian randomization analysis demonstrate a discernible link between the levels of Helicobacter pylori IgG antibodies and an augmented susceptibility to GERD. However, it is imperative to expand the sample size further in order to corroborate the correlation between Helicobacter pylori infection and GERD.

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Hynes, Sean O., Susann Teneberg, Niamh Roche, and Torkel Wadström. "Glycoconjugate Binding of Gastric and Enterohepatic Helicobacter spp." Infection and Immunity 71, no. 5 (May 2003): 2976–80. http://dx.doi.org/10.1128/iai.71.5.2976-2980.2003.

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ABSTRACT Helicobacter pylori is able to utilize several lectin-like, protein-carbohydrate interactions for binding to mucins, cell surfaces, and extracellular matrix proteins. As determined by hemagglutination assays and binding of radiolabeled bacteria to glycosphingolipids on thin-layer chromatograms, strains of gastric helicobacters and enterohepatic helicobacters, including Helicobacter canis, Helicobacter hepaticus, and Helicobacter bilis, also demonstrated evidence for the presence of lectin-hemagglutinin adhesins. In addition, in H. hepaticus and H. bilis, binding may be sialic acid dependent. The presence or absence and differences in the levels of activity of lectin adhesins may reflect the species' ecological niche.

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Lemke, Laura B., Zhongming Ge, Mark T. Whary, Yan Feng, Arlin B. Rogers, Sureshkumar Muthupalani, and James G. Fox. "Concurrent Helicobacter bilis Infection in C57BL/6 Mice Attenuates Proinflammatory H. pylori-Induced Gastric Pathology." Infection and Immunity 77, no. 5 (February 17, 2009): 2147–58. http://dx.doi.org/10.1128/iai.01395-08.

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ABSTRACT Because coinfections can alter helicobacter gastritis, we investigated whether enterohepatic Helicobacter bilis modulates Helicobacter pylori gastritis in C57BL/6 mice. Thirty mice per group were sham dosed, H. bilis or H. pylori infected, or H. bilis infected followed in 2 weeks by H. pylori and then evaluated at 6 and 11 months postinfection (mpi) for gastritis and premalignant lesions. Compared to H. pylori-infected mice, H. bilis/H. pylori-infected mice at 6 and 11 mpi had less severe gastritis, atrophy, mucous metaplasia and hyperplasia (P < 0.01) and, additionally, at 11 mpi, less severe intestinal metaplasia and dysplasia (P < 0.05). H. bilis/H. pylori-infected mice at 11 mpi exhibited less Ki67 labeling of proliferating epithelial cells, reduced numbers of FoxP3+ T-regulatory (TREG) cells, and lower FoxP3+ mRNA levels than did H. pylori-infected mice (P < 0.05). Proinflammatory interleukin-1β (IL-1β), gamma interferon, and tumor necrosis factor alpha mRNA levels were attenuated in H. bilis/H. pylori-infected mice at 6 and 11 mpi (P < 0.01), although anti-inflammatory IL-10, IL-13, and transforming growth factor β1 mRNA levels were not consistently impacted by H. bilis coinfection. Decreased pathology in H. bilis/H. pylori-infected mice correlated with higher gastric H. pylori colonization at 6 mpi (P < 0.001) and lower Th1-associated immunoglobulin G2c responses to H. pylori at 6 and 10 mpi (P < 0.05). We hypothesized that reduced pathology in H. bilis/H. pylori-infected mice was due to H. bilis-primed TREG cells in the lower bowel that migrated to the gastric compartment and inhibited Th1 responses to subsequent H. pylori infection. Thus, H. pylori-induced gastric lesions may vary in mouse models of unknown enteric helicobacter infection status and, importantly, variable sequelae to human H. pylori infection, particularly in developing countries, may occur where coinfection with lower bowel helicobacters and H. pylori may be common.

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Nisa, Intan Chairun, and Brilliant Margalin. "Optimasi dan uji efektivitas ekstrak Ganoderma lucidum sebagai anti-Helicobacter pylori." Bioma : Jurnal Ilmiah Biologi 10, no. 2 (October 11, 2021): 217–28. http://dx.doi.org/10.26877/bioma.v10i2.8236.

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Helicobacter pylori diketahui sebagai penyebab utama tukak lambung dengan melemahkan lapisan pelindung pada lambung dan duodenum. Sejumlah obat anti tukak lambung yang sering digunakan dapat menyebabkan resistensi pada H. pylori. Ganoderma lucidum diketahui dapat menghambat dan mendukung penyembuhan tukak lambung yang disebabkan oleh asam asetat. Akan tetapi, kemampuan G. lucidum dalam menghambat tukak lambung yang disebabkan H. pylori belum banyak diungkap. Penelitian ini bertujuan untuk mengetahui efektivitas ekstrak G. lucidum dalam menghambat pertumbuhan H. pylori penyebab tukak lambung. Penelitian merupakan ekperimental dua faktorial yaitu jenis pelarut fraksinasi dan konsentrasi ektrak G. lucidum. Ekstrak G. lucidum difraksinasi menggunakan dua jenis pelarut yaitu etanol 60% dan akuades. Konsentrasi ekstrak G. lucidum yang digunakan adalah 1, 5, 10, 20, 30 mg/mL. Efektivitas ekstrak G. lucidum diuji dengan metode difusi cakram. Berdasarkan analisis statistik didapat bahwa jenis pelarut berpengaruh terhadap aktivitas daya hambat H. pylori dengan nilai pada pelarut etanol 60% signifikan lebih tinggi dibandingkan akuades. Konsentrasi ekstrak G. lucidum baik etanol maupun akuades berpengaruh signifikan terhadap aktivitas daya hambat. Aktivitas daya hambat tertinggi adalah pada perlakuan ekstrak etanol G. lucidum konsentrasi 20 mg/ml. Kata kunci: akuades; difusi cakram; etanol; Helicobacter pylori; Ganoderma lucidum ABSTRACTOptimization and effectiveness assay of Ganoderma lucidum extract as Anti-Helicobactor pylori. Helicobacter pylori is known to be the main cause of gastric ulcers by weakening the protective lining of the stomach and duodenal. A number of gastric anti-ulcer drugs can cause resistance to H. pylori. Ganoderma lucidum is known to inhibit and support the healing of gastric ulcers caused by acetic acid. G. lucidum's ability to inhibit H. pylori growth has not been revealed much. This research aims to find out the effectiveness of G. lucidum extract in inhibiting the growth of H. pylori which causes gastric ulcers. This study is an experimental two factorial namely the type of fractionation solvent and the concentration of G. lucidum extract. Ganoderma lucidum extract is diffractionated using two types of solvents namely 60% ethanol and akuades. The concentration of G. lucidum extract used is 1, 5, 10, 20, 30 mg/mL. The effectiveness of G. lucidum is tested using the disc diffusion method. Based on statistical analysis found that the type of solvent affects the activity of H. pylori's resistance with a value in ethanol solvents 60% significantly higher than akuades On the other hand the concentration of G. lucidum extract in both ethanol and aquades has a significant effect on the activity of the slave. The highest inhibitory activity is in the treatment of ethanol extract G. lucidum concentration 20 mg / ml. Keywords: aquades; diffusion disc; ethanol; Helicobacter pylori; Ganoderma lucidum

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Samad, Khurshida, Md Nazrul Islam Chowdhury, Kazi Nishat Ara Begum, Imtiaz Ahmed, Touhid Uddin Rupom, and Md Saheduzzaman. "Detection Capacity of Helicobacter pylori Infection by Stool Antigen Test Comparing with Rapid Urease Test among Peptic Ulcer Disease Patients." Journal of National Institute of Neurosciences Bangladesh 7, no. 2 (February 6, 2022): 161–64. http://dx.doi.org/10.3329/jninb.v7i2.58113.

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Background: Rapid urease test and stool antigen test are both important diagnostic tools for the detection of Helicobacter pylori infection among peptic ulcer disease patients. Objective: The purpose of the present study was to compare the detection capacity of Helicobacter pylori infection with stool antigen test by comparing with rapid urease test among peptic ulcer disease patients. Methodology: This cross-sectional study was conducted in the Department of Clinical Pathology with the collaboration of Department of Gastroenterology at Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh from October 2011 to September 2012 for a period of one year. All the clinically suspected Helicobactor pylori infected peptic ulcer patients attending in the Department of Gastroenterology at Bangabandhu Sheikh Mujib Medical University (BSMMU) for upper GI endoscopy were selected as study population. Stool antigen test for Helicobactor pylori specific antigen from stool sample was done with “ABON-One Step Helicobactor pylori antigen test device”. Endoscopy of upper GIT was performed in the Department of Gastroenterology. Biopsy taken during endoscopy for RUT. Rapid urease test (RUT) of endoscopic biopsy was performed. Result: A total 86 patients were recruited for this study. The mean (±SD) age was found 38.53(±10.40) years. Out of 86 patients 76 cases were SAT positive and 10 cases were negative. The sensitivity, specificity, positive predictive values and negative predictive values and accuracy of SAT with RUT are 85.53%, 90.0%, 98.48%, 45.0%, 86.05% respectively. The area under the curve was 0.283 with the lower and upper limits of 95% confidence interval of 0.133 and 0.432. This was statistically significant (p=0.003). Conclusion: In conclusion the stool antigen test is an effective method for the diagnosis of Helicobacter pylori infection. Journal of National Institute of Neurosciences Bangladesh, July 2021, Vol. 7, No. 2, pp. 161-164

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Rosenberg, J. J., and H. M. Adam. "Helicobacter pylori." Pediatrics in Review 31, no. 2 (February 1, 2010): 85–86. http://dx.doi.org/10.1542/pir.31-2-85.

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Akram, Muhammad, E. Mohiuddin, HM Asif, and Khan Usmanghani. "Helicobacter Pylori." Kansas Journal of Medicine 4, no. 4 (November 23, 2011): 119–23. http://dx.doi.org/10.17161/kjm.v4i4.11396.

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Tytgat, G. N. J., L. Noach, and E. A. J. Rauws. "Helicobacter Pylori." Scandinavian Journal of Gastroenterology 26, sup187 (January 1991): 1–8. http://dx.doi.org/10.3109/00365529109098219.

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Lambert, J. R., S. K. Lin, and J. Aranda-Michel. "Helicobacter pylori." Scandinavian Journal of Gastroenterology 30, sup208 (January 1995): 33–46. http://dx.doi.org/10.3109/00365529509107760.

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Hussain, Zahoor, Zulfiqar Ali Shar, and Abdul Malik Sangri. "HELICOBACTER PYLORI." Professional Medical Journal 25, no. 12 (December 8, 2018): 1928–32. http://dx.doi.org/10.29309/tpmj/18.4959.

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Objectives: To determine the frequency of helicobacter pylori in gallbladder in patient with gall stones disease. Study Design: Cross-sectional study. Place and Duration of Study: This study was conducted at Surgical Unit-I Civil Hospital Karachi, March 2013 to August 2013. Methodology: A total of 281 patients diagnosed to have gall stone on basis of clinical history of pain in right upper abdomen with fatty intolerance confirmed on ultrasoundwho were operated rather by laparoscopic procedure or open surgery were included in the study. Immediately following gallbladder removal, the specimen was collected in a sterile cup. The specimen was sent to Laboratory for presence of H. Pylori using GEIMSA staining and for routine histopathology. Data was collected by a resident in predesigned proforma. Results: A total of 281 Patients diagnosed to have gall stone. Operated most of the cases were 21 to 50 years of age with mean age was 38.41±9.86 years. Out of 281 cases, 170 (60.5%) were female and 111 (39.5%) male. Seventy eight patients (27.76%) was observed obsess (BMI > 30kg/m2). Similarly duration of illness of 58.4% was below and equal to 6 months and 41.6% cases above six months. Frequency of helicobacter pylori in gallbladder of patients with gall stones disease was positive in 72(25.62%) cases. Conclusion: We conclude that H. pylori are also found in the biliary system, suggesting that these bacteria are of etiological importance in gallstoneformation. Early detection of helicobacter pylori and its eradication can prevent development of gall stones.

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NASEER, FAIZA, FATIMA JAVED, and IRUM IRSHAD. "HELICOBACTER PYLORI;." Professional Medical Journal 20, no. 04 (May 25, 2013): 489–94. http://dx.doi.org/10.29309/tpmj/2013.20.04.1025.

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Ansari, Shuaib, Irfan Murtaza Shahwani, Aqeel Ahmed Channa, Syed Zulfiquar Ali Shah, and Tarachand Devrajani. "HELICOBACTER PYLORI." Professional Medical Journal 21, no. 04 (December 8, 2018): 679–83. http://dx.doi.org/10.29309/tpmj/2014.21.04.2232.

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Objective: To determine the frequency of H. pylori in patients with functionaldyspepsia. Patients and methods: This six months multidisciplinary study was conducted attertiary care teaching hospital as well as at private hospital Hyderabad from February 2012 to July2012. All patients presented with history of dyspepsia were admitted and evaluated for functionaldyspepsia by performing endoscopy. After confirmation of functional dyspepsia the subjectswere further evaluated for H. pylori infection by taking the biopsy specimen, label it and sent tolaboratory for histopathological examination. The data was entered, saved and analyzed in SPSSversion 11.00. Results: During six month study period, total 100 patients with functionaldyspepsia were recruited. Majority of patients were from low socioeconomic class (78%), havehistory of spicy food intake (68%) and epigastric pain (94%). The associated symptoms observedwere nausea and vomiting (87%), anorexia (88%), early satiety (84%) and regurgitation (84%).The mean ±SD for age of patients with functional dyspepsia was 37.95±10.85. The mean age±SD of H. pylori identified patients was 35.81±7.72. Majority of the subjects was 30-40 years ofage and the male population predominant 64% (p-value 0.02, statistically significant). The H.pylori was identified in 62% of patients, of which 35 (56.5%) were males and 27(43.5%) werefemales (p-value 0.04, statistically significant) respectively.

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Rodríguez Ferrer, Marena Luz. "Helicobacter Pylori." Biociencias 6, no. 1 (June 1, 2011): 89–96. http://dx.doi.org/10.18041/2390-0512/bioc..1.2766.

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En 1982, Marshall y Warren descubrieron una bacteria que sobrevive en medio ácido y coloniza la mucosa gás- trica, llamada Helicobacter pylori, presente en pacientes con gastritis y úlcera péptica; su prevalencia en adultos de países occidentales está entre 20 y 40% y en países en vías de desarrollo en aproximadamente 80%. El conoci- miento de sus características inmunológicas, metabólicas y patogénicas, ha facilitado avanzar en el diagnóstico y prevención de enfermedades gastroduodenales relacionadas con ella. La infección se ha asociado con expresión de alelos específicos HLA-DR del tracto gastrointestinal humano, sugiriendo un papel en el desarrollo de gastritis crónica. Actualmente existen muchas pruebas para su detección, destacándose el test del aliento, por ser la más sensible y específica. El objetivo de esta revisión es el de evidenciar los conocimientos en la inmunogenética de la bacteria y los avances en las metodologías para su diagnóstico.

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Dunn, B. E., H. Cohen, and M. J. Blaser. "Helicobacter pylori." Clinical microbiology reviews 10, no. 4 (1997): 720–41. http://dx.doi.org/10.1128/cmr.10.4.720-741.1997.

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26

Nedrud, John G., and Steven J. Czinn. "Helicobacter pylori." Current Opinion in Gastroenterology 13, no. 1 (January 1997): 71–78. http://dx.doi.org/10.1097/00001574-199701000-00013.

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LANG, DIANE BERNEATH. "Helicobacter pylori." Radiology 179, no. 3 (June 1991): 680. http://dx.doi.org/10.1148/radiology.179.3.680.

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28

Moss, Steven F., and Shivani Sood. "Helicobacter pylori." Current Opinion in Infectious Diseases 16, no. 5 (October 2003): 445–51. http://dx.doi.org/10.1097/00001432-200310000-00011.

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Moss, Steven F., and Shivani Sood. "Helicobacter pylori." Current Opinion in Internal Medicine 2, no. 6 (December 2003): 553–59. http://dx.doi.org/10.1097/00132980-200302060-00002.

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Moss, Steven F., and Shivani Sood. "Helicobacter pylori." Current Opinion in Internal Medicine 2, no. 6 (December 2003): 553–59. http://dx.doi.org/10.1097/00132980-200312000-00002.

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31

Wyle, Frederic A. "Helicobacter pylori." Journal of Clinical Gastroenterology 13 (December 1991): S114—S124. http://dx.doi.org/10.1097/00004836-199112001-00019.

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32

Wood, David W., and Kevin P. Block. "Helicobacter Pylori." American Journal of Therapeutics 5, no. 4 (July 1998): 253–62. http://dx.doi.org/10.1097/00045391-199807000-00008.

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Schulz, Christian, and Peter Malfertheiner. "Helicobacter pylori." Gastroenterologie up2date 10, no. 01 (March 27, 2014): 11–22. http://dx.doi.org/10.1055/s-0033-1359236.

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34

Drumm, B. "Helicobacter pylori." Archives of Disease in Childhood 65, no. 11 (November 1, 1990): 1278–82. http://dx.doi.org/10.1136/adc.65.11.1278.

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Malfertheiner, Peter, and Michael Selgrad. "Helicobacter pylori." Current Opinion in Gastroenterology 30, no. 6 (November 2014): 589–95. http://dx.doi.org/10.1097/mog.0000000000000128.

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Malfertheiner, Peter, Michael Selgrad, and Jan Bornschein. "Helicobacter pylori." Current Opinion in Gastroenterology 28, no. 6 (November 2012): 608–14. http://dx.doi.org/10.1097/mog.0b013e32835918a7.

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37

CALAM, J. "Helicobacter pylori." European Journal of Clinical Investigation 24, no. 8 (August 1994): 501–10. http://dx.doi.org/10.1111/j.1365-2362.1994.tb01099.x.

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38

Korman, Melvin G., I. N. Marks, Richard H. Hunt, Anthony Axon, Martin J. Blaser, Dennis M. McCarthy, and Guido N. J. Tytgat. "Helicobacter pylori." European Journal of Gastroenterology & Hepatology 5, no. 11 (November 1993): 963–68. http://dx.doi.org/10.1097/00042737-199311000-00013.

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39

MOSS, S. "Helicobacter pylori." Gut 41, no. 5 (November 1, 1997): 723.6–723. http://dx.doi.org/10.1136/gut.41.5.723-f.

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MOSS, S. "Helicobacter pylori." Gut 41, no. 5 (November 1, 1997): 723. http://dx.doi.org/10.1136/gut.41.5.e723.

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41

Covacci, Antonello, and Rino Rappuoli. "Helicobacter pylori." Journal of Experimental Medicine 197, no. 7 (March 31, 2003): 807–11. http://dx.doi.org/10.1084/jem.20030063.

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42

Chen, S., V. Groves, and D. G. MacLellan. "HELICOBACTER PYLORI." ANZ Journal of Surgery 63, no. 5 (May 1993): 419–20. http://dx.doi.org/10.1111/j.1445-2197.1993.tb00417.x.

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Cats, Annemieke, Stephan G. M. Meuwissen, David Forman, Mikael E. Craanen, and Ernst J. Kuipers. "Helicobacter pylori." European Journal of Gastroenterology & Hepatology 10, no. 6 (June 1998): 447–50. http://dx.doi.org/10.1097/00042737-199806000-00001.

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Blaser, Martin J. "Helicobacter pylori." European Journal of Gastroenterology & Hepatology 10, Supplement (June 1998): S19. http://dx.doi.org/10.1097/00042737-199806001-00004.

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Pellicano, Rinaldo, Nathalie Broutet, Antonio Ponzetto, and Francis Mégraud. "Helicobacter pylori." European Journal of Gastroenterology & Hepatology 11, no. 11 (November 1999): 1335–38. http://dx.doi.org/10.1097/00042737-199911000-00027.

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46

Fisher, G., C. Lerch, J. Symonds, and M. Cooper. "Helicobacter pylori." Anaesthesia 53, no. 2 (February 1998): 209–10. http://dx.doi.org/10.1111/j.1365-2044.1998.tb00017.x.

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Seifrit, Barbara. "Helicobacter pylori." AORN Journal 65, no. 3 (March 1997): 614–20. http://dx.doi.org/10.1016/s0001-2092(06)63082-2.

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Peterson, Walter L. "Helicobacter pylori." Gastroenterology 114, no. 1 (January 1998): 224. http://dx.doi.org/10.1016/s0016-5085(98)70657-2.

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de Korwin, Jean Dominique. "Helicobacter pylori." Gastroentérologie Clinique et Biologique 31, no. 12 (December 2007): 1110–17. http://dx.doi.org/10.1016/s0399-8320(07)78346-x.

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Blaser, M. J. "HELICOBACTER PYLORI." Pediatric Infectious Disease Journal 12, no. 5 (May 1993): 422. http://dx.doi.org/10.1097/00006454-199305000-00027.

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