scholarly journals Detection of Helicobacter pylori in gastric biopsy and resection specimens

2005 ◽  
Vol 62 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Tatjana Babic ◽  
Hakija Basic ◽  
Biljana Selimovic-Miljkovic ◽  
Branislava Kocic ◽  
Gordana Tasic
Keyword(s):  
Duodenal Ulcer ◽  
Alkaline Phosphatase ◽  
Helicobacter Pylori ◽  
Gastric Biopsy ◽  
Giemsa Stain ◽  
Biopsy Specimens ◽  
H Pylori ◽  
Antral Biopsy ◽  
Better Than ◽  
Immunohistochemical Identification

Aim. To compare the sensitivity of detecting H. pylori in gastric biopsy and resection specimens using modified Giemsa stain and immunohistochemistry, using a commercially available anti-H. pylori antibody (Dako, Denmark). Methods. Gastric antral biopsy specimens showing chronic gastritis (28 cases) together with tissue blocks from gastrectomy specimens for duodenal ulcer (2 cases) were stained with modified Giemsa and immunoenzymatic alkaline phosphatase - anti-alkaline phosphatase (APAAP) method, and were carefully examined for the presence of H. pylori. Results. Using a modified Giemsa stain, the spiral shaped bacteria of H. pylori stained blue, were attached to the brush border of the gastric foveolar epithelial cells. However, the specificity of modified Giemsa stain depended on the morphological appearance of H. pylori. The specificity of immunostaining permitted detection of low numbers or even single organisms. In all cases bacteria were more prominent and easier to detect in immunostained preparations. H. pylori was identified in 22 (73.3%) of 30 sections stained with modified Giemsa stain, but it could be identified with greater frequency in sections stained with APAAP, in 27 (90%) of 30 sections. Conclusion. Immunohistochemical identification of H. pylori was better than Giemsa stain for detecting that organism.

Helicobacter pylori in gastric biopsy specimens. Comparison of culture, modified Giemsa stain, and immunohistochemistry. A retrospective study

1991 ◽  
Vol 165 (1) ◽  
pp. 69-73 ◽  
Author(s):  
R. J. L. F. Loffeld ◽  
E. Stobberingh ◽  
J. A. Flendrig ◽  
J. W. Arends
Keyword(s):  
Helicobacter Pylori ◽  
Retrospective Study ◽  
Gastric Biopsy ◽  
Giemsa Stain ◽  
Biopsy Specimens

scholarly journals Effect of Acid-Suppressive Therapy onHelicobactor pyloriProduction of Interleukin-8 in Gastric Mucosa

2000 ◽  
Vol 14 (4) ◽  
pp. 277-282 ◽  
Author(s):  
Masahiro Yoshinaga ◽  
Akira Ohtani ◽  
Satoru Tsuruta ◽  
Tetsuya Kato ◽  
Eishi Higashi ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Reflux Esophagitis ◽  
Serum Gastrin ◽  
Histological Finding ◽  
Gastric Biopsy ◽  
Suppressive Therapy ◽  
Biopsy Specimens ◽  
Gastric Corpus ◽  
Colonization Density ◽  
H Pylori

BACKGROUND: Recent studies have shown that acid-suppressive therapy increases the severity ofHelicobacter pylori- associated gastritis in the corpus.PURPOSE: To evaluate interleukin (IL)-8 production in the gastric corpus mucosa before and during acid-suppressive therapy inH pylori-infected patients.PATIENTS AND METHODS: Ten patients with reflux esophagitis (fiveH pylori-positive and fiveH pylori-negative) were treated with omeprazole 20 mg. Serum gastrin concentrations,H pyloricolonization density and mucosal IL-8 levels in the corpus were investigated at entry and two weeks after starting therapy. IL-8 levels were measured by ELISA. The organism density was determined, and scored according to area occupied by the bacterial colonies. The presence ofH pyloriwas assessed by rapid urease testing and histological finding of gastric biopsy specimens.RESULTS: InH pylori-positive patients, concentrations of IL-8 during therapy significantly exceeded those before therapy (36.2±6.8 versus 18.3±3.8 pg/mg protein; P<0.05) without alteringH pyloridensity. InH pylori-negative patients, IL-8 levels were similar before and during therapy (6.1±2.7 versus 6.3±3.0 pg/mg protein). Concentrations of gastrin during therapy were significantly higher than those before therapy in all patients.CONCLUSIONS: The results suggest that acid suppression increases mucosal IL-8 levels inH pylori-infected patients with reflux esophagitis.

scholarly journals Antibiotic Susceptibilities ofHelicobacter pyloriStrains Isolated in the Province of Alberta

1998 ◽  
Vol 12 (4) ◽  
pp. 295-298 ◽  
Author(s):  
Diane E Taylor ◽  
Qin Jiang ◽  
Richard N Fedorak
Keyword(s):  
Helicobacter Pylori ◽  
Antibiotic Resistance ◽  
Gastric Biopsy ◽  
Minimal Inhibitory Concentrations ◽  
Antibiotic Susceptibilities ◽  
Biopsy Specimens ◽  
Metronidazole Resistance ◽  
Agar Dilution ◽  
Resistant Strains ◽  
H Pylori

The incidence of antibiotic resistance to amoxicillin, clarithromycin, erythromycin, metronidazole and tetracycline inHelicobacter pyloristrains isolated from gastric biopsy specimens obtained in Alberta was investigated. Results for all antibiotics were obtained using agar dilution, and in addition to metronidazole, the E test was used. Resistance to amoxicillin and tetracycline was not detected. Metronidazole resistance determined using agar dilution was approximately 12% (95% CI 4% to 26%) when minimal inhibitory concentrations (MICs) were at least 8 µg/mL, but fell to 2% (95% CI 0.1% to 13%) when MICs were set at 32 µg/mL or greater. The E test for metronidazole resistance (MIC 8 µg/mL or greater) yielded a slightly higher percentage of resistant strains compared with agar dilution tests (14%, 95% CI 5% to 29%). One of the 31 strains was resistant to clarithromycin (MIC 8 µg/mL) and erythromycin (MIC 16 µg/mL). Thus, the incidence of resistance to clarithromycin, part of the currently used triple therapy for eradication ofH pylori, was 3% (95% CI 0.1% to 17%).

scholarly journals Role of apoptosis induced by Helicobacter pylori infection in the development of duodenal ulcer

Gut ◽  
1999 ◽  
Vol 44 (4) ◽  
pp. 456-462 ◽  
Author(s):  
K Kohda ◽  
K Tanaka ◽  
Y Aiba ◽  
M Yasuda ◽  
T Miwa ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Clinical Stage ◽  
Endoscopic Examination ◽  
Gastric Epithelium ◽  
Antral Mucosa ◽  
Biopsy Specimens ◽  
A Cell ◽  
H Pylori

BACKGROUNDHelicobacter pylori affects gastric epithelium integrity by acceleration of apoptosis. However, it remains unclear what product of the bacteria causes apoptosis, or whether or not the apoptosis is involved in the development of ulcers.AIMSTo elucidate the factor from H pylori that causes acceleration of apoptosis and the role of apoptosis in the development of duodenal ulcer in H pylori infection.PATIENTSFiveH pylori negative healthy volunteers, 47H pylori positive patients with duodenal ulcer, and 35 H pylori positive patients with gastric ulcer.METHODSAn endoscopic examination was carried out to diagnose ulcers and determine their clinical stage. To analyse apoptosis, a cell cycle analysis was performed using biopsy specimens.RESULTSThere was a significant correlation between the urease activity of theH pylori strain and the level of apoptosis induced by this bacterial strain. Moreover, in duodenal ulcer patients infected with H pylori, the patients with an active ulcer exhibited a significantly higher level of apoptosis than those with ulcers at both the healing and scarring stages.CONCLUSIONThese findings suggest that acceleration of apoptosis in the antral mucosa caused by the urease of H pylori plays a crucial role in the development of ulcers in the duodenum.

scholarly journals Transcriptional Profile of Helicobacter pylori Virulence Genes in Patients with Gastritis and Gastric Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Manouchehr Ahmadi Hedayati ◽  
Saeed Salavati
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Carcinoma ◽  
Clinical Outcomes ◽  
Virulence Genes ◽  
Gastric Biopsy ◽  
Transcriptional Profile ◽  
Statistical Correlations ◽  
H Pylori ◽  
Antral Biopsy

Introduction. Numerous molecular epidemiology studies have been performed about the frequency of Helicobacter pylori virulence genes in patients with H. pylori infection so far. This study was conducted to detect transcriptional profile by cDNA of H. pylori virulence genes in gastric biopsy samples of gastritis and gastric carcinoma patients. Materials and Methods. In a case-control study, based on the prevalence of gastritis and gastric cancer in Sanandaj city during 2018 and 2019, 23 and 11 gastric antral biopsy samples with H. pylori infection were collected from gastritis and gastric carcinoma patients by the consecutive and available sampling method. Pathological characters, including tumor grades and tumor areas for gastric carcinoma biopsy samples prepared from gastric cancer areas, were determined by the pathologist. Total RNA of gastric antral biopsy samples was extracted, and their cDNA was synthesized by TaKaRa kit. H. pylori virulence genes’ cDNA using specific primers and PCR was detected. This study’s results were analyzed by SPSS version 25 and statics chi-square tests for determination of relationship and correlation between cDNAs of H. pylori transcriptional profile and clinical outcomes of H. pylori infection, including gastritis, gastric carcinoma, tumor grades, and tumor area. Results. The positive statistical correlations were observed between transcripts of cagA, cagA-EPIYAC, cagE, and cagY genes and H. pylori infection clinical outcomes ( P < 0.05 ). Conclusion. Detection of the H. pylori virulence genes’ cDNA in gastric biopsy samples can help provide the prognosis of clinical outcomes.

Diagnosis of Helicobacter pylori infection and determination of clarithromycin resistance by fluorescence in situ hybridization from formalin-fixed, paraffin-embedded gastric biopsy specimens

2005 ◽  
Vol 51 (7) ◽  
pp. 569-573 ◽  
Author(s):  
Fusun Can ◽  
Zerrin Yilmaz ◽  
Muge Demirbilek ◽  
Banu Bilezikci ◽  
Ganiye Kunefeci ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Biopsy ◽  
Test Method ◽  
Biopsy Specimens ◽  
Clarithromycin Resistance ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
H Pylori ◽  
Formalin Fixed

A reliable diagnostic test for Helicobacter pylori is important in clinical practice and research. The ideal diagnostic test for H. pylori should be sensitive, specific, and cost-effective. Helicobacter pylori resistance to clarithromycin is a common reason for failure of eradication therapy. The aim of this study was to evaluate the fluorescent in situ hybridization (FISH) method to detect H. pylori and determine clarithromycin resistance in formalin-fixed, paraffin-embedded gastric biopsy specimens. One hundred seventeen gastric biopsy specimens from patients with dyspepsia were examined for the presence of H. pylori by conventional culture, FISH, and histopathological methods. A set of fluorescent-labeled oligonucleotide probes binding to either H. pylori 16S rRNA or 23S rRNA sequences were used for FISH analysis. Phenotypic antibiotic susceptibilities of the isolates were tested using the Epsilometer test method (E test). Helicobacter pylori was detected in 70 of 117 biopsy specimens by histopathological examination and FISH, whereas it was detected in 47 specimens by culturing. Histopathology and FISH techniques failed to identify H. pylori in 1 biopsy sample isolated by culture. Clarithromycin resistance was found in 11 of 46 H. pylori isolates using the E test method. All of the phenotypic resistance measurements of isolates were correlated with genotypic clarithromycin resistance. Eleven clarithromycin-resistant strains were identified by FISH. The diagnosis of H. pylori infection and the determination of clarithromycin resistance in formalin-fixed, paraffin-embedded specimens using FISH is promising because it provides a rapid, reliable, and culture-independent diagnosis.Key words: Helicobacter pylori, clarithromycin resistance, FISH.

scholarly journals Determination of Helicobacter pylori Virulence Genes in Gastric Biopsies by PCR

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Tamer Essawi ◽  
Wail Hammoudeh ◽  
Israr Sabri ◽  
Walid Sweidan ◽  
Mohammad A. Farraj
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Genes ◽  
Gastric Biopsy ◽  
Strong Indication ◽  
Specific Primers ◽  
Biopsy Specimens ◽  
Pcr Identification ◽  
Gastric Biopsies ◽  
H Pylori

Aim. The aim of this study was to identify the presence of H. pylori in biopsy specimens from symptomatic patients by PCR. In addition, the rate of cagA, vacA, iceA1, and iceA2 virulence genes was determined. Materials and Methods. One hundred antral gastric biopsy specimens were collected during endoscopy from patients suffering from gastroduodenal symptoms. The samples were collected by the gastroenterologists in their own clinics in Ramallah, Palestine. DNA was extracted from the biopsies and subsequently used for PCR identification of H. pylori and the virulence genes using specific primers. Results. The rate of positive H. pylori in the collected biopsies was 44%. The rates of the virulence genes in this sample: cagA, vacA, iceA1, and iceA2 were 65.9%, 40.9%, 63.6%, and 84.1%, respectively. Conclusion. The iceA2 gene was the most frequent in this study. Much research is necessary to determine the presence of an association of this gene with gastric pathology. Variation in the rates of the iceA gene in different countries is a strong indication of its geographical distribution. This study would provide important information regarding the prevalence of virulence genes (vacA, cagA, iceA1, and iceA2) in H. pylori strains in the sample tested in this country.

scholarly journals Interleukin-17C in Human Helicobacter pylori Gastritis

2017 ◽  
Vol 85 (10) ◽  
Author(s):  
Shingo Tanaka ◽  
Hiroyuki Nagashima ◽  
Modesto Cruz ◽  
Tomohisa Uchida ◽  
Takahiro Uotani ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Gastric Biopsy ◽  
Interleukin 17 ◽  
Human Gastric Mucosa ◽  
Mrna Levels ◽  
Content Type ◽  
Biopsy Specimens ◽  
H Pylori

ABSTRACT The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P = 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of IκB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.

Sign in / Sign up

Export Citation Format

Share Document