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gastritis

در نشریات گروه پزشکی
  • Divya Tejaswi Gopidesi*, Madhuri Recharla, Thejaswini Vallapureddy, Pratima Jonnadula, Durga K, Mohan Rao Nandam, Vaheda Begam
    Background & Aims

    Helicobacter pylori (H. pylori) infection, a common organic cause of dyspepsia, often lacks macroscopic mucosal lesions, necessitating distinction from functional dyspepsia. This study assessed H. pylori prevalence, optimal biopsy sites, histopathological changes, and infection density in dyspeptic patients.

    Materials & Methods

    Gastric mucosal biopsies from 100 dyspeptic patients were formalin-fixed, paraffin-embedded, and sectioned (5μm). Hematoxylin and eosin (H&E) and Giemsa stains were used for histopathological evaluation, with Giemsa specifically applied for H. pylori grading.

    Results

    Patients (mean age: 44.37 years; range: 11–80) showed peak H. pylori prevalence in the fourth (28%, n=28) and fifth (29%, n=29) decades, with a male-to-female ratio of 1.26:1. Common symptoms included nausea (76%, n=76), epigastric discomfort, abdominal pain, and bloating. Chronic gastritis was identified in 89% (n=89), with 82% (n=82) testing H. pylori-positive, all exhibiting chronic active gastritis. The pyloric antrum was the predominant colonization site (86.58%, n=71/82), followed by the fundus (84.14%, n=69/82) and body (74.39%, n=61/82). Per the Sydney System, inflammation severity was mild (42.68%, n=35), moderate (48.78%, n=40), or severe (8.54%, n=7). H. pylori density was graded as mild (36.59%, n=30), moderate (54.88%, n=45), or dense (8.53%, n=7).

    Conclusion

    Early H. pylori detection and eradication alleviate symptoms and prevent complications. Giemsa stain proved optimal for H. pylori identification due to its cost-effectiveness and rapidity. The pyloric antrum, followed by the fundus and body, is the primary biopsy site for diagnosing H. pylori-associated gastritis. These findings emphasize targeted biopsy protocols and efficient diagnostic methods in managing dyspepsia.

    Keywords: Dyspepsia, Gastritis, Haematoxylin, Eosin, H.Pylori, Sydney System
  • Abdollah Safikhani Mahmoodzadeh, Elham Moazamian, Seyedeh Azra Shamsdin, Gholam Abbas Kaydani
    Background

    Helicobacter pylori is a gram-negative pathogen. The infection caused by this pathogen may result in gastritis and can increase the risk of gastric cancer. This study investigated the relationship between H. pylori infection as the main risk factor for gastritis and changes in serum inflammatory cytokine levels.

    Methods

    Blood samples from 85 patients with stomach pain, including 46 H. pylori-positive (Hp+) and 39 H. pylori-negative (Hp- ) cases, were collected and referred to a gastroenterologist. After isolation and identification of H. pylori, the severity of gastritis was determined for each patient based on the histopathological findings. Finally, the serum levels of cytokines were measured using the multiplex kit and flow cytometry methods.

    Results

    There were significant differences in the levels of interleukin-2 (IL-2), IL-4, IL-17A, IL-17F, IL-22, tumor necrosis factoralpha (TNF-α), and interferon-gamma (IFN-γ) between the Hp- and the Hp+specimens (P≤0.05). The levels of IL-2, IL-17A, IL-17F, IL-22, TNF-α, and IFN-γ were significantly higher in patients with mild and moderate gastritis than Hp- group (P≤0.05). In addition, IL-4 significantly increased in patients with moderate gastritis compared with Hp- individuals (P=0.008).

    Conclusion

    Among the inflammatory cytokines evaluated in this study, IL-17A, IL-17F, and IL-22 may play a crucial role in developing moderate gastritis in infected patients with H. pylori.

    Keywords: Cytokines, Inflammation, Gastritis, Helicobacter Pylori
  • Mahmoudali Abdi
    Background

    Antibiotic resistance and adverse effects pose significant challenges to the effectiveness of Helicobacter pylori eradication therapies, such as clarithromycin-based triple therapy. Alternative treatments, including bismuth quadruple therapy, are effective in cases of clarithromycin resistance. Levofloxacin and metronidazole-based triple therapy have demonstrated high success rates with fewer side effects, making it a preferred option following clarithromycin treatment failure.

    Objectives

    This study aimed to evaluate the effectiveness of levofloxacin and metronidazole in eradicating H. pylori among patients with chronic epigastric pain in Zakho, Iraq. It also assessed the accuracy of diagnostic tests, patient history, and post-treatment confirmation of eradication.

    Methods

    A prospective study was conducted involving 100 patients with chronic epigastric pain at Zakho General Teaching Hospital. Diagnosis was performed using the fecal antigen test, urea breath test (UBT), and endoscopy with biopsy. Patients were treated with a 14-day regimen comprising levofloxacin, metronidazole, and either esomeprazole or pantoprazole.

    Results

    Of the 100 participants, 66% were female, with a mean age of 37.85 years. The fecal antigen test, performed on 60 patients, showed a positivity rate of 96.5%, while the UBT, conducted on 40 patients, revealed a positivity rate of 97.5%. The highest infection rate was observed in the 51 - 60 age group. The 14-day levofloxacin and metronidazole regimen achieved a 99% eradication rate with minimal side effects.

    Conclusions

    This study underscores the high efficacy of levofloxacin and metronidazole-based therapy for H. pylori eradication. It highlights the importance of non-invasive diagnostic methods, enhanced patient follow-up, and international collaboration to achieve optimal treatment outcomes.

    Keywords: Helicobacter Pylori, Levofloxacin, Metronidazole, 14C-Urea Breath Test, Gastritis, Stool Antigen Test (SAT)
  • Suresh Jaiswal*, Bijay Subedi, Ashmita Sapkota, Pushpa Sharma, Manisha Timilsina, Maheshwor Timilsina, Bishnu Raj Tiwari
    Background

    Intestinal infections with Helicobacter pylori mainly occur during childhood. If contracted, these infections may cause chronic gastritis, frequently leading to peptic ulcer disease in later life. This study aims to detect the prevalence of H. pylori infections in patients with active gastritis.

    Methods

    The study included 150 participants who were consuming daily anti-gastritis drugs to reduce the gas and were considered active gastritis patients and were recruited from Lekhnath 12, now known as Pokhara metropolitan-30, from May 2018 to March 2019. They were screened for H. pylori antibodies for detection of infection by the immunochromatographic rapid detection kit, and the data were analyzed using SPSS 2016.

    Results

    Serum anti-Helicobacter pylori antibodies were used to detect the presence of Helicobacter pylori in these participants. Among the 150 participants, 54 were males (36%) and 96 were females (64%). The results showed that 47 (31.3%) of the patients were positive for anti-Helicobacter pylori test. The age group 30 to 40 had the highest prevalence of 21 (14.0%). Using public water showed the highest prevalence with a P value of 0.04.

    Conclusion

    There should be an additional aspect required for the diagnosis and treatment of gastritis, which is the healthcare providers' and patients' awareness of the cause and most efficient treatments for this medical condition. Using only anti-gastritis drugs is not sufficient; treatment against Helicobacter pylori requires the right pathway of treatment by the use of several antibiotics.

    Keywords: Gastritis, Burns, Helicobacter Pylori
  • فروغ حیدری، غلامرضا حقیقی، عباس گنجعلی*
    مقدمه و هدف

    هلیکوباکتر پیلوری یکی از شایع ترین عفونت های باکتریایی واز عوامل مهم اتیولوژیک زخم های گوارشی شناخته شده و یکی از پاتوژن های اصلی که با ایجاد التهاب مزمن و پیشرونده منجر به سرطان معده می شود. این مطالعه با هدف بررسی مکانیسم های دخیل در پیشرفت بیماری سرطان معده ناشی از هلیکوباکتر پیلوری انجام شد.

    مواد و روش‏ها:

     این مطالعه مروری با هدف مرور نظام مند بر اساس پروتکل پریزما و جستجو در پایگاه های بین المللی Scopus، PubMed، Google Scholar، Science Direct و پایگاه های ملی SID، Magiran و MedLib انجام شد. با توجه به استراتژی PICOS، تمام مقالات منتشر شده به زبان فارسی و انگلیسی از سال 2011 تا 2021 با استفاده از کلمات کلیدی فارسی «مکانیسم»، «سرطان معده» و «هلیکوباکتر پیلوری» و معادل انگلیسی این واژه ها و ترکیب این کلمات در صفحه جستجوی هر یک از پایگاه های مد نظر با استراتژی لازم جستجو و در گام نهایی مقالات با کیفیت، متناسب با هدف مطالعه مورد ارزیابی قرار گرفتند.

    یافته‏ ها: 

    بر اساس نتایج، علت شناسی سرطان معده چند عاملی است ولی با تحقیق حاضر می توان گفت که نقش هلیکوباکتر پیلوری در ایجاد زخم و سرطان معده توسط مکانیسم ها، عوامل محیطی و پاسخ ایمنی میزبان تعیین می گردد.

    نتیجه ‏گیری: 

    بررسی دقیق مکانیسم ها و مسیرهای ایجاد بیماری توسط هلیکوباکتر پیلوری می تواند منجر به گسترش روش های جدیدتر و موثرتری برای پیشگیری و درمان سرطان معده شود.

    کلید واژگان: مکانیسم، گاستریت، سرطان معده، هلیکو باکتر پیلوری، ایران
    Heydari Forough, Gholamreza Haghighi, Abbas Ganjali *
    Background and Aims

    One of the most common bacterial infections is Helicobacter pylori (H.pylori), which causes chronic and progressive inflammation and is considered one of the important etiological and pathogenic factors of gastric ulcer and gastric cancer (GC). The aim of this study investigating the mechanisms related to H.pylori in causing gastric cancer.

    Materials and Methods

    This systematic review study was conducted based on the Prisma protocol and searching in international databases Scopus, PubMed, Google Scholar, Science Direct and national databases SID, Magiran and MedLib. According to the PICOS strategy, all articles published in Persian and English from 2011 to 2021 using the Persian keywords " Mechanism ", "Gastric Cancer" and "Helicobacter pylori" and the English equivalent of these words and the combination of these words in The search page of each of the databases in question was searched with the necessary strategy. Finally, the quality articles were evaluated based on the purpose of the study.

    Results

    Based on the results, The etiology of gastric cancer is multifactorial, but with the present research, it can be said that the role of H.pylori in causing ulcer and gastric cancer is determined by mechanisms, environmental factors, and the host's immune response.

    Conclusion

    Examining the mechanisms and pathways of disease caused by Helicobacter pylori can lead to the development of newer and more effective methods for the prevention and treatment of gastric cancer.

    Keywords: Mechanism, Gastritis, Stomach Neoplasms, Helicobacter pylori, Iran
  • Sanaz Mami, Saeedeh Khaleghnezhad, Masoud Mami, Masoud Dadashi, Mehdi Goudarzi, Hossein Ghahremanpour, Bahareh Hajikhani*
    Backgrounds

    Helicobacter pylori infections vary in severity and virulence in different populations for various reasons. There are different H. pylori strains with varying degrees of virulence. The genetic diversity of H. pylori strains in gastritis patients in different areas has not been well understood. This study aimed to evaluate the prevalence rate and different genotypes of H. pylori strains in clinical specimens of patients with gastritis in Ilam, Iran.

    Materials & Methods

    Saliva and gastric biopsy samples were collected from 81 patients (55 males and 26 females in the age range of 20 to 90 years) referring to Ilam medical centers. After DNA extraction, the prevalence of H. pylori as well as vacA, cagA, and ureC genes was evaluated using PCR, and then each vacA-positive sample was further evaluated for m1m2 and s1s2 variants.

    Findings

    The cagA and vacA genes were found in 27 (71%) and 36 (94.7%) H. pylori-positive samples, respectively. The cagA gene was detected in patients with gastric pain (44.4%) and anorexia (18.51%). Also, the results showed that the vacA s2m2 genotype and m2 allele were present in 32.9% of H. pylori isolates. Moreover, s2m2 and s1m2 genotypes were detected in 42.1 and 26.3% of vacA-positive samples, respectively. The lowest frequency was related to the m1 allele (17.18%).

    Conclusion

    This study results indicate a plausible relationship between the presence of some genotypes of H. pylori and the progression of gastritis, suggesting these markers as promising biomarkers to predict the disease severity.

    Keywords: Helicobacter pylori, Gastritis, Genotyping, vacA, cagA, PCR
  • Mandana Rafeey, Pardis Nikmanesh, Farshad Javadzadeh
    Background

    Fecal calprotectin (FC) is suggested as a novel biomarker for the diagnosis of gastrointestinal (GI) diseases; however, few studies have investigated its diagnostic value for Helicobacter pylori (H. pylori). Therefore, the current study evaluated the level of FC and its diagnostic value in patients with H. Pylori and its related conditions including gastritis and duodenitis.

    Methods

    In this case‑control study, 120 children with upper GI symptoms, who were indicated to undergo upper GI endoscopic examination, were consecutively included. Patients were categorized into different groups based on their endoscopic findings including H. pylori, gastritis, duodenitis or normal.

    Results

    Patients with gastritis (P = 0.014) and those with duodenitis (P < 001) had significantly higher FC. The level of FC was higher in patients with H. pylori but this difference was marginally significant (P = 0.054). The level of FC had poor ability to diagnose the presence of H. pylori (P = 0.054) and gastritis (area under the curve, AUC = 0.639, P = 0.014). However, it had acceptable power to diagnose patients with or duodenitis (AUC = 0.718, P < 0.001). The sensitivity and specificity of FC for diagnosis of gastritis were 64 and 65 percent (cut‑off = 45.2 µg/g), and for duodenitis were 77 and 61 percent (cut‑off = 46.2 µg/g), respectively.

    Conclusions

    FC can be considered as an objective and diagnostic tool for duodenitis. However, due to the low sensitivity and specificity, it is suggested to consider it as an objective supplementary test beside other established diagnostic modalities.

    Keywords: Calprotectin, diagnosis, duodenitis, gastritis, Helicobacter pylori
  • سیده زهره میرباقری، مسعود آل بویه، روناک بختیاری*، هاشم فخر یاسری، عباس رحیمی فروشانی، مرضیه قنبریان، فاطمه رضایی، امیر ابراهیمی
    زمینه و هدف

    شناخت الگوی جمعیتی میکروب های معده و ارتباط تفاوت های آن در ایجاد و پیشرفت گاستریت می تواند کمک زیادی به فهم مکانیسم ایجاد این بیماری و طراحی مسیرهای درمانی پیشگیرانه از پیشرفت آن کند. در این مطالعه تالش شده است تا کلونیزاسیون همزمان عوامل باکتریایی در گروه بیماران دچار گاستریت مزمن مورد بررسی قرار بگیرد.

    روش بررسی

    در این مطالعه، تعداد 168 نمونه ی بیوپسی معده از بیماران مراجعه کننده به بخش گوارش بیمارستان فیروزگر تهران که دچار ناراحتی های گوارشی بودند جمع آوری گردید. نمونه های بیوپسی در بخش پاتولوژی با روش رنگ آمیزی هماتوکسیلین- ایوزین مورد بررسی هیستولوژیکی قرار گرفتند و در محیط کشت اختصاصی هلیکوباکتر تحت شرایط رشد میکروایروفیل و محیط کشت های بالد آگار و مک کانکی آگار تحت شرایط هوازی از نظر حضور هلیکوباکتر پیلوری و سایر باکتری ها بررسی شدند. تعیین هویت ایزوله های هلیکوباکتر پیلوری با استفاده از روش های تست اوره آز سریع، کشت و روش مولکولی PCR و تعیین هویت سایر باکتری ها توسط بررسی بیوشیمیایی و فنوتیپی انجام شد.

    یافته ها

    در این مطالعه فراوانی عفونت هلیکوباکتر پیلوری 4/27 درصد تخمین زده شد. میانگین سنی بیماران در دو گروه مبتال و غیر مبتال به عفونت هلیکوباکتر پیلوری یکسان بود. 5/87 درصد از کل بیماران مبتال به گاستریت مزمن بودند که بین وجود گاستریت مزمن و ابتال به عفونت هلیکوباکتر پیلوری از نظر آماری تقریبا ارتیاط معنادار بوده است)001.0: <value-P .)از میان 140 ایزوله از نمونه های بیوپسی معده بیماران مبتال و غیر مبتال به هلیکوباکتر پیلوری، باکتری های جدا شده متعلق به 12 جنس و 3 شاخه باکتریایی بودند. بیشترین باکتری های جدا شده بر حسب جنس به ترتیب شامل استرپتوکوکوس، استافیلوکوکوس، میکروکوکوس، اشرشیا کلی، باسیلوس، انتروکوکوس، کلبسیال، سودوموناس، انتروباکتر، سیتروباکتر و پروویدنسیا بودند. شاخه های پروتیوباکتریا و فرمی کوتس غالب ترین و شاخه اکتینوباکتریا کمترین شاخه باکتریایی شناسایی شده بودند. همزمانی عفونت هلیکوباکتر پیلوری با سایر باکتری های ایزوله شده بویژه با جنس های استرپتوکوکوس و استافیلوکوکوس دیده شد.

    نتیجه گیری

    حضور جنس های مختلف باکتریایی در بافت معده بیماران مبتال به گاستریت در غیاب هلیکوباکتر پیلوری پیشنهادکننده نقش احتمالی آنها در بروز یا پیشرفت این بیماری است. انجام مطالعات تکمیلی جهت تعیین ارتباط استقرار این باکتری ها با مصرف داروهای تعدیل کننده اسیدیته معده و تغییرات پاتولوژیک می تواند در پیشگیری و درمان بیماری گاستریت مفید باشد.

    کلید واژگان: گاستریت، هلیکوباکتر پیلوری، میکروبیوتای معده
    Seyedeh Zohre Mirbagheri, Masoud Alebouyeh, Ronak Bakhtiari*, Hashem Fakhre Yaseri, Marzieh Ghanbarian, Fatemeh Rezaei, Amir Ebrahimi
    Background

    Understanding the bacterial community composition of gastric microbes and the relationship between its differences in the development and progression of gastritis can be of great help in the perception of the mechanism of this disease and designing preventive treatment pathways for its progression. We aimed to investigate the simultaneous colonization of bacterial agents in patients with chronic gastritis.

    Materials and Methods

    The study was performed on 168 gastric biopsy specimens of patients with gastric complaints who were referred to the endoscopic ward of Firoozgar hospital in Tehran. Biopsy specimens in the pathology department were examined histologically by the hematoxylin-eosin staining method and in the specific culture medium of Helicobacter under microaerophilic growth conditions and in general culture medium under aerobic conditions for the presence of Helicobacter and other bacteria. Identification of Helicobacter pylori (H. pylori) isolates was performed by analyzing colony morphology, gram staining, positive reactions of oxidase and catalase, rapid urease test, and polymerase chain reaction (PCR). Other bacteria were identified by biochemical and phenotypical analysis.

    Results

    In our study, the recovery rate of H. pylori infection was 27.4 %. The mean age of patients in the two groups with and without H. pylori infection was almost the same. 87.5% of all patients had chronic gastritis, which showed significant associations with H. pylori infection (p-value: 0.00). We identified 140 bacterial colonies that belonged to 12 genera and 3 phyla. At the genus level, Streptococcus and Staphylococcus were predominant followed by Micrococcus, Escherichia coli, Bacillus, Enterococcus, Klebsiella, Pseudomonas, Enterobacter, Citrobacter, and Providencia. The predominant phyla were Proteobacteria and Firmicutes while Actinobacteria was less frequent. Co-infection of H. pylori with other isolated bacteria, especially Streptococcus and Staphylococcus was observed.

    Conclusion

    The presence of different bacterial genera in the gastric tissue of patients with gastritis in the absence of H. pylori suggests their possible role in the occurrence or progression of this disease. Additional studies to determine the association of the persistence of these bacteria with the use of drugs that modulate gastric acidity and pathological changes can be useful in the prevention and treatment of gastritis.

    Keywords: Gastritis, Helicobacter pylori, Gastric microbiota
  • Ramina Mahboobi, Fatemeh Fallah, Abbas Yadegar, Naghi Dara, Maryam Kazemi Aghdam, Behnoush Asgari, Mojdeh Hakemi-Vala
    Background and Objectives

    Helicobacter pylori, is a major etiologic agent associated with gastritis. There is more evidence of noncoding microRNAs (miRs) dysregulation in gastrointestinal diseases, including inflammation caused by Helicobacter pylori. Also, the classification of gastrointestinal malignancies using the miRs profile is better than the protein profile. MiRNA-155(miRNA-155) among other miRs plays an important role in control of inflammation and gastric malignancy, so it can be remarkable prognosis marker of gastric cancer in the phase of chronic gastritis. The aim of this study was to compare the expression of miRNA-155 in gastric biopsy and serum samples of adult patients with chronic gastritis.

    Materials and Methods

    Biopsy and blood samples were collected from endoscopy candidates at Taleghani hospital, Tehran, during 2019. H. pylori infection was detected using histology, culture and molecular PCR methods. Based on cagA and vacA genotyping, the toxicity of H. pylori isolates were determined. After RNA extraction, the expression rate of miRNA-155 was evaluated by real-time polymerase chain reaction (RT-PCR) in gastric tissue and serum of adults infected by H. pylori (n = 30) compared with control group without infection (n = 20). RNU6 housekeeping miRNA were used as endogenous control and statistical analyses were performed using SPSS, ANOVA and Student’s t-test.

    Results

    miRNA-155 expression in H. pylori infected adult patients increased significantly by 5.61 and 10.11 fold in serum and tissue respectively, compared to that observed in the control group. Evaluation of miRNA-155 expression pattern in relation to bacterial virulence factors showed that the increase in miRNA-155 expression is independent of CagA and VacA toxins.

    Conclusion

    According to the differential expression patterns of miRNA-155 in serum samples of the infected adult patients, miRNA-155 has the potential to evaluate as chronic gastritis marker.

    Keywords: Helicobacter pylori, Gastritis, Serum marker, MicroRNA
  • Ghulam Rasool *, Muhammad Usman Shams, Muhammad Rashid Siraj, Waqas Latif, Rubina Sheikh, Shah Jahan
    Background

    Helicobacter pylori colonizes gastric tissue in obese patients and mostly remains undetected clinically, as histological and molecular analysis is seldom ordered in such cases.

    Objectives

    This study aimed to detect the frequency of H. pylori using different techniques in sleeve gastrectomy specimens of obese patients with minimal or no symptoms suggestive of gastritis.

    Methods

    This longitudinal study was carried out at Farooq Hospital Westwood Lahore, Morbid Anatomy and Histopathology Department and Resource Laboratory at the University of Health Sciences, Lahore, Pakistan, from February 2021 to September 2021. This study selected 80 cases who underwent sleeve gastrectomy within six months. Helicobacter pylori was detected by rapid urease test (RUT), modified Giemsa staining, and polymerase chain reaction (PCR) techniques.

    Results

    Most patients (83.7%) were clinically asymptomatic, while 10% had mild and 6.3% had moderate to severe gastritis symptoms. Of the asymptomatic patients, 56.7% of biopsies showed chronic gastritis. Rapid urease test and modified Giemsa staining showed positive evidence for H. pylori in 47.3% of cases, whereas an additional 13.2% of biopsies that were negative on conventional methods showed the amplification of H. pylori DNA by PCR. Patients were discharged with proton-pump inhibitors therapy (40 mg/day) that showed no adverse post-surgical event over a follow-up of six months.

    Conclusions

    Persistent obesity and other socioeconomic factors may lead to colonizing asymptomatic H. pylori infection. More sensitive techniques for detecting H. pylori may be employed in resource-constrained settings for better patient outcomes and to minimize the complications after sleeve gastrectomy.

    Keywords: Polymerase Chain Reaction, Obesity, Helicobacter pylori, Gastritis, Body Mass Index
  • فرید زندی، امین طالبی بزمین آبادی*، اشرف محبتی مبارز، محمد عبدی
    زمینه و هدف

    هلیکوباکتر پیلوری، باکتری مسبب مشکلات گوارشی و سوء هاضمه می باشد که در نهایت می تواند منجر به سرطان معده شود. ژنهای مربوط به فاکتورهای بیماریزای هلیکوباکتر پیلوری عبارتند از : vacA، cagA، oipA و .iceA این مطالعه در  غرب ایران و در بیماران مبتلا به سوء هاضمه، با در نظر گرفتن فراوانی فاکتورهای بیماری زای هلیکوباکترپیلوری، به ارتباط این فاکتورها با یافته های پاتولوژیک مربوطه تمرکز کرده است.

    مواد و روش ها

    در این مطالعه از 120 بیماران مبتلا به سوء هاضمه (60 بیمار دارای التهاب معده و 60 بیمار دارای پپتیک اولسر) نمونه های بیوپسی معده به عمل آمد. ژنوتایپ فاکتورهای بیماری زای هلیکوباکترپیلوری با استفاده از روش واکنش زنجیره ای پلیمراز  انجام گردید. تجزیه و تحلیل داده ها با استفاده از نرم افزار SPSS 16.0  انجام شد. مقادیر  0/05≤ p از نظر آماری معنی دار در نظر گرفته شد.

     یافته ها

    فراوانی ژنوتایپ های بررسی شده در این مطالعه به ترتیب عبارتند از: vacA (%51/7s1  ، %21/7s2 ، 15/8%s1s2 ، 32/51%m1 ، %45m2 ،7/5% m1m2 ، %29/2s1m1 ، % 27/5s1m2 ،7/5%s2m1 ،7/5 %  s2m2)، 64/2 % cagA، 57/5%oipA ، 55 % iceA2 و 15 % iceA1/iceA2. همچنین بین حضور فاکتورهای بیماری زایcagA  (0/013 =p)، vacA (p=0/041) و  iceA (p=0/035) و نوع بیماری (گاستریت و پپتیک اولسر) از سوی دیگر ارتباط معنی داری مشاهده گردید. ارتباط معنی دار بین فاکتورهای بیماری زا و یافته های پاتولوژیک عبارتند از: فاکتور iceA با التهاب حاد (039/0 p=) و همچنین فاکتورهای oipA(p=0/00) و vacA (p=0/011) با میزان تراکم باکتریایی هلیکوباکترپیلوری به ترتیب (p=0/00)  و(p=0/011)را دارند.

    کلید واژگان: هلیکوباکترپیلوری، گاستریت، VacA، CagA، IceA
    Amin Talebi Abadi
    Background and Aim

    H. pylori can cause digestive problems and eventually can lead to gastric cancer. This study deals with the relationship between H. pylori virulence factors and pathological findings in the patients with gastroduodenal disorders in a particular geographical area in the west of Iran.

    Materials and Methods

    In this study, gastric biopsies were taken from 120 patients with indigestion (60 patients with gastritis and 60 patients with peptic ulcer). H. pylori virulence factors, vacA, cagA, oipA and iceA were determined by polymerase chain reaction (PCR). SPSS 16.0 software was used for data analysis. p≤0.05 was considered statistically significant.

    Results

    The frequencies of the genotypes were as following: vacA (s1 51.7 %, s2 21.7%, s1s2 15.8 %, m1 32.51 %, m2 45 %, m1m2 7.5 %, s1m1 29.2 %, s1m2 27.5%, s2m1 7.5 %, s2m2 7.5 %), cagA 64.2%, oipA 57.5 %, iceA2 55% and iceA1/iceA2 15% respectively. Also, a significant relationship was observed between virulence factors such as cagA (p=0.013), vacA (p=0.041) and iceA (p=0.035) on one hand, and type of disorder (gastritis and peptic ulcer) on the other hand. Considering the relationships between the virulence factors and pathological findings, a significant relationship was found between iceA and acute inflammation (p=0.039). Also oipA and vacA showed significant relationships with bacterial density of H. pylori (p=0,000) and (p=0.011) respectively.

    Conclusion

    The results of this study showed role of vacA and cagA in the type of disease and the impact of oipA and iceA in microscopic findings.

     

    Keywords: H. pylori, Gastritis, VacA, CagA, IceA
  • Sanjeev K. Jha*, Ravikant Kumar, Amitesh Kumar, Shubham Purkayastha, Ravi Keshri, Saurabh Kumar, Aditya Vardhan Singh
    BACKGROUND

    The increasing prevalence of antibiotic-resistant strains of Helicobacter pylori (H. pylori) led to reduced success with traditional H. pylori treatments. This warrants further evaluation of other treatment options. One such treatment regimen of interest is nitazoxanide containing regimen. In this study, we evaluated the efficacy of the addition of nitazoxanide to clarithromycin-based triple therapy in patients with H. pylori infection.

    METHODS

    In this single-center prospective observational trial, patients with H. pylori infection were treated with a regimen comprising of nitazoxanide 1000 mg, amoxicillin 2000 mg, clarithromycin 1000 mg, and esomeprazole 80 mg per day (NACE regimen) for14 days. Eradication of H. pylori infection was assessed 4 weeks after completion of therapy by using stool antigen assay. Treatment compliance and adverse effects were also evaluated.

    RESULTS

    Out of 111 patients who entered into the study for final analysis, H. pylori eradication was achieved in 93.7% (104 out of 111) patients in per-protocol analysis and 90.4% (104 out of 115) patients in intention to treat analysis. The treatment regimen was well tolerated.

    CONCLUSION

    The addition of nitazoxanide to standard clarithromycin-based triple therapy effectively eradicates H. pylori infection. This regimen is safe and well tolerated.

    Keywords: H. pylori infection, Nitazoxanide, NACE, Gastritis, Eradication
  • Abdollah Safikhani Mahmoodzadeh, Elham Moazamian *, Seyedeh Azra Shamsedin, GholamAbbas Kaydani
    Background/ Aims

    The worldwide prevalence of Helicobacter pylori is about 50%. This bacterium needs a number of virulence factors for pathogenesis. This study aimed to determine the prevalence of virulence genes (ureB, cytotoxin-associated gene A [cagA], and vacuolating cytotoxin [vacA]), as well as the antigenic profile in H. pylori strains.

    Materials and methods

    Eighty-five patients with abdominal pain, including 46 H. pylori-positive (Hp+) and 39 H. pylori-negative (Hp-) cases, were enrolled in this study. The serum levels of interleukin (IL)-17F, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) cytokines were measured by multiplex kits and flow cytometry. After molecular identification by the ureC gene, vacA, cagA, and ureB genes were detected by polymerase chain reaction (PCR). Finally, after antigenic extraction, the whole-cell protein was exhibited by sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS-PAGE).

    Results

    The prevalence of vacA, ureB, and cagA genes were 91.3%, 67.39%, and 50%, respectively. The frequency of genes and cell surface antigens were not significantly different based on the gastritis severity (p > 0.05). IL-17F significantly (p = 0.046) increased in the presence of 19.5 kDa (outer membrane protein [OMP]). Moreover, the OMP antigen significantly enhanced immunoglobulin A (IgA; p = 0.013). In the presence of the 66-kDa (ureB) antigen, the serum level of IFN-γ increased (p = 0.041). Finally, the CagA protein led to increased IgG antibody levels (p = 0.027).

    Conclusion

    Early detection of H. pylori infection can play a crucial role in managing it. Our results suggest that IL-17F, TNF-α, and IFN-γ cytokines could be diagnostic markers. However, further studies are required to fully investigate this suggestion.

    Keywords: Helicobacter Pylori, Cytokines, Gastritis, Virulence Genes, Antigenic profile
  • Yongjian Li, Qiong Chen *, Shasha Wang, Shichao Zhang
    Background

     Stomach disorders, including gastric cancer and gastritis, are associated with the pathogenic bacterium Helicobacter pylori. Enhanced inflammation is the characteristic of H. pylori-induced gastritis. Ligustrazine exerts anti-inflammatory properties in mouse asthma models and acute kidney injury.

    Objectives

     To determine the role of ligustrazine in H. pylori-induced gastritis.

    Methods

     Normal gastric epithelial cell line (GES-1) was cultured with H. pylori at a multiplicity of infection (MOI) of 100: 1 for 24 hours. GES-1 cell line under H. pylori condition was incubated with 100 or 200 μM ligustrazine for 24 hours. Cell viability and apoptosis were investigated by MTT and flow cytometry assays, respectively. Inflammation was assessed by determining the levels and mRNA expression of interleukins (IL)-6/8, tumor necrosis factor-α (TNF-α), and monocyte chemotactic protein 1 (MCP-1) using ELISA and qRT-PCR analysis, respectively.

    Results

     Helicobacter pylori infection reduced the viability and promoted the apoptosis of GES-1 cell line, accompanied by the enhanced activities of caspases 3 and 9. However, ligustrazine reversed the H. pylori-induced infection decreased viability, while increased apoptosis and caspases 3/9 activities in GES-1 cell line. Moreover, ligustrazine attenuated H. pylori-induced secretions of pro-inflammatory factors, IL-6/8, TNF-α, and MCP-1, in GES-1 cell line. The protein expression of inhibitor of NF-κB (IκBα) was downregulated in GES-1 cell line after H. pylori infection, while the protein expression levels of p65 and phosphorylation of IκBα were upregulated by H. pylori infection. On the contrary, ligustrazine decreased H. pylori-induced protein expression of IκBα, whereas increased protein expression of p65 and phosphorylation of IκBα.

    Conclusions

     Ligustrazine exerted protective effects on H. pylori-induced gastric epithelial cells through inhibition of gastric inflammation and apoptosis and inactivation of NF-κB pathway.

    Keywords: Inflammation, Apoptosis, Helicobacter pylori, NF-κB, Gastritis, Ligustrazine
  • Fatemeh Heidari, Tahereh Komeili-Movahhed, Zeinab Hamidizad, Azam Moslehi*
    Background and purpose

    Gastritis is one of the most current gastrointestinal disorders worldwide. Alcohol consumption is one of the major factors, which provides gastritis. Rosmarinic acid (RA) is found in many plants and has powerful antioxidant and anti-inflammatory effects. In this study, the protective effect of RA was evaluated on the histopathological indices, antioxidant ability, and prostaglandin E2 (PGE2) secretion in male rats.

    Experimental approach

    Forty-two animals were divided into control, ethanol-induced gastritis, and RA groups, 6 each. The protective groups included RA administration before gastritis induction at 50 mg (R-G50), 100 mg (R-G100), 150 mg (R-G150), and 200 mg (R-G200) doses. Gastritis was induced by gavage of 1 mL pure ethanol in fasted animals. After 1 h of gastritis induction, the rats were sacrificed and stomach tissue was removed.

    Findings/ Results

    Histological evaluation revealed that RA significantly attenuated gastric ulcers, leucocyte infiltration, and hyperemia. It also increased mucosal layer thickness and restored gastric glands. Furthermore, RA decreased malondialdehyde level, increased superoxide dismutase, catalase, and glutathione in the stomach tissue, and raised gastric PGE2 level.

    Conclusion and implications

    Our study demonstrated that rosmarinic acid has a notable effect on gastritis protection that could be due to increased antioxidant defense and PGE2 secretion, eventually maintenance of mucosal barrier integrity and gastric glands.

    Keywords: Alcohol, Gastritis, Oxidative stress, PGE2, Rosmarinic acid
  • Mehmet Nuri ACIK *, Aykut ULUCAN, Pınar Cakan, Tugce Atcali, Seda Yakut, Emre Sahin, Burhan CETINKAYA
    Stress has been suggested to play an important role in the pathogenesis of gastric damage by either acting as a predisposing factor or a primary factor. Arcobacter species have frequently been isolated from stomach ulcer cases of pigs, but the role of these agents in the pathogenesis of the disease remains unclear.The primary aim of the present study was, to reveal the role of Arcobacter butzleri and stress in the etiology of gastric damage by establishing an experimental mouse design. Infection was induced by intra-gastric gavage of A. butzleri in two experimental groups comprising five weeks old specific pathogen-free (SPF) Balb/c mice. At 1, 2, 3, 4, and 7th weeks of the experiment, the animals were euthanized and examined for lesions occurring in the stomach. Histopathology, culture, and Polymerase Chain Reaction (PCR) were employed to detect development and severity of lesions and pathogens. In addition, serum corticosterone levels indicating the presence of stress in the mice were investigated by an ELISA method. Microscopic examination showed that the stomach of the experimental group had inflammatory reactions to varying degrees, but ulcers were not observed in the gastric mucosa of the animals exposed to A. butzleri and stress groups. The results suggested that A. butzleri and stress were predisposing factors in the formation of gastric ulcer, but failed to provide evidence for their causative role.
    Keywords: Arcobacter butzleri, BALB, c mice, Stress, Corticosterone, gastritis
  • آرمین قامشلو*، علی رشیدی نژاد، مسعود آل بویه، عباس شکوری
    مقدمه

    گاستریت یا ورم معده، یکی از رایج‌ترین بیماری‌های درگیرکننده معده است. عفونت با Helicobacter pylori می‌تواند به آسیب‌های DNA و به دنبال آن، فعال شدن مسیرهای ترمیم DNA مستعد خطا منجر گردد که متعاقب آن، تجمع آسیب‌ها در محل شکست‌های دو رشته DNA و تشدید بی‌ثباتی ژنوم و تسهیل در روند ایجاد سرطان معده می‌شود. در این مطالعه، بیان ژن‌های ATM، POLM و TP53 که در سیستم ترمیم DNA و توقف چرخه سلولی نقش دارند، در مراحل پیش‌سرطانی معده بررسی گردید.

    مواد و روش‌ها

    از 180 نمونه بیوپسی جمع‌آوری‌شده، 30 نمونه که گاستریت مزمن متوسط آلوده با هلیکوباکتر پیلوری داشتند، به‌عنوان گروه مورد و 30 نمونه دیگر که گاستریت مزمن خفیف بدون آلودگی با هلیکوباکتر پیلوری داشتند، به‌عنوان گروه شاهد در نظر گرفته شدند. پس از استخراج RNA، ساخت cDNA انجام و بیان ژن‌های ATM، POLM و TP53 با روش Real Time PCR در دو گروه سنجیده گردید.

    یافته‌های پژوهش

    ژن‌های ATM، POLM و TP53 در گروه مورد نسبت به گروه شاهد، به ترتیب 07/4، 35/3 و 13/5 افزایش بیان در سطح نسخه‌برداری را نشان دادند.

    بحث و نتیجه‌گیری

    درمجموع، ژن‌های ATM، POLM و TP53 بیان بالاتری را در گروه مورد نسبت به گروه شاهد نشان دادند که ممکن است بیانگر فعال شدن این ژن‌ها پس از عفونت هلیکوباکتر پیلوری و به دنبال آن، فعال شدن مسیر ترمیم DNA مستعد خطا و نوترکیبی غیرهومولوگ شود.

    کلید واژگان: گاستریت، هلیکوباکترپیلوری، شکست های دو رشته DNA، ATM، POLM، TP53
    Armin Ghameshloo*, Ali Rashidi-nezhad, Masoud Alebouyeh, Abas Shakouri
    Introduction

    Gastritis is one of the most common diseases affecting the stomach. Helicobacter pylori infection could lead to DNA damage in gastric epithelial cells, followed by error-prone DNA repair pathways that increase the accumulation of damage at the site of DNA double-stranded breaks, exacerbate genome instability, and facilitate the emergence of gastric cancer. This study aimed to examine the expression level of ATM, POLM, and TP53 genes involving in the DNA Damage Response and the cell cycle arrest in the gastric precancerous stage.

    Materials & Methods

    Among 180 gastric biopsy specimens, 30 samples taken from patients with moderate chronic gastritis infected by H. Pylori were regarded as the case group, and 30 other samples taken from non-infected patients with mild chronic gastritis were regarded as control. Following that, RNA extraction and cDNA synthesis was performed. Afterward, the expression levels of ATM, POLM, and TP53 genes were evaluated by the Real-Time PCR method. Ethics code: 98-02-27-43392

    Findings

    The ATM, POLM, and TP53 genes in the cases showed a 4.07, 3.35, and 5.13 increase in the gene expression at the transcriptional level, compared to the controls.

    Discussion & Conclusions

    In general, ATM, POLM, and TP53 genes showed a higher increased expression level in the case group, compared to the controls, which might indicate the activation of noted genes after H. pylori infection. This may subsequently activate the error-prone DNA repair and non-homologous recombination pathways.

    Keywords: ATM, POLM, TP53 genes, DNAdouble stranded breaks, Gastritis, H. pylori
  • Behnaz Eslami, Majid Iranshahi, Latif Gachkar, Fahimeh Hadavand *
    Background

     Identification of the causes of gallstone would result in better planning for the prevention of this disease. One of the proposed risk factors for this problem is Helicobacter pylori(H. pylori) infection.

    Objectives

     The purpose of this study was to determine the incidence rate of gallstone in patients with H. pylori gastritis.

    Methods

     This was an observational study performed as a descriptive-comparative cross-sectional survey. We enrolled 169 consecutive patients with H. pylori gastritis admitted to Imam-Hossein Hospital, Tehran, Iran, in 2018, and gallstone frequency in them was determined and compared with other variables.

    Results

     Overall, 14 (8.3%) patients had gallstone, and all the patients had H. pylori gastritis. There was no significant association between gallstone and H. pylori gastritis (P = 0.561).

    Conclusions

     It may be concluded that gallstone frequency in patients with H. pylori gastritis is low, and there is no significant association between these two conditions.

    Keywords: Gallstone, Helicobacter pylori, Gastritis
  • Noor Muhammad, Jehanzeb Afridi, Nourin Mahmood, Sajid Ali*
    Background

    There are studies on Helicobacter pylori infection in Khyber Pakhtunkhwa. However, district Buner is far away, and most people have the least access to more developed techniques for the diagnosis of different diseases, and no study has been conducted in this region. Therefore, this study was conducted to determine the frequency of H. pylori infection in patients presenting with upper gastrointestinal symptoms.

    Objectives

    This study aimed to determine the frequency of H. pylori antigen in the stool of patients with upper gastrointestinal symptoms.

    Methods

    A cross-sectional study was conducted at Bilal Medical Trust Hospital from February 2018 to November 30, 2019. A total of 111 patients presenting with upper gastrointestinal symptoms were included in this study. A purposive (non-probability) sampling technique was used. All of the patients were screened for H. Pylori in stool specimens using a specific stool H. pylori device.

    Results

    Out of 111 patients, 74 (66.66%) were reported positive for H. pylori infection, among whom, females had a higher ratio (54.05%) than had males (45.94%). The infection was more prevalent in patients aged 20 - 30 years (43.67%). Patients who consumed fresh milk had higher rates of infection than those who used powdered milk/packed milk (52.54% vs. 15.25%). Patients who consumed water from water wells had a higher infection rate (72.87%) than those who used water from tube wells (27.11%).

    Conclusions

    The present study revealed a higher prevalence of H. pylori in females than in males. The maximum prevalence was noticed in the age group of 20 - 30 years. The study indicated a significantly higher rate of H. pylori infection in patients who used uncooked milk and water from contaminated sources.

    Keywords: Age, Gender, Helicobacter pylori, Milk, Gastritis, Dyspepsia
  • محدثه زجاجی، علیرضا شریفی، احمد حرمتی*، فائزه عالمی، محبوبه عفیفیان، سید حسن عابدی
    Mohaddeseh Zojaji, Alireza Sharifi, Ahmad Hormati*, Faezeh Alemi, Mahboubeh Afifian, Seyed Hassan Abedi
    Background

    Helicobacter pylori infection is one of the most common bacterial infections that is affecting approximately half of the world's population. This bacterial infection causes gastrointestinal diseases, including gastritis and peptic ulcers. It is also the only microbial agent with definite association with gastrointestinal cancers such as adenocarcinoma and gastric mucosal lymphoma. The prevalence of this infection in Iran is reported to be 36% to 90% in different regions. Therefore, eradication of this germ is of great importance and has always been of interest to clinical researchers.

    Objective

    The aim of this study was to evaluate the antibiotic resistance of Helicobacter pylori infection in different regions of Iran based on previous studies. Also, introducing the most effective antibiotics based on antibiotic susceptibility in Iran is the ultimate goal of this study.

    Material and Methods

    Many studies have been done in different regions of Iran to show the antibiotic resistance of Helicobacter pylori, but no comprehensive review of these studies has been done until 2019. It is worth noting that the prevalence of resistance to antimicrobial therapies is increasing. Therefore, we conducted a review of these studies to obtain comprehensive results on the antibiotic susceptibility of Helicobacter pylori. We searched the databases of Google Scholar, Scopus, and PubMed and reviewed the studies in Iran until 2019 with more emphasis on the last five years.

    Results

    A total of 48 articles were reviewed, the results are summarized in the tables, and the best antibiotics to affect on Helicobacter pylori infection were also identified. It is worth noting that eradication rates in different regions of Iran based on different treatment regimens of three, four, and concomitant drugs in different studies have also been shown in tables, separately.

    Conclusions

    According to available data, the best first-line eradication regimen in Iran appears to be a 14-day quadruple therapy with amoxicillin, clarithromycin, bismuth, and a proton pump inhibitor (PPI). Cases of treatment failure should also be treated with a combination of amoxicillin and levofloxacin, or amoxicillin and rifabutin in combination with a PPI after evaluation and determination of antibiotic resistance.

    Keywords: Helicobacter pylori, Gastritis, Antibiotic resistance, Eradication, Iran
نکته
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