Absence Of Helicobacter Pylori Research Articles

A Novel Characteristic Gastric Mucus Named "Web-like Mucus" Potentially Induced by Vonoprazan.

Background: In the absence of Helicobacter pylori (HP) infection, a characteristic gastric mucus adhesion may appear during the use of vonoprazan. We named this novel characteristic mucus "web-like mucus" (WLM). This study aimed to determine the incidence and risk factors for WLM. Methods: Between January 2017 and January 2022, 5665 patients were enrolled in this study. The patients were divided into a proton-pump inhibitor (PPI)-prescribed group (n = 2000), a vonoprazan-prescribed group (n = 268), and a no-PPI/vonoprazan-prescribed (n = 3397) group, and the presence of WLM was examined. After excluding four patients with autoimmune gastritis, the remaining 264 patients in the vonoprazan group were divided into WLM and non-WLM groups, and their clinical features were analyzed. Results: A total of 55 (21%) patients had WLM, all in the vonoprazan-prescribed group. There were no significant differences in factors such as, sex, age, chronic kidney disease, diabetes mellitus, HP eradication history, smoking, or alcohol consumption between the WLM and non-WLM groups. The median duration from the start of vonoprazan administration to the endoscopic detection of WLM was 2 (1-24) months. Conclusions: WLM appears to be a characteristic feature in patients treated with vonoprazan.

Esophagogastric cancer after sleeve gastrectomy and roux-en-Y gastric bypass, its prevalence and risk factors: A meta-analysis

Abstract Purpose: In light of the increasing prevalence of esophagogastric cancer (EGC), the altered anatomy after bariatric surgery (BS) (mainly laparoscopic sleeve gastrectomy [LSG] and roux-en-Y gastric bypass [RYGB]) presents difficulties in treating these cancers. The article focuses on the risk factors associated with the development of EGC post-LSG and RYGB. Methods: Relevant articles were identified from databases such as SCOPUS, PubMed, and Web of Science (from 2010 to May 2022). From the selected and screened articles, a meta-analysis was performed using different statistical methods by calculating odds ratios, the t-test, and the discrepancies (95% confidence interval), to estimate the incidence of GC. Publication bias was estimated based on Cochrane risk tool and Newcastle–Ottawa Quality Assessment Scale. Results: The study included case reports (26), random control trials (RCT) (2), case series (6), and prospective (2) and retrospective studies (5). The current article also includes one each of epidemiological and medical administrative database studies. The 43 selected articles comprised 807,458 patients with BS, where 57.5% underwent LSG and 42.5% underwent RYGB. The average age and body mass index (BMI) were 48.11 and 43.53 ± 8.97 in the case of LSG, respectively. The average age was 52.77 and BMI was 42.62 ± 9.21 for RYGB. The obtained results suggested that cancer development is at higher risk in LSG among patients with comorbidities, absence of Helicobacter pylori, and delayed diagnosis, irrespective of their smoking habit. The incidence of the tumor or cancer and its severity is higher after LSG with 41.17% in comparison to RYGB 9.52%. A significant variation was observed in the period of cancer diagnosis. A minimum of 2 and 4 months and a maximum of 96 and 252 months variation have been observed for LSG and RYGB, respectively. No publication bias was noticed based on the selected articles. Furthermore, no direct correlation was identified or measured between the development of ECG and LSG/REYGB surgeries from the collected literature. EGC therapy following BS is complex and requires a personalized strategy that carefully balances optimal treatment with anatomical limitations. Conclusions: The risk factors like obesity, comorbidities, smoking, H. pylori infection, tumor stage, and diagnostic tests must be evaluated before BS. Although the current evidence-based practice does not advocate for a routine preoperative endoscopy, we highly advise for a preoperative endoscopic procedures before BS in the presence of the highlighted EGC risk factors.

ASSOCIATION OF HELICOBACTER PYLORI WITH PEPTIC PERFORATION

Background: Helicobacter pylori infections have been proved to be associated with peptic ulcer disease, gastritis, gastric adenocarcinoma, gastric lymphoma. The role of Helicobacter pylori is not well established in cases of peptic perforation. The objective of this study is to observe the presence or absence of Helicobacter pylori in cases of perforated peptic ulcer. Methods: We have done a cross sectional observational study with data from patients presenting to the emergency of a tertiary care hospital with perforated peptic ulcer and undergoing emergency exploratory laparotomy followed by omental patch repair. We collected mucosal biopsy samples from gastric/duodenal mucosa along margin of perforation site of these patients and performed rapid urease test using Rapid Urease Test kit. Of the 50 participants in our study, 48 (96%) were males Results: and 2 (4%) were females. 37 (74%) cases had perforation at pre pyloric region, and in 13 (26%) cases perforation was present at rst part of duodenum. Rapid urease test by Rapid Urease Test kit was found to be positive in 6 (12%) cases and negative among 44 (88%) cases. Conclusion: In our study, frequency of Helicobacter pylori in perforated peptic ulcer cases was found to be only 12% which proves that there may be other contributing factors in perforated peptic ulcer cases, which need further evaluation. Objective: To assess the presence of Helicobacter pylori in mucosal surface of stomach and duodenum in patients undergoing emergency exploratory laparotomy followed by omental patch repair in patients of peptic perforation.

Dysregulation of Expression of the FOXO3 Transcription Factors Pathway in Helicobacter pylori Associated Gastric Cancer

The transcription factor FOXO3 acts as a tumor suppressor and is the major target of AKT kinases pathway. The protein encoded by FOXO3, prevents the activation of genes that are important for proliferation, differentiation and death cell. In addition, FOXO3 interacts with BCL-2 family proteins; and among them, BBC3 (PUMA) and BCL2L (BIM) are responsible for regulating apoptosis through the BAX and BAK chains. This study investigated the expression of FOXO3a, BBC3 and BCL2L in gastric cancer considering the presence of Helicobacter pylori and its involvement in the modulation of gene and protein expression. A total of 225 gastric biopsy samples were evaluated from individuals with normal gastric mucosa (n=54), gastritis (n=108), and gastric cancer (n=63), of both genders and over 18 years old. Samples were subclassified according to the presence or absence of Helicobacter pylori, detected by PCR. Real-time quantitative RT-PCR (qRT-PCR) and western blotting, were used to detect the expression. FOXO3 showed increased gene (p<0.0001) and protein (p=0.036) expression in patients with gastric cancer, who also exhibited a boost in mRNA expression through H. pylori infection. BCL2L had a subtle increase in its expression independent of the presence of H. pylori (p<0.0001), while the BBC3 gene showed no alterations. Our results suggested that increase FOXO3 expression may play an important role in carcinogenesis by performing positive feedback in an attempt to eliminate neoplastic cells. FOXO3 could be suggested a prognostic marker as well as a potential molecular therapy target for gastric cancer patients.

Overexpressions of RHOA, CSNK1A1, DVL2, FZD8, and LRP5 genes enhance gastric cancer development in the presence of Helicobacter pylori

Background and study aimsIntestinal metaplasia (IM), and Helicobacter pylori (HP) infection can be shown as risk factors in the development of gastric cancer (GC). WNT signaling pathway plays a critical role in carcinogenesis. However, the literature studies are limited on the significance of this pathway for the transition from IM to GC. Patients and methodsWe aimed to investigate the importance of the genes of WNT signaling pathways diagnostic and prognostic markers in the presence and absence of HP in conversion from IM to GC. 104 patients, (GC group n = 35, IM group n = 45, control group n = 25) were included in this case-control study. Expression of genes in WNT signalling were searched in study groups with qRT-PCR array and qRT-PCR method. Data were analysed using PCR array data analysis software. ResultsStatistically significant overexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes was detected in the GC and IM groups compared to the control group (p < 0.05). Statistically significant overexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes was observed in patients with metastatic GC compared to patients with GC without metastasis (p < 0.05). It was found that the RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes were statistically significantly over-expressed in diffuse GC patients compared to non-diffuse GC patients (p < 0.05). Statistically significant overexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes was detected in HP positive IM patients compared to HP negative IM patients (p < 0.05). ConclusionOverexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes in IM may suggest that these genes are important markers in the development of IM and inflammation with HP. In addition, these genes are linked to tumor burden in the GC group. Consequently, we can conclude that these genes are poor prognosis biomarkers for GC and have the potential to be used as markers for future treatment monitoring.

Relationship between tumor infiltrating lymphocytes and clinicopathological features in Peruvian gastric cancer.

e16080 Background: Role of tumor-infiltrating lymphocytes (TIL) over clinicopathological features including Mismatch Repair (MMR), HER2 status, Epstein Barr Virus (EBV) and Helicobacter pylori (HP) infection is not well understood in gastric cancer (GC). Methods: TIL level and HP infection was also evaluated in H&amp;E from 503 Peruvian GC patients who underwent surgery. Density of CD3+ T cells, CD8+ cytotoxic T cells, CD163 M2 macrophages, as well as MMR and HER2 status were determined by immunohistochemistry. HP and EBV infection was also detected by qPCR in a 234 cases subset. Results: Median age was 62 years and 50.1% were female, most tumors were grade 3 (59.1%), intestinal subtype (44.8%) and stage III (59.8%). MMR loss was found in 29.4% and HER2+ in 4.7%. HP+ was detected by H&amp;E in 55.7% and by qPCR in 63.7%. EBV+ by qPCR was found in 20.5% and co-infection along with HP in 9.4% (22/234). Stage (p &lt; 0.001), intestinal histology (IH) (p = 0.019), grade (p = 0.006) and lymphovascular invasion (p &lt; 0.001) were associated with longer survival. Median TIL was higher in invasive border (IB) and stromal (ST) than intratumoral (IT) compartment but there were significantly correlated (p &lt; 0.001). High IT TIL was associated with absence of HP H&amp;E (p = 0.009). High ST TIL was associated with older age (p &lt; 0.001), IH (p &lt; 0.001), grade 1 (p = 0.009), lower stage (p = 002), MMR loss (p = 0.019) and EBV+ (p = 0.001). Density of CD3 and CD8 were significantly correlated in IT and ST compartments (p &lt; 0.001). High CD3 density in IT compartment was associated with grade 3 (p = 0.001) and HP- (p = 0.02), and in ST was associated with IH (p = 0.005), grade 1- 2 (p = 0.002) and MMR loss (p = 0.04). High IT CD8 was associated with HER2- (p = 0.016), HP- (p = 0.014) and EBV+ (p = 0.012). High ST CD8/CD3 ratio was associated with diffuse histology (p = 0.034), grade 3 (p = 0.013), more advanced stage (p = 0.022) and recurrence (p = 0.014). High ratio of IT CD8/CD3 was associated with MMR loss (p = 0.007). High ST TIL was associated with longer DFS (p = 0.007). Lower ratio of CD8/CD3 was associated with longer OS (p = 0.024) and DFS (p = 0.02). Conclusions: TIL levels and infiltrating immune subpopulations differs by clinicopathological features in GC including MMR loss, HER2 expression EBV and HP infection. ST CD8/CD3 was associated with recurrence and shorter DFS.

Intestinal microbiota and immunity. Possibilities of multistrain probiotics in the correction of immune status in children

On the basis of the analysis of foreign and Russian scientific studies the current data on the role of the intestinal microbiota in the formation of immunity and changes in its qualitative composition in the formation of various diseases are presented: For example, a decrease or absence of Helicobacter pylori is associated with bronchial asthma and reflux esophagitis in childhood, a change in Firmicutes/Actinobacteria ratio in psoriasis, and Bacteroidetes/Firmicutes ratio in the gastrointestinal tract in obesity, inflammatory bowel diseases are accompanied by an increase in Enterobacteriaceae, functional disorders of the gastrointestinal tract by a growth of Veillonella bacteria. The article shows the mechanisms of influence of the microbiota of the gastrointestinal and respiratory tracts on reducing the frequency of repeated infections by induction of antiviral defense genes, which in studies of probiotic therapy is confirmed by significant clinical effects. A discussion of the benefits of multistrain probiotics with comprehensive effects on the intestinal microbiota is provided. The importance of including probiotic strains in the complex therapy of acute respiratory infections is confirmed by the studies proving their positive effect on the child’s immunity, reducing the severity of the disease and the frequency of complications and relapses. The results of modern scientific research prove the importance of the optimal ratio of probiotic strains in the combination of lactoand bifidobacteria, as well as their strain specificity. The article presents information on a synbiotic created using an innovative protective technology of each sachet microgranule including a combination of 9 probiotic strains of lactoand bifidobacteria. The presence of fructooligosaccharide in the prebiotic component enhances the effect of the probiotic component.

Relationship between time-varying status of reflux esophagitis and Helicobacter pylori and progression to long-segment Barrett\u2019s esophagus: time-dependent Cox proportional-hazards analysis

BackgroundReflux esophagitis (RE) and absence of Helicobacter pylori (non-H. pylori) are considered to be associated with the progression to long-segment Barrett’s esophagus (LSBE). However, it is difficult to assess this association because RE and H. pylori status can change during follow-up. Additionally, the association between H. pylori eradication and LSBE remains unclear.MethodsA total of 11,493 asymptomatic Japanese subjects who underwent medical check-ups and were endoscopically diagnosed with short-segment Barrett’s esophagus (SSBE) between May 2006 and December 2015 were enrolled. The hazards of progression to LSBE were compared between time-varying RE and H. pylori infection/eradication by time-dependent multivariable Cox proportional hazards models.ResultsA total of 7637 subjects who underwent additional medical check-ups after being diagnosed with endoscopic SSBE were analyzed. Subjects with RE and without current/past H. pylori infection were strongly associated with a higher rate of progression to LSBE (adjusted hazard ratio [HR]: 7.17, 95% confidence interval [CI]: 2.48–20.73, p < 0.001 for RE and non-H. pylori vs. non-RE and H. pylori groups). Subjects with H. pylori had a lower rate of progression to LSBE (adjusted HR: 0.48, 95% CI: 0.22–1.07, p = 0.07 for H. pylori vs. non-H. pylori). Hazards of progression to LSBE were still lower in the H. pylori eradication group than that of the non-H. pylori group (adjusted HR: 0.51, 95% CI: 0.18–1.46, p = 0.21).ConclusionsRE and non-H. pylori were associated with the progression to LSBE, considering the changes in exposures. H. pylori infection was associated with the prevention of the development of LSBE irrespective of RE. The environment preventive of the development of LSBE persists for at least a few years after H. pylori eradication.

Abstract 1261: Detection of autophagy in gastric mucosae of Chilean individuals residing in a geographic region characterized by high rates of gastric cancer-related death

Abstract Gastric cancer is the fourth most common cancer worldwide. In Chile, gastric cancer is the first cause of cancer-related deaths, affecting most prominently the southern provinces. Therefore, the elucidation of molecular pathways that might be exploited to improve prognosis and therapies remains an important challenge. There is emerging evidence pointing to the role of autophagy in tumorigenesis. Autophagy, a lysosome-mediated catabolic process, represents a prosurvival process implemented by neoplastic cells in response to stressful stimuli. So far, markers of autophagy have been used as prognosis determinants in early stages of gastric cancer, or have been associated to recurrence and reduced survival in patients with advanced disease. However, the role of autophagy in precursor lesions (chronic gastritis, metaplasia, dysplasia) has not been explored. Our goal was to examine the presence of autophagy (cleaved-LC3A) and proliferation (Ki-67) markers in gastric biopsies obtained from healthy individuals residing in a Chilean geographic zone characterized by a high gastric cancer-related mortality. Toward this goal, 165 asymptomatic individuals, aged 40 to 70, from the Molina area in the south of Chile were subjected to endoscopy and biopsy sampling according to the Operative Link on Gastritis Assessment (OLGA) staging system. Each tissue section was processed for immunohistochemical detection of cleaved-LC3A and Ki67, and the results were correlated with the histopathological findings and the presence or absence of Helicobacter pylori. Our preliminary analyses indicate that 60% of individuals harbor at least one out of five biopsies with the highest score values for cleaved-LC3A staining. Most of these high-scored samples involved the gastric antrum (73.3%) and were also positive for the Ki67 proliferation marker (63.3%). Of note, tissue samples showing the highest score values for cleaved-LC3A staining occurred almost always (93.3%) in the context of chronic gastritis or a combination of chronic gastritis and intestinal metaplasia, even though only 56.7% of cleaved-LC3A positive tissues showed signs of Helicobacter pylori infection. These results seem to indicate that autophagy may allow gastric epithelial cells to circumvent inflammatory stress, highlighting this process as a potential target for the development of anti-cancer or preventive therapies.Grant Support: FIC-30388034-0, CONICYT-FONDAP 115130011, Fondecyt 1151411, PIA-Gastric cancer UTALCA Citation Format: Alejandro Corvalan, Hernan Pulgar, Claudio Cruzat, Nicole Cespedes, Francisco Ruiz, Rodrigo Prado, Nelson E. Brown. Detection of autophagy in gastric mucosae of Chilean individuals residing in a geographic region characterized by high rates of gastric cancer-related death [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1261.

Conventional Therapy vs Nitazoxanide Plus Omeprazole for the Eradication Of Helicobacter Pylori : A Randomized Control Trial

Helicobacter pylori has an important association with Peptic Ulcer Disease (PUD). Numerous trials have proved that eradication of Helicobacter pylori results in healing of PUD and a very low recurrence rate. Attempts at eradication in Bangladesh with different regimens showed poor results. In Bangladesh there is no study with regimen containing Nitazoxanide and Omeprazole that showed to be very effective in several trails in different countries. This study was conducted in the Medicine department, Chittagong Medical College Hospital, from December 2008 to November 2009 to evaluate the efficacy of Nitazoxanide and Omeprazole in the eradication of Helicobacter pylori in PUD patients of Bangladesh. 130 endoscopically proven PUD patients were enrolled in this study when rapid urease test gave positive result &amp; randomized into two halves for comparison of treatment regimens. After six weeks endoscopy was done. Ulcer healing, rapid urease test negativity and absence of Helicobacter pylori in histology was considered as cure. Conventional group treated with Clarithromycin, Amoxicillin, Lansoprazole for 14 days showed cure rate of 80%, whereas nitazoxanide group showed 76% cure, the difference is not statistically significant. This study shows that two regimens are effective and comparable though newer regimen failed to show superiority over conventional treatment. JCMCTA 2016 ; 27 (1) : 33 - 39

Acquired Small Bowel Mucosa-Associated Lymphoid Tissue Lymphoma in the Absence of Helicobacter pylori

Acquired Small Bowel Mucosa-Associated Lymphoid Tissue Lymphoma in the Absence of Helicobacter pylori

Preventive effect of rebamipide on N-methyl-N′-nitro-N-nitrosoguanidine-induced gastric carcinogenesis in rats

Chemoprevention strategies against gastric cancer (GC) need to be explored in light of the fact that stomach cancer still occurs in the absence of Helicobacter pylori (HP) infection and following HP eradication. We evaluated the effect of rebamipide on N-methyl-N′-nitro-N-nitrosoguanidine (MNNG)-induced carcinogenesis in SD rats. Thirty-nine male rats were divided into four groups based on whether or not they were treated with rebamipide and/or MNNG: Control, Rebamipide, Control-M, and Rebamipide-M groups. From 8 weeks of age, rats in the Control-M and Rebamipide-M groups received MNNG in drinking water for 30 weeks. The Rebamipide and Rebamipide-M groups were administered 5mg/kg/day of rebamipide. At 50 weeks, cancerous lesions were not observed in either the Control or Rebamipide groups. Nine rats in the Control-M group had developed GC, while four rats in the Rebamipide-M group had developed GC. The incidence of cancer in the Rebamipide-M group was significantly less than in the Control-M group (p<0.05), with a trend toward a lower incidence of invasive carcinoma in the Rebamipide-M group. Carcinomatous invasion into the muscularis propria was not observed in the Rebamipide-M group. In conclusion, the present study demonstrates that rebamipide suppresses. MNNG-induced carcinogenesis and may also inhibit progression of cancer in rats.

AB0896 Characteristics of Systemic Sclerosis and Localized Scleroderma in Children and Adolescents

BackgroundSystemic sclerosis (SS) is a connective tissue disease with inflammation, fibrosis and vascular damage. Early diagnosis may be difficult if disease expression is oligosymptomatic, presenting with only Raynaud's phenomenon or...

No evidence for Helicobacter pylori in oral lichen planus.

Oral lichen planus is a T-cell-mediated mucosal disease of unknown etiology. Numerous predisposing factors have been put forward in the etiology of this disease. This includes stress, drugs, genetic susceptibility, certain viruses, and bacterial infections. Recently, there have been studies published on possible role of Helicobacter pylori infection in pathogenesis of mucocutaneous diseases including oral lichen planus (OLP). The aim of this study was to detect immunohistochemically the presence of Helicobacter pylori in oral lichen planus. Paraffin-embedded tissue blocks of 50 cases of OLP and 10 cases of normal buccal mucosal biopsies and 6 endoscopic biopsies of patients with peptic ulcer (control group) were sectioned and stained by hematoxylin and eosin. Serial sections of same were stained immunohistochemically using Anti-Helicobacter pylori antibody and observed under microscope for presence or absence of Helicobacter pylori. Except for the control group, none of the cases of OLP and normal buccal mucosal biopsies showed positivity for Helicobacter pylori. As we did not detect the presence of Helicobacter pylori in any of the OLP cases, we question the role of these organisms in the pathogenesis of OLP planus if any.

Effects of IL-1β on the proliferation and apoptosis of gastric epithelial cells and acid secretion from isolated rabbit parietal cells

The aim of the present study was to explore the effects of IL-1β on the proliferation and apoptosis of gastric epithelial cells and acid secretion from isolated rabbit parietal cells. The mechanisms by which these effects are mediated were also investigated. Parietal cells were isolated from rabbit gastric mucosa by elutriation. The AGS human gastric cancer cell line, the GES-1 human gastric epithelial cell line and parietal cells were treated with interleukin (IL)-1β in the presence or absence of Helicobacter pylori (H.pylori) for the times indicated. MTT assay and flow cytometry (FCM) were used to determine the levels of proliferation and apoptosis. The expression levels of cyclooxygenase-2 (COX-2) mRNA and protein were examined by RT-PCR and FCM. Acid secretion by parietal cells was examined using 14C-aminopyrine (14C‑AP) accumulation. H+/K+ATPaseα subunit mRNA expression was assessed by RT-PCR. The results demonstrated that IL-1β (10ng/ml) stimul-ated cellular proliferation and inhibited H.pylori-induced apoptosis in GES-1 and AGS cell lines. IL-1β (10ng/ml) upregulated the mRNA and protein expression of COX‑2 in GES-1 and AGS cells. Acid secretion stimulated by histamine was identified as significantly inhi-bited and mRNA expression of H+/K+ATPaseα subunit was downregulated by treatment with IL-1β (10ng/ml) for 30min and 16h compared with the control in isolated rabbit parietal cells. The present study demonstrates that IL-1β plays a significant role in H.pylori-induced gastric carcinogenesis through 2main mechanisms: i) IL-1β may interfere in gastric epithelial cell growth by upregulating COX-2 expression; ii)IL-1β may inhibit the acid secretion from parietal cells by downregulating H+/K+ATPase expression.

The Association between Helicobacter Pylori and Laryngopharyngeal Reflux in Laryngeal Pathologies

We conducted a study to determine the presence or absence of Helicobacter pylori and laryngopharyngeal reflux (LPR) in 43 previously untreated patients who had presented with a laryngeal lesion. Our aim was to determine if there was any association among H pylori, LPR, and laryngeal lesions. H pylori status was determined by real-time polymerase chain reaction (PCR) assays of biopsy tissue obtained during direct laryngoscopy. The presence or absence of LPR was determined on the basis of patients' reflux symptom index (RSI) and reflux finding score (RFS), which were based on their questionnaire responses and findings on endoscopic examination of the larynx, respectively. Patients with an RSI of 14 or more and/or an RFS of 8 or more were considered to have LPR. H pylori was present in 24 patients (55.8%) and absent in 19 (44.2%)-not a statistically significant difference. The prevalence of LPR was higher than the prevalence of H pylori; it was present in 30 patients (69.8%) and absent in 13 (30.2%). The difference was statistically significant (p = 0.01). We found no association between H pylori status and LPR status. Additionally, we analyzed two subgroups based on whether their lesions were benign or malignant/premalignant and found a significant relationship between LPR positivity and the presence of malignant/premalignant laryngeal lesions (p = 0.03). We found no association between H pylori status and either of the two subgroup categories.

Absence of Helicobacter pylori in the river waters in the north of Iran

Helicobacter pylori is a helical shaped bacterium that predominantly resides in stomach and duodenal epithelia. It is believed to be responsible for localized inflammations resulting in peptic ulcers as well as other digestive tract complications. Although half of the world’s population are carriers of the bacterium, its exact mode of transmission and pathogenic mechanisms are yet to be elucidated. The major purpose of this study was isolation and identification of H. pylori from river waters in north of Iran. The preT-KB method was used for isolation and PCR technique for detection of DNA. The presence of the bacterium was not observed in any of the 235 samples of water analyzed. The results of the PCR on the water samples confirmed the absence of Helicobacter´s DNA. Considering that the applied technique could identify the number of 102 bacteria and 0.1 µg of DNA in each milliliter, we believe that the samples collected from this geographical region were not contaminated with H. pylori. Key words: Helicobacter, river waters, north of Iran

Comparison of enzyme immunoassays detecting Helicobacter pylori specific IgG in serum and saliva with endoscopic and biopsy findings in patients with dyspepsia

Purpose: To compare the performance of two indirect enzyme-linked immunosorbent assays (ELISA) detecting Helicobacter pylori (HP)-specific IgG antibodies in serum and saliva with endoscopic observations and histologic findings of biopsies from dyspeptic patients, in an area of high HP prevalence. Materials and Methods: Sera, saliva and antral biopsies were obtained from 55 dyspeptic patients. IgG antibodies against HP were assayed in sera and saliva utilizing two indirect ELISAs. Biopsies were processed according to standard procedures in order to detect histological changes and the presence or absence of Helicobacter pylori. Laboratory data thus obtained were compared and statistically analyzed. Results: Forty-two (76.36%) biopsies were positive for HP. The organisms were detected in 4 of 16 (25%) cases with normal endoscopic findings, in all 16 cases of gastritis and in 22 of the 23 (95.6%) cases of duodenal ulcers (DU). Serum and saliva HP-specific IgG antibodies were detected in 4 normal cases with positive biopsies, in 12 and 14 cases of gastritis, respectively, and in all 22 (100%) biopsy positive cases of DU. The sensitivities of the serum and saliva tests were 90.5% and 95%, respectively, while the specificities were 84.5% and 70%, respectively. Conclusion: Due to their high sensitivity and specificity in diagnosing HP-associated DU and gastritis, serum and saliva antibody testing seems to offer a valuable alternative to invasive procedures especially in areas of high HP prevalence such as ours; saliva antibody testing is simple and practical especially in children and in difficult patients who resent venipuncture.

What are Predictive Factors for Developing of Barrett\s Esophagus in Patients with Gerd - our Experience

Introduction:Barrett’s esophagus (BE) is a condition in which the normal squamous epithelium of the esophagus is replaced with metaplastic intestinal-type epithelium. This epithelium can progress sequentially from metaplasia to low-grade dysplasia, then to high-grade dysplasia and finally to invasive adenocarcinoma. Many factors that appear to be risk factors for the presence of BE include obesity, the presence of hiatal hernia, and interestingly, the absence of Helicobacter pylori infection.The aim:The aim of this study was to determine the predictive factors for progression of gastroesophageal reflux disease (GERD) to BE.Methods:42 patients with endoscopically diagnosed and histopathologically verified BE were included in this prospective study. We analysed predictive factors such as: age, sex, obesity, alcohol consumption and smoking, reflux symptom duration in this patients, prevalence of short and long segment of BE, and the presence of hiatal hernia. After endoscopic examination of these patients, the presence of BE was verified with histopathological examination and finally, infection with H. pylori was determined.Results:Among 42 subjects, 25 (59%) were males and 17 (41%) were females, with mean age of 52.8±3.28 years. Obesity was present in 24 of 42 patients (57%). 27 of 42 patients (64%) were smokers. Symptom duration in this patients was approximately 9.4 years. From total number of patients, 52% were with SSBE and 48% patients were with LSBE. Hiatal hernia was present in 64% of patients, of which 66% were with LSBE and 34% with SSBE. In these patients, prevalence of infection with H. pylori was present in 12% of cases, 9.5% in patients with SSBE and 2.5% in patients with LSBE.Conclusions:The important risk factors for appearance of BE in GERD patients were male sex, middle age, smooking and alcohol consumption. Obesity is an important factor for development of BE. Most of patients with BE also had hiatal hernia, in majority of cases these were patients with LSBE. The prevalence of infection with H. Pylori in patients with BE was lower and this may predict a protective role of this microorganism.

Relationship between Kyphosis and Barrett's Esophagus in Japanese Patients

Kyphosis is a risk factor for the presence of hiatal hernia, which is a strong predictor of Barrett's esophagus. However, the association between kyphosis and Barrett's esophagus has not yet been clarified. To investigate this relationship, the Cobb angle, a marker of kyphosis, was measured in patients with and without Barrett's esophagus. From January 2006 to December 2010, 26 patients with long-segment Barrett's esophagus (LSBE) were retrospectively enrolled. As the comparative groups, 100 consecutive patients with short-segment Barrett's esophagus (SSBE) and 100 consecutive control patients without Barrett's esophagus were also enrolled in this study. Cobb angles were measured on lateral chest radiographs, and kyphosis was defined as a Cobb angle of greater than 50°. Kyphosis, along with other patient characteristics, were evaluated as possible predictors for SSBE and LSBE. The mean Cobb angles in the non-BE, SSBE, and LSBE groups were 31.6° (95% CIs, 29.3°-33.9°), 34.8° (32.1°-37.4°) and 49.4° (44.9°-53.9°), respectively. Statistically significant differences were found between the LSBE and the other 2 groups (p<0.001). The mean Cobb angles were 33.3°±12.4° and 37.0°±14.1°, respectively in patients without and with hiatal hernia (p=0.039). Predictors for Barrett's esophagus of any length were erosive esophagitis and hiatal hernia. Kyphosis had the highest odds ratio for the presence of LSBE (OR, 1.50; 95% CI, 1.05-1.94; p=0.033). Other predictors were hiatal hernia and the absence of Helicobacter pylori infection. Kyphosis is a risk factor for the presence of LSBE in Japanese patients.