Acute pancreatitis in Turkey: Results of a nationwide multicenter study.

BACKGROUND: Acute pancreatitis (AP) is the most common gastrointestinal disease requiring hospitalization, with significant mortality and morbidity. We aimed to evaluate the clinical characteristics of AP and physicians' compliance with international guidelines during its management. METHODS: All patients with AP who were hospitalized at 17 tertiary centers in Turkey between April and October 2022 were evaluated in a prospective cohort study. Patients with insufficient data, COVID-19 and those aged below 18 years were excluded. The definitions were based on the 2012 revised Atlanta criteria. RESULTS: The study included 2144 patients (median age:58, 52 % female). The most common etiologies were biliary (n = 1438, 67.1 %), idiopathic (n = 259, 12 %), hypertriglyceridemia (n = 128, 6 %) and alcohol (n = 90, 4.2 %). Disease severity was mild in 1567 (73.1 %), moderate in 521 (24.3 %), and severe in 58 (2.6 %) patients. Morphology was necrotizing in 4.7 % of the patients. The overall mortality rate was 1.6 %. PASS and BISAP had the highest accuracy in predicting severe pancreatitis on admission (AUC:0.85 and 0.81, respectively). CT was performed in 61 % of the patients, with the majority (90 %) being within 72 h after admission. Prophylactic NSAIDs were not administered in 44 % of the patients with post-ERCP pancreatitis (n = 86). Antibiotics were administered to 53.7 % of the patients, and 38 % of those received them prophylactically. CONCLUSIONS: This prospective study provides an extensive report on clinical characteristics, management and outcomes of AP in real-world practice. Mortality remains high in severe cases and physicians' adherence to guidelines during management of the disease needs improvement in some aspects.

Molecular analyses of ADAMTS-1, -4, -5, and IL-17 a cytokine relationship in patients with ulcerative colitis.

BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory bowel disease that develops due to the impaired immune response in genetically susceptible individuals, and its etiopathogenesis is not fully elucidated. IL-17 A is a cytokine that is produced by a type of immune cell called Th17 cells and is involved in the immune response and inflammation. On the other hand, ADAMTS-1, -4, and - 5 are enzymes that are involved in the breakdown of extracellular matrix proteins, including proteoglycans, which are important components of the intestinal wall. This study aimed to evaluate the relationship between interleukin 17 (IL-17 A) cytokine, which plays a role in the pathogenesis of ulcerative colitis, and the inflammation-controlled a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-1, -4, and - 5 protein members. METHODS: Bowel tissue samples and blood serum from 51 patients with UC and 51 healthy controls were included in this study. mRNA expression levels of the ADAMTS-1, -4, -5, and IL-17 A were analyzed by RT-qPCR, and immunohistochemical analyses were performed to evaluate ADAMTS-1, -4, -5, and IL-17 A proteins in tissue samples. In addition, ELISA analysis determined serum levels of the ADAMTS-1, -4, -5, and IL-17 A. RESULTS: RT-qPCR results reveal that the expression of ADAMTS-1, -4, -5, and IL-17 A genes in the UC tissue samples were significantly high according to the control tissue samples. Also, ADAMTS-1, -4, -5, and IL-17 A proteins revealed enhanced expression pattern UC groups according to the control. Also, ADAMTS-1, -4, -5, and IL-17 A protein showed cytoplasmic localization patterns in both control and UC groups. The serum levels of ADAMTS-1,-5, and IL-17 A were significantly higher in UC samples than in the control group. CONCLUSIONS: We observed a positive correlation between the ADAMTS-1, -5 and IL17A cytokine expression in UC samples. These results provide a new understanding of controlling crucial ADAMTS family protein members by IL-17 A cytokines with UC.

The Role of Endoplasmic Reticulum Stress in Gastroesophageal Reflux Disease Symptoms and Treatment.

BACKGROUND: Gastroesophageal reflux disease is a common condition worldwide. There is no curative treatment for gastroesophageal reflux disease. Endoplasmic reticulum stress leads to the activation of the unfolded protein response and has an important role in inflammation. The aim is to determine the role of endoplasmic reticulum stress in the follow-up of individuals with gastroesophageal reflux disease and the temporal changes of endoplasmic reticulum stress markers with treatment. METHODS: Twenty-four subjects in total were recruited prospectively, of whom 15 had nonerosive reflux disease. Two biopsies from 2 cm above the esophagogastric junction, 2 biopsies from gastric antrum mucosa, and 2 biopsies from gastric corpus mucosa were taken. Simultaneously, 2 tubes of venous blood samples were drawn from each individual (1 tube for studying the genetic markers and 1 tube for analyzing the CYP2C19 polymorphism). RESULTS: The mean age was 42.3 ± 17.6 for women and 34.66 ± 11.2 for men. Pantoprazole, esomeprazole, rabeprazole, and lansoprazole preparations were used for treatment. There was no significant difference between tissue and blood samples for panel genes ATF-6, XBP-1, DDIT-3, DNAJC-10, and EIF-2-AK before treatment. There was a significant decrease in the level of ATF-6, XBP-1, DNAJC-9, EIF2-AK, and NF-2L-2 genes in blood after treatment. In the comparison of proton pump inhibitors, significant decreases in the expression of the ATF-6, XBP-1, and DNAJC-9 mRNAs were detected in blood from individuals after treatment. CONCLUSION: Endoplasmic reticulum stress can be for evaluating the clinical improvement and the effectiveness of treatment in gastroesophageal reflux disease.

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

BACKGROUND AND STUDY AIMS: Intestinal 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 METHODS: We 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. RESULTS: Statistically 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). CONCLUSION: Overexpression 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.

Prognostic Significance of Hemoglobin/Prognostic Nutritional Index and Hemoglobin/Red Blood Cell Distribution in Rectal Cancer.

BACKGROUND: We aimed to investigate the effect of hemoglobin/prognostic nutritional index and hemoglobin/red blood cell distribution, which are indicators of inflammation and nutrition, on prognosis and survival in patients with rectal cancer. METHODS: The retrospective study reviewed medical records of 138 patients with rectal cancer who were followed up between 2010 and 2021. The effects of hemoglobin/red blood cell distribution, hemoglobin/prognostic nutritional index, tumor stage, and lymph node status on survival and prognosis were evaluated using univariate and multivariate analyses. Overall survival and disease-free survival were calculated for both groups. RESULTS: Survival and prognosis were found to be significantly better in nonanemic patients with the hemoglobin/prognostic nutritional index higher than the cut-off value than in anemic patients with a normal or lower hemoglobin/prognostic nutritional index. Similarly, survival and prognosis were found to be significantly better in nonanemic patients with a hemoglobin/red blood cell distribution higher than the cut-off value than in anemic patients with a normal or lower hemoglobin/red blood cell distribution. CONCLUSION: The results indicated that nutrition and inflammatory markers have independent prognostic significance in rectal cancer. These markers are simple, inexpensive, and useful biomarkers commonly used in clinical practice, and they were found to predict overall survival and disease-free survival independently.

A No-Biopsy Approach for the Diagnosis of Celiac Disease in Adults: Can It Be Real?

Background and objective Pediatric guidelines on the diagnosis of celiac disease (CD) have reported that the positivity of anti-endomysium antibodies in the presence of anti-transglutaminase antibodies (TGA) 10 times higher than normal is sufficient for the diagnosis. In this study, we aimed to evaluate whether this diagnostic process for children can also be applied to adult patients. Materials and methods We retrospectively examined patients aged >18 years who were diagnosed with CD. The results of serological tests and endoscopic biopsy were evaluated. Patients with more than one month of duration between celiac serology and endoscopy, those diagnosed with CD before admission, those on a gluten-free diet, and those with selective IgA deficiency were excluded from the study. Results A total of 269 patients were included in the study. TGA value was significantly higher in patients with villous atrophy (p<0.001) and positively correlated with mucosal damage (r=0.60, p<0.01). Considering the cut-off value of 100 U/mL (>10 ULN) for the TGA antibodies, in line with the criteria regulated by the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) for the diagnosis of CD, the sensitivity was 71.64%, the specificity was 100%, and the positive predictive value (PPV) was 100%. When the cut-off value was taken as 29.42 U/mL, the sensitivity was 100% and the specificity was 99.5%. For a TGA cut-off value of 52.7 U/mL (5.27 ULN), which determines the presence of partial or complete villous atrophy in the evaluation made considering mucosal damage, the sensitivity was 90%, the specificity was 100%, and the PPV was 100%. Conclusion Based on our findings, TGA titers were highly effective in demonstrating CD-related mucosal damage. This study endorses a biopsy-free strategy in adult patients in line with the ESPGHAN criteria. Local validation of test-specific thresholds will ensure that this approach has a significant impact on adult patients.

Potential role of chromatin remodeling factor genes in atrophic gastritis/gastric cancer risk.

BACKGROUND/AIMS: Atrophic gastritis (AG), intestinal metaplasia (IM), and Helicobacter pylori (HP) are the risk factors for the development of gastric cancer (GC). Chromatin remodeling is one of the epigenetic mechanisms involved in the carcinogenesis of GC. The purpose of this study was to investigate the expression profiles of defined chromatin remodeling genes in gastric mucosal samples and their values as gastric carcinogenesis biomarkers. MATERIALS AND METHODS: In total, 95 patients were included in the study. Patients were divided into 3 groups as: GC group (n=34), AG group (n=36), and control group (n=25). AG group was further divided into subgroups based on the presence of HP and IM in gastric mucosa. Chromatin remodeling gene expressions were analyzed using real-time PCR (RT-PCR) array in all groups. Data were evaluated using the RT-qPCR primer assay data analysis software. RESULTS: EED, CBX3, and MTA1 were more overexpressed, whereas ARID1A, ING5, and CBX7 were more underexpressed in the AG and GC groups compared with the controls. No significant differences were observed between the AG and GC groups concerning the expression of these 6 genes, although the fold change levels of these genes in the GC group were well above than in the AG group. EED, CBX3, and MTA1 were significantly more overexpressed in HP- and IM-positive AG subgroup compared with the HP- or IM-negative AG subgroup. CONCLUSION: In conclusion, our results provide an evidence of epigenetic alterations in AG. Expressions of EED, CBX3, MTA1, ARID1A, ING5, and CBX7 may be considered as promising markers to be used in GC screening for patients with AG.

Expression profiles of histone modification genes in gastric cancer progression.

Gastric cancer (GC) development can be attributed to several risk factors including atrophic gastritis (AG), intestinal metaplasia (IM), and the presence of Helicobacter pylori (HP). Also, histone modification is an epigenetic mechanism that plays a pivotal role in GC carcinogenesis. In this preliminary study, we aimed to describe the expression profiles of histone modification in the AG, IM, and GC patient groups. A total of 80 patients with AG (n = 27), IM (n = 25), and GC (n = 28) with an additional 20 control subjects were included in the study. Expression profiles of three histone phosphorylation genes (PAK1, NEK6, and AURKA) and five histone deacetylation genes (HDACs 1, 2, 3, 5, and 7) were examined based on the results of Real Time qPCR method. It was observed that AURKA and HDAC2 genes were significantly overexpressed in all groups compared to the control (P < 0.05). In GC patients, overexpression of HDAC2 gene was detected in the absence of metastasis, and overexpression of AURKA, HDAC2, and NEK6 genes was detected in the presence of metastasis. When cancer involvements were compared, significant overexpression of the HDAC2 gene was noted in overall and corpus involvements (P < 0.05). In addition, overexpression of AURKA, NEK6, HDAC1, and HDAC2 genes and underexpression of HDAC5 gene were detected in the antrum involvement (P < 0.05). In conclusion, decreased expression of HDAC5 in GC is reported for the first time in this study, while supporting the existing literature in AURKA, NEK6, HDAC1, and HDAC2 up regulations during GC development.

[Determination of drug resistance mutations of NS3 inhibitors in chronic hepatitis C patients infected with genotype 1]. / Genotip 1 ile enfekte kronik hepatit C hastalarinda NS3 inhibitörü ilaçlarin direnç mutasyonlarinin belirlenmesi.

Direct-acting antiviral agents (DAA) such as NS3 protease inhibitors is the first class of drugs used for chronic hepatitis C (CHC) treatment. NS3 inhibitors (PI) with low genetic barrier have been approved to be used in the CHC genotype 1 infections, and in the treatment of compensated liver disease including cirrhosis together with pegile interferon and ribavirin. Consequently, the development of drug resistance during DAA treatment of CHC is a major problem. NS3 resistant variants can be detected before treatment as they can occurnaturally. The aim of this study was to investigate new and old generation NS3 inhibitors resistance mutations before DAA treatment in hepatitis C virus (HCV) that were isolated from CHC. The present study was conducted in 2015 and included 97 naive DAA patients infected with HCV genotype 1, who were diagnosed in Manisa and Kocaeli cities of Turkey. Magnetic particle based HCV RNA extraction and than RNA detection and quantification were performed using commercial real-time PCR assay QIASypmhony + Rotorgene Q/ArtusHCV QS-RGQ and COBAS Ampliprep/COBAS TaqMan HCV Tests. HCV NS3 viral protease genome region was amplified with PCR and mutation analysis was performed by Sanger dideoxy sequencing technique of NS3 protease codons (codon 32-185). HCV NS3 protease inhibitors; asunaprevir, boceprevir, faldaprevir, grazoprevir, pariteprevir, simeprevir and telaprevir were analysed for resistant mutations by Geno2pheno-HCV resistance tool. HCV was genotyped in all patients and 88 patients (n= 88/97, 91%) had genotype 1. Eight (n= 8/97, 8.2%) and 80 (n= 80/97, 82.4%) HCC patients were subgenotyped as 1a and 1b, respectively. Many aminoacid substitutions and resistance mutations were determined in 39/88 (44%) patients in the study group. Q80L, S122C/N, S138W were defined as potential substitutions (6/88 patients; 7%); R109K, R117C, S122G, I132V, I170V, N174S were described as potential resistance (34/88 patients; 39%); V36L, T54S, V55A, Q80H were characterized as resistance (7/88 patients; 8%) and Q80K, A156S were defined as high resistance (3/88 patients; 3%) mutations. Based on resistance and high resistance mutations, clinically significant mutations were defined in 10/88 (11%) of the patients. Our study shows that it is essential to analyse HCV NS3 protease inhibitors drug resistance before DAA treatment of CHC patients. On the other hand, our results pointed out that analysis of NS5A and NS5B genome region mutations may also be required in the near future.

Treatment of inflammatory bowel disease by leukocytapheresis.

Studies about leukocytapheresis have emerged with the need of search for alternatives to conventional treatment in inflammatory bowel diseases (IBD). Leukocytapheresis is a novel non-pharmacologic approach for active ulcerative colitis (UC) and Crohn's disease (CD), in which leukocytes are mechanically removed from the circulatory system. Patients with active IBD treated with leukocytapheresis using a Cellsorba E column between 2012 and 2015, were enrolled in Turkey. In our experience, the results of leukocytapheresis therapy in 6 patients with CD and 20 patients with active UC were overviewed. Leukocytapheresis (10 sessions for remission induction therapy, 6 sessions for maintenance therapy) was applied to the patients with their concomitant medications. Intensive leukocytapheresis (≥4 leukocytapheresis sessions within the first 2 weeks) was used in 30% patients with active severe UC. The overall clinical remission rate in patients with UC was 80%, and the mucosal healing rate was 65%. Patients were followed for an average of 24 months. It was observed that clinical remission has continued in 65% of patients with UC. Mild relapse was observed in 3 patients with UC during follow up period. In 5 patients with CD significant clinical remission was achieved except only one patient. Surgical needs were disappeared in 3 patients with obstructive type Crohn's disease. Adverse events were seen in only 4.3% of 416 sessions. Any concomitant medications did not increase the incidence of adverse events. Our results indicate that leukocytapheresis is efficacious in improving remission rates with excellent tolerability and safety in patients with IBD.

Prevalence of gastroesophageal reflux disease in a country with a high occurrence of Helicobacter pylori.

AIM: To evaluate the prevalence of gastroesophageal reflux disease (GERD) with additional symptoms, relationship with Helicobacter pylori (H. pylori) of this country-wide study. METHODS: Data from 3214 adults were obtained with validated questionnaire. Eight hundred and forty-one subjects were randomized to be tested for H. pylori via the urea breath test. "Frequent symptoms" were defined heartburn and/or regurgitation occurring at least weekly. RESULTS: The prevalence of GERD was 22.8%, frequent and occasional heartburn were 9.3%-12.7%, regurgitation were 16.6%-18.7%, respectively. Body mass index (BMI) ≤ 18.5 showed a prevalence of 15%, BMI > 30 was 28.5%. The GERD prevalence was higher in women (26.2%) than men (18.9%) (P < 0001). Overall prevalence of H. pylori was 75.7%. The prevalence was 77.1% in subjects without symptoms vs 71.4% in subjects with GERD (χ2 = 2.6, P = 0.27). Underprivileged with the lowest income people exhibit a higher risk. CONCLUSION: GERD is common in Turkey which reflects both Western and Eastern lifestyles with high rate of H. pylori. The presence of H. pylori had no effect on either the prevalence or the symptom profile of GERD. Subjects showing classical symptoms occasionally exhibit more additional symptoms compared with those without classical symptoms.

Alteration in Methylation Pattern of Retinoblastoma 1 Gene Promotor Region in Intestinal Metaplasia with or without Helicobacter pylori and Gastric Cancer Patients.

BACKGROUND: Helicobacter pylori, intestinal metaplasia (IM), and gene methylation play important roles in gastric carcinogenesis. However, the association among H. pylori infection, IM, gastric cancer (GC), and gene methylation is not fully understood. Cell cycle control involving retinoblastoma 1 (RB1) gene is one of the main regulatory pathways reported to be altered in gastric carcinogenesis. OBJECTIVES: The purpose of this research is to assess the methylation status of RB1 gene in GC and IM with or without H. pylori infection, and to discuss the possible role of H. pylori-induced RB1 gene methylation in the mechanism of gastric carcinogenesis. MATERIAL AND METHODS: The methylation profile of RB1 gene was analyzed by sodium bisulfite modification and methylation-specific PCR in GC (n = 24), IM patients with H. pylori positive (n = 20) and negative (n = 20), and control subjects (n = 20). RESULTS: According to methylation levels in RB1 gene; the high correlation values were detected between H. pylori positive-IM group and GC group, and between H. pylori positive-IM and H. pylori negative-IM groups (p < 0.05). No correlations between H. pylori negative-IM and GC groups and between GC and control groups were detected in methylation status of RB1 gene. CONCLUSIONS: High methylation levels in RB1 gene in H. pylori positive individuals may suggest an elevated risk of gastric cancer occurrence.

The potential role of the NEK6, AURKA, AURKB, and PAK1 genes in adenomatous colorectal polyps and colorectal adenocarcinoma.

Colorectal adenomatous polyp (CRAP) is a major risk factor for the development of sporadic colorectal cancer (CRC). Histone modifications are one of the epigenetic mechanisms that may have key roles in the carcinogenesis of CRC. The objective of the present study is to investigate the alternations in the defined histone modification gene expression profiles in patients with CRAP and CRC. Histone modification enzyme key gene expressions of the CRC, CRAP, and control groups were evaluated and compared using the reverse transcription PCR (RT-PCR) array method. Gene expression analysis was performed in the CRAP group after dividing the patients into subgroups according to the polyp diameter, pathological results, and morphological parameters which are risk factors for developing CRC in patients with CRAP. PAK1, NEK6, AURKA, AURKB, HDAC1, and HDAC7 were significantly more overexpressed in CRC subjects compared to the controls (p < 0.05). PAK1, NEK6, AURKA, AURKB, and HDAC1 were significantly more overexpressed in the CRAP group compared to the controls (p < 0.005). There were no significant differences between the CRAP and CRC groups with regards to PAK1, NEK6, AURKA, or AURKB gene overexpression. PAK1, NEK6, AURKA, and AURKB were significantly in correlation with the polyp diameter as they were more overexpressed in polyps with larger diameters. In conclusion, overexpressions of NEK6, AURKA, AURKB, and PAK1 genes can be used as predictive markers to decide the colonoscopic surveillance intervals after the polypectomy procedure especially in polyps with larger diameters.

Never in mitosis gene A-related kinase 6 and aurora kinase A: New gene biomarkers in the conversion from ulcerative colitis to colorectal cancer.

Ulcerative colitis (UC) is an important risk factor for colorectal cancer (CRC). Histone modifications are one of the epigenetic mechanisms that may have key roles in the carcinogenesis of CRC. At present, there are no studies comparing histone modification patterns of UC and CRC in the literature. Therefore the aim of the present study was to investigate whether genes, particularly those involved in histone modification, have value in patient monitoring with regards to CRC development in UC. Key gene expressions of the histone modification enzyme were assessed and compared in CRC, UC and control groups using the RT-PCR array technique. Patients were divided into subgroups based on the extent and duration of the disease and inflammatory burden, which are considered risk factors for CRC development in UC patients. In UC and CRC groups, a significantly higher overexpression of the NEK6 and AURKA genes compared to the control group was identified. In addition, there was a significantly higher overexpression of HDAC1 and PAK1 genes in the UC group, and of HDAC1, HDAC7, PAK1 and AURKB genes in the CRC group. NEK6, AURKA, HDAC1 and PAK1 were significantly overexpressed in patients with a longer UC duration. Overexpression of AURKA and NEK6 genes was significantly more pronounced in UC patients with more extensive colon involvement. HDAC1, HDAC7, PAK1, NEK6, AURKA and AURKB are important diagnostic and prognostic markers involved in the carcinogenesis of CRC. HDAC1, PAK1, NEK6 and AURKA may be considered as diagnostic markers to be used in CRC screening for UC patients.

Schizophrenia and gastroesophageal reflux symptoms.

BACKGROUND: Psychological factors and psychiatric disorders play a role in a variety of gastrointestinal illnesses, including esophageal diseases. AIM: The aim of the present study was to evaluate the frequency of gastroesophageal reflux disease symptoms in patients with schizophrenia in Turkey. PATIENTS AND METHODS: Ninety-eight patients with schizophrenia and one hundred control individuals were enrolled in the study, which was undertaken at the Manisa State Hospital for Mental Health and Neurological Disorders and Celal Bayar University Gastroenterology Department. Case and control subjects alike underwent 30-45 min oral interviews conducted by a designated study coordinator (E.K.). The coordinator gathered information about demographic characteristics, social habits, and a large variety of symptoms suggestive of reflux disease or other gastrointestinal conditions. RESULTS: In terms of reflux symptoms, cough was the only significant association in schizophrenic patients than controls. Heartburn and regurgitation were more frequent in schizophrenic patients who smoked than in controls who were smokers. However, the prevalence of reflux symptoms in cigarette smokers versus nonsmoker patients with schizophrenia was similar. Heartburn and/or regurgitation occurred more frequently in patients with schizophrenic than controls with alcohol use. CONCLUSIONS: Psychiatric disorders might indirectly affect esophageal physiology through increased consumption of alcohol and nicotine.

Aurora kinase A (AURKA) and never in mitosis gene A-related kinase 6 (NEK6) genes are upregulated in erosive esophagitis and esophageal adenocarcinoma.

Gastroesophageal reflux disease is a risk factor for esophageal adenocarcinoma yet studies that have investigated the relationship between erosive esophagitis and esophageal adenocarcinoma have usually focused on symptom-related evidence or polymorphisms. There are no epigenetic gene expression studies on this topic. In this study, we aimed to evaluate the relationship between erosive esophagitis and esophageal adenocarcinoma to identify whether there is a genetic predisposition for esophageal adenocarcinoma. The Human Epigenetic Chromatin Modification Enzyme RT(2) Profiler(™) PCR array (PAHS-085A) was used to detect the expression of 84 key genes encoding enzymes. This was carried out prospectively for samples from 60 patients (20 patients as a control group, 20 patients with erosive esophagitis and 20 patients with esophageal adenocarcinoma). AURKA, AURKB, NEK6 were expressed at significantly higher levels in esophageal adenocarcinoma compared to the control group. MBD2 was expressed at significantly lower levels in the esophageal adenocarcinoma group compared to the control group. AURKA, AURKC, HDAC9 and NEK6 were expressed at significantly higher levels in erosive esophagitis compared to the control group. There was no difference in upregulated gene expression between the erosive esophagitis and esophageal adenocarcinoma. MBD2 was significantly downregulated in esophageal adenocarcinoma compared to erosive esophagitis. NEK6 and AURKA were significantly upregulated in esophageal adenocarcinoma and erosive esophagitis compared to the control group. This is a novel study on the genetic predisposition for erosive esophagitis and esophageal adenocarcinoma. AURKA and NEK6 are two promising genetic markers for erosive esophagitis and esophageal adenocarcinoma.

GSTP1 gene methylation profiles in Helicobacter pylori (+) and (-) antral intestinal metaplasia and distal gastric tumour patients in Turkish population.

BACKGROUND/AIMS: Gastric cancer (GC) is the second most common malignancy worldwide, with a high mortality rate. The incidence of GC has declined in the western countries during the last decades. The glutathione S-transferases comprise a group of enzymes that are critical in the detoxification of carcinogens. In this study we aimed at the relationship GSTP-1 methylation in patients with intestinal metaplasia with and without Helicobacter pylori infection, gastric cancer and controls. METHODOLOGY: The methylation status of GSTP1 gene was analyzed by methylation specific PCR after bisulfate modification in H. pylori (+) (n=25) and (-) (n=25) intestinal metaplasia (IM) patients, GC (n=25) and control subjects (n=15) between September 2009 to November 2011. RESULTS: During the study period 90 patients who underwent endoscopic examination were included in the study. When we considered the GSTP1 gene methylation profile in all of the groups; 26 (28%)patients had methylated GSTP1 gene, 31 (34%) patients had unmethylated GSTP1 gene and 33 (36%) patients had heterogeneously methylated GSTPI gene. CONCLUSIONS: GSTP1 gene methylation profile is not appropriate for early diagnosis of cases with gastric cancer.

Does Helicobacter pylori treatment improve the symptoms of globus hystericus?

BACKGROUND/AIMS: Globus hystericus is a feeling of tension in the throat, irrelevant of swallowing, persisting for at least 12 weeks. Since the cause of globus hystericus is not fully described, the treatment is controversial. We aimed in this study to determine the symptoms of gastroesophageal reflux disease, upper gastrointestinal endoscopic findings, prevalence of Helicobacter pylori,and post-treatment symptoms (symptoms of gastroesophageal reflux and/or Helicobacter pylori) in patients with a diagnosis of globus hystericus. MATERIALS AND METHODS: One hundred twenty three patients were recruited from the archives of the Department of Gastroenterology and Endoscopy at Celal Bayar University Medical School between January 2009 and August 2010. RESULTS: Helicobacter pylori was positive in 75 (60%) of 123 patients with globus hystericus. Helicobacter pylori (+) patients had significantly more heartburn, regurgitation, and inlet patch in upper esophagus than Helicobacter pylori (-) patients. Significantly more Helicobacter pylori (-) patients had normal endoscopy findings when compared to Helicobacter pylori (+) patients. While 27 (50%) of Helicobacter pylori-eradicated patients had regressing globus symptoms, 12 (17.3%) of them did not have any regression in globus symptoms. Improvement in symptoms showed a positive correlation with Helicobacter pylori eradication (p=0.001). CONCLUSIONS: Helicobacter pylori rate among cases with globus sensation was similar to values in the general population. Helicobacter pylori eradication was found to decrease globus symptoms.

Correlation among standard endoscopy, narrow band imaging, and histopathological findings in the diagnosis of nonerosive reflux disease.

BACKGROUND AND AIMS: Gastroesophageal reflux disease (GERD) is caused by the reflux of gastric contents into the esophagus. Narrow band imaging (NBI) facilitates mucosal surface evaluation and may improve the endoscopic diagnosis of GERD. The diagnosis of GERD is based on the combination of clinical symptoms, endoscopic findings, and histological changes. In this study we aimed to show the differences between standard white light endoscopy and the NBI technique in squamo-columnar junction evaluation. We also evaluated the patients with NERD, as determined by standard white light endoscopy, using the NBI technique and histopathological mucosa examination (inflammation or normal mucosa). METHODS: A total of 60 subjects were recruited prospectively: 40 with nonerosive reflux disease (NERD) and 20 with erosive reflux disease (ERD). Patients were subjected to esophagogastroduodenoscopy and, in all of them, two biopsies were taken 2 cm above the esophagogastric junction. RESULTS: NBI was more sensitive than standard white light endoscopy in distinguishing normal endoscopic findings. Histopathological findings were more prevalent than the mucosal changes diagnosed by the standard white light endoscopy and NBI. CONCLUSION: NBI is more sensitive than white light endoscopy in detecting inflammation in NERD patients. However, histopathological evaluation is the most sensitive, therefore taking a biopsy will remain useful.