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 aim of this study was to determine the resistance status and to identify the point mutations conferring resistance to clarithromycin and fluoroquinolones among dyspeptic patients in Manisa, Turkey. The study included a sample of 140 patients with an indication for upper gastrointestinal endoscopy randomly selected from 2100 dyspeptic patients attending to the Gastroenterology and Endoscopy Unit at Manisa Celal Bayar University Hafsa Sultan Hospital between April 2016 and May 2018. A commercially available GenoType Helico DR test was used to detect the presence of Helicobacter pylori and mutations associated with resistance to clarithromycin and fluoroquinolones in biopsy specimens. In total, 116 (82.9%) of 140 biopsies obtained from the same number of dyspeptic patients were positive for H pylori and 82 (approximately 71%) of them harbored resistance mutations in 23SrRNA and/or gyrA. Resistance to clarithromycin, levofloxacin, or both were detected in 43.1% (50/116), 27.6% (32/116), and 16/116 (13.8%) of tested biopsies, respectively. The most common mutation conferring resistance to clarithromycin was A2147G (96%, 48/50). Resistance to fluoroquinolones was frequently due to mutation in codon 91 and the most common mutation detected was D91G (34.4%). Heteroresistance patterns were observed in 48.0% (24/50) of clarithromycin-resistant samples and 28.1% (9/32) of levofloxacin-resistant samples. The resistance rates and detected mutations in this study are in line with the country data. However, to achieve better H pylori eradication and to prevent the spread of multidrug-resistant strains in Turkey, the molecular-based susceptibility tests should be considered routinely. Further studies are needed to determine the various mutations among resistant strains.

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. Cite this article as: Kasap E, Buran T, Toraman Avcu A, et al. The role of endoplasmic reticulum stress in gastroesophageal reflux disease symptoms and treatment. Turk J Gastroenterol. 2023;34(5):533-541.

Mide kanseri, dünyada en sık görülen 5 kanserden biridir. Görülme sıklığı dünya genelinde büyük coğrafi farklılıklar göstermektedir. Mide Kanseri Japonya’da kanserden ölümlerin başlıca nedenlerindendir, bu ülkede erken tanı için endoskopideki gelişmelerle birlikte ulusal tarama programları uygulanarak mide kanserine erken tanı konmaya başlanmıştır. Mide kanseri sebepleri arasında: Helikobakter pilori, atrofik gastrit, intestinal metaplazi ve displazi, aşırı tuzlu gıda ile beslenme ve genetik yatkınlık gösterilmektedir. Mide kanserlerinin %90’dan fazlası adenokanser tipinde olup genellikle tanı anında ileri evrededir. 5 yıllık yaşam bu grupta %15-20’dir. Erken mide kanserinde endoskopik olarak submukozal rezeksiyon yapılarak kür sağlanabilmektedir. Eğer evre 2 ve üzeri mide kanseri ise geç kabul edilmektedir. Geç mide kanserinde hastalığın durumuna göre cerrahi rezeksiyon, kemoterapi veya radyoterapi yapılabilmektedir.

Background/Aim: JAK2 is a gene that provides instructions for making a protein called Janus kinase 2, which is involved in the signaling process that regulates the growth and division of cells. Variations in the JAK2 gene have been associated with several different diseases, including certain blood disorders like myeloproliferative neoplasms (MPNs) and ulcerative colitis (UC). The exact reason for ulcerative colitis is not fully understood. This study aimed to examine the possible role of JAK2 V617F mutation in the etiopathogenesis of ulcerative colitis. Methods: The included patients were selected with UC and with signs of thrombosis. The DNA isolation was carried out from peripheral blood for all included patients. RT-qPCR methods were used to find JAK2 V617F mutations in UC patients with signs of thrombosis. Results: 73.3% of the included patients in this study had bloody diarrhea and 80% had abdominal pain. 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