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 73.3% bloody diarrhea and 80% had abdominal pain. Also, the JAK2 V617F mutation rate was detected in 6.6 % of the patients included in the study. Conclusion: In this study, it was found that the V617F mutation was relatively rare in ulcerative colitis patients and there was no correlation with the JAK2 V617F mutation in most of the ulcerative colitis cases with thrombotic symptoms.

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. This study aimed to evaluate the relationship between interleukin 17 (IL-17A) cytokine, which plays a role in the pathogenesis of ulcerative colitis, and the inflammation-controlled matrix enzymes 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-17A were analyzed by RT-PCR, and immunohistochemical analyses were performed to evaluate ADAMTS-1, -4, -5, and IL-17A proteins in tissue samples. In addition, ELISA analysis determined serum levels of the ADAMTS-1, -4, -5, and IL-17A. Results: RT-qPCR results reveal that the expression of ADAMTS-1, -4, -5, and IL-17A genes in the UC tissue samples were significantly high according to the control tissue samples. Also, ADAMTS-1, -4, -5, and IL-17A proteins revealed enhanced expression pattern UC groups according to the control. Also, ADAMTS-1, -4, -5, and IL-17A protein showed cytoplasmic localization patterns in both control and UC groups. The serum levels of ADAMTS-1,-5, and IL-17A 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-17A 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.