Turkish Journal of Gastroenterology最新文献

Upper gastrointestinal bleeding (UGIB) is a major cause of morbidity and mortality. Clinical symptoms that patients may present with include: hematemesis, coffee-ground emesis, melena, and hematochezia. Clinical signs can range from tachycardia to shock. The anatomical landmark that differentiates upper gastrointestinal (GI) bleeds from lower bleeds is the ligament of Treitz. The first steps of treating a patient who presents with signs of UGIB are resuscitation with appropriate fluids and blood products as necessary. The consideration of endoscopy and the urgency at which it should be performed is also vital during initial resuscitation. Endoscopic therapy should ideally be performed within 24 hours of presentation after initial stabilization with crystalloids and blood products. Intravenous proton pump inhibitors are the mainstay in the initial management of upper GI bleeding from a non-variceal etiology, and they should be administered in the acute setting to decrease the probability of high-risk stigmata seen during endoscopy. Pro-kinetic agents can be given 30 minutes to an hour before endoscopy and may aid in the diagnosis of UGIB. There are 3 broad categories of endoscopic management for UGIB: injection, thermal, and mechanical. Each endoscopic method can be used alone or in combination with others; however, the injection technique with epinephrine should always be used in conjunction with another method to increase the success of achieving hemostasis. In this review article, we will review the steps of triage and initial resuscitation in UGIB, causes of UGIB and their respective management, several endoscopic techniques and their effectiveness, and prognosis with a primary focus limited to non-variceal bleeding.

Esophageal cancer (ESCA) is a high-incidence disease worldwide, of which the 5-year survival rate remains dismal since the cellular basis of ESCA remains largely unclear. Herein, we attempted to examine the manifestation of fucosyltransferase-6 (FUT6) in ESCA and the associated mechanisms.The GSE161533 dataset was used to analyze a crucial gene in ESCA. The expression of FUT6 was investigated in normal esophageal epithelial cells and ESCA cell lines. Following FUT6 knockdown or overexpression, cell proliferation, migration, invasion, and levels of epithelial–mesenchymal transition (EMT)-related and epidermal growth factor receptor (EGFR)/extracellular signal-regulated kinase (ERK) signaling pathway-related proteins were evaluated using CCK-8, Transwell, and Western blotting with antibodies against EGFR, p-EGFR, E-cadherin, Vimentin, N-cadherin, ERK1/2, and p-ERK1/2), respectively. EGF was administered to stimulate the EGFR/ERK signaling pathway, followed by the assessment of cellular activity.Database analysis revealed that FUT6 was downregulated in the ESCA cells. Our study indicated that FUT6 is suppressed in various ESCA cell lines. Moreover, cell proliferation, invasion, migration, and EMT-related protein levels were conspicuously enhanced or restrained by FUT6 disruption or overexpression. FUT6 overexpression suppressed the malignant activities of the cells when stimulated by EGF, including inhibition of cell growth, movement, invasion, and EMT advancement, as well the reduction the levels of EGFR/ERK pathway proteins.In conclusion, FUT6 can suppress the EGFR/ERK signaling pathway activated by EGF, leading to the potential attenuation of ESCA cell proliferation, invasion, migration, and EMT.

Familial mediterranean fever (FMF) is a genetic autoinflammatory disease typically diagnosed in childhood. In this study, we aimed to investigate the demographic, clinical, and genetic characteristics of patients aged 18 years and older who were diagnosed with FMF. Patients diagnosed with FMF between 2014 and 2022 at Karadeniz Technical University Faculty of Medicine Hospital were included in the study. Patients were divided into 2 groups based on the age of disease onset. Group I included patients with adult-onset (ages 18-40), while group II comprised patients with late onset (ages 40 and above). Subsequently, the 2 groups were compared. A total of 150 patients with a mean age of 32 (18-79) were included in the study. There were 116 patients in group I and 34 (22.7%) in group II. The most common presenting complaint was abdominal pain (91.3%), and the most prevalent complication was amyloidosis (4.7%). No significant differences were observed between age groups regarding clinical findings and symptoms. The most frequent homozygous mutations were M694V (9.3%) and R202Q (1.8%), while the heterozygous mutations were M694V (37.3%) and R202Q (35.5%), respectively. The rate of M694V gene positivity in the adult-onset group was significantly higher compared to the lateonset group (52.9% and 25%, respectively, P = .020). There does not appear to be a significant difference in clinical signs and symptoms between adult-onset and late-onset FMF patients. The higher rate of M694V gene positivity in the adult-onset group suggests that the M694V mutation may be responsible for the early expression of the disease.

Cite this article as: Yüksekyayla O, Batıbay E, Efe C. Unusual cause of gastrointestinal bleeding in an elderly adult: Gastric kissing ulcers. Turk J Gastroenterol. 2024;35(5):421-422.

Background/aims:  We aimed to compare the effectiveness of the polyethylene glycol (PEG) and sennoside A+B regimens after clear fluid diet and fasting in bowel preperation of capsule endoscopy.

Materials and methods:  In this retrospective single-center study, patients who were consecutively examined with small bowel capsule endoscopy (SBCE) between May 2010 and March 2023 were evaluated. Patients who underwent PEG 4 L and sennoside A+B calcium 250 mL for small bowel preparation were assigned. The quality of the small bowel cleaning and the diagnostic yield in detecting of small bowel lesions were compared.

Results:  Two hundred forty-two patients who underwent SBCE for various indications (PEG 74.4%, sennoside A+B 25.6%) were included in the study. The mean proximal small bowel cleaning scores was 1.97 ± 0.77 for PEG and 1.98 ± 0.04 (P = .83) for sennoside A+B; the mid small bowel cleaning scores was 1.76 ± 0.84 for PEG and 1.59 ± 0.05 (P = .108) for sennoside A+B; the mean distal small bowel cleaning scores was 1.27 ± 0.08 for PEG and 1.3 ± 0.54 (P = .805) for sennoside A+B; and the total small bowel cleaning scores was 1.66 ± 0.06 and 1.62 ± 0.04 (P = .622) for PEG and sennoside A+B, respectively. There were no significant differences regarding small bowel cleaning scores both segmentally and totally. At the same time, the diagnostic value of SBCE was similar in both groups.

Conclusion:  The effectiveness of sennoside A+B in SBCE preparation is similar to that of PEG and can be used in intestinal cleansing.

Hepatocellular carcinoma (HCC) represents a common neoplasm that presents a substantial worldwide health challenge. Nevertheless, the involvement of HPN-AS1 in HCC remains unknown. The quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay was utilized to measure HPN-AS1 expression in HCC. The GABPA effects on the HPN-AS1 promoter were analyzed through chromatin immunoprecipitation and luciferase reporter assays. Cell proliferation potential was determined by deploying CCK-8 assay, Ki-67 immunofluorescence staining, and colony formation assay. Cell apoptosis was detected using acridine orange/ethidium bromide staining and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Western blotting was utilized to measure the protein levels of proliferation factors and apoptosis regulators. HPN-AS1 binding to eIF4A3 was accessed by RNA-binding protein immunoprecipitation assay. HPN-AS1 was significantly downregulated in both HCC cells and tissues. Lower HPN-AS1 levels indicate a poorer HCC prognosis. Moreover, we found that GABPA functions as a transcription factor for HPN-AS1. Functional studies revealed that HPN-AS1 displayed inhibitory effects on HCC cell proliferation and promoted apoptosis. Mechanically, HPN-AS1 bound to and facilitated translation initiation factor eIF4A3 degradation. Loss of HPN-AS1 augmented eIF4A3 protein levels rather than eIF4A3 mRNA levels. Exogenous expression of eIF4A3 could restore eIF4A3 protein levels and reverse HPN-AS1 overexpression-induced cell proliferation inhibition and cell apoptosis. Our study elucidated that HPN-AS1 downregulation was mediated by GABPA. HPN-AS acted as a tumor suppressor within HCC through binding and facilitating eIF4A3 degradation. The study provides a novel insight into the biological function of HPN-AS1 in HCC, suggesting that HPN-AS1 could be a promising biomarker and a potential target for HCC diagnosis and treatment.

Background/aims: In this study, we evaluated the efficacy and safety of transcatheter arterial chemoembolization (TACE) combined with hepatic arterial infusion chemotherapy (HAIC) compared to TACE monotherapy for the treatment of unresectable hepatocellular carcinoma (HCC).

Materials and methods: Relevant studies were systematically searched in PubMed, Embase, Web of Science, and Cochrane Library databases until September 1, 2023. Our analysis included 7 cohort studies encompassing a total of 630 patients.

Results: The results demonstrated that the TACE plus HAIC group exhibited significantly improved prognosis compared to the TACE alone group, as evidenced by superior rates of complete response, partial response, progressive disease, objective response rate, and disease control rate. Moreover, the TACE group displayed a lower risk of platelet reduction and vomiting when compared to the TACE plus HAIC group. None of the 7 studies reported any intervention-related mortality.

Conclusion: In conclusion, the combination of TACE and HAIC may be recommended as a viable option for patients with unresectable HCC, given its evident enhancements in survival and tumor response rates without significant differences in adverse events when compared to TACE monotherapy. Nevertheless, additional randomized controlled trials and studies involving Western cohorts are warranted to further validate these findings.

Background/aims:  Anti-programmed cell death protein 1 (PD-1) treatment has exhibited clinical benefits in colorectal cancer (CRC). However, the low response rate of CRC to immunotherapy is an urgent problem that needs to be solved.

Materials and methods:  MC-38 tumor cells was challenged subcutaneously in the flank of 7-week-old male C57BL/6 mice. The mice were randomly divided into 3 groups, and 200µg/mouse anti-PD-1 antibody and 100 mg/kg RAS-Seletive Lethal 3 (RSL) or phosphate buffer saline (PBS) were intraperitoneally injected every 2 days. The expression of oxidative stress and ferroptosis-related genes was measured by Western blotting, real-time reverse transcription-polymerase chain reaction, Prussian blue staining, and enzyme-linked immunosorbent assay.

Results:  Anti-PD-1 treatment-unresponsive tumors showed stronger immunosuppression than responsive tumors. Notably, the responsive tumors showed higher levels of H2O2 and reactive oxygen species, both of which could impair the antitumor effect of cytotoxic CD8+ T cells. The anti-PD-1 treatment-responsive tumors showed a higher expression of pro-ferroptosis genes and Fe2+ accumulation than those of anti-PD-1 nonresponsive tumors, indicating the potential role of ferroptosis in the efficacy of anti-PD-1 treatment. In MC-38 syngeneic tumor model, (1S, 3R)-RSL3 (RSL), a glutathione peroxidase 4 inhibitor, effectively promoted the antitumor effect of anti-PD-1 treatment in vivo. However, anti-PD-1 treatment did not affect the levels of ferroptosis-related genes in tumor model. Mechanistically, RSL treatment significantly upregulated the frequency of proliferating (ki67+) and cytotoxic (GZMB+) CD8+ T cells. Furthermore, the frequency of tumor neoantigen-specific interferon (IFN)-γ CD8+ T cells showed a significant increase after RSL plus anti-PD-1 treatment.

Conclusion:  RSL may be a promising drug for potentiating the antitumor efficiency of anti-PD-1 treatment in CRC.

Background/aims:  The relationship between neutrophil-to-lymphocyte ratio (NLR) and liver fibrosis in nonalcoholic fatty liver disease remains controversial. The aim of this study was to examine the association between NLR and liver fibrosis.

Materials and methods:  We conducted a cross-sectional analysis using the National Health and Nutrition Examination Survey. Vibration-controlled transient elastography was used to assess liver fibrosis and its severity. Neutrophil-to-lymphocyte ratio was calculated as the ratio of neutrophil count to lymphocyte count.

Results:  This study included 1620 US adults with a mean age of 52.9 years, of which 53.3% were male. The obese population accounted for 62.5%, 68.5% had hypertension, 31.1% had diabetes, and 16% had significant liver fibrosis. After adjusting for all covariates, a positive correlation was observed between NLR and the severity of liver fibrosis (β = 0.57, 95% CI = 0.22-0.92, P = .001), which remained stable across different subgroups.

Conclusion:  This study suggests that elevated NLR levels are positively correlated with the severity of liver fibrosis in patients with nonalcoholic fatty liver disease, and these results can be well generalized to the US adult population.