Turkish Journal of Gastroenterology最新文献

Background/aims: Ulcerative colitis (UC) represents a persistent inflammatory condition that influences millions of people worldwide, with rising prevalence and limited treatment options. Current therapies, such as corticosteroids and immunosuppressants, offer symp tom relief but are associated with significant adverse effects. Fecal microbiota transplantation (FMT) is being increasingly viewed as an effective alternative, but the molecular basis for its benefits in UC is still not fully understood. This study aimed to explore the function of the transforming growth factor-beta 1 (TGF-β1)/Smad signaling cascade in FMT-induced remission of UC.

Materials and methods: Stable Smad3-knockdown and Smad3-overexpression Caco2 cell lines were established via lentivirus-medi ated transduction. These modified Caco-2 cells were co-incubated with RAW264.7 macrophages to mimic intestinal inflammation in vitro. Following FMT treatment, the expression of major components of the TGF β1/Smadsignaling cascade was assessed.

Results: The results demonstrated that FMT markedly downregulated TGF-β1, Smad2, and Smad3 expression, while enhancing Smad7 expression in both Smad3-knockdown and overexpression cell lines. In addition, FMT treatment attenuated the phosphorylation of Smad2 and Smad3, indicating a decrease in the activation of the TGF-β1/Smad signaling pathway.

Conclusion: These findings suggest that optimizing FMT protocols targeting this pathway could improve therapeutic outcomes for UC patients.   Cite this article as:Qiu J, Wu C, Li S, Yang X. Fecal microbiota transplantation attenuated inflammation through TGF-β1/Smad signaling pathway in Caco-2 and RAW264.7 cells. Turk J Gastroenterol. 2026;37(2):161-169.

Background/aims: Idiopathic achalasia is a rare esophageal motility disorder of unknown etiology. Although its neuromuscular aspects are well described, little is known about the role of the esophageal epithelium. This study aimed to evaluate the activation status of key cell signaling pathways and assess esophageal epithelial barrier function in achalasia patients.

Materials and methods: Biopsy samples from 37 achalasia patients and 15 healthy volunteers (HVs) were analyzed. Tissue resistance and permeability were measured using a mini-Ussing chamber system. Gene expression related to epithelial integrity and signaling was assessed via quantitative reverse transcription polymerase chain reaction, and corresponding protein levels were evaluated using enzyme-linked immunosorbent assay (ELISA) and multiplex ELISA.

Results: No significant differences were observed in epithelial resistance (achalasia: 187.3 ± 25.6 Ω vs. HVs: 166.8 ± 20.1 Ω, P = .18) or permeability (achalasia: 35.76 ± 5.4 pmol vs. HVs: 36.9 ± 4.7 pmol, P = .67) between the 2 groups. Thirty-two genes involved in key sig naling pathways were found to be significantly deregulated (P < .05), and 6 key signaling proteins (Akt (Ser473), c-Jun (Ser63), Erk1/2 (Th202/Tyr204), Thr185/Tyr187), IκB-α (Ser32/Ser36), MEK1 (Ser217/Ser221), mTOR (Ser2448)) were downregulated at the protein level (P < .05).

Conclusion: The findings reveal that major signaling pathways, including MAPK, PI3K/AKT/mTOR, and JAK/STAT, are significantly sup pressed in the esophageal epithelium of achalasia patients, despite preserved epithelial barrier integrity. These molecular alterations may represent a previously unrecognized component of achalasia pathogenesis. Furthermore, the preserved barrier function suggests that endoscopic therapies such as peroral endoscopic myotomy may not exacerbate reflux-related epithelial injury in these patients.   Cite this article as:Kipcak S, Ergun P, Gunel NS, Bor S. Epithelial barrier function and altered cell signaling pathways in the esophageal epithelium of achalasia patients. Turk J Gastroenterol. 2026;37(2):170-178.

Background/aims: To assess the correlation between indocyanine green retention rate at 15 minutes (ICG-R15), liver stiffness mea surement (LSM), and other clinical indicators in cirrhotic patients, using hepatic venous pressure gradient (HVPG) as a reference and to evaluate the predictive capability of ICG-R15 for clinically significant portal hypertension (CSPH).

Materials and methods: From February 2023 to September 2024, 80 cirrhotic patients were recruited. Data collected included baseline information, laboratory results, HVPG measurements, and ICG-R15 via the ICG clearance test. Patients were classified into non-CSPH (n = 33) and CSPH (n = 47) groups based on HVPG. Pearson's correlation analyzed relationships between HVPG, ICG-R15, LSM, and other indicators. Logistic regression was used to identify risk factors for CSPH and develop a predictive model, evaluated by receiver operating characteristic curve.

Results: The CSPH patients showed lower white blood cell count, red blood cell count, hemoglobin, platelet count (PLT), and albumin, with higher total bilirubin (TBil), prothrombin time, LSM, and ICG-R15. Significant correlations were found between HVPG and ICG-R15 (r = 0.662) and LSM (r = 0.633) (both P < .001). The ICG-R15, LSM, PLT, and TBil were independent risk factors for CSPH. The model had an AUC of 0.947, sensitivity of 78.72%, and specificity of 96.97%.

Conclusion: The ICG-R15 is a significant predictor of CSPH, and a model incorporating ICG-R15 can effectively assess disease severity and predict prognosis in cirrhotic patients.   Cite this article as: Hu H, Lai W, Zhou T, Zhu J, Yan H. Indocyanine green retention rate at 15 minutes as a key predictor of clinically significant portal hypertension in cirrhosis: development and validation of a superior non-invasive diagnostic model. Turk J Gastroenterol. 2026;37(2):215-222.

Background/aims: Ulcerative colitis (UC) is a chronic inflammatory bowel disease known for mucosal inflammation and dysbiosis of gut microbiota. The association between mucosa-related microecological imbalance and UC severity is a crucial aspect in unraveling the disease's pathogenesis. The relationship between mucosa-related microecological imbalance and different levels of UC severity was investigated, as defined by Mayo score, and its association with mucosal mechanical barrier damage.

Materials and methods: The composition of mucosa-associated bacterial and fungal populations in UC patients and healthy controls was analyzed using Illumina MiSeq sequencing. The analysis focused on changes in the diversity of bacteria and fungi, along with their distribution at phylum and genus levels. Additionally, the potential relationship between microecological imbalance and damage to the mucosal mechanical barrier was assessed.

Results: Patients with severe UC exhibited elevated abundance indexes, increased numbers of phyla, and higher proportions of specific phyla (Actinobacteria, Acidobacteria, Chloroflexi, Gemmatimonadetes, Nitrospirae, and an unclassified phylum) compared to patients with mild or moderate UC. Conversely, the proportions of dominant bacterial phyla (Firmicutes, Bacteroidetes, and Proteobacteria) displayed an inverse relationship with UC severity. In the fungal microbiota, moderate and severe UC cases showed a greater prevalence of negative genera compared to mild cases. Notably, changes in microflora composition were associated with the extent of mucosal mechanical barrier damage.

Conclusion: The progression of mucosa-associated microecological imbalance is associated with increasing inflammation in UC, potentially contributing to disruptions in the intestinal mucosal mechanical barrier.   Cite this article as: Shang Y, Wang X, Diao X, Li L, Zuo X. The degree of mucosa-associated microecological imbalance in ulcerative colitis patients with different mayo score and its relationship with mucosal mechanical barrier damage. Turk J Gastroenterol. 2026;37(1):26-34.

Cite this article as: Durmaz O, Ozkahraman A, Kayar Y. Rare side effect due to vedolizumab in a patient with ulcerative colitis: Catatonic depression. Turk J Gastroenterol. 2026;37(1):139-141.

Background/aims: Early diagnosis of cytomegalovirus gastrointestinal disease (CMV-GID) is often deemed critical for the appropriate management of the disease. Although histopathological examination is the gold standard for diagnosis, non-invasive and early diagnostic methods may be needed to predict CMV-GID. As a rapid and non-invasive method, the detection of CMV DNA in plasma by polymerase chain reaction (PCR) can be utilized. In this study, the aim was to determine the optimal plasma CMV DNA cut-off value and to develop a scoring system as an adjunct diagnostic method for predicting CMV-GID.

Materials and methods: In this methodological study, the records of patients who underwent gastrointestinal biopsy and plasma CMV PCR testing were retrospectively reviewed. A scoring system based on multivariate analysis was established as a predictive model for CMV-GID. Receiver operating characteristic analysis was performed to determine the optimal plasma CMV DNA cut-off using the Youden Index and to evaluate the performance measures related to the proposed methods for predicting CMV-GID.

Results: A total of 302 patients (125 with the diagnosis of CMV-GID and 177 without CMV-GID, based on their endoscopic biopsy reports and plasma CMV PCR results) were included. The optimal CMV DNA cut-off value in plasma to predict CMV-GID was determined to be 272 copies/mL. A total score of 28.1 obtained from the predictive model was set to be the optimal value for predicting CMV-GID.

Conclusion: The use of a scoring system and an optimal CMV DNA cut-off may help to predict CMV-GID and facilitate early diagnosis and treatment.

Background/aims: There are still many controversies about whether antiviral therapy should be administered to patients with chronic hepatitis B (CHB) in the indeterminate phase. Thus, this study aimed to investigate the histopathological features and antiviral efficacy of HBeAg-negative CHB patients aged over 30 in the indeterminate phase.

Materials and methods: The clinical, laboratory, and histopathological characteristics of 666 CHB patients were assessed through a retrospective study. To identify factors associated with significant liver inflammation and fibrosis, inter-group differential analysis and binary logistic regression were conducted. Receiver operating characteristic curve analysis was used to determine the area under the curve and optimal cut-off values for relevant indicators. The antiviral efficacy was analyzed in 62 patients who received antiviral treat ment by inter-group differential analysis.

Results: A total of 70 patients were enrolled in the study. The median age was 40.5 years and 38 patients (54.28%) were male. Significant liver inflammation and significant liver fibrosis represented 30% and 55.7% of the patient cohort, respectively. Multivariate logistic regression analysis revealed that red blood cell count (RBC) and aspartate aminotransferase (AST) were independent predictors of sig nificant liver inflammation (odds ratio [OR] (95%CI): 0.34 (0.13,0.90), P = .03; OR (95%CI): 1.19 (1.05,1.34), P = .006). Aspartate amino transferase was also an independent predictor of significant liver fibrosis (OR (95%CI): 1.24 (1.06,1.47), P = .01). The negative conversion rate of hepatitis B virus (HBV) DNA was above 80% from 24 weeks after antiviral treatment, and low-level viremia (LLV) accounted for 6.5% (4/62) at 48 weeks after antiviral treatment.

Conclusion: Among HBeAg-negative CHB patients aged over 30 in the indeterminate phase, over half had significant liver inflamma tion or fibrosis. In addition, RBC was a protective factor for significant liver inflammation, and AST was a risk factor for significant liver inflammation and fibrosis in such patients. Notably, antiviral treatment was effective. However, long-term monitoring of HBV DNA and the occurrence of LLV and drug resistance should be conducted during treatment.   Cite this article as: Ou K, Ma Y, Yuan C, et al. Histopathological Features and Antiviral Efficacy in Patients Over 30 Years Old with Chronic Hepatitis B in the Indeterminate Phase. Turk J Gastroenterol. 2026;37(2):186-195.

Background/Aims: Colorectal polyps are precursor lesions of colorectal cancer, and their histopathological types are critical for determining malignant potential. Predicting polyp histopathological types may support early and appropriate clinical management. Machine learning (ML) algorithms based on accessible demographic, clinical, and lifestyle data can contribute to individualized screening strategies. Materials and Methods: This retrospective cross-sectional study included 491 individuals who underwent colonoscopy for the first time between 2022 and 2025 at University of Health Sciences, Antalya Training and Research Hospital. Demographic and clinical data were recorded, and dietary habits were assessed using the Food Frequency Questionnaire. Patients were classified into 3 groups according to histopathology: adenomatous polyp, hyperplastic polyp, and no polyp. Four ML algorithms-decision tree, random forest, support vector machines (SVMs), and extreme gradient boosting-were applied. Model performance was evaluated using accuracy, sensitivity, specificity, kappa statistic, and McNemar's test. Variable contributions were further analyzed with SHapley Additive exPlanations. Results: Accuracy ranged from 70.9% to 76.4%, with the highest performance from SVM (76.4%) and random forest (75.7%). Extreme gradient boosting showed lower overall accuracy (70.9%) but was the only model that identified hyperplastic polyps. The no polyp group was consistently predicted with high accuracy (sensitivity 85.6%-95.9%). Precision for adenomatous polyps was highest with SVM (71.4%). SHapley Additive exPlanations analysis highlighted frequent bulgur consumption (>2 times/week), red meat intake, age, and body mass index as major predictors. Conclusion: Machine learning algorithms can predict colorectal polyp histopathological types using routine demographic, clinical, and dietary data, enabling more personalized and effective screening beyond age-based protocols.

Liver fibrosis is a key intermediate stage in the progression of chronic liver disease to end-stage liver cirrhosis. Mortality rises exponentially once it reaches decompensated liver disease. In a healthy liver microenvironment, hepatocytes, Kupffer cells, hepatic stellate cells (HSCs), liver sinusoidal endothelial cells, and other cells interact with extracellular matrix (ECM) to maintain cell stability and liver function. Different types of liver injury (such as viral hepatitis and alcoholic liver injury) can cause liver fibrosis. Liver injury signals activate Kupffer cells and recruit immune cells, leading to liver inflammation. This inflammation, together with liver injury, stimulates the activation of HSCs. Activated HSCs migrate to injury sites and secrete ECM. The ECM increase and stiffening contribute to fibrosis. Microenvironment changes alter cell phenotypes, perpetuating HSC activation. This article explores liver fibrosis mechanisms, reviews cellular and microenvironmental changes, summarizes fibrosis characteristics, and provides insights for clinical treatment.

Background/aims: Gold standard diagnostic methods, such as invasive procedures and serum biomarkers, have limited sensitivity and specificity for the detection of colorectal cancer (CRC). Thus, the development of more accurate and noninvasive detection approaches is imperative. Emerging research elucidating the intricate role of the gut microbiota in CRC pathogenesis underscores the need for precision screening tailored to high-risk cohorts to improve early detection and intervention strategies and comprehensively address this challenging clinical problem.

Materials and methods: Fecal metagenomic sequencing datasets were employed to identify potential bacterial biomarkers for CRC diagnosis and selected relevant microbial taxa for subsequent validation. A total of 180 participants were enrolled: 65 healthy controls (HC), 65 colorectal adenoma patients, and 50 CRC patients, and fecal samples were analyzed using fluorescence quantitative polymerase chain reaction to confirm biomarker relative abundance, culminating in the establishment of an evolutionary model for CRC progression; furthermore, a treatment efficacy and prognostication model supported by comprehensive statistical methodologies was established.

Results: This study analyzed fecal microbial biomarkers associated with CRC progression and identified differentially abundant bacterial species across HCs, adenoma, and CRC patient groups. Notably, Fusobacterium nucleatum (Fn) and Peptostreptococcus anaerobius (P. anaerobius) showed significant correlations with CRC stage and metastasis, highlighting their potential as diagnostic biomarkers. Among individual microbes, P. anaerobius exhibited the highest diagnostic value when combined with Fn.

Conclusion: The results underscore the potential application of fecal microbial markers, particularly Fn and P. anaerobius, for diagnosing CRC and monitoring its progression.   Cite this article as: Shen F, Xu C, Wang C. Gut microbiome diagnostic biomarkers for colorectal cancer. Turk J Gastroenterol. 2026;37(1):62-74.