Turkish Journal of Gastroenterology最新文献

Background/aims: The biopsy-free diagnostic approach for celiac disease (CD) in children, recommended by ESPGHAN guidelines, is not widely implemented in pediatric gastroenterology centers across Türkiye. This study aimed to retrospectively evaluate patients who met ESPGHAN biopsy-free criteria but were nonetheless diagnosed through biopsy.

Materials and methods: Of 180 pediatric patients diagnosed with CD in the authors' department over 5 years, 79 (43.8%) met the ESPGHAN biopsy-free criteria. All patients underwent routine biopsies of the duodenum, bulb, antrum, corpus, and esophagus at diagnosis. Clinical presentations, celiac serology, and endoscopic and histopathological findings were retrospectively analyzed.

Results: The mean age at diagnosis was 7.48 ± 4 years (range, 2-17; M/F: 38/41). Presenting symptoms included growth failure (32.9%), abdominal pain (22.8%), constipation (8.9%), diarrhea (7.6%), anemia (6.3%), vomiting (5%), and elevated liver enzymes (1.3%). Fourteen patients (17.7%) were diagnosed via screening; 9 (64.3%) had type 1 diabetes. Endoscopy findings were consistent with CD in 77 patients; 2 had normal results. Non-celiac endoscopic findings were seen in 19 patients. Histopathology confirmed Marsh 3 lesions in 78 patients; 1 had normal findings, with tTG IgA levels normalizing at a 4-month follow-up. The positive predictive value of biopsy-free criteria was 98.7%. Non-celiac findings (in 24 patients) included Helicobacter pylori gastritis (n = 7) and eosinophilic esophagitis (n = 2).

Conclusion: The biopsy-free diagnostic approach accurately identifies CD in most cases but may miss treatable conditions like eosinophilic esophagitis or H. pylori infection, especially in endemic regions. Misdiagnoses, though rare, highlight the need for careful evaluation in populations with diverse clinical presentations.

Background/aims: There is evidence suggesting an association between hepatitis B virus (HBV) RNA and hepatic fibrosis in treatmentnaïve chronic hepatitis B (CHB) patients. However, few studies have delved into the relevance between HBV RNA and HBV-related cirrhosis. The purpose of this article is to elucidate the connection between HBV RNA and cirrhosis in patients undergoing nucleos(t)ide analogs (NAs).

Materials and methods: This study included 381 patients. Logistic regression was employed to investigate the variables linked to the development of cirrhosis. Propensity score matching was used to correct for confounders.

Results: In this cross-sectional study, multivariable logistic regression showed HBV RNA detectability was associated with cirrhosis. Multivariate regression suggests that the variables associated with cirrhosis were: older age, HBV RNA above the lower limit of quantification, shorter duration of treatment, higher level of serum bilirubin, and treatment strategy. Among patients with quantifiable HBV RNA (n = 242), cirrhotic patients exhibit lower median serum HBV RNA titers compared to those with CHB patients. Furthermore, qHBsAg ≤ 3.3 lg IU/mL and qHBV RNA ≤ 3.7 lg copies/mL may be linked to cirrhosis.

Conclusion: Nucleos(t)ide analogs treatment may result in varying degrees of decrease in HBV RNA levels. Lower levels of HBV RNA may be linked to the development of cirrhosis.

Background/aims: The study analyzed the roles of circulating omentin-1 and irisin in patients with type 2 diabetes mellitus (T2DM) concomitant with metabolic-associated fatty liver disease (MAFLD).

Materials and methods: This cross-sectional study included 80 patients with T2DM but no MAFLD, 62 patients with MAFLD but no T2DM, 50 T2DM patients having MAFLD (T2DM/MAFLD), and 80 healthy individuals.

Results: The serum levels of omentin-1 and irisin were both significantly reduced in patients with T2DM coexisting with MAFLD compared to T2DM or MAFLD patients alone. In T2DM patients, the level of omentin-1 decreased as the level of fasting plasma glucose (FPG) increased and the level of high-density lipoprotein cholesterol (HDL-C) reduced; the level of irisin decreased as the levels of FPG and fasting insulin (FINS) increased. In MAFLD patients, a lower level of omentin-1 was correlated with a lower level of HDL-C but with a greater waist-to-hip ratio (WHR), alanine aminotransferase and aspartate aminotransferase levels; a lower level of irisin was correlated with higher WHR and FINS level. In patients with T2DM coexisting with MAFLD, those with a lower level of omentin-1 were found to have a lower level of HDL-C concurrent with lower WHR and triglyceride level; and those with a lower level of irisin showed lower WHR, FPG and FINS levels. Combined evaluation of omentin-1 and irisin for diagnosing T2DM coexisting with MAFLD yielded an area under the curve of 0.943.

Conclusion: These findings suggest the assessment potential of omentin-1 and irisin for T2DM coexisting with MAFLD.

Background/aims: Obesity correlates with a higher prevalence of gastroesophageal reflux disease (GERD) and ineffective esophageal motility (IEM); however, the connection between metabolic obesity phenotype and these symptoms is poorly explored. Here, empirical data were used to explore the relationships between phenotypes of metabolic obesity and GERD and IEM.

Materials and methods: The present retrospective study involved 605 patients demonstrating typical reflux symptoms, categorized into 4 phenotypes: metabolically healthy obesity (MHO), metabolically healthy non-obesity (MHNO), metabolically unhealthy obesity (MUO), and metabolically unhealthy non-obesity (MUNO). The study excluded cases who were underweight, with severe comorbidities, prior gastric surgeries, or an absence of complete data. A 24-hour multichannel intraluminal impedance-pH system was used for monitoring.

Results: Patients exhibiting MUO, MHO, and MUNO phenotypes demonstrated a higher risk of GERD (pathological acid exposure time (AET), >6%) and IEM compared to those with the MHNO phenotype. Potential confounders, such as sex, age, body mass index, waist-hipratio, smoking status, alcohol intake, psychosocial stress, socioeconomic status, dietary practices, and opioid usage were adjusted, with the results indicating that the MUO phenotype was linked to the highest risk of pathological AET [15.78 (95% CI: 4.72-52.73)]; IEM [3.00 (95% CI: 1.31-6.87)].

Conclusion: The effects of obesity on GERD and IEM incidence could exceed those of metabolic diseases.

Background/aims: Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases and is characterized by extensive deposition of fat in hepatocytes. This study aims to elucidate iron responsive element binding protein 2's (IREB2) role in highfat diet (HFD)-induced NAFLD and the regulatory mechanisms of the TLR4/NF-κB cascade.

Materials and methods: Male rats were fed an HFD to induce the NAFLD in vivo model. Changes in body weight and liver tissue weight were measured. Liver tissue damage and hepatic steatosis were monitored by hematoxylin-eosin staining in rats. Fat droplet size of rat liver tissue was detected by oil red O staining kit to evaluate fat deposition. Total cholesterol (TC), triglycerides (TG), alanine transaminase (ALT), Aspartate transaminase (AST), fatty acid synthase (FAS, and PPARα were detected by enzyme-linked immunosorbent assay (ELISA) kit and western blot. Interleukin-1-beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were detected by ELISA. Finally, glucose tolerance and insulin sensitivity were measured by glucose analyzer.

Results: IREB2 was highly expressed in the liver tissue of NAFLD rats. The body weight and liver tissue weight of rats with knockdown of IREB2 were lower than those fed HFD, and the liver tissue was severely damaged, serum ALT/AST activity, glucose, TG, and TC levels were increased. In addition, overexpressing IREB2 increased IL-1β, IL-6, and TNF-α, promoting HFD-induced metabolic disorders, hepatic steatosis, and inflammation. Knocking down IREB2 had the opposite effect. Blocking the TLR4/NF-κB cascade reversed the promoting effect of IREB2 on steatosis and inflammatory response.

Conclusion: NAFLD treatment and prevention could benefit from IREB2, which may be closely related to TLR4/NF-κB signaling in lipid metabolism and glucose tolerance.

Background/aims: Hepatocellular carcinoma (HCC) is a molecularly heterogeneous solid malignancy that carries a dismal prognosis. Tanshinone IIA (Tan-IIA) is involved in the regulation of N6-methyladenosine (m6A) modification and plays an anti-tumor role in HCC, but whether Tan-IIA regulates HCC by mediating m6A modification is unclear.

Methods and materials: Cell apoptosis, invasion, proliferation, viability, and stemness were estimated with flow cytometry, transwell, 5-ethynyl-2'-deoxyuridine, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide, and sphere-forming assays. Methyltransferase-like 14 (METTL14) and 3 (METTL3) mRNA and protein levels were detected with reverse transcription-quantitative polymerase chain reaction and western blotting. Total m6A levels were measured using an m6A RNA methylation quantification kit. A possible regulation of tribbles pseudokinase-3 (TRIB3) expression by METTL3 in an m6A-modified manner was predicted through RM2Target and SRAMP and verified by m6A methylated RNA immunoprecipitation (MeRIP) and RIP. Mouse xenograft models assessed the action of Tan-IIA in HCC tumorigenesis.

Results: Tanshinone IIA restrained HCC cell viability, proliferation, invasion, and stemness, and induced HCC cell apoptosis invitro, as well as repressed tumor growth in xenograft models. METTL3 and TRIB3 were upregulated in HCC samples and downregulated in TanIIA-treated HCC cells and xenograft tumors. METTL3 facilitated HCC cell viability, proliferation, invasion, and stemness by enhancing TRIB3 mRNA stability through m6A modification. Tan-IIA played its role by downregulating TRIB3, and Tan-IIA mediated TRIB3 expression by METTL3.

Conclusion: Tanshinone IIA restrained HCC progression by regulating METTL3-mediated m6A modification of TRIB3 mRNA, offering evidence to support the clinical translation of Tan-IIA.