BMC Gastroenterology最新文献

Objective: This study investigates the protective effects of citraconic acid (CA) on radiation-induced intestinal injury (RIII) and elucidates its relationship with the interleukin-17 (IL-17) signaling pathway.

Methods: A mouse model of whole-abdominal irradiation (IR) was established, and CA (10, 20, 40 mg/kg) was administered intraperitoneally as an intervention. Assessments included body weight, Disease Activity Index (DAI), and colon length measurements. Serum and tissue inflammatory markers were quantified using enzyme-linked immunosorbent assay. Histological analysis was performed using Hematoxylin and Eosin (HE) staining, Ki67 and Lgr5 immunohistochemistry, Alcian Blue-Periodic Acid-Schiff (AB-PAS) staining, and immunofluorescence for Zonula Occludens-1 (ZO-1) and Occludin. Transcriptomic sequencing with functional enrichment analyses was conducted, followed by Western blot validation of IL-17 A, CCL7, CXCL2, and MMP13 protein expression. IL-17 inhibitor experiments were performed to validate the causal relationship.

Results: CA administration attenuated body weight loss and reduced DAI scores in a dose-dependent manner while preserving colon length. CA treatment suppressed the elevation of IL-6 and TNF-α levels induced by irradiation. Furthermore, CA enhanced the abundance of Ki67-positive and Lgr5-positive cells, increased goblet cell numbers and mucus secretion, and restored the expression of tight junction proteins ZO-1 and Occludin, thereby improving histological damage. Transcriptomic analysis revealed significant enrichment of IL-17 signaling pathways associated with regeneration and inflammation. Protein levels of IL-17 A, CCL7, CXCL2, and MMP13 were upregulated following CA treatment. Importantly, IL-17 inhibition abolished the protective effects of CA, confirming the dependence on IL-17 signaling.

Conclusion: CA exerts protective effects against radiation-induced intestinal injury by modulating the IL-17-related signaling network, thereby promoting intestinal epithelial regeneration and barrier repair. These findings suggest that CA may represent a potential metabolic intervention strategy for the prevention and treatment of radiation-induced gastrointestinal damage.

Current indicators lack the precision required to accurately predict the PM(peritoneal metastasis) of gastric cancer (GC). The accurate prediction of GC with PM and the implementation of targeted therapeutic strategies hold substantial clinical significance. This study aimed to evaluate the prognostic value of galectin-1 expression and peritoneal fibrosis in predicting PM in GC patients. Immunohistochemical and Masson's trichrome staining were conducted on GC tissues and peritoneal tissues from 125 patients who underwent radical gastrectomy. The correlations among galectin-1 expression in GC tissues, peritoneal fibrosis, and PM were analyzed. Univariate and multivariate regression analyses were performed, incorporating clinicopathological parameters, to assess predictors of PM of GC. Both univariate and multivariate analyses revealed significant correlations among pathological Tumor (pT) stage, galectin-1 expression, peritoneal fibrosis, and PM. Patients with pathological pT3-4 stage GC, who had high galectin-1 expression and who were positive for peritoneal fibrosis had a greater risk of PM after pairwise superposition. This study represents the first to systematically elucidate that galectin-1 expression in GC tissues and peritoneal fibrosis are independent predictors of the risk of PM in patients with GC. These two indicators coordinate with pT stage, and the combination of these two indicators increases their predictive accuracy.

Background: Gastric bronchogenic cyst constitutes a rare form of ectopic bronchogenic cyst, with an estimated incidence of less than 1 in 68,000 to 1 in 42,000. This study reported a case who was preoperatively misdiagnosed as gastrointestinal stromal tumor and reviewed the literature on gastric bronchogenic cyst to summarize its clinical features, diagnosis, treatment, pathological manifestations, and prognosis.

Methods: A systematic search of the literature in the PubMed, Embase, Cochrane Library, Web of Science and Scopus databases was conducted by two independent reviewers focusing on cases of gastric bronchogenic cyst.

Results: Firstly, we report a rare case of bronchogenic cyst in a middle-aged female, with the lesion located near the gastric fundus. After literature review, 48 cases of gastric bronchogenic cyst (male-to-female ratio of 1:1.67, mean age was 47.54 ± 15.83 years) derived from 46 studies were enrolled. Abdominal pain (45.8%) was the most prevalent symptom, whereas 15 patients (31.3%) remained asymptomatic. Gastric bronchogenic cysts predominantly affected the gastric fundus (33.3%) and cardia (27.1%). Gastrointestinal stromal tumor (37.5%) was the most frequent misdiagnosis, while 9 patients (18.8%) were misdiagnosed as cysts originating from other abdominal organs. Laparoscopic surgery was the primary treatment (50.0%), followed by laparotomy (35.4%). Median follow-up was 10 months, no postoperative recurrence or mortality was reported in the pooled cases.

Conclusion: Gastric bronchogenic cyst is a rare and diagnostically challenging congenital abnormality with limited evidence to guide preoperative diagnosis. It should be incorporated into the differential diagnosis of gastrointestinal neoplasms, surgical resection is regarded as the effective approach for definitive diagnosis treatment.

Background: The underlying mechanisms of incomplete response to ursodeoxycholic acid (UDCA) therapy in patients with primary biliary cholangitis (PBC) remain unclear. This study aimed to investigate the clinicopathological characteristics and potential mechanisms of hepatobiliary (HB) cells in PBC patients with an incomplete response to UDCA.

Methods: A total of 132 PBC patients who underwent ultrasound-guided liver biopsy were enrolled. Liver tissue samples were processed using multiple histochemical staining methods. Demographic, clinical, hematological, autoantibody, and biochemical data were retrospectively analyzed. The therapeutic response to UDCA was evaluated according to the Paris II criteria. Additionally, bile acid metabolomic profiling was performed using liquid chromatography-mass spectrometry (LC-MS) on paraffin-embedded liver tissues from 25 randomly selected PBC patients.

Results: Among the 132 patients, 58 (43.9%) exhibited an incomplete response to UDCA. The number of CK7⁺ HB cells, degree of hepatocellular copper deposition, levels of alkaline phosphatase (ALP), total bile acid (TBA), and anti-GP210 antibody were significantly associated with incomplete response to UDCA. These factors exhibited AUC values of 0.745, 0.678, 0.809, 0.770 and 0.588, respectively. Hepatic levels of TBA (p = 0.010) and glycoursodeoxycholic acid (GUDCA, p = 0.037) were significantly higher in the incomplete response group compared with the complete response group. Moreover, the abundance of CK7⁺ HB cells was positively correlated with hepatic TBA (r = 0.544, p < 0.01) and GUDCA (r = 0.480, p < 0.05) levels.

Conclusions: PBC patients with an incomplete response to UDCA exhibited a significant increase in CK7⁺ HB cells, which were independently associated with treatment incomplete response. Although biochemical parameters such as ALP and TBA remain key predictors of incomplete response to UDCA, CK7⁺ HB cells provide additional histological insights into the mechanisms underlying incomplete therapeutic response.

Background: Peptic ulcer disease (PUD) remains a cause of gastrointestinal mortality despite advances in Helicobacter pylori eradication and gastroprotection.

Methods: We analyzed U.S. death certificates in CDC WONDER from 1999 to 2023, using Underlying Cause-of-Death files. Age-adjusted mortality rates (AAMRs; per 100,000) were standardized to the 2000 U.S.

Population: Trends used average annual percent change (AAPC). Analyses were stratified by sex, age, race/ethnicity, region, urban-rural status, and ICD-10 subtype (K25-K28).

Results: From 1999 to 2023, there were 87,574 PUD deaths. Annual deaths fell from 4,575 (1999) to 3,850 (2023; - 15.85%). AAMR declined from 3.30 (95% CI 3.20-3.39) to 1.78 (1.73-1.84) (AAPC - 2.66%, 95% CI - 3.80 to - 1.51). In 2023, AAMR was 2.09 (2.00-2.19) in males and 1.46 (1.39-1.52) in females; rates rose with age from 0.25 (35-44 years) to 14.71 (≥ 85 years). By race/ethnicity, AAMR was 1.81 (non-Hispanic [NH] White), 1.70 (NH Black), 1.57 (NH Other), and 1.47 (Hispanic). The West reached its highest point in 1999 and 2023. By 2013, NCHS (through 2020), the metropolitan AAMR was 1.74 (1.67-1.80) compared to 2.07 (1.91-2.23) in nonmetropolitan areas. Duodenal and gastric ulcers predominated; subtype AAPCs showed the steepest decline for unspecified-site ulcers.

Conclusions: PUD mortality declined over a 25-year period but plateaued or increased in selected strata in the late 2010s and during the pandemic. Findings support sustained H. pylori control, evidence-based gastroprotection for high-risk medication users, and timely endoscopy-especially for older adults, men, rural residents, and regions with a high burden. Continuous surveillance should monitor post-pandemic rebound risks and equity in access.