Journal of Gastrointestinal and Liver Diseases最新文献

Background and aims: Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. Studies evaluated the effect of several diets on inflammatory markers in IBD patients. Nevertheless, the results have been inconsistent. Therefore, we conducted this review to evaluate the effectiveness of dietary interventions on inflammatory markers in IBD.

Methods: A comprehensive electronic literature search strategy using the PubMed, Embase, and Scopus was conducted in March 2023 and evaluated inflammatory markers included C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and fecal calprotectin (FC), as well as disease severity scores. We included full-text articles that met our inclusion and exclusion criteria. To evaluate the included studies, we used the NHLBI quality evaluation tools.

Results: A total of 16 studies were included in our qualitative synthesis. Elemental and polymeric diets showed similar efficacy in reducing Crohn's disease activity index (CDAI) and CRP levels. On the other hand, most studies evaluating the effects of omega 3 fatty acids reported no significant improvement. Moreover, protein supplementation was not seen to improve ESR or CRP levels. Except for improvements in FC levels with IgG4-guided exclusion diet in CD patients with elevated CDAI levels, restrictive diets were successful in controlling functional abdominal symptoms but did not appear to have an impact on inflammation in most studies. Furthermore, disease severity scores, CRP, ESR, and FC levels did not significantly change when eating a high-fiber, low-refined-carb, low-fat diet.

Conclusions: Diet plays a vital role in managing IBD by impacting the inflammatory response. Among the interventions studied, enteral nutrition showed the most promising results, improving patients' inflammatory status. Restrictive diets effectively managed symptoms and clinical remission but had limited impact on inflammatory markers. Supplementing the diet with fatty acids, omega 3, or proteins did not definitively improve patients' condition or inflammation.

Background and aims: Non-alcoholic fatty liver disease (NAFLD) is a common hepatic condition that can progress to hepatocellular carcinoma (HCC) in non-cirrhotic livers. To better understand the development of NAFLD-associated HCC, we performed an integrated morphological and molecular analysis to identify new insights that can improve the follow-up of NAFLD patients.

Methods: Our study included a cohort of 14 NAFLD-associated HCC and 41 NAFLD patients. We analyzed clinical parameters, a four-microRNA (miRNA) panel (miR-21-5p, miR-34a-5p, miR-130a-3p, and miR-155-3p) panel and their relationship with p53 and β-catenin expression.

Results: In the study cohort, the NAFLD-associated HCC patients were predominantly male, older, had significantly altered hepatic function, and a higher incidence of hypertension, type 2 diabetes, and dyslipidemia. Morphologically, the NAFLD-HCC group had substantially higher steatosis, ballooning, and fibrosis grades than the NAFLD group. The β-catenin expression was higher in both adjacent non-tumoral liver tissue (ANT) from NAFLD-associated HCC patients and in HCC tissue com-pared with NAFLD samples. The 4 miRNAs panel showed a dysregulated expression profile between NAFLD, ANT and HCC samples.

Conclusions: This study provides important insights regarding the molecular mechanisms underlying HCC progression in NAFLD patients, allowing for the development of better screening strategies for the early detection of NAFLD-associated HCC.

Background and aims: Hepatic encephalopathy (HE) remains one of the most debilitating complications of liver cirrhosis. Changes in gut microbiome composition have been linked to liver diseases and its complications including HE. Recent randomized controlled trials showed fecal microbiota transplantation to be safe and effective in HE treatment, however transferring unidentified live bacteria could cause various complications, including infections, especially in immunocompromised patients. This study aimed to evaluate the safety and efficacy of sterile fecal filtrate transfer (SFFT) for the modulation of the intestinal microbiome of patients with cirrhosis and HE.

Methods: A custom-made air pressure filtration device was used for the sterile fecal filtrate preparation. Seven patients received SFFT from the same healthy donor. Patients were monitored at least 30 days after the procedure. Cognition tests, blood and stool sampling were performed to assess the safety and efficacy of SFFT on HE, liver function, and stool microbiome composition on follow-up days 7 and 30.

Results: SFFT was well tolerated and resulted in fluctuations in the microbial composition of study participants: α-diversity increased in 4/7 of the patients, without robust engraftment of donors' microbial composition as assessed by β-diversity analysis. No significant effect on cognition tests or liver function was noted after the procedure. One death occurred three months after the procedure, however, it was not related to the SFFT.

Conclusions: Despite the effect on the gut microbiome, we did not observe robust improvement in patients' liver function or HE cognition tests after the procedure.

Chemokines play a critical role in cell migration and activation through binding to G-protein coupled cell- surface receptors with seven transmembrane domains. Chemokines are subdivided into four superfamilies including the CC, the CXC, the CX3C and the C families and the receptors of chemokines also segregate into four families including the CCR, CXCR, CX3CR and XCR families. Most chemokine receptors can bind to more than one chemokine and some chemokines also can bind to more than one receptor. There is ligand- receptor restriction during the binding of chemokines and special receptors. Interaction between chemokines and their receptors exerts a critical role in liver fibrogenesis through recruiting a variety of inflammatory cells into injured liver. The roles of chemokines including the CC, CXC and CX3C families on liver inflammation and fibrosis were described by the Wasmuth HE team ten years ago. Abundant evidence for pro-fibrotic or anti-fibrotic roles of chemokines and their receptors in liver fibrosis has been provided in the past decade. This paper is drawing on new evidence that has come up over the past 10 years, and uses that evidence to advance the understanding of chemokines' roles.

A 74-year-old woman was admitted for weight loss, abdominal pain and diarrhea for a year. Blood tests showed elevated transaminases, cholestasis and hyperbilirubinemia. Capsule endoscopy revealed extensively scattered lymphangiectasias, shortened villi and erosions in the jejunum and ileum. The histological examination of the small bowel mucosa biopsies evidenced severe mucosal atrophy and crypt hyperplasia, without significant intraepithelial lymphocytosis. The clinical picture, lack of response to a gluten-free diet and endoscopic and histopathologic findings were compatible with autoimmune enteropathy. Simultaneously, autoimmune hepatitis was also diagnosed. The patient showed significant improvement after starting treatment with prednisolone and azathioprine. To our knowledge, this is the first case of autoimmune enteropathy diagnosed simultaneously with autoimmune hepatitis.

Background and aims: High-grade gastrointestinal neuroendocrine neoplasms (GI-NENs) are divided into well-differentiated G3 neuroendocrine tumors (NETs G3) and neuroendocrine carcinomas (NECs), having identical cut-offs of proliferation, but different biomolecular origins. This translates in distinct treatment choices. Our aim was to establish if p53/Rb1 immunohistochemical status in GI-NENs with Ki67 index >20% can predict the histopathological diagnosis.

Methods: p53/Rb1 immunolabelling was performed on 42 cases of high-grade GI-NENs, diagnosed as NET G3, NEC and mixed neuroendocrine-non-neuroendocrine neoplasms (MiNEN) with NEC component. Immunolabeled slides were digitally scanned, with automatic quantification of p53 and Rb1, blind to the diagnosis.

Results: The p53 positive percentage was stratified; two cut-offs were selected, naming the intervals as N (null, <1%), T (tumor, 1%-20%) and C (carcinoma, >20%). The Rb1 expression loss in >90% of neoplastic cells was considered mutational. NETs G3 mainly showed the T status (14/16, 87.5%), followed by N (1/16, 6.25%) and C (1/16, 6.25%); NECs and NEC components in MiNENs predominantly expressed the C status (19/26, 73.08%), followed by N (5/26, 19.23%) and T (2/26, 7.69%) (p<0.001, χ 2 =27.017). NET G3s showed positive expression for Rb1; 73.08% of NECs expressed negative Rb1 (p<0.001, χ 2 =21.351). NECs and NEC components in MiNENs showed Rb1 mutational status in 13 C cases (13/19, 68.42%), 4 N cases (4/5, 80%) and in both the T cases (p=0.002, χ 2 =11.187).

Conclusions: Our results highlight the correlations between the p53/Rb1 immunostainings and the histopathological diagnosis of high-grade GI-NENs. NECs and NEC components in MiNENs showed a p53 mutational status (0% or 21-100%) and predominantly negative Rb1 expression. NETs G3 showed a p53 wild-type status (1-20%) and retained Rb1 expression. These findings suggest that the differential diagnosis of high-grade GI-NENs may benefit from p53/Rb1 immunohistochemical tests in everyday practice.

Background and aims: To compare the efficacy and safety of transarterial chemoembolization (TACE) + lenvatinib (TACE+L) versus lenvatinib (L) monotherapy in the treatment of advanced hepatocellular carcinoma by a meta-analysis.

Methods: PubMed, Embase, the Cochrane Library, CNKI, VIP e-Journals Database, and Wanfang Data were systematically searched to collate literature comparing TACE+L with L alone for the treatment of advanced liver cancer. The literature search, quality assessment, and data extraction were performed independently by two reviewers. The Stata 16 software package was used to process and analyze the data. We assessed heterogeneity using both I2 and the p-value, performed a publication bias assessment, and conducted a sensitivity analysis.

Results: Five studies were finally included, including one randomized controlled study and four retrospective studies; these involved a total of 1,167 patients, including 523 patients in the TACE+L combination group and 644 patients in the L monotherapy group. In this meta-analysis, the TACE+L group showed a significantly better objective response rate (ORR) (OR=2.54, 95%CI: 1.34 - 4.80) and disease control rate (DCR) compared to the L monotherapy group (OR=2.68, 95%CI: 1.75 - 4.08). The combined group had significantly improved progression-free survival (PFS) (HR=0.47, 95%CI: 0.40 - 0.56) and overall survival (OS) (HR=0.48, 95%CI: 0.39-0.59). In addition, there was no significant difference found in the overall adverse events of any grade between the two groups (OR=1.13, 95%CI: 0.99 - 1.29).

Conclusions: Compared to L alone, TACE+L treatment resulted in better tumor response, better long-term survival, and was accompanied by controllable adverse events.