This letter critically evaluates Jiang et al's article on the differentiation of benign and malignant liver lesions using Emax and platelet count.Despite notable findings,significant methodological and interpretat...This letter critically evaluates Jiang et al's article on the differentiation of benign and malignant liver lesions using Emax and platelet count.Despite notable findings,significant methodological and interpretative limitations are identified.The study lacks detailed assay conditions for Emax measurement,employs inadequate statistical methods without robust multivariate analysis,and does not provide clinically relevant threshold values.The nomogram's reliance on Emax as a major diagnostic contributor is questionable due to attenuation in hepatocellular carcinoma patients with cirrhosis.Moreover,the study's limitations,such as selection bias and confounding factors,are not adequately addressed.Future research should adopt more rigorous methodologies,including prospective studies with larger cohorts and standardized protocols for biomarker measurement,to enhance validity and clinical applicability.展开更多
Once considered a concern solely for the gut,gluten is now recognized as an important factor in the pathogenesis of metabolic dysfunction-associated steatotic liver disease.Studies estimate that 18%-40%of individuals ...Once considered a concern solely for the gut,gluten is now recognized as an important factor in the pathogenesis of metabolic dysfunction-associated steatotic liver disease.Studies estimate that 18%-40%of individuals with gluten-related diseases have elevated liver enzyme levels,with 9%of patients with unexplained hypertransaminasemia ultimately diagnosed with gluten sensitivity.Hepatic manifestations of gluten sensitivity range from mild transaminase elevations to autoimmune liver diseases,metabolic dysfunction-associated steatotic liver disease,and even cirrhosis.Up to 50%of untreated cases of gluten-induced liver dysfunction show significant hepatic injury,which can lead to liver failure in severe cases.The pathophysiology is multifaceted and involves increased intestinal permeability,immune dysregulation,and shared genetic risk factors.A gluten-free diet leads to normalized liver enzymes in 75%-90%of cases within 1 year.Long-term gluten-free diet adherence has been paradoxically linked to higher body mass index,insulin resistance and increased hepatic steatosis risk,which raise concerns about its metabolic impact.Our review dissects the gluten-liver axis,emphasizing a need for early recognition,targeted screening,and personalized dietary interventions.Ultimately,given the increasing global burden of metabolic and autoimmune liver diseases,understanding gluten’s role is essential for optimizing liver health and preventing progressive hepatic injury.展开更多
Functional gastrointestinal disorders,now termed“disorders of gut-brain interaction”(DGBI),are characterized by a spectrum of chronic gastrointestinal symptoms driven by dysregulated gut-brain interaction.DGBIs freq...Functional gastrointestinal disorders,now termed“disorders of gut-brain interaction”(DGBI),are characterized by a spectrum of chronic gastrointestinal symptoms driven by dysregulated gut-brain interaction.DGBIs frequently coexist with liver diseases,including cirrhosis,thereby exacerbating clinical manifestations and complicating management;this overlap is underpinned by shared mechanisms,including gut dysbiosis,increased intestinal permeability,systemic inflammation,and altered neuroimmune signaling.Portal hypertension in cirrhosis promotes small intestinal bacterial overgrowth and microbial translocation,thereby triggering inflammatory pathways that worsen gut and liver function.This minireview explores the gut-liver axis as a central mediator in the interplay between DGBIs and liver disease/cirrhosis.Clinically,these interactions manifest as refractory gastrointestinal symptoms,nutritional deficiencies,and impaired quality of life.Emerging research emphasizes the need for integrative diagnostic approaches,such as combining advanced imaging,microbiome analysis,and biomarker profiling,to unravel the complex interplay between DGBIs and liver disease/cirrhosis.Therapeutic interventions targeting the gut microbiome,neuroimmune pathways,and lifestyle modification can mitigate disease burden.This review underscores the importance of a multidisciplinary framework for enhancing patient outcomes and guiding future research in this intersectional field.展开更多
This letter critically evaluates the effects of proton pump inhibitors(PPIs)on inflammatory bowel disease,particularly focusing on Crohn's disease(CD)and ulcerative colitis(UC),as discussed in Liang et al’s recen...This letter critically evaluates the effects of proton pump inhibitors(PPIs)on inflammatory bowel disease,particularly focusing on Crohn's disease(CD)and ulcerative colitis(UC),as discussed in Liang et al’s recent review.While the review provides significant insights,it relies heavily on cross-sectional and observational studies,which limits the ability to draw causal inferences.The heterogeneous study populations and inconsistent definitions of long-term PPI use further complicate the findings.This letter also highlights the need for rigorous control of confounding factors and considers the potential publication bias in the existing literature.The implications of these issues are discussed in the context of both CD and UC,and future research directions are proposed to address these shortcomings.展开更多
文摘This letter critically evaluates Jiang et al's article on the differentiation of benign and malignant liver lesions using Emax and platelet count.Despite notable findings,significant methodological and interpretative limitations are identified.The study lacks detailed assay conditions for Emax measurement,employs inadequate statistical methods without robust multivariate analysis,and does not provide clinically relevant threshold values.The nomogram's reliance on Emax as a major diagnostic contributor is questionable due to attenuation in hepatocellular carcinoma patients with cirrhosis.Moreover,the study's limitations,such as selection bias and confounding factors,are not adequately addressed.Future research should adopt more rigorous methodologies,including prospective studies with larger cohorts and standardized protocols for biomarker measurement,to enhance validity and clinical applicability.
文摘Once considered a concern solely for the gut,gluten is now recognized as an important factor in the pathogenesis of metabolic dysfunction-associated steatotic liver disease.Studies estimate that 18%-40%of individuals with gluten-related diseases have elevated liver enzyme levels,with 9%of patients with unexplained hypertransaminasemia ultimately diagnosed with gluten sensitivity.Hepatic manifestations of gluten sensitivity range from mild transaminase elevations to autoimmune liver diseases,metabolic dysfunction-associated steatotic liver disease,and even cirrhosis.Up to 50%of untreated cases of gluten-induced liver dysfunction show significant hepatic injury,which can lead to liver failure in severe cases.The pathophysiology is multifaceted and involves increased intestinal permeability,immune dysregulation,and shared genetic risk factors.A gluten-free diet leads to normalized liver enzymes in 75%-90%of cases within 1 year.Long-term gluten-free diet adherence has been paradoxically linked to higher body mass index,insulin resistance and increased hepatic steatosis risk,which raise concerns about its metabolic impact.Our review dissects the gluten-liver axis,emphasizing a need for early recognition,targeted screening,and personalized dietary interventions.Ultimately,given the increasing global burden of metabolic and autoimmune liver diseases,understanding gluten’s role is essential for optimizing liver health and preventing progressive hepatic injury.
文摘Functional gastrointestinal disorders,now termed“disorders of gut-brain interaction”(DGBI),are characterized by a spectrum of chronic gastrointestinal symptoms driven by dysregulated gut-brain interaction.DGBIs frequently coexist with liver diseases,including cirrhosis,thereby exacerbating clinical manifestations and complicating management;this overlap is underpinned by shared mechanisms,including gut dysbiosis,increased intestinal permeability,systemic inflammation,and altered neuroimmune signaling.Portal hypertension in cirrhosis promotes small intestinal bacterial overgrowth and microbial translocation,thereby triggering inflammatory pathways that worsen gut and liver function.This minireview explores the gut-liver axis as a central mediator in the interplay between DGBIs and liver disease/cirrhosis.Clinically,these interactions manifest as refractory gastrointestinal symptoms,nutritional deficiencies,and impaired quality of life.Emerging research emphasizes the need for integrative diagnostic approaches,such as combining advanced imaging,microbiome analysis,and biomarker profiling,to unravel the complex interplay between DGBIs and liver disease/cirrhosis.Therapeutic interventions targeting the gut microbiome,neuroimmune pathways,and lifestyle modification can mitigate disease burden.This review underscores the importance of a multidisciplinary framework for enhancing patient outcomes and guiding future research in this intersectional field.
文摘This letter critically evaluates the effects of proton pump inhibitors(PPIs)on inflammatory bowel disease,particularly focusing on Crohn's disease(CD)and ulcerative colitis(UC),as discussed in Liang et al’s recent review.While the review provides significant insights,it relies heavily on cross-sectional and observational studies,which limits the ability to draw causal inferences.The heterogeneous study populations and inconsistent definitions of long-term PPI use further complicate the findings.This letter also highlights the need for rigorous control of confounding factors and considers the potential publication bias in the existing literature.The implications of these issues are discussed in the context of both CD and UC,and future research directions are proposed to address these shortcomings.
