Pub Date : 2024-01-23DOI: 10.1038/s41575-024-00897-1
Katrina Ray
{"title":"A role for the gut microbiota in immune checkpoint inhibitor-induced colitis","authors":"Katrina Ray","doi":"10.1038/s41575-024-00897-1","DOIUrl":"10.1038/s41575-024-00897-1","url":null,"abstract":"","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139522490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-19DOI: 10.1038/s41575-023-00884-y
Shuibin Lin, Ming Kuang
Malignant liver cancer is characterized by rapid tumour progression and a high mortality rate, whereas the molecular mechanisms underlying liver cancer initiation and progression are still poorly understood. The dynamic and reversible RNA modifications have crucial functions in gene expression regulation by modulating RNA processing and mRNA translation. Emerging evidence has revealed that alterations in RNA modifications facilitate the selective translation of oncogenic transcripts and promote the diverse tumorigenic processes of liver cancer. In this Review, we first highlight the current progress on the functions and mechanisms underlying RNA modifications in the regulation of mRNA translation and then summarize the exciting discoveries on aberrant RNA modification-mediated mRNA translation in the regulation of tumour initiation, metastasis, metabolism, tumour microenvironment, and drug and radiotherapy resistance in liver cancer. Finally, we discuss the diagnostic and therapeutic potentials of targeting RNA modifications and mRNA translation for the clinical management of liver cancer. RNA modifications are crucial in regulating mRNA translation. This Review provides a comprehensive overview of the molecular mechanisms underlying RNA modifications in mRNA translation regulation, and discusses the diagnostic and therapeutic potentials of targeting RNA modifications for liver cancer management.
{"title":"RNA modification-mediated mRNA translation regulation in liver cancer: mechanisms and clinical perspectives","authors":"Shuibin Lin, Ming Kuang","doi":"10.1038/s41575-023-00884-y","DOIUrl":"10.1038/s41575-023-00884-y","url":null,"abstract":"Malignant liver cancer is characterized by rapid tumour progression and a high mortality rate, whereas the molecular mechanisms underlying liver cancer initiation and progression are still poorly understood. The dynamic and reversible RNA modifications have crucial functions in gene expression regulation by modulating RNA processing and mRNA translation. Emerging evidence has revealed that alterations in RNA modifications facilitate the selective translation of oncogenic transcripts and promote the diverse tumorigenic processes of liver cancer. In this Review, we first highlight the current progress on the functions and mechanisms underlying RNA modifications in the regulation of mRNA translation and then summarize the exciting discoveries on aberrant RNA modification-mediated mRNA translation in the regulation of tumour initiation, metastasis, metabolism, tumour microenvironment, and drug and radiotherapy resistance in liver cancer. Finally, we discuss the diagnostic and therapeutic potentials of targeting RNA modifications and mRNA translation for the clinical management of liver cancer. RNA modifications are crucial in regulating mRNA translation. This Review provides a comprehensive overview of the molecular mechanisms underlying RNA modifications in mRNA translation regulation, and discusses the diagnostic and therapeutic potentials of targeting RNA modifications for liver cancer management.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139494760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-15DOI: 10.1038/s41575-024-00894-4
Jordan Hindson
{"title":"Effect of expectation of gluten intake on non-coeliac gluten sensitivity","authors":"Jordan Hindson","doi":"10.1038/s41575-024-00894-4","DOIUrl":"10.1038/s41575-024-00894-4","url":null,"abstract":"","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139468695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-12DOI: 10.1038/s41575-024-00892-6
Seung-min Park
Our Ig Nobel Prize-winning smart toilet research confronts societal taboos and uses humour as a gateway to advance serious dialogue about health technology. It is a call to action to embrace innovation, foster richer scientific discussions and support pioneering research for tangible health advancements.
{"title":"Contrasting aspects of human excreta","authors":"Seung-min Park","doi":"10.1038/s41575-024-00892-6","DOIUrl":"10.1038/s41575-024-00892-6","url":null,"abstract":"Our Ig Nobel Prize-winning smart toilet research confronts societal taboos and uses humour as a gateway to advance serious dialogue about health technology. It is a call to action to embrace innovation, foster richer scientific discussions and support pioneering research for tangible health advancements.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139432565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-05DOI: 10.1038/s41575-023-00889-7
Silvio Danese, Laurent Peyrin-Biroulet
A substantial percentage of patients with inflammatory bowel disease (IBD) exhibit biologic treatment failure or loss of response over time. This article explores the effectiveness and safety of monoclonal antibodies targeting the IL-23 pathway in treating IBD; continued research is needed to address lingering questions regarding long-term safety and efficacy.
{"title":"Are all the IL-23 blockers the same in inflammatory bowel disease?","authors":"Silvio Danese, Laurent Peyrin-Biroulet","doi":"10.1038/s41575-023-00889-7","DOIUrl":"10.1038/s41575-023-00889-7","url":null,"abstract":"A substantial percentage of patients with inflammatory bowel disease (IBD) exhibit biologic treatment failure or loss of response over time. This article explores the effectiveness and safety of monoclonal antibodies targeting the IL-23 pathway in treating IBD; continued research is needed to address lingering questions regarding long-term safety and efficacy.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139101381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-04DOI: 10.1038/s41575-023-00883-z
Julieta Argüero, Daniel Sifrim
Gastro-oesophageal reflux disease (GERD) is a common gastrointestinal disorder in which retrograde flow of gastric content into the oesophagus causes uncomfortable symptoms and/or complications. It has a multifactorial and partially understood pathophysiology. GERD starts in the stomach, where the refluxate material is produced. Following the trajectory of reflux, the failure of the antireflux barrier, primarily the lower oesophageal sphincter and the crural diaphragm, enables the refluxate to reach the oesophageal lumen, triggering oesophageal or extra-oesophageal symptoms. Reflux clearance mechanisms such as primary and secondary peristalsis and the arrival of bicarbonate-rich saliva are critical to prevent mucosal damage. Alterations of the oesophageal mucosal integrity, such as macroscopic oesophagitis or microscopic changes, determine the perception of symptoms. The intensity of the symptoms is affected by peripheral and central neural and psychological mechanisms. In this Review, we describe an updated understanding of the complex and multifactorial pathophysiology of GERD. It is now recognized that different GERD phenotypes have different degrees of reflux, severity of mucosal integrity damage and type, and severity of symptoms. These variations are probably due to the occurrence of a predominant pathophysiological mechanism in each patient. We also describe the main pathophysiological mechanisms of GERD and their implications for personalized diagnosis and management. In this Review, Argüero and Sifrim describe the core pathophysiological mechanisms involved in gastro-oesophageal reflux disease (GERD). They also discuss the implications for clinical management of GERD.
{"title":"Pathophysiology of gastro-oesophageal reflux disease: implications for diagnosis and management","authors":"Julieta Argüero, Daniel Sifrim","doi":"10.1038/s41575-023-00883-z","DOIUrl":"10.1038/s41575-023-00883-z","url":null,"abstract":"Gastro-oesophageal reflux disease (GERD) is a common gastrointestinal disorder in which retrograde flow of gastric content into the oesophagus causes uncomfortable symptoms and/or complications. It has a multifactorial and partially understood pathophysiology. GERD starts in the stomach, where the refluxate material is produced. Following the trajectory of reflux, the failure of the antireflux barrier, primarily the lower oesophageal sphincter and the crural diaphragm, enables the refluxate to reach the oesophageal lumen, triggering oesophageal or extra-oesophageal symptoms. Reflux clearance mechanisms such as primary and secondary peristalsis and the arrival of bicarbonate-rich saliva are critical to prevent mucosal damage. Alterations of the oesophageal mucosal integrity, such as macroscopic oesophagitis or microscopic changes, determine the perception of symptoms. The intensity of the symptoms is affected by peripheral and central neural and psychological mechanisms. In this Review, we describe an updated understanding of the complex and multifactorial pathophysiology of GERD. It is now recognized that different GERD phenotypes have different degrees of reflux, severity of mucosal integrity damage and type, and severity of symptoms. These variations are probably due to the occurrence of a predominant pathophysiological mechanism in each patient. We also describe the main pathophysiological mechanisms of GERD and their implications for personalized diagnosis and management. In this Review, Argüero and Sifrim describe the core pathophysiological mechanisms involved in gastro-oesophageal reflux disease (GERD). They also discuss the implications for clinical management of GERD.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139091420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-19DOI: 10.1038/s41575-023-00857-1
Lin Y. Hung, Kara Gross Margolis
Autism spectrum disorders (ASDs) are recognized as central neurodevelopmental disorders diagnosed by impairments in social interactions, communication and repetitive behaviours. The recognition of ASD as a central nervous system (CNS)-mediated neurobehavioural disorder has led most of the research in ASD to be focused on the CNS. However, gastrointestinal function is also likely to be affected owing to the neural mechanistic nature of ASD and the nervous system in the gastrointestinal tract (enteric nervous system). Thus, it is unsurprising that gastrointestinal disorders, particularly constipation, diarrhoea and abdominal pain, are highly comorbid in individuals with ASD. Gastrointestinal problems have also been repeatedly associated with increased severity of the core symptoms diagnostic of ASD and other centrally mediated comorbid conditions, including psychiatric issues, irritability, rigid–compulsive behaviours and aggression. Despite the high prevalence of gastrointestinal dysfunction in ASD and its associated behavioural comorbidities, the specific links between these two conditions have not been clearly delineated, and current data linking ASD to gastrointestinal dysfunction have not been extensively reviewed. This Review outlines the established and emerging clinical and preclinical evidence that emphasizes the gut as a novel mechanistic and potential therapeutic target for individuals with ASD. Gastrointestinal issues are common in autism spectrum disorders (ASDs). This Review provides a comprehensive overview of the clinical and mechanistic connections between ASDs and gastrointestinal disorders and how these data might be utilized for future research and novel therapeutic targets.
{"title":"Autism spectrum disorders and the gastrointestinal tract: insights into mechanisms and clinical relevance","authors":"Lin Y. Hung, Kara Gross Margolis","doi":"10.1038/s41575-023-00857-1","DOIUrl":"10.1038/s41575-023-00857-1","url":null,"abstract":"Autism spectrum disorders (ASDs) are recognized as central neurodevelopmental disorders diagnosed by impairments in social interactions, communication and repetitive behaviours. The recognition of ASD as a central nervous system (CNS)-mediated neurobehavioural disorder has led most of the research in ASD to be focused on the CNS. However, gastrointestinal function is also likely to be affected owing to the neural mechanistic nature of ASD and the nervous system in the gastrointestinal tract (enteric nervous system). Thus, it is unsurprising that gastrointestinal disorders, particularly constipation, diarrhoea and abdominal pain, are highly comorbid in individuals with ASD. Gastrointestinal problems have also been repeatedly associated with increased severity of the core symptoms diagnostic of ASD and other centrally mediated comorbid conditions, including psychiatric issues, irritability, rigid–compulsive behaviours and aggression. Despite the high prevalence of gastrointestinal dysfunction in ASD and its associated behavioural comorbidities, the specific links between these two conditions have not been clearly delineated, and current data linking ASD to gastrointestinal dysfunction have not been extensively reviewed. This Review outlines the established and emerging clinical and preclinical evidence that emphasizes the gut as a novel mechanistic and potential therapeutic target for individuals with ASD. Gastrointestinal issues are common in autism spectrum disorders (ASDs). This Review provides a comprehensive overview of the clinical and mechanistic connections between ASDs and gastrointestinal disorders and how these data might be utilized for future research and novel therapeutic targets.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138770395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-18DOI: 10.1038/s41575-023-00871-3
Camille Danne, Jurate Skerniskyte, Benoit Marteyn, Harry Sokol
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract that results from dysfunction in innate and/or adaptive immune responses. Impaired innate immunity, which leads to lack of control of an altered intestinal microbiota and to activation of the adaptive immune system, promotes a secondary inflammatory response that is responsible for tissue damage. Neutrophils are key players in innate immunity in IBD, but their roles have been neglected compared with those of other immune cells. The latest studies on neutrophils in IBD have revealed unexpected complexities, with heterogeneous populations and dual functions, both deleterious and protective, for the host. In parallel, interconnections between disease development, intestinal microbiota and neutrophils have been highlighted. Numerous IBD susceptibility genes (such as NOD2, NCF4, LRRK2, CARD9) are involved in neutrophil functions related to defence against microorganisms. Moreover, severe monogenic diseases involving dysfunctional neutrophils, including chronic granulomatous disease, are characterized by intestinal inflammation that mimics IBD and by alterations in the intestinal microbiota. This observation demonstrates the dialogue between neutrophils, gut inflammation and the microbiota. Neutrophils affect microbiota composition and function in several ways. In return, microbial factors, including metabolites, regulate neutrophil production and function directly and indirectly. It is crucial to further investigate the diverse roles played by neutrophils in host–microbiota interactions, both at steady state and in inflammatory conditions, to develop new IBD therapies. In this Review, we discuss the roles of neutrophils in IBD, in light of emerging evidence proving strong interconnections between neutrophils and the gut microbiota, especially in an inflammatory context. In this Review, Danne and colleagues describe the roles of neutrophils in inflammatory bowel disease, as well as their functions in host–microbiota interactions.
{"title":"Neutrophils: from IBD to the gut microbiota","authors":"Camille Danne, Jurate Skerniskyte, Benoit Marteyn, Harry Sokol","doi":"10.1038/s41575-023-00871-3","DOIUrl":"10.1038/s41575-023-00871-3","url":null,"abstract":"Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract that results from dysfunction in innate and/or adaptive immune responses. Impaired innate immunity, which leads to lack of control of an altered intestinal microbiota and to activation of the adaptive immune system, promotes a secondary inflammatory response that is responsible for tissue damage. Neutrophils are key players in innate immunity in IBD, but their roles have been neglected compared with those of other immune cells. The latest studies on neutrophils in IBD have revealed unexpected complexities, with heterogeneous populations and dual functions, both deleterious and protective, for the host. In parallel, interconnections between disease development, intestinal microbiota and neutrophils have been highlighted. Numerous IBD susceptibility genes (such as NOD2, NCF4, LRRK2, CARD9) are involved in neutrophil functions related to defence against microorganisms. Moreover, severe monogenic diseases involving dysfunctional neutrophils, including chronic granulomatous disease, are characterized by intestinal inflammation that mimics IBD and by alterations in the intestinal microbiota. This observation demonstrates the dialogue between neutrophils, gut inflammation and the microbiota. Neutrophils affect microbiota composition and function in several ways. In return, microbial factors, including metabolites, regulate neutrophil production and function directly and indirectly. It is crucial to further investigate the diverse roles played by neutrophils in host–microbiota interactions, both at steady state and in inflammatory conditions, to develop new IBD therapies. In this Review, we discuss the roles of neutrophils in IBD, in light of emerging evidence proving strong interconnections between neutrophils and the gut microbiota, especially in an inflammatory context. In this Review, Danne and colleagues describe the roles of neutrophils in inflammatory bowel disease, as well as their functions in host–microbiota interactions.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138740533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-18DOI: 10.1038/s41575-023-00872-2
Luca Elli, Daniel Leffler, Christophe Cellier, Benjamin Lebwohl, Carolina Ciacci, Michael Schumann, Knut E. A. Lundin, Stefania Chetcuti Zammit, Reena Sidhu, Leda Roncoroni, Julio C. Bai, Anne R. Lee, Melinda Dennis, Marie E. Robert, Kamran Rostami, Sherine Khater, Isabel Comino, Angel Cebolla, Federica Branchi, Elena F. Verdu, Juan Pablo Stefanolo, Randi Wolf, Sheba Bergman-Golden, Nick Trott, Luigia Scudeller, Fabiana Zingone, Lucia Scaramella, David S. Sanders
Coeliac disease (CeD) is an immunological disease triggered by the consumption of gluten contained in food in individuals with a genetic predisposition. Diagnosis is based on the presence of small bowel mucosal atrophy and circulating autoantibodies (anti-type 2 transglutaminase antibodies). After diagnosis, patients follow a strict, life-long gluten-free diet. Although the criteria for diagnosis of this disease are well defined, the monitoring phase has been studied less and there is a lack of specific guidelines for this phase. To develop a set of clinical guidelines for CeD monitoring, we followed the Grading of Recommendations Assessment, Development and Evaluation methodology. Statements and recommendations with the level of evidence were developed and approved by the working group, which comprised gastroenterologists, pathologists, dieticians and biostatisticians. The proposed guidelines, endorsed by the North American and European coeliac disease scientific societies, make recommendations for best practices in monitoring patients with CeD based on the available evidence. The evidence level is low for many topics, suggesting that further research in specific aspects of CeD would be valuable. In conclusion, the present guidelines support clinicians in improving CeD treatment and follow-up and highlight novel issues that should be considered in future studies. Coeliac disease is a chronic inflammatory disease triggered by gluten consumption in individuals with a genetic susceptibility. These Evidence-Based Guidelines provide recommendations for improving the health care of the patients and discuss future perspectives.
{"title":"Guidelines for best practices in monitoring established coeliac disease in adult patients","authors":"Luca Elli, Daniel Leffler, Christophe Cellier, Benjamin Lebwohl, Carolina Ciacci, Michael Schumann, Knut E. A. Lundin, Stefania Chetcuti Zammit, Reena Sidhu, Leda Roncoroni, Julio C. Bai, Anne R. Lee, Melinda Dennis, Marie E. Robert, Kamran Rostami, Sherine Khater, Isabel Comino, Angel Cebolla, Federica Branchi, Elena F. Verdu, Juan Pablo Stefanolo, Randi Wolf, Sheba Bergman-Golden, Nick Trott, Luigia Scudeller, Fabiana Zingone, Lucia Scaramella, David S. Sanders","doi":"10.1038/s41575-023-00872-2","DOIUrl":"10.1038/s41575-023-00872-2","url":null,"abstract":"Coeliac disease (CeD) is an immunological disease triggered by the consumption of gluten contained in food in individuals with a genetic predisposition. Diagnosis is based on the presence of small bowel mucosal atrophy and circulating autoantibodies (anti-type 2 transglutaminase antibodies). After diagnosis, patients follow a strict, life-long gluten-free diet. Although the criteria for diagnosis of this disease are well defined, the monitoring phase has been studied less and there is a lack of specific guidelines for this phase. To develop a set of clinical guidelines for CeD monitoring, we followed the Grading of Recommendations Assessment, Development and Evaluation methodology. Statements and recommendations with the level of evidence were developed and approved by the working group, which comprised gastroenterologists, pathologists, dieticians and biostatisticians. The proposed guidelines, endorsed by the North American and European coeliac disease scientific societies, make recommendations for best practices in monitoring patients with CeD based on the available evidence. The evidence level is low for many topics, suggesting that further research in specific aspects of CeD would be valuable. In conclusion, the present guidelines support clinicians in improving CeD treatment and follow-up and highlight novel issues that should be considered in future studies. Coeliac disease is a chronic inflammatory disease triggered by gluten consumption in individuals with a genetic susceptibility. These Evidence-Based Guidelines provide recommendations for improving the health care of the patients and discuss future perspectives.","PeriodicalId":18793,"journal":{"name":"Nature Reviews Gastroenterology &Hepatology","volume":null,"pages":null},"PeriodicalIF":65.1,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41575-023-00872-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138714129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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