Search results for "030211 gastroenterology & hepatology"

showing 10 items of 1275 documents

The Role of Laboratory Tests in Crohn's Disease.

2016

In the past, laboratory tests were considered of limited value in Crohn's disease (CD). In the era of biologics, laboratory tests have become essential to evaluate the inflammatory burden of the disease (C-reactive protein, fecal calprotectin) since symptoms-based scores are subjective, to predict the response to pharmacological options and the risk of relapse, to discriminate CD from ulcerative colitis, to select candidates to anti-tumor necrosis factors [screening tests looking for hepatitis B virus and hepatitis C virus status and latent tuberculosis], to assess the risk of adverse events (testing for thiopurine metabolites and thiopurine-methyltransferase activity), and to personalize a…

0301 basic medicineOncologyCrohn’s diseasemedicine.medical_specialtyDiseaseReviewlaboratory testsBioinformaticsInflammatory bowel disease03 medical and health sciences0302 clinical medicineinflammatory bowel diseaseInternal medicinemedicinelcsh:RC799-869Crohn's diseaseLatent tuberculosisThiopurine methyltransferasebiologybusiness.industryGastroenterologymedicine.diseaseUlcerative colitis030104 developmental biologybiology.proteinlcsh:Diseases of the digestive system. Gastroenterology030211 gastroenterology & hepatologyCalprotectinbusinessPharmacogeneticsClinical medicine insights. Gastroenterology
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Non-invasive stratification of hepatocellular carcinoma risk in non-alcoholic fatty liver using polygenic risk scores

2021

Background & Aims: Hepatocellular carcinoma (HCC) risk stratification in individuals with dysmetabolism is a major unmet need. Genetic predisposition contributes to non-alcoholic fatty liver disease (NAFLD). We aimed to exploit robust polygenic risk scores (PRS) that can be evaluated in the clinic to gain insight into the causal relationship between NAFLD and HCC, and to improve HCC risk stratification. Methods: We examined at-risk individuals (NAFLD cohort, n = 2,566; 226 with HCC; and a replication cohort of 427 German patients with NAFLD) and the general population (UK Biobank [UKBB] cohort, n = 364,048; 202 with HCC). Variants in PNPLA3-TM6SF2-GCKR-MBOAT7 were combined in a hepatic …

0301 basic medicineOncologyLiver CirrhosisMaleMultifactorial InheritanceCirrhosis0302 clinical medicineRisk FactorsNon-alcoholic Fatty Liver DiseaseHepatic fatAdiposityeducation.field_of_studyFatty liverLiver NeoplasmsMiddle AgedPrognosisEuropeCirrhosisLiverCohort030211 gastroenterology & hepatologyBiomarker; Cirrhosis; Genetics; Hepatic fat; Non-alcoholic fatty liver diseaseFemaleLiver cancerCohort studymedicine.medical_specialtyCarcinoma HepatocellularSettore MED/12 - GASTROENTEROLOGIAPopulationRisk Assessment03 medical and health sciencesBiomarker Cirrhosis Genetics Hepatic fat Non-alcoholic fatty liver disease Cross-Sectional Studies Europe Female Genetic Predisposition to Disease Humans Liver Liver Cirrhosis Male Mediation Analysis Middle Aged Multifactorial Inheritance Predictive Value of Tests Prognosis Risk Assessment Risk Factors Adiposity Carcinoma Hepatocellular Non-alcoholic Fatty Liver DiseaseGeneticPredictive Value of TestsInternal medicinemedicineGenetic predispositionGeneticsHumansGenetic Predisposition to DiseaseeducationCirrhosiMediation AnalysisHepatologybusiness.industryCarcinomaCase-control studyHepatocellularBiomarkermedicine.diseasedigestive system diseases030104 developmental biologyCross-Sectional StudiesbusinessJournal of Hepatology
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Associations of Pathogenic Variants in MLH1, MSH2, and MSH6 With Risk of Colorectal Adenomas and Tumors and With Somatic Mutations in Patients With L…

2020

Contains fulltext : 220040.pdf (Publisher’s version ) (Closed access) BACKGROUND & AIMS: Lynch syndrome is caused by variants in DNA mismatch repair (MMR) genes and associated with an increased risk of colorectal cancer (CRC). In patients with Lynch syndrome, CRCs can develop via different pathways. We studied associations between Lynch syndrome-associated variants in MMR genes and risks of adenoma and CRC and somatic mutations in APC and CTNNB1 in tumors in an international cohort of patients. METHODS: We combined clinical and molecular data from 3 studies. We obtained clinical data from 2747 patients with Lynch syndrome associated with variants in MLH1, MSH2, or MSH6 from Germany, the Net…

0301 basic medicineOncologyMaleColorectal cancerDNA Mutational Analysisgenetic analysisHEREDITARYcancer riskGUIDELINESDNA Mismatch Repair0302 clinical medicineGermanyTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Prospective Studiesprognostic factorFinlandbeta CateninNetherlandsOutcomePrognostic FactorGastroenterologyGenetic AnalysisColonoscopyMiddle AgedCANCERLynch syndromeCancer Risk3. Good healthDNA-Binding ProteinsDEFICIENCYMutS Homolog 2 Proteinsyöpägeenitoutcome030211 gastroenterology & hepatologyDNA mismatch repairFemaleMutL Protein Homolog 1geenitutkimusAdenomaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdenoma3122 CancersAdenomatous Polyposis Coli ProteinINSTABILITYSOCIETYMLH103 medical and health sciencesInternal medicinemedicineMANAGEMENTHumansLynchin oireyhtymäneoplasmspaksusuolisyöpäHepatologybusiness.industryCancernutritional and metabolic diseasesennusteetmedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesMSH6030104 developmental biologyMSH2Mutationbusiness
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Optimized Mouse Models for Liver Fibrosis

2017

Fibrosis is the excessive accumulation of extracellular matrix components due to chronic injury, with collagens as predominant structural components. Liver fibrosis can progress to cirrhosis, which is characterized by a severe distortion of the delicate hepatic vascular architecture, the shunting of the blood supply away from hepatocytes and the resultant functional liver failure. Cirrhosis is associated with a highly increased morbidity and mortality and represents the major hard endpoint in clinical studies of chronic liver diseases. Moreover, cirrhosis is a strong cofactor of primary liver cancer. In vivo models are indispensable tools to study the cellular and molecular mechanisms of li…

0301 basic medicinePathologymedicine.medical_specialtyCirrhosisbusiness.industryLiver fibrosismedicine.diseaseVascular architectureExtracellular matrix03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinechemistryIn vivoFibrosisMedicine030211 gastroenterology & hepatologyThioacetamidebusinessPrimary liver cancer
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A "systems medicine" approach to the study of non-alcoholic fatty liver disease

2016

a b s t r a c t The prevalence of fatty liver (steatosis) in the general population is rapidly increasing worldwide. The progress of knowledge in the physiopathology of fatty liver is based on the systems biology approach to studying the complex interactions among different physiological systems. Similarly, translational and clinical research should address the complex interplay between these systems impacting on fatty liver. The clinical needs drive the applications of systems medicine to re-define clinical phenotypes, assessing the multiple nature of disease susceptibility and progression (e.g. the definition of risk, prognosis, diag- nosis criteria, and new endpoints of clinical trials).…

0301 basic medicinePathologymedicine.medical_specialtyFatty liver; Medicine; NAFLD; NASH; Personalized; Systems medicine; Gastroenterology; HepatologySystems AnalysisSystems biologyPersonalizedPopulationDiseaseBioinformatics03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsInternal medicineFatty liverNAFLDFatty liver; Medicine; NAFLD; NASH; Personalized; Systems medicinemedicineHumansFatty liver; Medicine; NAFLD; NASH; Personalized; Systems medicine; Hepatology; GastroenterologyeducationFatty liver; Medicine; NAFLD; NASH; Personalized; Systems medicine; Disease Progression; Humans; Non-alcoholic Fatty Liver Disease; Phenotype; Risk Factors; Systems Biology; Systems Analysis; Medicine (all); Hepatology; Gastroenterologyeducation.field_of_studyHepatologybusiness.industrySystems BiologySettore MED/09 - MEDICINA INTERNAFatty liverGastroenterologyNASHHepatologymedicine.diseaseSystems medicineClinical trial030104 developmental biologyPhenotypeSystems medicineDisease ProgressionMedicine030211 gastroenterology & hepatologySteatosisbusiness
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Guidelines are silver, but a multidisciplinary team discussion may be golden?

2018

0301 basic medicinePatient Care TeamMedical educationCarcinoma HepatocellularSilverHepatologybusiness.industryLiver NeoplasmsMultidisciplinary teamCombined Modality Therapy03 medical and health sciences030104 developmental biology0302 clinical medicineMedicineHumans030211 gastroenterology & hepatologybusinessLiver international : official journal of the International Association for the Study of the Liver
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Phenotypic spectrum and diagnostic pitfalls of ABCB4 deficiency depending on age of onset.

2017

Genetic variants in the adenosine triphosphate-binding cassette subfamily B member 4 (ABCB4) gene, which encodes hepatocanalicular phosphatidylcholine floppase, can lead to different phenotypes, such as progressive familial intrahepatic cholestasis (PFIC) type 3, low phospholipid-associated cholelithiasis, and intrahepatic cholestasis of pregnancy. The aim of this multicenter project was to collect information on onset and progression of this entity in different age groups and to assess the relevance of this disease for the differential diagnosis of chronic liver disease. Clinical and laboratory data of 38 patients (17 males, 21 females, from 29 families) with homozygous or (compound) heter…

0301 basic medicinePediatricsmedicine.medical_specialtyHepatologybusiness.industryProgressive familial intrahepatic cholestasisMedizinOriginal ArticlesABCB4Jaundicemedicine.diseaseChronic liver disease03 medical and health sciencesLiver disease030104 developmental biology0302 clinical medicineBiliary atresiamedicine030211 gastroenterology & hepatologyOriginal ArticleAge of onsetmedicine.symptombusinessCholestasis of pregnancyHepatology communications
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Nutritional Wheat Amylase-Trypsin Inhibitors Promote Intestinal Inflammation via Activation of Myeloid Cells.

2016

Background & Aims Wheat amylase-trypsin inhibitors (ATIs) are nutritional activators of innate immunity, via activation of the toll-like receptor 4 (TLR4) on myeloid cells. We aimed to characterize the biologic activity of ATIs in various foods and their effect on intestinal inflammation. Methods We selected 38 different gluten-containing and gluten-free products, either unprocessed (such as wheat, rye, barley, quinoa, amaranth, soya, lentils, and rice) or processed (such as pizza, pasta, bread, and biscuits). ATIs were extracted and their biological activities determined in TLR4-responsive mouse and human cell lines. Effects of oral ATIs on intestinal inflammation were determined in health…

0301 basic medicinePharmacologyAdaptive Immunitychemistry.chemical_compoundMice0302 clinical medicineMesenteric lymph nodesMesenteryMyeloid CellsTriticumPlant ProteinsToll-like receptorDextran SulfateGastroenterologyfood and beveragesColitisIntestinesmedicine.anatomical_structureAmylases030211 gastroenterology & hepatologymedicine.symptomTrypsin InhibitorsInterferon InducersGlutensColonDuodenumInflammationIleumBiologyCell Line03 medical and health sciencesDiet Gluten-FreeIleummedicineAnimalsHumansColitisInflammationInnate immune systemHepatologymedicine.diseaseImmunity InnateMice Inbred C57BLToll-Like Receptor 4Celiac Disease030104 developmental biologyPoly I-CchemistryPolyinosinic:polycytidylic acidImmunologyLymph NodesWheat allergyGastroenterology
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Niemann-Pick type C2 protein supplementation in experimental non-alcoholic fatty liver disease

2017

BACKGROUND AND AIMS: Hepatic cholesterol deposition drives inflammation and fibrosis in non-alcoholic steatohepatitis (NASH). The Niemann-Pick type C2 (NPC2) protein plays an important role in regulating intracellular cholesterol trafficking and homeostasis. We hypothesized that intravenous NPC2 supplementation reduces cholesterol accumulation, hepatic inflammation and fibrogenesis in a nutritional NASH rat model.METHODS: Rats were fed a high-fat, high-cholesterol (HFHC) diet for four weeks resulting in moderately severe NASH. Animals were treated with intravenous NPC2 or placebo twice weekly for either the last two weeks or the entire four weeks. End-points were liver/body- and spleen/body…

0301 basic medicinePhysiologyGene Expressionlcsh:MedicinePathology and Laboratory MedicineBiochemistrychemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseSterol Regulatory Element Binding ProteinsInnate Immune SystemMultidisciplinarybiologyLiver DiseasesReverse cholesterol transportFatty liverIntracellular Signaling Peptides and ProteinsLipidsCholesterolLiverCytokinesLiver FibrosisFemale030211 gastroenterology & hepatologylipids (amino acids peptides and proteins)Research Articlemedicine.medical_specialtyImmunologyBiological Transport ActiveGastroenterology and HepatologyCollagen Type I03 medical and health sciencesSigns and SymptomsDiagnostic MedicineInternal medicineGeneticsmedicineAnimalsRats WistarGlycoproteinsNutritionInflammationbusiness.industryCholesterollcsh:RBiology and Life Sciencesnutritional and metabolic diseasesMolecular Developmentmedicine.diseaseDietary FatsFibrosisRatsDietCollagen Type I alpha 1 ChainPPAR gammaFatty LiverDisease Models Animal030104 developmental biologyEndocrinologychemistryImmune SystemABCA1LDL receptorbiology.proteinlcsh:QSteatohepatitisCarrier ProteinsbusinessDevelopmental BiologyLipoprotein
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Nutritional Intake and the Risk for Non-Alcoholic Fatty Liver Disease (NAFLD)

2019

The prevalence of non-alcoholic fatty liver disease (NAFLD) is rising worldwide, and it is estimated that approximately one billion individuals may be afflicted with NAFLD globally [...]

0301 basic medicinePhysiologylcsh:TX341-641DiseaseGlobal Healthdigestive system03 medical and health sciences0302 clinical medicineFeeding behaviorNon-alcoholic Fatty Liver DiseaseGlobal healthMedicineHumans030109 nutrition & dieteticsNutrition and Dieteticsbusiness.industryFatty livernutritional and metabolic diseasesNon alcoholicFeeding BehaviorDietary patternmedicine.diseasedigestive system diseasesEditorialn/a030211 gastroenterology & hepatologybusinesslcsh:Nutrition. Foods and food supplyFood ScienceNutrients
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