Search results for " TUMOR NECROSIS FACTOR-a"

showing 10 items of 32 documents

Cancer in Elderly Onset Inflammatory Bowel Disease: A Population-Based Study.

2016

IF 10.383; International audience; OBJECTIVES: Cancer may be a complication of inflammatory bowel disease (IBD) or its treatment. In elderly onset IBD patients the risk of malignancy is of particular concern. We studied this risk in a population-based cohort of elderly onset IBD patients.METHODS: In a French population-based cohort, we identified 844 patients aged >60 years at IBD diagnosis from 1988 to 2006, including 370 Crohn's disease (CD) and 474 ulcerative colitis (UC). We compared incidence of cancer among IBD patients with that observed in the French Network of population-based Cancer Registries (FRANCIM). Confidence interval (CI) was estimated assuming a Poisson-specific law for ra…

MESH: CarcinomaMaleNonmelanoma Skin-CancerInflammatory bowel disease0302 clinical medicineAdrenal Cortex HormonesAzathioprineMESH: IncidenceAge of OnsetAged 80 and overeducation.field_of_studyMESH: Middle AgedRheumatoid-ArthritisIncidenceGastroenterologyMESH: Follow-Up StudiesMESH: Anti-Inflammatory Agents Non-Steroidal3. Good health030220 oncology & carcinogenesisCohort030211 gastroenterology & hepatology[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: Immunosuppressive Agentsmedicine.medical_specialtyMESH: Age of OnsetMESH: Colitis Ulcerativedigestive systemMESH: Adrenal Cortex Hormones03 medical and health sciencesIntestinal NeoplasmsHumansCrohns-DiseaseeducationMESH: Intestinal NeoplasmsMESH: Protective FactorsMESH: AzathioprineAgedRetrospective StudiesMESH: HumansMESH: Crohn DiseaseTumor Necrosis Factor-alphaMESH: Retrospective Studiesmedicine.diseaseMESH: Inflammatory Bowel DiseasesInflammatory Bowel Diseasesdigestive system diseasesLymphoproliferative DisordersMethotrexateMESH: Tumor Necrosis Factor-alphaColitis UlcerativeComplicationMESH: FemaleProspective Observational CohortTime FactorsMESH: RegistriesMESH: Proportional Hazards ModelsMaintenance TherapyMESH: Aged 80 and overMESH: Lymphoproliferative DisordersCrohn DiseaseMESH: Risk FactorsRisk FactorsNeoplasmsMESH: NeoplasmsRegistriesUlcerative-ColitisMesalamineMESH: AgedIncidence (epidemiology)Anti-Inflammatory Agents Non-SteroidalMetaanalysisMiddle AgedhumanitiesMESH: MethotrexateFemaleFranceFrench PopulationColorectal NeoplasmsImmunosuppressive AgentsMESH: Myeloproliferative DisordersPopulationColorectal-CancerIncreased RiskInternal medicinemedicineProportional Hazards ModelsMyeloproliferative DisordersHepatologybusiness.industryMESH: Time FactorsCarcinomaCancerRetrospective cohort study[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: MesalamineProtective FactorsMESH: MaleMESH: FranceAge of onsetbusinessMESH: Colorectal NeoplasmsFollow-Up StudiesThe American journal of gastroenterology
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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Advanced age is an independent risk factor for severe infections and mortality in patients given anti-tumor necrosis factor therapy for inflammatory …

2011

See related article, Oostlander AE et al, on page 116 in Gastroenterology. BACKGROUND & AIMS: Few data are available on effects of biologic therapies in patients more than 65 years old with inflammatory bowel disease (IBD). We evaluated the risk and benefits of therapy with tumor necrosis factor (TNF) inhibitors in these patients. METHODS: We collected data from patients with IBD treated with infliximab (n 2475) and adalimumab (n 604) from 2000 to 2009 at 16 tertiary centers. Ninety-five patients (3%) were more than 65 years old (52 men; 37 with ulcerative colitis and 58 with Crohn’s disease; 78 treated with infliximab and 17 with adalimumab). The control group comprised 190 patients 65 yea…

MaleAgingSettore MED/09 - Medicina InternaBiologicantagonists /&/ inhibitors/immunology Young AdultInflammatory bowel diseaseHumanized AntibodieElderlyNeoplasmsMonoclonalYoung adultAged 80 and overSettore MED/12 - GastroenterologiaCrohn's diseaseGastroenterologyAge FactorsAntibodies MonoclonalMiddle AgedUlcerative colitisepidemiology Opportunistic InfectionFemaleDrug ComplicationSafetymedicine.drugAdultmedicine.medical_specialtyAdolescentIBDOpportunistic InfectionsAntibodies Monoclonal HumanizedYoung AdultInternal medicinemedicineAdalimumab80 and over AntibodieHumansImmunologic FactorsRisk factoradverse effects/therapeutic use Inflammatory Bowel DiseaseAgedHepatologymortality/therapy Male Middle Aged Neoplasmepidemiology Tumor Necrosis Factor-alphabusiness.industryTumor Necrosis Factor-alphaAdalimumabmedicine.diseaseInflammatory Bowel DiseasesCrohn's Disease Activity IndexInfliximabInfliximabSurgeryInflammation Side Effects Drug ComplicationsSide Effectinflammationadverse effects/therapeutic use Female Humans Immunologic FactorAdolescent Adult Age Factors Aged Agedbusiness
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A 2-year comparative open label randomized study of efficacy and safety of etanercept and infliximab in patients with ankylosing spondylitis

2010

The signs and symptoms of ankylosing spondylitis (AS) respond inadequately to nonsteroidal antiinflammatory drugs, corticosteroids, and disease modifying antirheumatic drugs in quite a number of patients. Tumor necrosis factor inhibitors have demonstrated to be of value in reducing AS disease activity in clinical trials. The efficacy and safety of both etanercept and infliximab in patients with ankylosing spondylitis were compared in a 2-year open label randomised study. Our results are consistent with a significant more rapid clinical improvement in the infliximab treated group. Treatment with both etanercept and infliximab at the end of the study was effective, safe, and well tolerated. ©…

MaleAntibodieReceptors Tumor Necrosis FactorEtanerceptlaw.inventionEtanerceptRandomized controlled triallawimmune system diseasesOutcome Assessment Health CareMonoclonalImmunology and Allergyskin and connective tissue diseasesAntirheumatic AgentAntibodies MonoclonalAntirheumatic AgentsTreatment OutcomeAntirheumatic AgentsFemalemedicine.drugHumanReceptormusculoskeletal diseasesAdultAnkylosingmedicine.medical_specialtyImmunologyDrug Administration ScheduleOutcome Assessment (Health Care)RheumatologyInternal medicinemedicineHumansSpondylitis AnkylosingSpondylitisSpondylitiAnkylosing spondylitisbusiness.industryTumor Necrosis Factor-alphaAnkylosing spondylitis; Etanercept; Infliximab; Adult; Antibodies Monoclonal; Antirheumatic Agents; Drug Administration Schedule; Etanercept; Female; Humans; Immunoglobulin G; Infliximab; Male; Outcome Assessment (Health Care); Receptors Tumor Necrosis Factor; Spondylitis Ankylosing; Treatment Outcome; Tumor Necrosis Factor-alpha; Rheumatology; Immunology; Immunology and Allergymedicine.diseaseInfliximabRheumatologyInfliximabClinical trialAnkylosing spondylitistomatognathic diseasesImmunoglobulin GPhysical therapybusinessTumor Necrosis Factor
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TNF-alpha gene promoter polymorphisms and risk of venous thromboembolism in gastrointestinal cancer patients undergoing chemotherapy

2013

Abstract Background TNF-α has been proposed as a predictive factor for venous thromboembolism (VTE). Genetic polymorphisms could regulate TNF-α production. However, the relationship between TNFA gene variants and VTE is not clarified. This study aims to investigate the predictive role of five different TNFA gene promoter SNPs, or their haplotype combination(s), for a first VTE episode in gastrointestinal cancer out-patients treated with chemotherapy. Patients and methods Serum TNF-α levels and TNFA -863C/A, -857C/T, -376G/A, -308G/A and -238G/A gene promoter polymorphisms were retrospectively evaluated in 314 subjects, including 157 controls and 157 Caucasian patients with histologically di…

MaleAntimetabolitesSettore MED/06 - Oncologia Medicamedicine.medical_treatmentchemotherapyGastroenterologysingle nucleotide polymorphismschemotherapy; gastrointestinal cancer; single nucleotide polymorphisms; tumour necrosis factor-α; venous thromboembolismsingle nucleotide polymorphismPhytogenic80 and overtumour necrosis factor-αPromoter Regions GeneticGastrointestinal NeoplasmsAged 80 and overHazard ratioSingle NucleotideHematologyMiddle AgedAntineoplasticChemotherapy regimenOncologyFemaleFluorouracilmedicine.drugAdultRiskAntimetabolites Antineoplasticmedicine.medical_specialtygastrointestinal cancervenous thromboembolismAntineoplastic AgentsSingle-nucleotide polymorphismIrinotecanPolymorphism Single NucleotidePromoter RegionsGeneticInternal medicinemedicineHumansGenetic Predisposition to DiseaseGastrointestinal cancercardiovascular diseasesPolymorphismRetrospective StudiesAgedChemotherapyTumor Necrosis Factor-alphabusiness.industryHaplotypeOdds ratiomedicine.diseaseAntineoplastic Agents PhytogenicIrinotecanHaplotypesCase-Control StudiesImmunologyCamptothecinHuman medicinePolymorphism Single Nucleotide; Antimetabolites Antineoplastic; single nucleotide polymorphisms; Humans; Retrospective Studies; Aged; Promoter Regions Genetic; Haplotypes; Aged 80 and over; Adult; gastrointestinal cancer; Genetic Predisposition to Disease; Male; tumour necrosis factor-α; Tumor Necrosis Factor-alpha; Venous Thromboembolism; Camptothecin; chemotherapy; Risk; Fluorouracil; Case-Control Studies; Gastrointestinal Neoplasms; Middle Aged; venous thromboembolism; Antineoplastic Agents Phytogenic; Femalebusiness
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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Dietary polyunsaturated fatty acids reduce retinal stress induced by an elevation of intraocular pressure in rats.

2011

International audience; N-6 and n-3 polyunsaturated fatty acids (PUFAs) have been shown to prevent tissue release of inflammatory molecules. We have shown that a combination of n-6 and n-3 PUFAs is more efficient than single supplementations on the long-term consequences of intraocular pressure elevation. We hypothesized that such an association is also more effective during early retinal stress by modifying retinal proinflammatory prostaglandin and cytokine productions. Rats were supplemented for 3 months with n-6 PUFAs, n-3 PUFAs, or both n-6 and n-3 PUFAs. After 3 months, a surgical elevation of intraocular pressure was induced. Retinal morphometry and glial cell activation were evaluate…

MaleMESH : RNA MessengerMESH: Eicosapentaenoic AcidEndocrinology Diabetes and Metabolismmedicine.medical_treatment[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betaMESH: Dietary SupplementsMESH: Rats Sprague-DawleyRats Sprague-Dawleychemistry.chemical_compound0302 clinical medicineEndocrinologyMESH: Interleukin-1betaratMESH: AnimalsProstaglandin E2Prostaglandin E1MESH : Tumor Necrosis Factor-alphaMESH : Intraocular Pressure0303 health sciencesNutrition and DieteticsMESH : RatsMESH : NeurogliaMESH: RetinaMESH: Dinoprostonepression intraoculaireMESH: AlprostadilMESH: Docosahexaenoic AcidsBiochemistryEicosapentaenoic AcidDocosahexaenoic acidlipids (amino acids peptides and proteins)MESH: NeurogliaProstaglandin D2Cell activationNeurogliaMESH : Alprostadilmedicine.drugProstaglandin Emedicine.medical_specialtyMESH : DinoprostoneMESH : Interleukin-6Docosahexaenoic AcidsMESH: RatsMESH : MaleProstaglandinBiologyMESH : Interleukin-1betaDinoprostoneRetinaMESH : Diet03 medical and health sciencesMESH: DietMESH: Intraocular PressureInternal medicinemedicineMESH : Eicosapentaenoic AcidAnimalsMESH : Dietary SupplementsRNA MessengerAlprostadilprostanoids030304 developmental biologyMESH: RNA MessengerInterleukin-6Tumor Necrosis Factor-alphadietary polyunsatured fatty acidretinal stressMESH : RetinaRetinalN-6MESH: Interleukin-6MESH : Rats Sprague-Dawleyeye diseasesMESH: MaleMESH : Docosahexaenoic AcidsDietRatsN-3EndocrinologychemistryMESH: Tumor Necrosis Factor-alphaDietary Supplements030221 ophthalmology & optometryMESH : Animalssense organs[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionintraocular pressure
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Expression of Interleukin-32 in the Inflamed Arteries of Patients With Giant Cell Arteritis

2011

Objective Giant cell (temporal) arteritis (GCA) is a vasculitis that mainly affects the large and medium arteries, especially the branches of the proximal aorta. Interleukin-32 (IL-32) is a recently described Th1 proinflammatory cytokine, and is mainly induced by interferon-γ (IFNγ), IL-1β, and tumor necrosis factor α (TNFα). This study was undertaken to investigate the expression and tissue distribution of IL-32 in artery biopsy specimens from patients with GCA. Methods Quantitative gene expression analysis of IL-32, IL-1β, TNFα, IFNγ, IL-6, and IL-27 was performed in artery biopsy specimens obtained from 18 patients with GCA and 15 controls. Immunohistochemistry analysis was performed to …

MalePathologyInterleukin-1betaMessenger80 and overImmunology and AllergyPharmacology (medical)Giant Cell ArteritiAged 80 and overeducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionInterleukin-17StatisticsArteriesMiddle AgedFlow CytometryImmunohistochemistryTh1 responseFemaleInterleukin 17VasculitisInterleukin-32; Giant Cell Arteritis; Th1 responsemedicine.medical_specialtyGiant Cell ArteritisImmunologyPopulationBiologyStatistics NonparametricProinflammatory cytokineInterferon-gammaRheumatologymedicine.arterymedicineHumansNonparametricRNA MessengerArteritiseducationAgedAortaAged; Aged 80 and over; Arteries; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; Interferon-gamma; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukins; Male; Middle Aged; RNA Messenger; Reverse Transcriptase Polymerase Chain Reaction; Statistics Nonparametric; Th1 Cells; Tumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alphaInterleukinsTh1 Cellsmedicine.diseaseInterleukin-32Giant cell arteritisGiant cellImmunologyRNA
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Obesity and reduction of the response rate to anti-tumor necrosis factor α in rheumatoid arthritis: an approach to a personalized medicine.

2013

Objective Obesity is a mild, long-lasting inflammatory disease and, as such, could increase the inflammatory burden of rheumatoid arthritis (RA). The study aim was to determine whether obesity represents a risk factor for a poor remission rate in RA patients requiring anti–tumor necrosis factor α (anti-TNFα) therapy for progressive and active disease despite treatment with methotrexate or other disease-modifying antirheumatic drugs. Methods Patients were identified from 15 outpatient clinics of university hospitals and hospitals in Italy taking part in the Gruppo Italiano di Studio sulle Early Arthritis network. Disease Activity Score in 28 joints (DAS28), body mass index (BMI; categorized …

MaleSettore MED/16 - REUMATOLOGIAArthritisGastroenterologyReceptors Tumor Necrosis FactorEtanerceptEtanerceptArthritis RheumatoidRheumatoidMonoclonalReceptorsMedicineOutpatient clinicLongitudinal StudiesRegistriesPrecision Medicineskin and connective tissue diseasesHumanizedRemission InductionAntibodies MonoclonalIndividualized MedicineMiddle AgedTreatment OutcomeRheumatoid arthritisAntirheumatic AgentsFemaleDrugmedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyAdalimumab; Aged; Antibodies Monoclonal; Antibodies Monoclonal Humanized; Antirheumatic Agents; Arthritis Rheumatoid; Dose-Response Relationship Drug; Etanercept; Female; Humans; Immunoglobulin G; Infliximab; Longitudinal Studies; Male; Middle Aged; Obesity; Precision Medicine; Receptors Tumor Necrosis Factor; Registries; Remission Induction; Treatment Outcome; Tumor Necrosis Factor-alphaAntibodies Monoclonal HumanizedAntibodiesDose-Response RelationshipRheumatologyInternal medicineAdalimumabHumansObesityRisk factorAgedDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaArthritisAdalimumabmedicine.diseaseInfliximabRheumatologyInfliximabAged; Antibodies Monoclonal; Antibodies Monoclonal Humanized; Antirheumatic Agents; Arthritis Rheumatoid; Dose-Response Relationship Drug; Female; Humans; Immunoglobulin G; Individualized Medicine; Longitudinal Studies; Male; Middle Aged; Obesity; Receptors Tumor Necrosis Factor; Registries; Remission Induction; Treatment Outcome; Tumor Necrosis Factor-alphaImmunoglobulin GImmunologybusinessTumor Necrosis FactorArthritis careresearch
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Longterm Retention of Tumor Necrosis Factor-α Inhibitor Therapy in a Large Italian Cohort of Patients with Rheumatoid Arthritis from the GISEA Regist…

2012

Objective.To evaluate 4-year retention rates of tumor necrosis factor-α (TNF-α) inhibitors adalimumab, etanercept, and infliximab among patients with longstanding rheumatoid arthritis (RA), as derived from an Italian national registry.Methods.The clinical records of 853 adult patients with RA in the GISEA (Gruppo Italiano Studio Early Arthritis) registry were prospectively analyzed to compare drug survival rates and the baseline factors that may predict adherence to therapy.Results.In 2003 and 2004, 324 patients started treatment with adalimumab, 311 with etanercept, and 218 with infliximab. After 4 years, the global retention rate of anti-TNF-α therapy was 42%. Etanercept survival (51.4%) …

MaleTime FactorsHealth StatusArthritisKaplan-Meier EstimateReceptors Tumor Necrosis FactorEtanerceptlaw.inventionEtanerceptArthritis RheumatoidRandomized controlled triallawRheumatoidMonoclonalReceptorsImmunology and AllergyProspective StudiesRegistriesskin and connective tissue diseasesProspective cohort studyHumanizedAntibodies Monoclonal; Antibodies Monoclonal Humanized; Antirheumatic Agents; Arthralgia; Arthritis Rheumatoid; Biological Markers; Drug Substitution; Female; Health Status; Humans; Immunoglobulin G; Italy; Joints; Kaplan-Meier Estimate; Male; Middle Aged; Pain Measurement; Prospective Studies; Receptors Tumor Necrosis Factor; Survival Rate; Time Factors; Tumor Necrosis Factor-alpha; RegistriesPain MeasurementDrug SubstitutionAntibodies MonoclonalMiddle AgedArthralgiaAdalimumab; Antibodies Monoclonal; Antibodies Monoclonal Humanized; Antirheumatic Agents; Arthralgia; Arthritis Rheumatoid; Biomarkers; Drug Substitution; Etanercept; Female; Health Status; Humans; Immunoglobulin G; Infliximab; Italy; Joints; Kaplan-Meier Estimate; Male; Middle Aged; Pain Measurement; Prospective Studies; Receptors Tumor Necrosis Factor; Survival Rate; Time Factors; Tumor Necrosis Factor-alpha; RegistriesSurvival RateItalyRheumatoid arthritisAntirheumatic AgentsBiological MarkersAdalimumab; Drug survival; Etanercept; Infliximab; Adalimumab; Antibodies Monoclonal; Antibodies Monoclonal Humanized; Antirheumatic Agents; Arthralgia; Arthritis Rheumatoid; Biomarkers; Drug Substitution; Etanercept; Female; Health Status; Humans; Immunoglobulin G; Infliximab; Italy; Joints; Kaplan-Meier Estimate; Male; Middle Aged; Pain Measurement; Prospective Studies; Receptors Tumor Necrosis Factor; Survival Rate; Time Factors; Tumor Necrosis Factor-alpha; Registries; Rheumatology; Immunology; Immunology and AllergyFemalemedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyImmunologyAntibodies Monoclonal HumanizedAntibodiesRheumatologyDrug survivalInternal medicineAdalimumabmedicineHumansSurvival ratebusiness.industryTumor Necrosis Factor-alphaArthritisAdalimumabmedicine.diseaseInfliximabInfliximabSurgeryImmunoglobulin GJointsbusinessTumor Necrosis FactorBiomarkers
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