Search results for " Tumor necrosis factor-alpha"

showing 10 items of 31 documents

A Propensity Score-matched Comparison of Infliximab and Adalimumab in Tumour Necrosis Factor-α Inhibitor-naïve and Non-naïve Patients with Crohn's Di…

2019

Background and aims There is an unmet need to better understand the effectiveness of different biologics in inflammatory bowel diseases. We aimed at performing a multicentre, real-life comparison of the effectiveness of infliximab [IFX] and adalimumab [ADA] in Crohn's disease [CD]. Methods Data of consecutive patients with CD treated with IFX and ADA from January 2013 to May 2017 were extracted from the cohort of the Sicilian Network for Inflammatory Bowel Disease. We used propensity score-matching accounting for the main baseline characteristics in TNF-α inhibitor-naive and non-naive patients. Results A total of 632 patients [735 total treatments] were included. Among naive patients, a cli…

0301 basic medicineAdultMalemedicine.medical_specialtyInflammatory bowel diseaseGastroenterology03 medical and health sciencesYoung Adult0302 clinical medicineCrohn DiseaseGastrointestinal AgentsInternal medicinemedicineAdalimumabHumansYoung adultSicilypropensity scoreCrohn's diseasebusiness.industryTumor Necrosis Factor-alphaGastroenterologyAdalimumabGeneral MedicineOdds ratiomedicine.diseaseAdalimumab; infliximab; propensity score; Adalimumab; Adult; Crohn Disease; Female; Gastrointestinal Agents; Humans; Infliximab; Male; Propensity Score; Sicily; Treatment Outcome; Tumor Necrosis Factor-alpha; Young AdultInfliximab030104 developmental biologyTreatment OutcomeCohortPropensity score matching030211 gastroenterology & hepatologyFemalebusinessinfliximabmedicine.drug
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Characteristic of chronic plaque psoriasis patients treated with biologics in Italy during the COVID-19 pandemic. risk analysis from the PSO-BIO-COVI…

2021

Background The susceptibility of patients with chronic plaque psoriasis and the risks or benefits related to the use of biological therapies for COVID-19 are unknown. Few data about prevalence, clinical course and outcomes of COVID-19 among psoriatic patients were reported. The aims of this study were 1) to assess the prevalence and severity of COVID-19 in psoriatic patients treated with biologic agents during the first phase of the emergency (22 February to 22 April 2020) in Italy, and 2) to report the clinical outcomes of patients who have been exposed to individuals with confirmed SARS-CoV-2 infection. Methods Patients with moderate-to-severe chronic plaque psoriasis, aged ≥18 years and …

0301 basic medicineMaleClinical BiochemistryDiseaseCohort Studies0302 clinical medicineDrug DiscoveryReceptors80 and overMedicineAged 80 and overeducation.field_of_studyIncidence (epidemiology)IncidenceInterleukin-17psoriasisMiddle Ageddermatologysars-CoV-2Italybiological therapy030220 oncology & carcinogenesisCohortBiological ProductCOVID-19; biological therapy; dermatology; psoriasis; sars-CoV-2FemaleSettore MED/35 - MALATTIE CUTANEE E VENEREEbiological therapy; COVID-19; dermatology; psoriasis; sars-CoV-2; Adult; Aged; Aged 80 and over; Biological Products; Biological Therapy; COVID-19; Chronic Disease; Cohort Studies; Female; Humans; Incidence; Interleukin-17; Italy; Male; Middle Aged; Pandemics; Psoriasis; Receptors Interleukin; Risk Assessment; Tumor Necrosis Factor-alpha; Young AdultCohort studyHumanAdultmedicine.medical_specialtyPopulationRisk AssessmentCOVID-19; psoriasis; biological therapy; dermatology; sars-CoV-203 medical and health sciencesYoung AdultSettore MED/35Internal medicinePsoriasisPsoriasis.HumanseducationPandemicsAgedPharmacologyPsoriasiBiological ProductsPandemicbiological therapy; COVID-19; dermatology; psoriasis; sars-CoV-2business.industryTumor Necrosis Factor-alphaCOVID-19Receptors InterleukinBiological productInterleukinmedicine.diseaseClinical trial030104 developmental biologyChronic DiseaseCOVID-19; SARS-CoV-2; biological therapy; dermatology; psoriasisCohort Studiebusiness
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Amyotrophic Lateral Sclerosis, a Multisystem Pathology: Insights into the Role of TNFα

2017

Amyotrophic lateral sclerosis (ALS) is considered a multifactorial, multisystem disease in which inflammation and the immune system play important roles in development and progression. The pleiotropic cytokine TNFαis one of the major players governing the inflammation in the central nervous system and peripheral districts such as the neuromuscular and immune system. Changes in TNFαlevels are reported in blood, cerebrospinal fluid, and nerve tissues of ALS patients and animal models. However, whether they play a detrimental or protective role on the disease progression is still not clear. Our group and others have recently reported opposite involvements of TNFR1 and TNFR2 in motor neuron dea…

0301 basic medicinePathologymedicine.medical_specialtyAmyotrophic Lateral Sclerosis; Animals; Humans; Motor Neurons; T-Lymphocytes Regulatory; Tumor Necrosis Factor-alphamedicine.medical_treatmentT-LymphocytesCentral nervous systemImmunologyAmyotrophic lateral sclerosis inflammation TNFαInflammationReview ArticleT-Lymphocytes Regulatory03 medical and health sciences0302 clinical medicineImmune systemCerebrospinal fluidImmunology; Cell BiologyTNFαlcsh:PathologyMedicineAnimalsHumansAmyotrophic lateral sclerosisMotor Neuronsbusiness.industryTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisCell BiologyMotor neuronmedicine.diseaseRegulatory3. Good health030104 developmental biologymedicine.anatomical_structureCytokineinflammationImmunologyTumor necrosis factor alphamedicine.symptombusiness030217 neurology & neurosurgerylcsh:RB1-214
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Splenic Littoral Cell Hemangioendothelioma in a Patient With Crohn's Disease Previously Treated With Immunomodulators and Anti-TNF Agents: A Rare Tum…

2011

Th e risk of malignancy in Crohn ’ s disease (CD) has been well described. Moreover, immunomodulators, uch as azathioprine (AZA) and 6-mercaptopurine (6-MP), and biological agents, such as infl iximab and adalimumab, may promote carcinogenesis ( 1 – 3 ). Splenic littoral cell tumors are recently described tumors of vascular origin composed of endothelial cells, with typical microscopic and immunohistochemical features of splenic sinus lining cells ( 4 ). Clinical findings are not specific, and outcome is unpredictable but usually benign, although a few cases with a malignant behavior have been reported ( 5,6 ). We report a 58-year-old Caucasian man with a long history of ileocolonic CD.

6-MercaptopurineMalePathologymedicine.medical_specialtyColonic Diseasemedicine.medical_treatmentAzathioprineSplenic NeoplasmHemangioendotheliomaHemangiomaImmunosuppressive AgentImmunocompromised HostImmunologic FactorCrohn Disease6-Mercaptopurine; Azathioprine; Colonic Diseases; Crohn Disease; Gastrointestinal Agents; Hemangioendothelioma; Hemangioma; Humans; Ileal Diseases; Immunologic Factors; Immunosuppressive Agents; Male; Middle Aged; Splenic Neoplasms; Tumor Necrosis Factor-alpha; Immunocompromised Host; GastroenterologyAzathioprineGastrointestinal AgentMedicineGastrointestinal agentCrohn's diseaseHepatologyTumor Necrosis Factor-alphabusiness.industryGastroenterologyImmunosuppressionMiddle Agedmedicine.diseaseSplenic NeoplasmHemangioendotheliomaImmunologyIleal DiseaseTumor necrosis factor alphaHemangiomabusinessHumanmedicine.drugAmerican Journal of Gastroenterology
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Different effects of biological drugs in rheumatoid arthritis

2013

Biological drugs have brought new hope to patients with rheumatoid arthritis (RA) in whom previously existing treatments could not control inflammation, joint destruction, or the progression of disability. The five currently available TNF blockers are approved for treating RA patients, but they have different structures, morphology, pharmacokinetic properties, and activity. Randomised clinical trials (RCTs) have shown that they improve the signs and symptoms of both early and long-standing RA and other inflammatory arthritides, prevent radiographic progression, and improve the patients' health-related quality of life. However, they are more effective in combination with methotrexate (MTX) t…

Cartilage Articularmedicine.medical_specialtyDrug-Related Side Effects and Adverse ReactionsImmunologyArthritisPharmacologyArthritis Rheumatoidchemistry.chemical_compoundChondrocytesPharmacotherapyTocilizumabDrug TherapyRheumatoidInternal medicinemedicineHumansImmunology and AllergyArthritis Rheumatoid; Cartilage Articular; Chondrocytes; Drug Therapy Combination; Drug-Related Side Effects and Adverse Reactions; Humans; Inflammation Mediators; Pharmaceutical Preparations; Randomized Controlled Trials as Topic; Tumor Necrosis Factor-alphaAdverse effectRandomized Controlled Trials as TopicTumor Necrosis Factor-alphabusiness.industryArthritisAbataceptmedicine.diseaseClinical trialCartilagePharmaceutical PreparationschemistryRheumatoid arthritisCombinationDrug Therapy CombinationRituximabInflammation MediatorsbusinessArticularmedicine.drugAutoimmunity Reviews
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Dose adjustments and discontinuation in TNF inhibitors treated patients: when and how. A systematic review of literature.

2018

Objectives To review the available evidence concerning the possibility of discontinuing and/or tapering the dosage of TNF inhibitors (TNFi) in RA patients experiencing clinical remission or low disease activity. Methods A systematic review of the literature concerning the low dosage and discontinuation of TNFi in disease-controlled RA patients was performed by evaluation of reports published in indexed international journals (Medline via PubMed, EMBASE), in the time frame from 8 April 2013 to 15 January 2016. Results We analysed the literature evaluating the efficacy and the safety of two different strategies using TNFi, decreasing dosage or discontinuation, in patients experiencing clinica…

Drugmedicine.medical_specialtymedia_common.quotation_subjectMEDLINEArthritisEtanerceptDose-Response RelationshipArthritis Rheumatoid03 medical and health sciences0302 clinical medicineRheumatologyRheumatoidInternal medicinemedicineAdalimumabHumansPharmacology (medical)030212 general & internal medicinemedia_common030203 arthritis & rheumatologyDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaArthritisRemission Inductionmedicine.diseaseRheumatologyAntirheumatic Agents; Arthritis Rheumatoid; Dose-Response Relationship Drug; Humans; Remission Induction; Tumor Necrosis Factor-alpha; Rheumatology; Pharmacology (medical)DiscontinuationRheumatoid arthritisAntirheumatic AgentsDrugbusinessmedicine.drugRheumatology (Oxford, England)
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Updated insights into the mechanism of action and clinical profile of the immunoadjuvant QS-21: A review

2019

Background Vaccine adjuvants are compounds that significantly enhance/prolong the immune response to a co-administered antigen. The limitations of the use of aluminium salts that are unable to elicite cell responses against intracellular pathogens such as those causing malaria, tuberculosis, or AIDS, have driven the development of new alternative adjuvants such as QS-21, a triterpene saponin purified from Quillaja saponaria. Purpose The aim of this review is to attempt to clarify the mechanism of action of QS-21 through either receptors or signaling pathways in vitro and in vivo with special emphasis on the co-administration with other immunostimulants in new adjuvant formulations, called a…

InflammasomesT-Lymphocytesmedicine.medical_treatmentHerpes zosterPharmaceutical ScienceMonophosphoryl Lipid AAPCs antigen presenting cellsMiceCMI cell mediated immunity0302 clinical medicineDrug DiscoveryHerpes Zoster VaccineMedicineNSCLC non small cell lung carcinomaCancerImmunity CellularVaccines Synthetic0303 health sciencesImmunogenicityIl-2 interleukine 2HIV human immunodeficiency virusLipid A030220 oncology & carcinogenesisCytokinesMolecular MedicineDCs dendritic cellsNK natural killerAdjuvantTLR Toll-like receptorHerpes Zoster VaccineCD cluster of differentiationAntigen-Presenting CellsCTL cytotoxic T lymphocytesHZ herpes zosterMPL 3-deacylated monophosphoryl lipidVaccine adjuvantImmunoadjuvantArticleVZV varicella zoster virus03 medical and health sciencesImmune systemAdjuvants ImmunologicAntigenPAMPs pathogen-associated molecular patternsMalaria VaccinesPRRs pathogen recognition receptorsQS-21 Quillaja saponaria Molina-fraction 21AnimalsMHC major histocompatibility complexMtb Mycobacterium tuberculosis bacteriaSARS severe acute respiratory syndromeAntigen-presenting cellIFN-γ interferon-gamma030304 developmental biologyPharmacologybusiness.industryA-β amyloid-betaTNF-α tumor necrosis factor-alphaSaponinsQS-21MalariaQuillaja saponariaComplementary and alternative medicineTCR T-cell receptorLiposomesImmunologyKLH keyhole limpet hemocyaninbusinessdLN draining lymph nodesMAPK mitogen activated protein kinasePhytomedicine
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Choice of second-line disease-modifying antirheumatic drugs after failure of methotrexate therapy for rheumatoid arthritis: A decision tree for clini…

2009

Objective To survey rheumatologists' preferences for the choice of a second-line disease-modifying antirheumatic drug (DMARD) after inadequate response with methotrexate (MTX) therapy in rheumatoid arthritis (RA). Methods Thirty-six rheumatologists stated their preferences for RA treatment after inadequate response with MTX therapy (optimal dose at least 6 months). From the initial scenario, we derived 54 vignettes varying by rheumatoid factor or anti–cyclic citrullinated peptide antibody presence, swollen joint count, Disease Activity Score in 28 joints, and structural damage. Respondents stated their preference among 5 therapeutic options: MTX continuation, switch to another conventional …

MESH: Antirheumatic AgentsMESH: Decision TreesMESH: Treatment FailureArthritisMESH: Antibodies Anti-IdiotypicMESH: Logistic ModelsLogistic regressionSeverity of Illness IndexArthritis Rheumatoid0302 clinical medicineimmune system diseasesImmunology and AllergyMESH: Data CollectionPharmacology (medical)Treatment Failure030212 general & internal medicinePractice Patterns Physicians'skin and connective tissue diseasesMESH: Arthritis RheumatoidData CollectionAntibodies Anti-Idiotypic3. Good healthMESH: Interleukin 1 Receptor Antagonist ProteinMESH: Methotrexate[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemAntirheumatic AgentsRheumatoid arthritismedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyMESH: Rheumatoid FactorImmunologyPeptides Cyclic03 medical and health sciencesRheumatologyRheumatoid FactorMESH: Severity of Illness IndexInternal medicineSeverity of illnessmedicineHumansRheumatoid factorMESH: Physician's Practice PatternsMESH: Peptides Cyclic030203 arthritis & rheumatologyAnakinraMESH: HumansTumor Necrosis Factor-alphabusiness.industryDecision Treesmedicine.diseaseRheumatologyInterleukin 1 Receptor Antagonist ProteinLogistic ModelsMethotrexateMESH: Tumor Necrosis Factor-alphaPhysical therapyMethotrexatebusinessArthritis & Rheumatism
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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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