Search results for "arteritis"

showing 10 items of 48 documents

Unexpected death for takayasu aortitis associated with coronary ostial stenosis

2015

The differential diagnosis of vasculitis is often a difficult task due to the frequent morphological similarities that various vasculitic syndromes express when the heart is the target organ. The more the lesions are limited to the arterial tree with absent or almost silent coronary events, the less specific the anatomical and clinical frameworks. To create a series of clinical records and on the basis of these assumptions, the authors report a case concerning the sudden death of a 43-year-old woman which occurred while an ergonometric test was being carried out 28 days after the onset of the symptoms. A subsequent postmortem investigation/autopsy enabled us to detect a granulomatous aortit…

Adultunexpected sudden deathCoronary StenosiTakayasu aortitis2734coronary ostial stenosis; Takayasu aortitis; unexpected sudden death; Adult; Coronary Stenosis; Death Sudden Cardiac; Exercise Test; Female; Forensic Pathology; Humans; Takayasu Arteritis; 2734Coronary StenosisSuddenTakayasu ArteritisDeathDeath Sudden Cardiaccoronary ostial stenosiExercise TestHumansFemalecoronary ostial stenosisCardiacForensic PathologyTakayasu aortitiHuman
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Pathogénie de l’artérite à cellules géantes

2012

Giant-cell arteritis (GCA) involves larges arteries, especially aorta and extra-cranial branches of external carotid. Histo-pathological lesions affect all the layers of the artery leading to a segmental and focal panarteritis with a polymorphic cell infiltrate including T cells, macrophages and multinucleated giant cells, a fragmented internal elastic lamina and an intimal hyperplasia. The pathophysiology of GCA is not fully understood. After dendritic cell activation in the adventitia, CD4T cells are recruited in the arterial wall and polarized into Th1 and Th17 cells that produce IFN-γ and IL-17. These cytokines activate macrophages, giant cells and smooth muscle cells inducing vascular …

AortaPathologymedicine.medical_specialtyIntimal hyperplasiaGeneral MedicineDendritic cellBiologyInternal elastic laminamedicine.diseasemedicine.anatomical_structureGiant cellmedicine.arteryAdventitiacardiovascular systemmedicinecardiovascular diseasesArteritisArteryLa Presse Médicale
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Are IL-10+ regulatory Th17 cells implicated in the sustained response to glucocorticoid treatment in patients with giant cell arteritis? Comment on t…

2013

We have read with interest the recently published paper of Espigol-Frigole et al 1 in which the authors confirmed that interleukin (IL)-17 is highly expressed in giant cell arteritis (GCA) lesions.1–3 They also demonstrated for the first time that IL-17 expression in temporal artery biopsies (TABs) was correlated with a better outcome. Among other interesting results, the identification of Foxp3+IL-17+ T cells by confocal microscopy in TAB made the authors to hypothesize that these cells could be induced regulatory T cells (Treg) that may facilitate the remission of the disease under steroid therapy. …

BiopsyGiant Cell ArteritisImmunologyGeneral Biochemistry Genetics and Molecular Biologylaw.inventionRheumatologyRecurrenceConfocal microscopylawBiopsymedicineHumansImmunology and AllergyGlucocorticoidsmedicine.diagnostic_testbusiness.industryInterleukin-17InterleukinFOXP3Forkhead Transcription Factorsmedicine.diseaseInterleukin-10Temporal ArteriesGiant cell arteritisInterleukin 10ImmunologyTh17 CellsInterleukin 17businessGlucocorticoidmedicine.drugAnnals of the Rheumatic Diseases
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Is TNF-α really involved in giant cell arteritis pathogenesis?

2013

Giant cell arteritis (GCA) is the most frequent vasculitis in people >50 years, and glucocorticoids (GC) remain the cornerstone of the treatment. However, this long-term treatment is responsible for numerous GC-related complications.1 Thus, reliable GC-sparing drugs need to be explored. Seror et al 2 have recently reported the inefficacy of adalimumab, a humanised anti-TNF-α therapy, as a GC-sparing drug in the treatment of GCA. These clinical results contrast with previous studies reporting a production of TNF-α by giant cells and macrophages in GCA lesions.3 However, recent advance in the knowledge of GCA pathogenesis have shown that macrophages and giant cells are not involved in the fir…

CD4-Positive T-LymphocytesMaleImmunologyGiant Cell ArteritisGeneral Biochemistry Genetics and Molecular BiologyPathogenesisRheumatologyimmune system diseasesAdalimumabImmunology and AllergyMedicineHumanscardiovascular diseasesskin and connective tissue diseasesAgedAged 80 and overbusiness.industryTumor Necrosis Factor-alphaMiddle Agedmedicine.diseaseGiant cell arteritisGiant cellImmunologycardiovascular systemTumor necrosis factor alphaFemalebusinessVasculitismedicine.drugAnnals of the rheumatic diseases
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Rationale and evidence on the use of tocilizumab in COVID-19: a systematic review

2020

Abstract Background Tocilizumab is an IL-6 receptor-blocking agent proposed for the treatment of severe COVID-19. The aim of this systematic review was to describe the rationale for the use of tocilizumab for the treatment of COVID-19 and to summarize the available evidence regarding its efficacy and safety. Methods MEDLINE, PubMed, EMBASE, pre-print repositories (bioRxiv and medRxiv) and two trial Registries were searched for studies on the use of tocilizumab in COVID-19 or SARS-CoV-2 infection, viral pneumonia, and/or sepsis until 20th June 2020. Results We identified 3 indirect pre-clinical studies and 28 clinical studies including 5776 patients with COVID-19 (13 with a comparison group,…

Coronavirus COVID-19 Pneumonia SARS-CoV-2 TocilizumabGCA Giant cell arteritispJIA Pediatric juvenile idiopathic arthritislaw.inventionchemistry.chemical_compound0302 clinical medicineRandomized controlled triallawMedicine030212 general & internal medicineClinical efficacyCPAP Continuous positive airway pressureCOVID-19 Coronavirus disease 2019IDSA Infectious Diseases Society of AmericaRA Rheumatoid arthritisTocilizumabIMV Invasive mechanical ventilationsJIA Juvenile idiopathic arthritisAIFA Agenzia Italiana del FarmacoPulmonary and Respiratory Medicinemedicine.medical_specialtyCoronavirus disease 2019 (COVID-19)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)MEDLINEAntibodies Monoclonal HumanizedNIH U.S. National Institutes of HealthArticleWHO World Health OrganizationSIMIT Italian Society of Infectious and Tropical disease03 medical and health sciencesTocilizumabARDS Acute respiratory distress syndromeAnimalsHumansIn patientIntensive care medicineTocilizumab ; COVID-19 ; Pneumonia ; SARS-CoV-2 ; Coronaviruslcsh:RC705-779business.industryCRS CAR-T cell-induced cytokine release syndromeInterleukin-6SARS-CoV-2NIV Noninvasive mechanical ventilationTNF Tumor necrosis factorCOVID-19Pneumonialcsh:Diseases of the respiratory systemCOVID-19 Drug TreatmentClinical trialCoronavirus030228 respiratory systemchemistrybusinessICTRP International Clinical Trials Registry PlatformPulmonology
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EULAR/PRINTO/PRES criteria for Henoch-Schonlein purpura, childhood polyarteritis nodosa, childhood Wegener granulomatosis and childhood Takayasu arte…

2010

EULAR/PRINTO/PRES Objectives To validate the previously proposed classification criteria for Henoch-Schonlein purpura (HSP), childhood polyarteritis nodosa (c-PAN), c-Wegener granulomatosis (c-WG) and c-Takayasu arteritis (c-TA).Methods Step 1: retrospective/prospective webdata collection for children with HSP, c-PAN, c-WG and c-TA with age at diagnosis <= 18 years. Step 2: blinded classification by consensus panel of a representative sample of 280 cases. Step 3: statistical (sensitivity, specificity, area under the curve and.-agreement) and nominal group technique consensus evaluations.Results 827 patients with HSP, 150 with c-PAN, 60 with c-WG, 87 with c-TA and 52 with c-other were compar…

Genetics and Molecular Biology (all)myalgiaVasculitismedicine.medical_specialtyHenoch-Schonlein purpuraAdolescentIgA VasculitisClassification criteriaInternational CooperationImmunologychildhood polyarteritis nodosaBiochemistryGeneral Biochemistry Genetics and Molecular BiologyRheumatologyhemic and lymphatic diseasesTerminology as TopicSchoenlein-HenochmedicineHumansImmunology and Allergycardiovascular diseasesArteritisChildPurpurac-Wegener granulomatosisAdolescent; Child; Epidemiologic Methods; Granulomatosis with Polyangiitis; Humans; International Cooperation; Polyarteritis Nodosa; Purpura Schoenlein-Henoch; Takayasu Arteritis; Terminology as Topic; Rheumatology; Immunology; Biochemistry Genetics and Molecular Biology (all); Immunology and Allergycriteria; children; Henoch-Schönlein purpura; childhood polyarteritis nodosa; Wegener granulomatosis; Takayasu arteritis; EULAR; PRINTO; PRESPolyarteritis nodosabusiness.industryGranulomatosis with Polyangiitismedicine.diseaseTakayasu ArteritisDermatologyPolyarteritis NodosaSurgeryHenoch-Schönlein purpuraIgA vasculitisSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICAmedicine.symptomEpidemiologic MethodsGranulomatosis with polyangiitisVasculitisbusinessRheumatismc-Takayasu arteriti
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Glomerulonephritis und Hepatitis-B-Virus-Infektion

1990

Hepatitis B AntigensGlomerulonephritisbusiness.industryHumansMedicineGeneral MedicineHepatitis BPrognosisbusinessPolyarteritis NodosaDMW - Deutsche Medizinische Wochenschrift
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Difference in the expression of IL-9 and IL-17 correlates with different histological pattern of vascular wall injury in giant cell arteritis

2015

OBJECTIVE: GCA is a large- and medium-vessel arteritis characterized by a range of histological patterns of vascular wall injury. The aim of this study was to immunologically characterize the various histological patterns of GCA. METHODS: Thirty-five consecutive patients with biopsy-proven GCA and 15 normal controls were studied. IL-8, IL-9, IL-9R, IL-17, IL-4, TGF-β and thymic stromal lymphopoietin expression was evaluated by RT-PCR and immunohistochemistry on artery biopsy specimens. Confocal microscopy was used to characterize the phenotypes of IL-9-producing and IL-9R-expressing cells. Five additional patients who had received prednisone when the temporal artery biopsy was performed wer…

MalePathologyBiopsyT-LymphocytesSettore BIO/13 - Biologia ApplicataTransforming Growth Factor betaTh9Pharmacology (medical)Aged 80 and overMicroscopy Confocalmedicine.diagnostic_testSmall vessel vasculitisVasa vasorum vasculitiInterleukin-17vasa vasorum vasculitis Giant cell arteritiMiddle AgedTemporal Arteriesmedicine.anatomical_structurePhenotypeVasa vasorum vasculitisSmall vessel vasculitiCytokinesFemaleTh17medicine.symptomVasculitisgiant cell arteritimedicine.medical_specialtyThymic stromal lymphopoietinGiant Cell ArteritisInflammationThymic Stromal LymphopoietinRheumatologyBiopsyTh17; Th9; giant cell arteritis; small vessel vasculitis; vasa vasorum vasculitismedicineHumansInterleukin 9ArteritisGlucocorticoidsAgedbusiness.industryInterleukin-9Vascular System Injuriesmedicine.diseaseGiant cell arteritisSettore MED/16 - ReumatologiaVasa vasorumCase-Control StudiesImmunologyPrednisonebusinessBiomarkers
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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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Th1 and Th17 lymphocytes expressing CD161 are implicated in giant cell arteritis and polymyalgia rheumatica pathogenesis.

2012

International audience; OBJECTIVE: Giant cell arteritis (GCA) is the most frequently occurring vasculitis in elderly individuals, and its pathogenesis is not fully understood. The objective of this study was to decipher the role of the major CD4+ T cell subsets in GCA and its rheumatologic form, polymyalgia rheumatica (PMR). METHODS: A prospective study of the phenotype and the function of major CD4+ T cell subsets (Th1, Th17, and Treg cells) was performed in 34 untreated patients with GCA or PMR, in comparison with 31 healthy control subjects and with the 27 treated patients who remained after the 7 others withdrew. RESULTS: Compared with control subjects, patients with GCA and patients wi…

MalePathologyMESH: Th17 CellsCellMESH : AgedMESH : Prospective StudiesMESH: Flow CytometryT-Lymphocytes RegulatoryPathogenesisMESH : T-Lymphocytes Regulatory0302 clinical medicineimmune system diseasesMESH : Th1 CellsImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyPharmacology (medical)MESH : FemaleProspective Studiesskin and connective tissue diseasesCells CulturedMESH: Aged0303 health sciencesMESH: Middle Agedmedicine.diagnostic_testMESH: Giant Cell ArteritisCell DifferentiationMESH : AdultMiddle AgedFlow CytometryMESH : NK Cell Lectin-Like Receptor Subfamily B3. Good healthMESH: NK Cell Lectin-Like Receptor Subfamily Bmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleVasculitisMESH : Cell DifferentiationGlucocorticoidmedicine.drugNK Cell Lectin-Like Receptor Subfamily BMESH: Cells CulturedAdultMESH: Cell Differentiationmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Flow CytometryT cellMESH : MaleImmunologyGiant Cell ArteritisBiologyPolymyalgia rheumatica03 medical and health sciencesRheumatologyBiopsyMESH : Cells CulturedmedicineMESH : Th17 CellsHumansMESH : Middle Aged030304 developmental biologyAged030203 arthritis & rheumatologyMESH: HumansMESH: T-Lymphocytes RegulatoryMESH : HumansMESH: AdultTh1 Cellsmedicine.diseaseMESH : Giant Cell ArteritisMESH: Prospective StudiesMESH: MaleGiant cell arteritisMESH: Th1 CellsPolymyalgia RheumaticaMESH: Polymyalgia RheumaticaImmunologyTh17 CellsMESH : Polymyalgia RheumaticaMESH: Female
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