Search results for "030203 arthritis & rheumatology"

showing 10 items of 355 documents

The CD68+/H-ferritin+ cells colonize the lymph nodes of the patients with adult onset Still's disease and are associated with increased extracellular…

2015

Summary In this work, we aimed to evaluate the levels of ferritin enriched in H subunits (H-ferritin) and ferritin enriched in L subunits (L-ferritin) and the cells expressing these two molecules in the lymph node (LN) biopsies obtained from adult-onset Still's disease (AOSD) patients, and the possible correlation among these data and the severity of the disease. Ten patients with AOSD underwent LN biopsy. All the samples were stained by immunofluorescence. A statistical analysis was performed to estimate the possible correlation among both H-ferritin and L-ferritin tissue expression and the clinical picture of the disease. Furthermore, the same analysis was performed to evaluate the possib…

0301 basic medicineAdult-OnsetMalePathologyMacrophageApoferritinAdult-onset Still's disease; H-ferritin; Hyperferritinaemic syndrome; Macrophage; Adult; Aged; Antigens CD; Antigens Differentiation Myelomonocytic; Apoferritins; Biopsy; Female; Ferritins; Fluorescent Antibody Technique; Humans; Lymph Nodes; Macrophages; Male; Middle Aged; Still's Disease Adult-Onset; Immunology; Immunology and AllergyH-ferritinBiopsyFluorescent Antibody TechniquePathogenesis0302 clinical medicineMacrophageImmunology and AllergyLymph nodemedicine.diagnostic_testCD68Lymph NodeMiddle AgedCDmedicine.anatomical_structureAntigenDifferentiationFemaleLymphHyperferritinaemic syndromeStill's Disease Adult-OnsetHumanAdultmedicine.medical_specialtyImmunologyAntigens Differentiation MyelomonocyticBiologyImmunofluorescenceAdult-onset Still's disease03 medical and health sciencesAntigens CDBiopsymedicineHumansAntigensAged030203 arthritis & rheumatologyFerritinMacrophagesOriginal ArticlesMyelomonocyticStill's DiseaseFerritinSettore MED/16 - Reumatologia030104 developmental biologyImmunologyApoferritinsFerritinsbiology.proteinLymph Nodes
researchProduct

FMF is not always "fever": from clinical presentation to "treat to target".

2020

AbstractFamilial Mediterranean Fever, a monogenic autoinflammatory disease secondary to MEFV gene mutations in the chromosome 16p13, is characterized by recurrent self-limiting attacks of fever, arthritis, aphthous changes in lips and/or oral mucosa, erythema, serositis. It is caused by dysregulation of the inflammasome, a complex intracellular multiprotein structure, commanding the overproduction of interleukin 1. Familial Mediterranean Fever can be associated with other multifactorial autoinflammatory diseases, as vasculitis and Behçet disease.Symptoms frequently start before 20 years of age and are characterized by a more severe phenotype in patients who begin earlier.Attacks consist of …

0301 basic medicineAutoinflammatory diseasemedicine.medical_specialtyCanakinumabAutoinflammatory diseasesArthritisFamilial Mediterranean feverDiseaseReviewGene mutationFamilial Mediterranean feverDiagnosis Differential03 medical and health sciences0302 clinical medicineMedicineHumansChild030203 arthritis & rheumatologybusiness.industryAmyloidosislcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseMEFVDermatologyTubulin ModulatorsCanakinumab030104 developmental biologyPhenotypebusinessColchicineSerositisBiomarkersmedicine.drugItalian journal of pediatrics
researchProduct

H-ferritin and proinflammatory cytokines are increased in the bone marrow of patients affected by macrophage activation syndrome

2017

Summary Macrophage activation syndrome (MAS) is hyperinflammatory life-threatening syndrome, associated typically with high levels of serum ferritin. This is an iron storage protein including heavy (H) and light (L) subunits, categorized on their molecular weight. The H-/L subunits ratio may be different in tissues, depending on the specific tissue and pathophysiological status. In this study, we analysed the bone marrow (BM) biopsies of adult MAS patients to assess the presence of: (i) H-ferritin and L-ferritin; (ii) CD68+/H-ferritin+ and CD68+/L-ferritin+; and (iii) interleukin (IL)-1β, tumour necrosis factor (TNF) and interferon (IFN)-γ. We also explored possible correlations of these re…

0301 basic medicineBiopsymedicine.medical_treatment0302 clinical medicineBone MarrowcytokineImmunology and AllergyInterleukinBlood ProteinsSyndromeMiddle AgedC-Reactive ProteinCytokinemedicine.anatomical_structureCytokinesTumor necrosis factor alphaInflammation Mediatorsmedicine.symptommacrophage activation syndromeAdultImmunologyAntigens Differentiation MyelomonocyticInflammationmacrophageBiologyProinflammatory cytokine03 medical and health sciencesAntigens CDmedicineHumansAgedRetrospective StudiesInflammation030203 arthritis & rheumatologyMacrophagesferritinOriginal ArticlesMacrophage Activationmedicine.diseaseFerritinSettore MED/16 - Reumatologia030104 developmental biologyMacrophage activation syndromeApoferritinsImmunologybiology.proteinBone marrowCytokine; Ferritin; Hyperferritinaemic syndrome; Macrophage; Macrophage activation syndrome; Immunology and Allergy; Immunologycytokine; ferritin; hyperferritinaemic syndrome; macrophage; macrophage activation syndromehyperferritinaemic syndrome
researchProduct

Increased expression of interleukin-22 in patients with giant cell arteritis

2017

Objectives GCA is characterized by arterial remodelling driven by inflammation. IL-22 is an attractive cytokine which acts at the crosstalk between immune and stromal cells. We hypothesized that IL-22 might be induced in GCA and might be involved in disease pathogenesis. Methods Patients subjected to temporal artery biopsies (TABs) naive from therapy were enrolled: 27 biopsy-proven GCA, 8 biopsy-negative GCA, 21 biopsy-negative non-GCA patients. Expression of IL-22 was determined in TABs by immunohystochemistry, in plasma by ELISA, in peripheral blood mononuclear cells by real-time PCR and flow cytometry. Effects of IL-22 on viability and gene expression of primary cultures obtained from TA…

0301 basic medicineCD4-Positive T-LymphocytesMalearterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesismedicine.medical_treatmentMessengerInterleukin 220302 clinical medicineimmune system diseasesarterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesis; Aged; Aged 80 and over; CD4-Positive T-Lymphocytes; Calcium Ionophores; Carcinogens; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; In Vitro Techniques; Interleukins; Ionomycin; Leukocytes Mononuclear; Male; RNA Messenger; Real-Time Polymerase Chain Reaction; Temporal Arteries; Tetradecanoylphorbol Acetate80 and overLeukocytesPharmacology (medical)skin and connective tissue diseasesAged 80 and overIonomycinpathogenesisautoimmunityInterleukinFlow CytometryImmunohistochemistryTemporal ArteriesCalcium IonophoresCytokinecardiovascular systemTetradecanoylphorbol AcetateFemalemedicine.symptomgiant cell arteritiStromal cellMononuclearGiant Cell ArteritisInflammationEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellarterial remodelling03 medical and health sciencesRheumatologymedicineHumansViability assayRNA Messengercardiovascular diseasesAged030203 arthritis & rheumatologybusiness.industryInterleukinsinterleukin-22medicine.diseaseGiant cell arteritis030104 developmental biologyinflammationCase-Control StudiesImmunologyCarcinogensLeukocytes MononuclearRNAbusiness
researchProduct

Macrophage Migration Inhibitory Factor Induces Inflammation and Predicts Spinal Progression in Ankylosing Spondylitis

2017

Objectives: To understand the role of macrophage migration inhibitory factor (MIF) in the pathogenesis of Ankylosing Spondylitis (AS). Methods: AS patients satisfying the modified New York criteria were recruited for the study. Healthy volunteers, rheumatoid arthritis and osteoarthritis patients were included as controls. Based on the annual rate of increase in mSASSS scores, AS patients were classified as progressors or non-progressors. MIF levels were quantitated by ELISA in the serum and synovial fluid. Predictors of AS progression were studied by logistic regression analysis. Immunohistochemistry of ileal tissue was performed to identify MIF producing cells. Flow cytometry was used to r…

0301 basic medicineCD74animal diseasesImmunologychemical and pharmacologic phenomenaInflammationPathogenesis03 medical and health sciences0302 clinical medicineRheumatologyotorhinolaryngologic diseasesmedicineImmunology and AllergySynovial fluid030203 arthritis & rheumatologyAnkylosing spondylitisbusiness.industryrespiratory systemmedicine.diseasebiological factors3. Good health030104 developmental biologyRheumatoid arthritisImmunologyMacrophage migration inhibitory factorTumor necrosis factor alphamedicine.symptombusinessArthritis & Rheumatology
researchProduct

Genetics and pathophysiology of granulomatosis with polyangiitis (GPA) and its main autoantigen proteinase 3.

2016

Granulomatosis with polyangiitis (GPA) is a severe autoimmune disease and one of the small vessel anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides. Although its etiology and pathophysiology are still widely unknown, it is accepted that infections, environmental factors, epigenetic modifications, and a genetic predisposition provide the basis for this systemic disorder. GPA typically evolves into two phases: an initial phase characterized by ear, nose and throat (ENT) manifestations, such as chronic sinusitis and otitis, ulceration of the oral cavity and pharynx, as well as pulmonary nodules and a severe generalized phase, defined by the occurrence of rapidly progressive g…

0301 basic medicineCandidate geneMyeloblastinGenome-wide association studyAnti-Neutrophil Cytoplasmic Antibody-Associated Vasculitismacromolecular substancesBiologyAutoantigensAntibodies Antineutrophil CytoplasmicPTPN2203 medical and health sciencesMice0302 clinical medicinestomatognathic systemProteinase 3medicineGenetic predispositionRapidly progressive glomerulonephritisAnimalsHumansGenetic Predisposition to DiseaseMolecular Biology030203 arthritis & rheumatologyAutoimmune diseaseGranulomatosis with PolyangiitisCell Biologymedicine.disease030104 developmental biologyImmunologyGranulomatosis with polyangiitisGenome-Wide Association StudyMolecular and cellular probes
researchProduct

Chondroprotective effects of the combination chondroitin sulfate-glucosamine in a model of osteoarthritis induced by anterior cruciate ligament trans…

2016

[EN] Context: The efficacy of the combination chondroitin sulfate-glucosamine (CS-GlcN) in the treatment of knee osteoarthritis (OA) has been suggested in recent clinical studies. In vitro reports have also suggested anti-inflammatory and anti-resorptive effects of this combination. Objective: The aim of this study was to characterize the effects of CS-GlcN on joint degradation in vivo including the assessment of inflammation and bone metabolism in a model of OA. Materials and methods: We have used the OA model induced by anterior cruciate ligament transection (ACLT) in ovariectomised rats. CS-GlcN was administered daily (oral gavage) from week 0 until week 12 after ovariectomy at the dose …

0301 basic medicineCartilage Articularmedicine.medical_specialtyAnterior cruciate ligamentOvariectomyType II collagenOsteoarthritisProtective AgentsBone and BonesBone remodeling03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOsteoprotegerinGlucosamineInternal medicineOsteoarthritisMedicineAnimalsChondroitin sulfateAnterior cruciate ligament transectionAnterior Cruciate LigamentRats Wistar030203 arthritis & rheumatologyPharmacologyGlucosaminebusiness.industryCartilageAnterior Cruciate Ligament InjuriesChondroitin SulfatesGeneral MedicineX-Ray MicrotomographyOsteoarthritis Kneemedicine.diseaseChondroitin sulfate-glucosamine Ovariectomised ratscarbohydrates (lipids)Disease Models Animal030104 developmental biologymedicine.anatomical_structureEndocrinologychemistryDrug Therapy CombinationFemaleJointsInflammation MediatorsbusinessBiomarkersModel
researchProduct

Guidelines for biomarkers in autoimmune rheumatic diseases - evidence based analysis

2018

Autoimmune rheumatic diseases are characterised by an abnormal immune system response, complement activation, cytokines dysregulation and inflammation. In last years, despite many progresses in managing these patients, it has been shown that clinical remission is reached in less than 50% of patients and a personalised and tailored therapeutic approach is still lacking resulting in a significant gap between guidelines and real-world practice. In this context, the need for biomarkers facilitating early diagnosis and profiling those individuals at the highest risk for a poor outcome has become of crucial interest. A biomarker generally refers to a measured characteristic which may be used as a…

0301 basic medicineEvidence-based practiceImmunologyInflammationGuidelines as TopicSystemic lupus erythematosuBioinformaticsAntiphospholipid syndrome; Biomarker; Rheumatoid arthritis; Sjögren syndrome; Spondyloarthritides; Systemic lupus erythematosus; Systemic sclerosis;Autoimmune DiseaseAutoimmune DiseasesRheumatic Disease03 medical and health sciencesTherapeutic approachSystemic sclerosiEconomica0302 clinical medicineImmune systemSystemic lupus erythematosusAntiphospholipid syndromeEarly DiagnosiRheumatic DiseasesAntiphospholipid syndromemedicineImmunology and AllergyHumansRheumatoid arthritisRheumatoid arthritiAntiphospholipid syndrome; Biomarker; Rheumatoid arthritis; Sjögren syndrome; Spondyloarthritides; Systemic lupus erythematosus; Systemic sclerosis030203 arthritis & rheumatologySpondyloarthritidebusiness.industryBiomarkermedicine.diseaseClinical diseaseSjögren syndromeAntiphospholipid syndrome; Biomarker; Rheumatoid arthritis; Sjögren syndrome; Spondyloarthritides; Systemic lupus erythematosus; Systemic sclerosis; Autoimmune Diseases; Biomarkers; Early Diagnosis; Evidence-Based Practice; Guidelines as Topic; Humans; Rheumatic Diseases; Immunology and Allergy; ImmunologySettore MED/16 - Reumatologia030104 developmental biologyEarly DiagnosisRheumatoid arthritisEvidence-Based PracticeBiomarker (medicine)SpondyloarthritidesSystemic sclerosismedicine.symptombusinessBiomarkersHuman
researchProduct

Ectopic expression of CXCL13, BAFF, APRIL and LT-ß is associated with artery tertiary lymphoid organs in giant cell arteritis

2016

ObjectivesTo investigate whether artery tertiary lymphoid organs (ATLOs) are present in giant cell arteritis (GCA) and that their formation is associated with the ectopic expression of constitutive lymphoid tissue-homing chemokines.MethodsReverse transcriptase PCR, immunohistochemical and immunofluorescence analysis were used to determine the presence of ectopic ATLOs in GCA and the expression of chemokines/chemokine receptors and cytokines involved in lymphoneogenesis in the temporal artery samples obtained from 50 patients with GCA and 30 controls. The presence of lymphatic conduits, of follicular dendritic cells (FDCs) precursors and lymphoid tissue inducer cells was also investigated. F…

0301 basic medicineGenetics and Molecular Biology (all)ChemokineChemokines; Cytokines; Giant Cell Arteritis; Rheumatology; Immunology; Biochemistry Genetics and Molecular Biology (all); Immunology and AllergyHigh endothelial venulesImmunologyBiologyBiochemistryGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesChemokine receptor0302 clinical medicineRheumatologyChemokines; Cytokines; Giant Cell ArteritisImmunology and AllergyCXCL13B-cell activating factorCytokineGiant Cell Arteriti030203 arthritis & rheumatologyBiochemistry Genetics and Molecular Biology (all)Follicular dendritic cellsSettore MED/16 - Reumatologia030104 developmental biologyLymphatic systemChemokineImmunologybiology.proteinEctopic expression
researchProduct

Clinical efficacy of α4 integrin block with natalizumab in ankylosing spondylitis

2016

We describe the impact of α4-β1/7 blockade with natalizumab, a recombinant humanised immunoglobulin (Ig) G4κ monoclonal antibody (mAb) targeted to the α4 subunit of the α4β1 and α4β7 integrins, on the gut and spine inflammation in a patient with ankylosing spondylitis (AS) who developed multiple sclerosis after treatment with tumour necrosis factor (TNF)-blocking agents. A 45-year-old man with human leucocyte antigen (HLA)-B27-positive AS was admitted in January 2007. He had been diagnosed with AS 4 years earlier based on the presence of inflammatory back pain, peripheral arthritis, radiographic bilateral grade 2 sacroiliitis, HLA-B27 positivity. At that time, he had evidence of chronic int…

0301 basic medicineGenetics and Molecular Biology (all)medicine.drug_classImmunologyHuman leukocyte antigenMonoclonal antibodyBiochemistryGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineNatalizumabRheumatologymedicineAdalimumabImmunology and Allergy030203 arthritis & rheumatologyInflammationAnkylosing spondylitisBiochemistry Genetics and Molecular Biology (all)business.industryMultiple sclerosisMedicine (all)Sacroiliitismedicine.diseaseTreatmentSettore MED/16 - Reumatologia030104 developmental biologyImmunologyTumor necrosis factor alphaSpondyloarthritibusinessmedicine.drug
researchProduct