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Rhumatologue

Docteur Andre RAMON

📍 Dijon (21)HospitalierRPPS 10101358165
📊 Reconnaissance scientifique : 12/100📝 63 articles publiés📚 HAL (8)

Diplômes

🎓 DES & spécialité ordinale

  • DES Rhumatologie
  • Rhumatologie (SM)

🎓 Diplômes

  • DE Docteur en médecine

Source : Annuaire Santé ANS (FHIR Practitioner.qualification) · Mises à jour quotidiennes.

Thèses universitaires

Source : catalogue national des thèses theses.fr (ABES). Ne couvre que les doctorats / HDR — les thèses d'exercice (DES) sont archivées dans les SCD universitaires.

Activité de recherche & publications

Source : bases de données publiques (OpenAlex, PubMed).

h-index

12

h articles cités ≥ h fois chacun. Un h de 12 = 12 publications avec 12+ citations.

Citations

439

Publications

63

i10-index

18

Thématiques principales

  • Vasculitis and related conditions ×27
  • Rheumatoid Arthritis Research and Therapies ×10
  • Gout, Hyperuricemia, Uric Acid ×8
  • Otitis Media and Relapsing Polychondritis ×8
  • Spondyloarthritis Studies and Treatments ×7

Affiliations FR : Inserm · Université de Bourgogne · CHU Dijon Bourgogne

Voir sur OpenAlex ↗🆔 ORCID 0000-0002-7289-7916

Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.

Bibliographie

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

Lieu de consultation

  • HOPITAL LE BOCAGE CHRU DIJON

    1 Boulevard JEANNE D ARC, 21079 Dijon

    ☎ 0380293031Hospitalier

Tarifs & secteur de conventionnement

Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).

📊 Comprendre le remboursement

Prendre rendez-vous & contact

🗓 Trouver sur Doctolib📇 Ajouter à mes contacts

Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Top publications · les plus citées

  • 1
    New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation

    Journal of clinical medicine · 2022

    📚 43 citations🎯 RCR 4.21Top 10% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    The giant cell arteritis (GCA) pathophysiology is complex and multifactorial, involving a predisposing genetic background, the role of immune aging and the activation of vascular dendritic cells by an unknown trigger. Once activated, dendritic cells recruit CD4 T cells and induce their activation, proliferation and polarization into Th1 and Th17, which produce interferon-gamma (IFN-γ) and interleukin-17 (IL-17), respectively. IFN-γ triggers the production of chemokines by vascular smooth muscle cells, which leads to the recruitment of additional CD4 and CD8 T cells and also monocytes that differentiate into macrophages. Recent data have shown that IL-17, IFN-γ and GM-CSF induce the differentiation of macrophage subpopulations, which play a role in the destruction of the arterial wall, in neoangiogenesis or intimal hyperplasia. Under the influence of different mediators, mainly endothelin-1 and PDGF, vascular smooth muscle cells migrate to the intima, proliferate and change their phenotype to become myofibroblasts that further proliferate and produce extracellular matrix proteins, increasing the vascular stenosis. In addition, several defects in the immune regulatory mechanisms probably contribute to chronic vascular inflammation in GCA: a defect in the PD-1/PD-L1 pathway, a quantitative and qualitative Treg deficiency, the implication of resident cells, the role of GM-CSF and IL-6, the implication of the NOTCH pathway and the role of mucosal-associated invariant T cells and tissue-resident memory T cells.

  • 2
    Do JAK inhibitors affect immune response to COVID-19 vaccination? Data from the MAJIK-SFR Registry

    The Lancet. Rheumatology · 2022

    📚 28 citations🎯 RCR 2.01🔓 Open Access📄 PDF gratuit ↗
  • 3
    PET/CT of cranial arteries for a sensitive diagnosis of giant cell arteritis

    Rheumatology (Oxford, England) · 2023

    📚 27 citations🎯 RCR 5.32Top 7% NIH🩺 Clinique
    Lire l'abstract Crossref ↓

    AbstractObjectivesTo investigate the performance of cranial PET/CT for the diagnosis of GCA.MethodsAll patients with a suspected diagnosis of GCA were prospectively enrolled in this study and had a digital PET/CT with evaluation of cranial arteries if they had not started glucocorticoids >72 h previously. The diagnosis of GCA was retained after at least 6 months of follow-up if no other diagnosis was considered by the clinician and the patient went into remission after at least 6 consecutive months of treatment. Cranial PET/CT was considered positive if at least one arterial segment showed hypermetabolism similar to or greater than liver uptake.ResultsFor cranial PET/CT, sensitivity (Se), specificity (Sp), positive predictive value (PPV) and negative predictive value (NPV) were 73.3%, 97.2%, 91.7% and 89.7%, respectively. For extracranial PET/CT, diagnostic performance was lower (Se = 66.7%, Sp = 80.6%, PPV = 58.8%, NPV = 85.3%). The combination of cranial and extracranial PET/CT improved overall sensitivity (Se = 80%) and NPV (NPV = 90.3%) while decreasing overall specificity (Sp = 77.8%) and PPV (PPV = 60%).ConclusionCranial PET/CT can be easily combined with extracranial PET/CT with a limited increase in examination time. Combined cranial and extracranial PET/CT showed very high diagnostic accuracy for the diagnosis of GCA.Trial registrationClinicalTrials.gov, https://clinicaltrials.gov, NCT05246540.

Publications scientifiques (41) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

Transversal28

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Goutte6

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Épidémiologie & registres4

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Essai clinique1

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Maladie de Horton1

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Pharmacovigilance1

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Vascularites des gros vaisseaux1

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Vraie vie / RWE1

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