Aller au contenu principal
Retour à l'annuaire
RhumatologueMédecins généralistes et spécialistes👤 Libéral intégral

M. Docteur AZZEDINE ARIF

📍 Argelès-sur-Mer (66)Libéral💶 Secteur 1RPPS 10003243028

✨ Profil synthétique

IA · 06/05/2026

Le Dr Azzedine Arif est un rhumatologue exerçant à Argelès-sur-Mer. Ses publications sur PubMed couvrent diverses pathologies, notamment le lupus et les vascularites des gros vaisseaux. Il a également contribué à des revues générales et à des méta-analyses dans le domaine de la rhumatologie.

Expertises présumées

  • Lupus
  • Vascularites des gros vaisseaux
  • SAPL
  • Pathologies auto-immunes
  • Rhumatologie systémique
  • Évaluation des cas cliniques complexes
  • Méta-analyse en rhumatologie

Synthèse automatique à partir des sources publiques (HAL, OpenAlex, theses.fr, ClinicalTrials.gov, FAI²R, ANS). Pas une évaluation clinique. Le médecin peut corriger via son compte.

Diplômes

🎓 DES & spécialité ordinale

  • Rhumatologie (SM)

🏅 DU / DIU

  • Médecine et Biologie du sport
  • Médecine et Biologie du sport (CAPA)

🎓 Diplômes

  • Diplôme équivalent d'un pays hors EEE profession Médecin

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

Localisation

Adresses géocodées via la Base Adresse Nationale (api-adresse.data.gouv.fr). Précision indicative.

Lieu de consultation

Tarifs & secteur de conventionnement

🟢 Secteur 1 — Tarif conventionnéSource CNAM (Annuaire santé Ameli)
💳 Carte VitaleLibéral intégral

Prendre rendez-vous & contact

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
    A Meta-analysis and Systematic Review of Valvular Heart Disease in Systemic Lupus Erythematosus and Its Association With Antiphospholipid Antibodies

    Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases · 2021

    📚 21 citations🎯 RCR 1.88
    Lire l'abstract Crossref ↓

    Background Valvular heart disease (VHD) is a known cardiac manifestation of systematic lupus erythematosus (SLE). This systematic review aims to pool data from studies to estimate the frequency of valvular lesions in SLE patients. It also aims to demonstrate the association between VHD in SLE and antiphospholipid antibodies positivity. Methods We included 27 studies after identifying relevant abstracts from PubMed, Scopus, and Google Scholar from the time of inception of database to 2019. Inclusion criteria consisted of English-language case-control and cohort studies. Three reviewers independently performed study selection, data extraction, and quality assessment using the Newcastle-Ottawa Scale for assessing risk for bias. Results For VHD in SLE patients, the most commonly involved valve was the mitral valve, with 19.7% lesions being mitral regurgitation. In terms of morphological lesions, valve thickening (11.06%) and vegetations (11.76%) were among the most prevalent. Other commonly encountered lesions were mitral valve prolapse and tricuspid regurgitation in 9.25% and 10.86% of patients, respectively. A meta-analysis of 21 studies with 2163 SLE patients, of which 23.3% had valvular lesions, showed a significant association of anticardiolipin antibodies positivity with VHD (relative risk, 1.55; confidence interval, 1.10–2.18). Conclusions Systemic lupus erythematosus is associated with VHD, and it should be considered a clinical manifestation of SLE in the absence of other valvular pathologies. There is a clear association between VHD in SLE and immunoglobulin G anticardiolipin antibodies positivity. This association suggests that this subgroup of SLE patients might benefit from a screening echocardiogram.

  • 2
    Chronic exposure to TNF reprograms cell signaling pathways in fibroblast-like synoviocytes by establishing long-term inflammatory memory

    Scientific reports · 2020

    📚 19 citations🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    Abstract Fibroblast-like synoviocytes (FLS) play a critical role in the pathogenesis of rheumatoid arthritis (RA). Chronic inflammation induces transcriptomic and epigenetic modifications that imparts a persistent catabolic phenotype to the FLS, despite their dissociation from the inflammatory environment. We analyzed high throughput gene expression and chromatin accessibility data from human and mouse FLS from our and other studies available on public repositories, with the goal of identifying the persistently reprogrammed signaling pathways driven by chronic inflammation. We found that the gene expression changes induced by short-term tumor necrosis factor-alpha (TNF) treatment were largely sustained in the FLS exposed to chronic inflammation. These changes that included both activation and repression of gene expression, were accompanied by the remodeling of chromatin accessibility. The sustained activated genes (SAGs) included established pro-inflammatory signaling components known to act at multiple levels of NF-kappaB, STAT and AP-1 signaling cascades. Interestingly, the sustained repressed genes (SRGs) included critical mediators and targets of the BMP signaling pathway. We thus identified sustained repression of BMP signaling as a unique constituent of the long-term inflammatory memory induced by chronic inflammation. We postulate that simultaneous targeting of these activated and repressed signaling pathways may be necessary to combat RA persistence.

  • 3
    Therapeutic Potential Of Foeniculum vulgare Mill. Derived Selenium Nanoparticles In Arthritic Balb/c Mice

    International journal of nanomedicine · 2019

    📚 13 citations🎯 RCR 1.04🔓 Open Access📄 PDF gratuit ↗

Publications scientifiques (15) — classées par pathologie

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

Transversal6

Lupus4

Revue générale2

Vascularites des gros vaisseaux2

Case report / série1

Revue / méta-analyse1

SAPL1

Vascularites1

Partager cette fiche

in LinkedIn🟢 WhatsApp✉ Email

Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.