M. Docteur THIBAULT VANDHUICK
✨ Profil synthétique
IA · 04/05/2026Le Dr Thibault Vandhuick est un rhumatologue exerçant à Rouen. Ses publications sur PubMed révèlent une expertise dans le domaine des biothérapies, notamment les traitements anti-TNF et non anti-TNF. Il a également publié des travaux sur les biomarqueurs et l'imagerie par résonance magnétique (IRM) ostéo-articulaire.
Expertises présumées
- Rhumeumatologie inflammatoire
- Thérapies biologiques
- Imagerie ostéo-articulaire
- Biomarqueurs en rhumatologie
- Traitement des maladies auto-immunes
- Utilisation des anti-TNF
- IRM 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
- DES Rhumatologie
- Rhumatologie (SM)
🎓 Diplômes
- DE Docteur en médecine
Source : Annuaire Santé ANS (FHIR Practitioner.qualification) · Mises à jour quotidiennes.
Bibliographie
Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
2015ArticleArthritis Research and Therapy
Switching from an anti-TNF monoclonal antibody to soluble TNF-receptor yields better results than vice versa: An observational retrospective study of 72 rheumatoid arthritis switchers
2015ArticleJoint Bone Spine
Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).
Localisation des cabinets
Adresses géocodées via la Base Adresse Nationale (api-adresse.data.gouv.fr). Précision indicative.
Lieux de consultation
THIBAULT VANDHUICK
26BIS BOULEVARD GAMBETTA, 76000 Rouen
LibéralTHIBAULT VANDHUICK
CLINIQUE SAINT HILAIRE — 2 PLACE SAINT HILAIRE, 76000 Rouen
LibéralGIE IRM II SAINT HILAIRE
7 Rue DE L'ABREUVOIR, 76000 Rouen
☎ 0235066626Libéral© OpenStreetMap · Photos Wikimedia Commons (CC)HOPITAL CHARLES NICOLLE CHU ROUEN
1 Rue DE GERMONT, 76000 Rouen
Tarifs & secteur de conventionnement
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
- 1Soluble VE-cadherin in rheumatoid arthritis patients correlates with disease activity: evidence for tumor necrosis factor α-induced VE-cadherin cleavage
Arthritis and rheumatism · 2012
📚 67 citations🎯 RCR 1.95Lire l'abstract Crossref ↓
AbstractObjectiveRheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that principally attacks synovial joints. However, accelerated atherosclerosis and increased cardiovascular morbidity and mortality are major clinical consequences of endothelial dysfunction in RA patients. Tumor necrosis factor α (TNFα) is the major mediator of inflammation in RA, related to vascular injury by targeting VE‐cadherin, an endothelium‐specific adhesion molecule of vital importance for endothelium integrity and angiogenesis. We undertook this study to examine the mechanisms regulating VE‐cadherin processing by TNFα and their occurrence in RA.MethodsHuman umbilical vein endothelial cells were used in primary culture and treated with recombinant TNFα to study VE‐cadherin cleavage. Cell lysates and conditioned media were analyzed by Western blotting for VE‐cadherin cytoplasmic domain and extracellular domain (VE‐90) generation, respectively. VE‐90 was analyzed at baseline and at the 1‐year followup in sera from 63 RA patients (from the Very Early Rheumatoid Arthritis cohort) with disease duration of <6 months.ResultsTNFα induced a time‐dependent shedding of VE‐90 in cell media. This effect was prevented by tyrosine kinase inhibitors (genistein and PP2) or by knocking down Src kinase. In contrast, tyrosine phosphatase blockade enhanced VE‐cadherin cleavage, confirming the requirement of tyrosine phosphorylation processes. In addition, using the matrix metalloproteinase (MMP) activator APMA and the MMP inhibitor GM6001, we demonstrated that MMPs are involved in TNFα‐induced VE‐cadherin cleavage. Of major importance, VE‐90 was detected in sera from the 63 RA patients and was positively correlated with the Disease Activity Score at baseline and after 1‐year followup.ConclusionThese findings provide the first evidence of VE‐cadherin proteolysis upon TNFα stimulation and suggest potential clinical relevance of soluble VE‐cadherin in management of RA.
- 2Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Arthritis research & therapy · 2015
- 3Switching from an anti-TNF monoclonal antibody to soluble TNF-receptor yields better results than vice versa: An observational retrospective study of 72 rheumatoid arthritis switchers
Joint bone spine · 2015
📚 17 citations🩺 Clinique
Publications scientifiques (7) — classées par pathologie
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Transversal3
▼
Transversal3
▼- Early phase clinical and biological markers associated with subclinical atherosclerosis measured at 7 years of evolution in an early inflammatory arthritis cohort
Clinical and experimental rheumatology · 2016 · Journal Article
Vandhuick T, Allanore Y, Borderie D, Louvel JP, et al.
📚 10 cit.🔬→🩺 Translationnel - Soluble VE-cadherin in rheumatoid arthritis patients correlates with disease activity: evidence for tumor necrosis factor α-induced VE-cadherin cleavage
Arthritis and rheumatism · 2012 · Journal Article
Sidibé A, Mannic T, Arboleas M, Subileau M, et al.
📚 67 cit.🎯 RCR 1.95🔬→🩺 Translationnel - [A painful hip after percutaneous nephrolithotomy]
La Revue de medecine interne · 2007 · Case Reports
Vandhuick T, Abboud P, Levesque H, Marie I
Anti-TNF1
▼
Anti-TNF1
▼- Switching from an anti-TNF monoclonal antibody to soluble TNF-receptor yields better results than vice versa: An observational retrospective study of 72 rheumatoid arthritis switchers
Joint bone spine · 2015 · Journal Article
Lequerré T, Farran É, Ménard JF, Kozyreff-Meurice M, et al.
📚 17 cit.🩺 Clinique
Biomarqueurs / Auto-Ac1
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Biomarqueurs / Auto-Ac1
▼- Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Arthritis research & therapy · 2015 · Clinical Trial
Golinski ML, Vandhuick T, Derambure C, Fréret M, et al.
📚 18 cit.🩺 Clinique
Biothérapies non-anti-TNF1
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Biothérapies non-anti-TNF1
▼- [Psoriatic arthritis during rituximab treatment of granulomatosis with polyangiitis: a new paradoxical side effect?]
La Revue de medecine interne · 2015 · Case Reports
Aussy A, Girszyn N, Vandhuick T, Marie I, et al.
📚 5 cit.
IRM ostéo-articulaire1
▼
IRM ostéo-articulaire1
▼- Role for magnetic resonance imaging in coccydynia with sacrococcygeal dislocation
Joint bone spine · 2013 · Case Reports
Trouvin AP, Goeb V, Vandhuick T, Michelin P, et al.
📚 3 cit.
Datasets & protocoles partagés
Additional file 6: of Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Image2015FigshareTNF receptor (TNFR)1 and TNFR2 have no effect on RasGRP1 and RasGRP3 gene expression level in T and B cells respectively. Quantitative PCR analysis was performed to measure RasGRP1 and RasGRP3 gene expression levels in T
Additional file 5: of Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Image2015FigshareT cell activation induces an increase of RasGRP1 gene expression level. After T cell negative selection, cells were cultured with IL-2 and anti-CD3 antibody for 4 days (n = 3). a To evaluate the T cell activation status,
Additional file 4: of Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Image2015FigshareT and B cell purity. After negative selection of peripheral blood mononuclear cells from healthy controls, buffy coat and rheumatoid arthritis patients, cytometric analysis of T and B cell purity was checked. a Cytometri
Additional file 6: of Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Image2015FigshareTNF receptor (TNFR)1 and TNFR2 have no effect on RasGRP1 and RasGRP3 gene expression level in T and B cells respectively. Quantitative PCR analysis was performed to measure RasGRP1 and RasGRP3 gene expression levels in T
Additional file 7: of Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Image2015FigshareTNFα has no effect on T cell apoptosis. After T cell negative selection, cells were cultured with or without TNFα for 48 and 72 hours. To measure apoptosis, a fluorescein isothiocyanate (FITC) annexin-V Apoptosis Detecti
Additional file 3: of Dysregulation of RasGRP1 in rheumatoid arthritis and modulation of RasGRP3 as a biomarker of TNFα inhibitors
Image2015FigshareModulation of RasGRP3 gene expression levels in peripheral blood mononuclear cells (PBMCs) from healthy controls (HC) incubated with TNFα and adalimumab, etanercept, infliximab, certolizumab or golimumab. Quantitative PC
Source : DataCite — DOIs pour datasets, logiciels, protocoles, registres patient. Hors articles (déjà couverts).