Letteratura scientifica selezionata sul tema "Sclérodermie systémique – physiopathologie"
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Articoli di riviste sul tema "Sclérodermie systémique – physiopathologie":
Allanore, Yannick. "Physiopathologie de la sclérodermie systémique". médecine/sciences 32, n. 2 (febbraio 2016): 183–91. http://dx.doi.org/10.1051/medsci/20163202012.
Mouthon, L. "Sclérodermie systémique : de la physiopathologie au traitement". La Revue de Médecine Interne 28 (dicembre 2007): S266—S272. http://dx.doi.org/10.1016/j.revmed.2007.09.020.
Allanore, Yannick, e Catherine Boileau. "Génétique et physiopathologie de la sclérodermie systémique". Bulletin de l'Académie Nationale de Médecine 195, n. 1 (gennaio 2011): 55–67. http://dx.doi.org/10.1016/s0001-4079(19)32136-3.
Blaise, S. "Physiopathologie de l’atteinte microcirculatoire de la sclérodermie systémique". Journal des Maladies Vasculaires 38, n. 2 (marzo 2013): 69–70. http://dx.doi.org/10.1016/j.jmv.2012.12.103.
Didier, K., A. Robbins, F. Antonicelli, B. N. Pham, D. Giusti e A. Servettaz. "Actualités dans la physiopathologie de la sclérodermie systémique : vers de nouvelles opportunités thérapeutiques". La Revue de Médecine Interne 40, n. 10 (ottobre 2019): 654–63. http://dx.doi.org/10.1016/j.revmed.2019.05.016.
Servettaz, Amélie, Christian Agard, Mathieu C. Tamby, Philippe Guilpain, Loïc Guillevin e Luc Mouthon. "Physiopathologie de la sclérodermie systémique: état des lieux sur une affection aux multiples facettes". La Presse Médicale 35, n. 12 (dicembre 2006): 1903–15. http://dx.doi.org/10.1016/s0755-4982(06)74924-7.
Tesi sul tema "Sclérodermie systémique – physiopathologie":
Tiev, Kiet Phong. "Rôle du monoxyde d'azote dans la physiopathologie des atteintes pulmonaires de la sclérodermie systémique". Thesis, Paris Est, 2008. http://www.theses.fr/2008PEST0081.
Interstitial lung disease (ILD) has become the main cause of death in systemic sclerosis (SSc). In ILD, immune activation leads to strong nitric oxide (NO) output by inducible NO synthase. Increased the whole fractional rate of NO in exhaled air has been reported in SSc patients with ILD and suggested that exhaled NO can be an accurate none-invasive marker of early alveolar inflammation in order to initiate in time treatment. The two compartment-model method partitioned exhaled NO into alveolar concentration (CANO) and conducting airway flux, We hypothesized that overproduction of NO in the lung eventually leads to ILD in SSc. We have found that CANO is significantly increased in SSc patients as compared with healthy controls. We have also demonstrated that high levels of CANO were related to alveolitis and the severity of ILD in SSc. Moreover, we have found that ILD could be ruled in (positive predictive value > 95%) when CANO = 10.8 ppb, and ruled out when CANO values = 3.8 ppb (negative predictive value > 95%). The two-compartment model neglected the trumpet shape of airway tree and the axial diffusion of NO that the advanced “trumpet model” takes account. We have found that CANO levels assessed by the two models were comparable (rho=0,98, p<0.001). Finally, we have found that the serum ability to induce lung fibroblast proliferation and myofibroblast transition was increased in SSc patients with high levels of CANO (>5ppb) as compared to SSc patients with low levels of CANO (=5ppb) and healthy controls. Our findings suggest a possible link between alveolar inflammation, and lung fibrosis in SSc. 1624 caractères avec espace
Sanges, Sébastien. "Intérêt de biomarqueurs immunologiques dans l'hypertension artérielle pulmonaire associée à la sclérodermie systémique". Electronic Thesis or Diss., Université de Lille (2022-....), 2023. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2023/2023ULILS038.pdf.
Pulmonary arterial hypertension (PAH) is now the leading cause of disease-related mortality in patients with systemic sclerosis (SSc). Two issues arise to improve its prognosis:• first, its pathogenesis is poorly elucidated. Interactions between the immunological and fibrosing components of SSc have been extensively investigated, but few studies have focused on the relationship between immunity and the vasculature in this disease;• second, its management is hindered by clinical heterogeneity, sub-optimal diagnostic strategies and limited therapeutic options (mostly based on vasodilator treatments).During this PhD project, our objective was to identify new biomarkers associated with SSc-PAH, in order to generate new pathophysiological hypotheses, to improve the clinical characterization of patients, and to open therapeutic avenues.To do this, we mined the serum proteome of SSc-PAH patients using a high-throughput technique (SOMAscan), allowing the simultaneous measurement of 1129 unselected proteins. Overall, 53 proteins were differentially expressed compared to SSc patients without PAH. Among them, 2 candidate biomarkers were further explored:• Chemerin and its receptor CMKLR1Among the 1129 proteins studied, serum levels of chemerin (an adipokine involved in various inflammatory, fibrosing and vascular processes) were the only ones correlated with pulmonary vascular resistance in 2 independent cohorts. A single-cell RNA sequencing study on SSc-PAH lungs localized the production of chemerin within fibroblasts, pulmonary arterial smooth muscle cells (PA-SMC)/pericytes and mesothelial cells. Confocal immunofluorescence did not detect any chemerin staining in the lungs; but its receptor CMKLR1 was overexpressed by PA-SMC. Serum from SSc-PAH patients increased the PASMC proliferation, and this effect was neutralized by a CMKLR1 inhibitor. These results plead for the involvement of the chemerin-CMKLR1 axis in the pathophysiology of SSc-PAH.• BAFF and B cellsSeveral B cell-associated proteins were differentially expressed between SSc patients with and without PAH in the SOMAscan dataset. A panel of 14 B-cell biomarkers (including 2-microglobulin, rheumatoid factor, immunoglobulin (Ig) G, IgA, IgM, BAFF, APRIL, soluble forms (s) of TACI and BCMA receptors, sCD21, sCD23, sCD25, sCD27, and CXCL13) was thus created; and the associations between their serum levels and various SSc characteristics were studied in 2 independent cohorts.Several correlations were observed between different B-cell biomarkers and parameters associated with PAH. Notably, a strong correlation was identified between the levels of BAFF, a cytokine essential for the survival of B cells, and markers of PAH severity. Finally, we demonstrated the capacity of SSc B cells to produce pro-angiogenic mediators, suggesting their contribution to the microangiopathy associated with the disease.The chemerin-CMKLR1 and BAFF-B cell axes are robust biomarker candidates of SSc-PAH, presenting diagnostic and prognostic potential, opening the way to new therapeutic possibilities and suggesting unsuspected pathophysiological interactions between immunity and the vasculature
Bussone, Guillaume. "Caractérisation des cibles antigéniques des auto-anticorps au cours de la sclérodermie systémique et de l'hypertension artérielle pulmonaire". Paris 5, 2011. http://www.theses.fr/2011PA05T038.
Introduction. Pathophysiology of systemic sclerosis (SSc) and idiopathic pulmonary arterial hypertension (PAH) is not clearly established. By identifying new targets of auto-antibodies from patients, we tried to better understand the pathophysiology of these conditions. Methods. Reactivities contained in intravenous immunoglobulin preparations and of serum IgG from patients with SSc and/or PAH were tested by indirect immunofluorescence, 1-D and 2-D immunoblots on HEp-2 cell, fibroblast, endothelial cell (EC) and vascular smooth muscle cell (VSMC) protein extracts, then identified by mass spectrometry and analysed using Pathway Studio software. ELISA using recombinant proteins and VSMC contraction assays were performed. Results. We characterized target antigens of normal human IgG on HEp-2 cell and EC protein extracts. In addition, new target antigens of anti-nuclear antibodies, involved in TGF-β pathway, were identified in patients with SSc. We also detected anti-fibroblast antibodies in the serum of patients with PAH, and lamin A/C and tubulin beta chain were identified as targets of anti-EC antibodies. Finally, we demonstrated that serum IgG from patients recognized VSMC, recognized well-defined targets and led to cellular contraction. Conclusion. New target antigens of auto-antibodies were identified in patients with SScand/or PAH, that could allow the development of diagnostic, prognostic and/or therapeutic tools