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Review [Therapeutic intensification and autologous stem cell transplantation in autoimmune diseases] 2005
Marjanovic Z, Gerber I, Toledano C, Hen-Solal J, Damade R, de Saint-Cyr I, Sarrot-Reynauld F, Ilié D, Daneshpouy M, Mounier N, Ruivard M, Tyndall C, Vidal E, Quere I, Durand JM, Constans J, Farge D. · Service de médecine interne, Service de greffe de moelle, Hôpital Saint-Louis, 1, avenue Claude Vellefaux, 75010 Paris, France. · Presse Med. · Pubmed #15798553 No free full text.
Abstract: THE PATHOPHYSIOLOGY of most autoimmune diseases is often poorly understood. EXPERIMENTAL CONSIDERATIONS and clinical experience suggest that high doses immunoablation followed by stem cell transplantation is a therapeutic option to consider for certain severe autoimmune disorders. THE CONCEPT OF RESTORING NORMAL IMMUNE REACTIVITY must in part br true since current results of 466 transplants (445 autologous, 21 allogeneic) patients suffering from various autoimmune diseases show a beneficial outcome in approximately 2/3 of the patients. TO IMPROVE THE EFFICACY AND SAFETY OF SUCH AN AGGRESSIVE PROCEDURE in patients with potentially affected vital organs by the underlying autoimmune disease, it is especially important to follow international consensus guidelines and to centrally collect clinical data for in depth analysis in the EBMT International Stem Cell Project for Autoimmune Disease in Basel, Switzerland. PHASE III STUDIES ARE RUNNING FOR SYSTEMIC SCLEROSIS (Astis, Autologous Stem cell Transplantation International Rheumatoid Arthritis Trial) started in 2003. A STUDY PROJECT IS PLANNED FOR MULTIPLE SCLEROSIS (Astims, Autologous Stem cell Transplantation International Multiple Sclerosis).
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Article Diagnostic and prognostic relevance of neuromuscular biopsy in primary Sjögren's syndrome-related neuropathy. free! 2007
Terrier B, Lacroix C, Guillevin L, Hatron PY, Dhote R, Maillot F, Diot E, Sarrot-Reynauld F, Sordet C, Dubourg O, Meyer L, Mariette X, Gottenberg JE, Anonymous00097. · Assistance Publique Hôpitaux de Paris, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France. · Arthritis Rheum. · Pubmed #18050172 links to free full text
Abstract: OBJECTIVE: To evaluate the clinicobiologic presentation in patients with primary Sjögren's syndrome (SS)-related peripheral neuropathy, the histologic results of neuromuscular biopsy (NMB), and clinical outcome, and to identify prognostic factors. METHODS: We retrospectively studied clinical and biologic presentation of 40 patients with primary SS-related neuropathy who underwent NMB. Prognostic factors of clinical outcome were assessed by univariate and multivariate analysis. RESULTS: Patients with vasculitis (lymphocytic [n = 8] or necrotizing [n = 14]) had a higher prevalence of acute-onset neuropathy, multiple mononeuropathy, sensorimotor involvement, vascular purpura, general symptoms, increased C-reactive protein level, positivity for rheumatoid factor, hypocomplementemia, and monoclonal gammopathy compared with those without vasculitis (n = 18). Comparison between patients with necrotizing or lymphocytic vasculitis did not reveal significant differences in clinical or biologic presentation except for the presence of general symptoms and rheumatoid factor. Regarding clinical evolution, the results of NMB (P < 0.0001), in particular the presence of necrotizing vasculitis (P < 0.001), an acute neuropathy onset (P < 0.0001), general symptoms (P < 0.0001), multiple mononeuropathy (P = 0.0007), presence of sensorimotor involvement (P = 0.002), and increased C-reactive protein level (P = 0.008), were significantly associated with a better outcome in univariate analysis. In multivariate analysis, NMB resulting in the identification of patients with necrotizing vasculitis was the only variable that remained significantly associated with a better outcome (P = 0.01). CONCLUSION: NMB is necessary to identify patients with necrotizing vasculitis, who have a better response to immunosuppressive therapy. NMB might therefore have both a diagnostic and prognostic relevance in primary SS-related neuropathy.
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Article Local hyperemia to heating is impaired in secondary Raynaud's phenomenon. free! 2005
Boignard A, Salvat-Melis M, Carpentier PH, Minson CT, Grange L, Duc C, Sarrot-Reynauld F, Cracowski JL. · Laboratory HP2, EA 3745 Inserm ESPRI, Grenoble Medical School, France. · Arthritis Res Ther. · Pubmed #16207327 links to free full text
Abstract: Accurate and sensitive measurement techniques are a key issue in the quantification of the microvascular and endothelial dysfunction in systemic sclerosis (SSc). Thermal hyperemia comprises two separate mechanisms: an initial peak that is axon reflex mediated; and a sustained plateau phase that is nitric oxide dependent. The main objective of our study was to test whether thermal hyperemia in patients with SSc differed from that in patients with primary Raynaud's phenomenon (RP) and healthy controls. In a first study, we enrolled 20 patients suffering from SSc, 20 patients with primary RP and 20 healthy volunteers. All subjects were in a fasting state. Post-occlusive hyperemia, 0.4 mg sublingual nitroglycerin challenge and thermal hyperemia were performed using laser Doppler flowmetry on the distal pad of the third left finger. In a second study, thermal hyperemia was performed in 10 patients with rheumatoid arthritis and 10 patients with primary RP. The thermal hyperemia was dramatically altered in terms of amplitude and kinetics in patients with SSc. Whereas 19 healthy volunteers and 18 patients with primary RP exhibited the classic response, including an initial peak within the first 10 minutes followed by a nadir and a second peak, this occurred only in four of the SSc patients (p < 0.0001). The 10 minutes thermal peak was 43.4 (23.2 to 63), 42.6 (31 to 80.7) and 27 (14.7 to 51.4) mV/mm Hg in the healthy volunteers, primary RP and SSc groups, respectively (p = 0.01), while the 44 degrees C thermal peak was 43.1 (21.3 to 62.1), 42.6 (31.6 to 74.3) and 25.4 (15 to 52.4) mV/mm Hg, respectively (p = 0.01). Thermal hyperemia was more sensitive and specific than post-occlusive hyperhemia for differentiating SSc from primary RP. In patients with rheumatoid arthritis, thermal hyperemia was also altered in terms of amplitude. Thermal hyperemia is dramatically altered in patients with secondary RP in comparison with subjects with primary RP. Further studies are required to determine the mechanisms of this altered response, and whether it may provide additional information in a clinical setting.
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