Rheumatoid Arthritis: Fain O

Fain O, Aras N, Morin AS, Stirnemann J. · Service de médecine interne, AP-HP, hôpital Jean-Verdier. Université Paris-13, 93140 Bondy. · Rev Prat. · Pubmed #17717938 No free full text.

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Gottenberg JE, Guillevin L, Lambotte O, Combe B, Allanore Y, Cantagrel A, Larroche C, Soubrier M, Bouillet L, Dougados M, Fain O, Farge D, Kyndt X, Lortholary O, Masson C, Moura B, Remy P, Thomas T, Wendling D, Anaya JM, Sibilia J, Mariette X, Anonymous00301. · Service de Rhumatologie, Hôpital de Bicêtre, 78 rue du Général Leclerc, 94275 Le Kremlin Bicêtre, France. · Ann Rheum Dis. · Pubmed #15550531 links to  free full text

Abstract: OBJECTIVE: To assess the tolerance and efficacy of rituximab in patients with various autoimmune diseases seen in daily rheumatological practice. METHODS: 866 rheumatology and internal medicine practitioners were contacted by e-mail to obtain the files of patients treated with rituximab for systemic autoimmune diseases. Patients with lymphoma were analysed if the evolution of the autoimmune disease could be evaluated. RESULTS: In all, 43 of 49 cases could be analysed, including 14 with rheumatoid arthritis (RA), 13 with systemic lupus erythematosus (SLE), six with primary Sjogren's syndrome (pSS), five with systemic vasculitis, and five with other autoimmune diseases. Rituximab was prescribed for lymphoma in two patients with RA and two with pSS. In the 39 other cases, rituximab was given because of the refractory character of the autoimmune disease. The mean follow up period was 8.3 months (range 2 to 26). There were 11 adverse events in 10 patients and treatment had to be discontinued in six. Efficacy was observed in 30 patients (70%): RA 11, SLE 9, pSS 5, vasculitis 2, antisynthetase syndromes 2, sarcoidosis 1. The mean decrease in corticosteroid intake was 9.5 mg/d (range 0 to 50) in responders. Seven patients experienced relapse after mean 8.1 months (5 to 15). Three patients died because of refractory autoimmune disease. CONCLUSIONS: Despite absence of marketing authorisation, rituximab is used to treat various refractory autoimmune diseases in daily rheumatological practice. This study showed good tolerance and short term clinical efficacy, with marked corticosteroid reduction in patients with SLE, pSS, vasculitis, and polymyositis.

Bibi-Triki T, Eclache V, Frilay Y, Stirnemann J, Frémeaux-Bacchi V, Fain O. · Laboratoire d'hématologie, hôpital Jean-Verdier (AP-HP), avenue du 14-juillet, 93143, université Paris-Nord UPRES 3409, Bondy cedex, France. · Rev Med Interne. · Pubmed #15363623 No free full text.

Abstract: INTRODUCTION: Acquired C1 inhibitor deficiency is sometimes associated with lymphoproliferative disorders. EXEGESIS: We report four cases of acquired C1 inhibitor deficiency in association with lymphoproliferative disorders. Three of them were asymptomatic; one was associated with abdominal pain. Four women (median age, 66 years) presented either two non-Hodgkin lymphoma or two chronic lymphocytic leukaemia. C1 inhibitor deficiency was detected fortuitous (n = 1) or during investigation of arthralgia (n = 2), or Gougerot-Sjogren syndrome (n = 1). The deficit was acquired in all cases type I. Auto-immune disorders were associated with: Gougerot-Sjogren syndrome (n = 1), cryoglobulinemia (n = 2), IgM lambda monoclonal gammopathy (n = 1), Coombs positive test (n = 2), IgG anti-cardiolipine antibodies (n = 1). C1 inhibitor deficiency was not modified after lymphoproliferative disorders treatment (radiotherapy, splenic ablation) in two cases but patients were not in complete remission. C1 inhibitor raised normal level in one case, after five chemotherapy regimens, but decreased complement level and C4 split persist. CONCLUSION: Acquired C1 inhibitor deficiency associated with lymphoproliferative disorders is sometimes asymptomatic. Diagnosis could be delay in spite of clinical manifestations. Deficit correction is not constant after lymphoproliferative disorders treatment.

Volter F, Fain O, Mathieu E, Thomas M. · Laboratoire de Physiologie Digestive and Service de Medecine Interne, AP-HP, Hôpital Jean-Verdier, 93143 Bondy Cedex, France. · Dig Dis Sci. · Pubmed #15104365 No free full text.

Abstract: The frequency and characteristics of esophageal dysmotility in Sjögren's syndrome (SS) are as controversial as their related symptoms. We evaluated esophageal function and gastroesophageal reflux (GER) in 21 SS patients using manometry and 24-hr esophageal pH monitoring. All patients complained of xerostomia, 33% of dysphagia, and 62% of heartburn. Compared to controls, the mean percentage abdominal length of their lower esophageal sphincters (LES) and resting LES pressures were significantly lower, with no difference in primary esophageal peristalsis. Tertiary waves without swallowing were detected in 29% of them and pathological GER in 67%. Symptoms, esophageal motor abnormalities, and reflux features were similar in primary and secondary SS. ANOVA indicated that dysphagia was unrelated to the esophageal impairments and GER analysis results, while heartburn was significantly associated with GER severity. Esophageal acid-exposure time was significantly longer in SS patients with distal tertiary waves, while proximal esophagus wave velocity was significantly lower. While SS patients have nonspecific esophageal motility disorders and frequently GER disease, early and accurate diagnosis of GER is essential to identify SS patients at risk for acidic reflux, especially because the acid-clearance capacity of the esophagus is already diminished by the lack of saliva.

Fain O. · Service de médecine interne, hôpital Jean Verdier (AP-HP), université Paris Nord, Bondy. · Rev Prat. · Pubmed #15008210 No free full text.

This publication has no abstract.

Guilpain P, Kettaneh A, Chamouard JM, Stirnemann J, Thomas M, Fain O. · Service de médecine interne, hôpital Jean-Verdier, Bondy, France. · Rev Med Interne. · Pubmed #12614860 No free full text.

Abstract: INTRODUCTION: Craniocervical junction damages may result in a compression of the spinal cord. They may be caused by infectious, tumoral or inflammatory processes. Rheumatoid arthritis is probably among rheumatic diseases the most frequent cause of atlantoaxial arthritis. Nevertheless involvement of the craniocervical junction as the presenting symptom of rheumatoid arthritis is a very rare feature. EXEGESIS: We report the case of a 61 years old woman who presented with atlantoaxial involvement and spinal cord compression one year before the diagnosis of a seronegative rheumatoid arthritis. CONCLUSION: Symptomatic craniocervical junction damages may appear. Patients with damages of the craniocervical junction and negative investigations should be followed long-term; an underlying inflammatory disease may become evident after significant delay.