86 research outputs found
La maladie de Whipple (à partir de quatre observations et revue de la littérature)
No full textANGERS-BU Médecine-Pharmacie (490072105) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF
Pneumomédiastin compliquant une pneumopathie interstitielle au cours des dermatomyosites et polymyosites (étude de 11 cas et revue de la littérature )
No full textLe pneumomédiastin spontané est une complication rare des myopathies inflammatoires avec une prévalence estimée à 2%. Sa survenue dans un tableau de connectivite doit faire évoquer le diagnostic de dermatomyosite ou polymyosite. Cette complication est plus fréquente chez l homme et dans les formes cliniquement amyopathiques de dermatomyosites. Une pneumopathie interstitielle est constante, jouant possiblement un rôle via la rupture d une alvéole ou de bulles paracardiaques. C est une complication sévère avec une mortalité de 40%. La gravité de la pneumopathie interstitielle et sa rapidité d évolution semblent être des facteurs de mauvais pronostic faisant discuter un traitement précoce. L indication d un traitement immunosuppresseur est à envisager rapidement, permettant parfois une évolution favorable sans séquelle.NANTES-BU Médecine pharmacie (441092101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF
Contributions à l'évaluation diagnostique, pronostique et thérapeutique des vascularites systéliques
No full textRENNES1-BU Santé (352382103) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF
Association of an IRF5 gene functional polymorphism with Sjögren's syndrome.
No full textInternational audienceOBJECTIVE: Interferon regulatory factor 5 (IRF-5) is a transcription factor involved in the regulation of the host defense. Previous studies have demonstrated a significant association of various IRF5 gene polymorphisms with systemic lupus erythematosus (SLE) in Caucasians. The purpose of this case-control study was to investigate whether IRF5 polymorphisms are involved in the genetic predisposition to primary Sj?n's syndrome (SS), an autoimmune disease closely related to SLE. METHODS: We analyzed IRF5 rs2004640, rs2070197, rs10954213, and rs2280714 polymorphisms in a cohort of 212 primary SS patients and 162 healthy blood donors, all of whom were of Caucasian origin. The 4 polymorphisms examined were genotyped by competitive allele-specific polymerase chain reaction using fluorescence resonance energy transfer technology. RESULTS: The IRF5 rs2004640 GT or TT genotype (T allele carriers) was identified in 87% of primary SS patients compared with 77% of controls (P = 0.01, odds ratio [OR] 1.93 [95% confidence interval (95% CI) 1.15-3.42]). The IRF5 rs2004640 T allele was found on 59% of chromosomes from primary SS patients compared with 52% of chromosomes from controls (P = 0.04, OR 1.36 [95% CI 1.01-1.83]). No significant association of primary SS with rs2070197, rs10954213, or rs2280714 was seen when they were analyzed independently. Nevertheless, haplotype reconstructions based on the 4 polymorphisms examined suggest that various allele combinations of rs2004640 and rs2070197 could define susceptibility or protective haplotypes. CONCLUSION: This study is the first to demonstrate a significant association between primary SS and the IRF5 rs2004640 T allele. These results, which require further replication on larger populations, suggest that besides their association with identical major histocompatibility complex gene polymorphisms, primary SS and SLE share IRF gene polymorphisms as a common genetic susceptibility factor
Tumour Necrosis Factor Receptor 2 (TNFRSF1B) Association Study in Sjögren's Syndrome [2]
No full textInternational audienc
Thromboangiitis obliterans and the inherited thrombophilias: Does an association merit consideration?
No full text[No abstract available]Almawi WY, 2004, AM J HEMATOL, V76, P85, DOI 10.1002-ajh.20047; Avcu F, 2000, THROMB RES, V100, P143, DOI 10.1016-S0049-3848(00)00310-8; BORDMANN M, 2000, THROMB RES, V99, P483; Franchini M, 2006, CRIT REV CL LAB SCI, V43, P249, DOI 10.1080-10408360600552678; Lazarides M K, 2006, Int J Low Extrem Wounds, V5, P89, DOI 10.1177-1534734606288817; Makita S, 1996, CIRCULATION, V94, P211; Mercie P, 1998, MICROVASC RES, V55, P271, DOI 10.1006-mvre.1998.2071; OLIN JW, 1990, CIRCULATION, V82, P3; Olin JW, 2006, CURR OPIN RHEUMATOL, V18, P18, DOI 10.1097-01.bor.0000198000.58073.aa; Puechal X, 2007, RHEUMATOLOGY, V46, P192, DOI 10.1093-rheumatology-kel388; Rosendaal FR, 1999, LANCET, V353, P1167, DOI 10.1016-S0140-6736(98)10266-0; Siguret V, 1997, THROMB RES, V86, P85, DOI 10.1016-S0049-3848(97)00049-2; Taher A, 2001, THROMB HAEMOSTASIS, V86, P7231
Randomised controlled trial of prolonged treatment in the remission phase of ANCA-associated vasculitis
No full textObjectives A prospective randomised trial to compare two different durations of maintenance immunosuppressive therapy for the prevention of relapse in anti-neutrophil cytoplasmic antibodies (ANCA)associated vasculitis (AAV). Methods Patients with AAV were recruited 18-24 months after diagnosis if they were in stable remission after cyclophosphamide/prednisolone-based induction followed by azathioprine/prednisolone maintenance therapy. They were randomised (1: 1) to receive continued azathioprine/prednisolone to 48 months from diagnosis (continuation group) or to withdraw azathioprine/prednisolone by 24 months (withdrawal group). The primary endpoint was the relapse risk, from randomisation to 48 months from diagnosis. Results One hundred and seventeen patients were randomised and 110 remained to the trial end. At entry, median serum creatinine was 116 mu mol/L (range 58-372), 53% were ANCA positive. The percentage of patients presenting with relapse was higher in the withdrawal than in the continuation treatment group (63% vs 22%, p Conclusions Prolonged remission maintenance therapy with azathioprine/prednisolone, beyond 24 months after diagnosis reduces relapse risk out to 48 months and improves renal survival in AAV
The CGGGG insertion/deletion polymorphism of the IRF5 promoter is a strong risk factor for primary Sjögren's syndrome.
No full textInternational audienceInterferon regulatory factor 5 is a transcription factor involved in type I interferon (IFN) secretion. This study was undertaken to investigate whether a 5-bp (CGGGG insertion/deletion) promoter polymorphism is involved in genetic predisposition to primary Sjögren's syndrome (SS) and to assess the functional consequences of this polymorphism.The exploratory cohort consisted of 185 patients with primary SS and 157 healthy controls, and the replication cohort consisted of 200 patients with primary SS and 282 healthy controls. Levels of IRF5 messenger RNA (mRNA) were assessed at baseline and after in vitro infection with reovirus in peripheral blood mononuclear cells (PBMCs) from 30 patients with primary SS and from salivary gland epithelial cells that had been cultured for 4 weeks from patients with primary SS or sicca symptoms.Carriage of the IRF5 4R CGGGG allele was associated with a greatly increased risk of primary SS in both cohorts (odds ratio 2.00 [95% confidence interval 1.5-2.7], P = 6.6 x 10(-6)). The CGGGG insertion/deletion polymorphism alone was sufficient to explain the association of primary SS with IRF5. The level of IRF5 mRNA in PBMCs depended significantly on genotype (P = 0.002) and was correlated with the levels of mRNA for the IFN-induced genes MX1 and IFITM1. Cultured salivary gland epithelial cells from patients carrying the 4R CGGGG IRF5 allele showed a high level of IRF5 mRNA (P = 0.04), which was amplified after reovirus infection (P = 0.026).Our findings indicate an association of the CGGGG insertion/deletion polymorphism of the IRF5 promoter with primary SS. Patients carrying the 4R CGGGG IRF5 allele had a high level of mRNA for IRF5 in PBMCs and salivary gland epithelial cells, mainly after in vitro viral infection. Patients with high levels of mRNA for IRF5 also had high levels of mRNA for type I IFN-induced genes in PBMCs
The CGGGG insertion/deletion polymorphism of the IRF5 promoter is a strong risk factor for primary Sjögren's syndrome.
No full textInternational audienceInterferon regulatory factor 5 is a transcription factor involved in type I interferon (IFN) secretion. This study was undertaken to investigate whether a 5-bp (CGGGG insertion/deletion) promoter polymorphism is involved in genetic predisposition to primary Sjögren's syndrome (SS) and to assess the functional consequences of this polymorphism.The exploratory cohort consisted of 185 patients with primary SS and 157 healthy controls, and the replication cohort consisted of 200 patients with primary SS and 282 healthy controls. Levels of IRF5 messenger RNA (mRNA) were assessed at baseline and after in vitro infection with reovirus in peripheral blood mononuclear cells (PBMCs) from 30 patients with primary SS and from salivary gland epithelial cells that had been cultured for 4 weeks from patients with primary SS or sicca symptoms.Carriage of the IRF5 4R CGGGG allele was associated with a greatly increased risk of primary SS in both cohorts (odds ratio 2.00 [95% confidence interval 1.5-2.7], P = 6.6 x 10(-6)). The CGGGG insertion/deletion polymorphism alone was sufficient to explain the association of primary SS with IRF5. The level of IRF5 mRNA in PBMCs depended significantly on genotype (P = 0.002) and was correlated with the levels of mRNA for the IFN-induced genes MX1 and IFITM1. Cultured salivary gland epithelial cells from patients carrying the 4R CGGGG IRF5 allele showed a high level of IRF5 mRNA (P = 0.04), which was amplified after reovirus infection (P = 0.026).Our findings indicate an association of the CGGGG insertion/deletion polymorphism of the IRF5 promoter with primary SS. Patients carrying the 4R CGGGG IRF5 allele had a high level of mRNA for IRF5 in PBMCs and salivary gland epithelial cells, mainly after in vitro viral infection. Patients with high levels of mRNA for IRF5 also had high levels of mRNA for type I IFN-induced genes in PBMCs
The CGGGG insertion/deletion polymorphism of the IRF5 promoter is a strong risk factor for primary Sjögren's syndrome.
No full textInternational audienceInterferon regulatory factor 5 is a transcription factor involved in type I interferon (IFN) secretion. This study was undertaken to investigate whether a 5-bp (CGGGG insertion/deletion) promoter polymorphism is involved in genetic predisposition to primary Sjögren's syndrome (SS) and to assess the functional consequences of this polymorphism.The exploratory cohort consisted of 185 patients with primary SS and 157 healthy controls, and the replication cohort consisted of 200 patients with primary SS and 282 healthy controls. Levels of IRF5 messenger RNA (mRNA) were assessed at baseline and after in vitro infection with reovirus in peripheral blood mononuclear cells (PBMCs) from 30 patients with primary SS and from salivary gland epithelial cells that had been cultured for 4 weeks from patients with primary SS or sicca symptoms.Carriage of the IRF5 4R CGGGG allele was associated with a greatly increased risk of primary SS in both cohorts (odds ratio 2.00 [95% confidence interval 1.5-2.7], P = 6.6 x 10(-6)). The CGGGG insertion/deletion polymorphism alone was sufficient to explain the association of primary SS with IRF5. The level of IRF5 mRNA in PBMCs depended significantly on genotype (P = 0.002) and was correlated with the levels of mRNA for the IFN-induced genes MX1 and IFITM1. Cultured salivary gland epithelial cells from patients carrying the 4R CGGGG IRF5 allele showed a high level of IRF5 mRNA (P = 0.04), which was amplified after reovirus infection (P = 0.026).Our findings indicate an association of the CGGGG insertion/deletion polymorphism of the IRF5 promoter with primary SS. Patients carrying the 4R CGGGG IRF5 allele had a high level of mRNA for IRF5 in PBMCs and salivary gland epithelial cells, mainly after in vitro viral infection. Patients with high levels of mRNA for IRF5 also had high levels of mRNA for type I IFN-induced genes in PBMCs
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