Rheumatoid Arthritis: Sordet C

Fabien N, Goetz J, Sordet C, Humbel RL, Sibilia J, Anonymous00070. · Laboratoire d'auto-immunité, Hospices Civils de Lyon, Centre hospitalier Lyon-Sud, F-69495 Pierre Bénite Cedex, France. · Presse Med. · Pubmed #18951757 No free full text.

Abstract: New treatment strategies require that rheumatoid arthritis (RA) be diagnosed as early as possible. New diagnostic markers were required, because rheumatoid factors (RF), until now criteria for classification of RA, are not sufficiently specific and sometimes appear late, thereby limiting their diagnostic usefulness. The objective of this review is to describe the current state of knowledge and more particularly to analyze the interest of new RA autoanti-bodies, called anti-peptide or anti-citrullinated protein anti-bodies (ACPA). Other autoanti-bodies have been described, including anti-Sa, anti-alpha enolase, and anti-calpastatin autoanti-bodies. Nonetheless, their diagnostic value remains limited compared to ACPA. Accordingly, in daily practice today, the only autoanti-bodies that must be tested for to diagnose RA are the ACPAs and RFs. The discovery of ACPA (initially called anti-keratin and anti-perinuclear anti-bodies) was a major step forward for the laboratory diagnosis of RA. The tests most often used routinely areenzyme-linked immunosorbent assays(ELISA) with cyclic citrullinated peptides, whence the name anti-CCP autoanti-bodies. Accordingly, the two terms ACPA and anti-CCP can both be used. The diagnostic value, in particular their specificity, is on the order of 95%, regardless of the method of identification. These markers are very useful and are often present earlier than RF. These ACPA also have prognostic value because they are associated with more aggressive forms of RA. On the other hand, their value over time, in particular, their fluctuation as a function of treatment, is more controversial. In practice, it is recommended to test for both RF and ACPA in a diagnostic work-up for early RA. During follow-up, the value of testing for these autoanti-bodies has not been demonstrated, but additional studies are still necessary with the anti-CCP autoanti-bodies and the new anti-citrullinated protein autoanti-bodies.

Sibilia J, Sordet C, Mrabet D, Wachsmann D. · Service de rhumatologie, CHU Strasbourg, EA physiopathologie des arthrites, Université Louis Pasteur. · Rev Prat. · Pubmed #16544924 No free full text.

Abstract: Rheumatoid arthritis is a common and severe inflammatory rheumatic disease, for which the immune mechanisms are being decoded little by little. The pathogenic ncludes significant cellular actors of innate immunity (fibroblastic synoviocytes, macrophages, mastocytes...) and adaptive immunity (T and B lymphocytes). These actors interact through the production of and response to specific (cytokines, chemokines and auto-antibodies) and non-specific (prostaglandins, nitrous oxide [NO], complement, proteases) mediators. The chronology of this rheumatoid synovitis is becoming progressively clearer. Its initiation could be the consequence of a precocious activation of the innate immunity, induced by bacterial agents or debris (PAMP). The activation of the synoviocytes and the macrophages via specific receptors (PPR) unleashes an intense inflammatory reaction that triggers a cascade of events. The ongoing nature of this synovitis leads to the intra-articular recruitment of different cells of immunity. This cellular afflux amplifies the macrophagic and synoviocytic activation and proliferation. All of these interactive phenomena end in the production of large quantities of pro-inflammatory cytokines (TNFa, IL1, IL6, IL15, IL17, IL18) but also other pathogenic mediators (auto-antibodies, complement, prostaglandins, nitrous oxide...). This synovitis persists, as it is no longer regulated by a sufficient production of physiological regulators (soluble receptors and inhibitors of cytokines). The consequence of this intense inflammation and synovial proliferation leads to osteo-articular destruction by the production of proteases and the activation of osteoclasts by the RANK/RANK-ligand pathway under the effect of cytokines (TNFa, IL5, IL1, IL6, IL17) and other mediators (prostaglandins) liberated by synoviocytes, macrophages and lymphocytes. The decryption of this puzzle has already created new therapeutic orientations. The identification of new targets is one of the major consequences of this progress in immuno-rheumatology.

Sordet C, Cantagrel A, Schaeverbeke T, Sibilia J. · Service de Rhumatologie, CHU de Strasbourg, France. · Joint Bone Spine. · Pubmed #16376804 No free full text.

Abstract: Primary immune deficiencies (PIDs) are characterized by functional and/or quantitative abnormalities of one or more immune system components. Several bone and joint abnormalities can occur in patients with PID, with arthritis being the most common. Joint manifestations, of which arthritis is the most common, occur chiefly in humoral PIDs (agammaglobulinemia, common variable immunodeficiency, hyper-IgM syndromes, and IgA deficiency) and occasionally in other PIDs (chronic granulomatous disease and Wiskott-Aldrich syndrome). Monoarthritis or oligoarthritis is the usual pattern, although polyarthritis may occur, occasionally with nodules suggesting rheumatoid arthritis. Arthritis in patients with PID is usually infectious in nature, the most common causative organism being Mycoplasma, followed by Staphylococcus, Streptococcus, and Haemophilus. These bacteria can induce not only synovial infections, but also aseptic arthritogenic inflammatory responses. Arthritis having no demonstrable relation to chronic infection has been reported also and ascribed to dysimmunity-driven mechanisms that exhibit a number of specific features. Bone lesions are far less common and usually due to infections complicating humoral PID. Distinctive bone manifestations occur in a number of rare PIDs (e.g., hyper-IgE syndrome and Di George syndrome) and in syndromes characterized by spondyloepiphyseal dysplasia. Familiarity with PID syndromes both enhances the diagnostic capabilities of physicians and provides insight into the pathophysiology of bone and joint abnormalities associated with immune dysfunction. In children and occasionally in adults, a combination of bone and/or joint manifestations and hypogammaglobulinemia may indicate PID. When there is no evidence of lymphoproliferative disease, infection, or iatrogenic complications, investigations for PID should be obtained. PID-related arthritis is a unique model for studying the pathogenesis of presumably postinfectious arthritis and of inflammatory joint diseases including rheumatoid arthritis.

Martinot M, Sordet C, Soubrier M, Puéchal X, Saraux A, Lioté F, Guggenbuhl P, Lègre V, Jaulhac B, Maillefert JF, Zeisel M, Coumaros G, Sibilia J. · Service de Pathologies Infectieuses et Tropicales, Médicale A - Hôpitaux Universitaires de Strasbourg and Service de Médecine Interne et de Rhumatologie, Hopital Pasteur, Colmar, France. · Clin Exp Rheumatol. · Pubmed #15971417 No free full text.

Abstract: OBJECTIVE: To determine the diagnostic value of serum and synovial procalcitonin (PCT) for bacterial arthritis and to determine the cellular origin of synovial PCT. METHODS: A prospective study enrolled 42 patients with acute arthritis including 11 bacterial arthritis, 18 rheumatoid arthritis and 13 crystal induced arthritis. Diagnostic values of serum and synovial PCT levels were determined by a immunoluminometric assay (Lumitest PCT) and compared to those of classical inflammatory markers (C-reactive protein, erythrocyte sedimentation rate, synovial fluid cellularity and both serum and synovial IL-6 and TNF alpha). Using fibroblast-like synoviocyte (FLS) cultures derived from rheumatoid arthritis (n = 4) and osteo-arthritis (n = 3) synovium, with or without stimulation by lipopolysaccharid or recombinant streptococcal protein 1/II, we attempted to determine whether synovial cells could be a source of PCT. RESULTS: Serum PCT was the best parameter to distinguish patients with acute bacterial arthritis from patients with crystal induced arthritis or rheumatoid arthritis. In setting of an acute arthritis serum PCT (> 0.5 ng/mL) achieved 55% sensitivity and 94% specificity for the diagnosis of bacterial arthritis, while CRP (> 50 mg/L) had 100% sensitivity but poor specificity (40%). Serum PCT appeared to be higher in patients with septic arthritis resulting from "systemic infection" than in cases resulting from direct inoculation. Synovial PCT was not useful to discriminate between infectious and non infectious arthritis in clinical practice. PCT could not be detected at significant levels in the conditioned medium from fibroblast-like synoviocyte cultures. CONCLUSION: Serum PCT is a poorly sensitive but specific marker of bacterial arthritis. Use of serum PCT in association with CRP could nevertheless be useful in an emergency situation for the diagnosis of bacterial arthritis.

El Bouchti I, Sordet C, Kuntz JL, Sibilia J. · Department of Rheumatology, Hautepierre Teaching Hospital, Strasbourg, France. · Joint Bone Spine. · Pubmed #18457979 No free full text.

Abstract: Rheumatoid arthritis (RA) is a chronic inflammatory joint disease whose main complication is accelerated atheroma responsible for high rates of cardiovascular morbidity and mortality. Hyperhomocysteinemia is among the factors incriminated in RA-associated atheroma. We managed a 46-year-old patient with RA who required admission to evaluate severe arterial and venous disease with involvement of the coronary, renal, and peripheral arteries. She had no laboratory evidence of rheumatoid vasculitis or conventional cardiovascular risk factors (diabetes and hypercholesterolemia) and had never smoked. Her serum homocysteine level was elevated to 20.9 micromol/L as a result of a homozygous C667T mutation in the methylenetetrahydrofolate (MTHFR) gene. Folate and vitamin B12 levels were normal. A circulating anticoagulant was identified. Hyperhomocysteinemia, which is defined as a homocysteine level greater than 15 micromol/L, is a risk factor for arterial and venous disease. Hyperhomocysteinemia is found in 20%-42% of patients with RA. Methotrexate therapy is the most common causative factor. Other causes include MTHFR deficiency, vitamin B12 deficiency, renal failure, old age, and smoking. Whatever the underlying cause, folic acid supplementation returns the homocysteine level to normal.

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.

Morel J, Deschamps V, Toussirot E, Pertuiset E, Sordet C, Kieffer P, Berthelot JM, Champagne H, Mariette X, Combe B. · Department of Immuno-Rheumatology, Montpellier I University and Lapeyronie Teaching Hospital, 34295 Montpellier, Cedex 5 France. · Ann Rheum Dis. · Pubmed #17604284 No free full text.

Abstract: OBJECTIVE: To date, only a few series of patients with paraneoplastic arthritis have been published. The charts of patients with cancer-associated arthritis were collected in order to describe characteristics of this rheumatism. METHODS: A questionnaire was created for this study and validated by experts based on specific criteria of inclusion and exclusion. Histology of neoplasia was included. RESULTS: In all, 16 males and 10 females with a mean (range) age of 57.5 years (28-85) were recruited from 17 nationwide centres in France. Patients presented with symmetric polyarthritis involving wrists and hands (85%) and extra-articular symptoms were frequent (84%). There was no specific biologic or radiographic feature. The mean (range) delay between the diagnosis of rheumatism and neoplasia was 3.6 months (0-21.2). Tumours were usually diagnosed after articular symptoms occurred (88.5%). Twenty patients had a solid cancer, and six a haematological malignancy. Adenocarcinoma of the lungs was the most frequent type of solid cancer (60%). Tumours were diagnosed at an early stage, which may explain the good median survival of 1.21 years (range 0.64-present) with a mean follow-up of 1.9 years (range 0.16-10). The percentage of articular symptoms resolution was significantly higher in patients with solid tumours, as compared to patients with haemopathy (p = 0.007). In cases of tumour relapse, rheumatic symptoms did not recur for 75% of patients. CONCLUSIONS: Underlying neoplasia should be considered in male patients with new onset polyarthritis, smokers, and particularly in patients chronically ill. Additional investigations should then be performed to diagnose cancer at an early stage.

Sordet C, Mrabet D, Ardizzone M, Marcellin L, Hirschorn P, Sibilia J. · Department of Rheumatology, CHU Strasbourg, 67098 Strasbourg Cedex, France; ORL, CHU Strasbourg, 67098 Strasbourg Cedex, France. · Eur J Intern Med. · Pubmed #17223048 No free full text.

Abstract: We report on a 65-year-old man who was hospitalized for polyarthritis with deterioration of his general state of health and chronic sinusitis. Clinical and biological signs led to the diagnosis of RA associated with localized Wegener's granulomatosis. Methotrexate and corticosteroids led to a distinct improvement in the patient's articular symptoms and in his general condition. One year after the start of treatment, a tumefaction of the right maxillary sinus appeared. Scans revealed a tumoral lesion in the right maxillary sinus. This proved to be a large B-cell lymphoma. The patient received chemotherapy (CHOP) and radiotherapy. This centrofacial lymphoma may be regarded as a B lymphoma of the MALT (mucosal associated lymphoma tumor) type, mimicking a relapse of Wegener's granulomatosis.

Seror R, Sordet C, Guillevin L, Hachulla E, Masson C, Ittah M, Candon S, Le Guern V, Aouba A, Sibilia J, Gottenberg JE, Mariette X. · Department of Rheumatology, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris, Université paris-Sud 11, INSERM U802, Le Kremlin Bicêtre, France. · Ann Rheum Dis. · Pubmed #16950808 No free full text.

Abstract: OBJECTIVE: To investigate the safety and efficacy of rituximab (RTX) for systemic symptoms in patients with primary Sjögren's syndrome (pSS), and changes in B cell biomarkers. PATIENTS AND METHODS: The records of 16 patients with pSS according to the American European consensus group criteria were reviewed retrospectively. RESULTS: Patients, all women, had a median age of 58.5 (range 41-71) years and a disease duration of 9.5 (range 0-25) years. RTX was prescribed for lymphoma (n = 5), refractory pulmonary disease with polysynovitis (n = 2), severe polysynovitis (n = 2), mixed cryoglobulinaemia (n = 5), thrombocytopenia (n = 1) and mononeuritis multiplex (n = 1). The median follow-up duration was 14.5 (range 2-48) months. Three patients experienced adverse events, including one mild serum sickness-like reaction with the presence of human antichimeric antibodies. Efficacy of treatment was observed in 4 of 5 patients with lymphomas and in 9 of 11 patients with systemic involvement. Dryness was improved in only a minority of patients. Corticosteroid dose was reduced in 11 patients. RTX induced decreased rheumatoid factor, gamma-globulin and beta2-microglobulin levels, and the level of B cell activating factor of the tumour necrosis factor family (BAFF) increased concomitantly with B cell depletion. Five patients were re-treated, with good efficacy and tolerance, except for one with probable serum sickness-like reaction. CONCLUSION: This study shows good efficacy and fair tolerance of RTX for systemic features. In addition, RTX allows for a marked reduction in corticosteroid use. Except for BAFF, the level of which increases, serum B cell biomarker levels decrease after taking RTX. Controlled trials should be performed to confirm the efficacy of RTX in pSS.

Danner S, Sordet C, Terzic J, Donato L, Velten M, Fischbach M, Sibilia J. · Department of Pediatry, Laboratory of Epidemiology, and Department of Rheumatology, CHU Hautepierre, Strasbourg, France. · J Rheumatol. · Pubmed #16821272 No free full text.

Abstract: OBJECTIVE: To determine the incidence, prevalence, and principal characteristics of the different forms of juvenile idiopathic arthritis (JIA) in the region of Alsace, northeastern France, using the new classification of the International League of Associations for Rheumatology (ILAR). METHODS: In 2002 we performed a retrospective epidemiologic study pertaining to the year 2001. The pediatricians, rheumatologists, ophthalmologists, orthopedic surgeons, and physicians involved in functional reeducation in the Alsace region were interviewed, and all patients were classified according to the new ILAR classification using the criteria revised in Durban in 1997. RESULTS: Among the 361 clinicians contacted, the participation rate was 97.8%. The study identified 67 children followed for JIA in Alsace in 2001, from a total population of 1.8 million inhabitants including 339,095 children under age 16 years. The incidence was calculated to be 3.2 cases/100,000/year and the prevalence 19.8 cases/100,000 children under age 16 years. Among these 67 cases of JIA, the most frequent forms were oligoarthritis (n = 27, 40.3%), polyarthritis without rheumatoid factor (RF; n = 15, 22.4%), and enthesitis related arthritis (n = 12, 17.9%). Other forms, notably systemic arthritis (n = 6, 8.9%) and psoriatic arthritis (n = 3, 4.5%), were more rare and in this study there was no case of polyarthritis with RF. Only 4 patients (6%) were classified in the undifferentiated arthritis group using the new classification. Antinuclear antibodies (ANA; by indirect immunofluorescence, HEp >/= 1/80) were detected in patients with oligoarthritis (81%) and polyarthritis without RF (79%). Uveitis occurred in 41% of children with oligoarthritis and in 14% of those with polyarthritis without RF. CONCLUSION: Our results are comparable to those of other studies carried out in Caucasian populations with regard to incidence and prevalence. This work also highlights the frequent presence of ANA and uveitis in patients with oligoarthritis or polyarthritis without RF.

Avouac J, Sordet C, Depinay C, Ardizonne M, Vacher-Lavenu MC, Sibilia J, Kahan A, Allanore Y. · René Descartes University, Medical Faculty, Hôpital Cochin, France. · Arthritis Rheum. · Pubmed #16802363 links to  free full text

Abstract: OBJECTIVE: To determine the prevalence of sicca symptoms and Sjögren's syndrome (SS) in a 2-center prospective series of patients with systemic sclerosis (SSc), using the American-European Consensus Group criteria for SS. METHODS: Consecutive SSc patients hospitalized for followup care were evaluated for sicca symptoms. When the initial clinical evaluation yielded positive findings, a labial salivary gland biopsy was performed; histologic analysis evaluated focal lymphocytic sialadenitis and/or glandular fibrosis. Computed tomography and respiratory function tests were used to assess pulmonary fibrosis. RESULTS: We included 133 SSc patients (mean +/- SD age 55 +/- 13 years; mean +/- SD disease duration 6.5 +/- 6 years). Eighty-one patients had limited cutaneous SSc (lcSSc). Ninety-one patients (68%) had sicca syndrome. Histologic analysis revealed fibrotic involvement in 50 of these 91 patients, but labial salivary gland fibrosis was not associated with any organ involvement we evaluated. Nineteen of the 133 patients (14%) had SS. In this subgroup, lcSSc was present at a significantly higher frequency (18 of 19 patients) than in the remaining patients with sicca syndrome (39 of 72 patients) and the patients without sicca syndrome (24 of 42 patients). This subgroup also had a significantly higher frequency of anticentromere antibodies (18 of 19 patients) than did the remaining patients with sicca syndrome (19 of 72 patients) and the patients without sicca syndrome (5 of 42 patients). In addition, this subgroup had a significantly lower prevalence of pulmonary fibrosis (2 of 19 patients) than did the remaining patients with sicca syndrome (29 of 72 patients) and the patients without sicca syndrome (19 of 42 patients). CONCLUSION: There was a 68% prevalence of sicca syndrome in this prospective series of SSc patients. Sicca syndrome was related primarily to glandular fibrosis, the hallmark of SSc. The prevalence of secondary SS, as defined by the American-European Consensus Group criteria, was 14% and was markedly associated with lcSSc. We believe that lcSSc should be regarded as a specific autoimmune subgroup of SSc.

Gottenberg JE, Aucouturier F, Goetz J, Sordet C, Jahn I, Busson M, Cayuela JM, Sibilia J, Mariette X. · Rhumatologie, Université Paris-Sud 11, INSERM U802, Hôpital Bicêtre, Assistance Publique des Hôpitaux de Paris, Le Kremlin Bicêtre, France. · Ann Rheum Dis. · Pubmed #16569685 No free full text.

Abstract: BACKGROUND: B cell activation may result in an increased secretion of immunoglobulin free light chains (FLCs) in autoimmune diseases. OBJECTIVE: To analyse serum FLC levels in patients with rheumatoid arthritis and in those with primary Sjögren's syndrome (pSS). PATIENTS AND METHODS: Blood samples were collected from 80 healthy blood donors, 50 patients with rheumatoid arthritis and 139 patients with pSS. Serum FLC level was measured using a new quantitative immunoassay. RESULTS: Mean (standard error (SE)) serum kappa and lambda FLC levels were significantly higher in patients with rheumatoid arthritis and in those with pSS than in controls (kappa : 18.9 (1.1) and 16.3 (1.4) v 10.5 (0.4) mg/l, p<0.001 and p = 0.001, respectively; lambda: 16.7 (1.2) and 19.3 (1.5) v 11.6 (0.6) mg/l, p<0.001 for both). 18 (36%) patients with rheumatoid arthritis and 31 (22.3%) patients with pSS had abnormal serum FLC levels (increased kappa or lambda levels and abnormal ratio of kappa:lambda). Serum kappa and lambda levels were correlated with other B cell activation markers in both diseases. FLC levels increased with disease activity, because, unlike total gammaglobulin and immunoglobulin G levels, they were significantly correlated with Disease Activity Score 28 in patients with rheumatoid arthritis (p = 0.004 for kappa, p = 0.05 for lambda) and with extraglandular involvement in pSS (p = 0.01 for kappa, p = 0.04 for lambda). CONCLUSION: FLC levels are increased and correlate with disease activity in patients with rheumatoid arthritis and in those with pSS, two diseases in which increased risk of lymphoma could result from persistent B cell activation and disease activity. Further studies are required to determine whether FLC assessment could represent a relevant biomarker for response to treatment (especially B cell depletion) and for the risk of lymphoma in autoimmune diseases.

Gottenberg JE, Sellam J, Ittah M, Lavie F, Proust A, Zouali H, Sordet C, Sibilia J, Kimberly RP, Mariette X, Miceli-Richard C. · Rhumatologie, INSERM E 109, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris, Université Paris-Sud 11, Le Kremlin Bicêtre, France. · Arthritis Res Ther. · Pubmed #16507129 links to  free full text

Abstract: Polyclonal B cell activation might be related to pathogenic over-expression of B-cell-activating factor (BAFF) in primary Sjögren's syndrome (pSS) and other autoimmune diseases. We therefore investigated whether BAFF over-expression in pSS could be a primary, genetically determined event that leads to the disease. The complete BAFF gene was sequenced in Caucasian pSS patients and control individuals. The only single nucleotide polymorphism frequently observed, namely -871 T/C in the promoter region, was then genotyped in 162 French patients with pSS and 90 French control individuals. No significant differences in allele (T allele frequency: 49.7% in patients with pSS versus 50% in controls; P = 0.94) and genotype frequencies of BAFF polymorphism were detected between pSS patients and control individuals. BAFF gene polymorphism was not associated with a specific pattern of antibody secretion either. T allele carriers had significantly increased BAFF protein serum levels (mean values of 8.6 and 5.7 ng/ml in patients with TT and TC genotypes, respectively, versus 3.3 ng/ml in patients with CC genotype; P = 0.01), although no correlation was observed between BAFF polymorphism and mRNA level. In conclusion, BAFF gene polymorphism is neither involved in genetic predisposition to pSS nor associated with a specific pattern of antibody production.

Andrès E, Blicklé F, Sordet C, Cohen-Solal J, Sibilia J, Sapin R. · No affiliation provided · Am J Med. · Pubmed #16750953 No free full text.

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Sordet C, Gottenberg JE, Goetz J, Bengoufa D, Humbel RL, Mariette X, Sibilia J. · No affiliation provided · Ann Rheum Dis. · Pubmed #16014693 links to  free full text

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Sordet C, Gottenberg JE, Hellmich B, Kieffer P, Mariette X, Sibilia J. · No affiliation provided · Ann Rheum Dis. · Pubmed #15647445 links to  free full text

This publication has no abstract.