Rheumatoid Arthritis: Vitali C

Vitali C. · Department of Internal Medicine and Section of Rheumatology, 'Villamarina' Hospital, Piombino, Italy. · Rheum Dis Clin North Am. · Pubmed #18984415 No free full text.

Abstract: Sjögren's syndrome (SS) is a systemic autoimmune disease that is characterized by an aggressive autoimmune response to epithelia, with consequent reduction of their secretions accompanied by sicca complaints. Systemic features may also be present in a subset of patients and may require more aggressive therapies. Improvements in knowledge concerning disease pathophysiology, combined with the availability of specifically targeted therapies able to modulate or block some of the most important pathologic mechanisms of the disease, may open totally new perspectives in the therapeutic approach to SS. The absence of reliable and validated outcome measures for SS is a major obstacle in performing clinical trials of new therapies in SS but studies devoted to defining outcome measurement instruments for this disorder have been performed or are in an advanced phases of completion.

Vitali C, Bombardieri S, Jonsson R, Moutsopoulos HM, Alexander EL, Carsons SE, Daniels TE, Fox PC, Fox RI, Kassan SS, Pillemer SR, Talal N, Weisman MH, Anonymous00126. · Department of Internal Medicine and Rheumatology, Ospedale Villamaria, Piombino, LI, Italy. · Ann Rheum Dis. · Pubmed #12006334 links to  free full text

Abstract: Classification criteria for Sjögren's syndrome (SS) were developed and validated between 1989 and 1996 by the European Study Group on Classification Criteria for SS, and broadly accepted. These have been re-examined by consensus group members, who have introduced some modifications, more clearly defined the rules for classifying patients with primary or secondary SS, and provided more precise exclusion criteria.

Bowman SJ, Pillemer S, Jonsson R, Asmussen K, Vitali C, Manthorpe R, Sutcliffe N, Anonymous00266. · Rheumatology Department, Division of Immunity and Infection, The Medical School, University of Birmingham, UK. · Rheumatology (Oxford). · Pubmed #11600750 links to  free full text

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Vitali C, Palombi G, Baldini C, Benucci M, Bombardieri S, Covelli M, Del Papa N, De Vita S, Epis O, Franceschini F, Gerli R, Govoni M, Bongi SM, Maglione W, Migliaresi S, Montecucco C, Orefice M, Priori R, Tavoni A, Valesini G. · Villamarina Hospital, Piombino, Italy. · Arthritis Rheum. · Pubmed #17599741 links to  free full text

Abstract: OBJECTIVE: To develop valid instruments for the assessment of disease-related damage and disease activity in Sjögren's syndrome (SS). METHODS: Data on 206 patients with primary SS were collected in 12 Italian centers. Each patient was scored by 1 investigator, on the basis of a global assessment of the degree of disease damage and disease activity. Patients judged to have active disease at the time of enrollment underwent a second evaluation after 3 months. Univariate and multivariate analyses were performed to select the clinical and serologic variables that were the best predictors of damage and of disease activity, and these variables were used to construct the Sjögren's Syndrome Disease Damage Index (SSDDI) and the Sjögren's Syndrome Disease Activity Index (SSDAI). The weight of each variable in the index was determined by the beta coefficients in multivariate regression models. Scores obtained using the SSDDI and the SSDAI were compared with scores initially given by the investigators. Finally, a receiver operating characteristic (ROC) curve was used to determine the cutoff value in the SSDAI with the highest level of accuracy in identifying patients with a significant level of disease activity. RESULTS: A multivariate model with 9 variables was the best predictor of investigator scores of damage. The scores obtained using the SSDDI were closely correlated with investigator ratings (R = 0.760, P < 0.0001). A model composed of 11 variables was the best predictor of investigator scores of disease activity. The scores obtained using the SSDAI were strongly correlated with the investigator ratings both at the time of enrollment and 3 months after enrollment (R = 0.872, P < 0.0001, and R = 0.817, P < 0.0001, respectively). The differences between scores given by investigators at study enrollment and after 3 months, a measure of variation of disease activity over time, were also closely correlated with the differences calculated using the SSDAI (R = 0.683, P < 0.0001). The ROC curve analysis showed that patients with the highest level of disease activity could be identified on the basis of an SSDAI score of >or=5. CONCLUSION: Our findings indicate that the SSDDI is an adequate instrument to objectively measure damage in patients with SS, and that the SSDAI is a valid tool to measure disease activity when used either as a single-state index or as a transition index.

Vaudo G, Bocci EB, Shoenfeld Y, Schillaci G, Wu R, Del Papa N, Vitali C, Delle Monache F, Marchesi S, Mannarino E, Gerli R. · University of Perugia, Perugia, Italy. · Arthritis Rheum. · Pubmed #16320337 links to  free full text

Abstract: OBJECTIVE: Systemic lupus erythematosus and rheumatoid arthritis represent independent risk factors for atherosclerosis (ATS), although this may be confounded by continuous pharmacologic treatment. Primary Sjögren's syndrome (SS) shares several features of these diseases and may therefore represent an interesting model for verifying the presence of accelerated ATS in the absence of pharmacologic interference. The present study therefore used this model to describe the presence of accelerated ATS in a group of young women. METHODS: Thirty-seven untreated white women with primary SS were evaluated clinically and serologically. Carotid and femoral artery intima-media thickness (IMT) was evaluated in the patients and in 35 age-matched healthy women who served as controls. RESULTS: The patients had a higher IMT than did the controls at both the carotid (mean +/- SD 0.82 +/- 0.24 mm versus 0.63 +/- 0.20 mm; P < or = 0.001) and the femoral (0.81 +/- 0.26 mm versus 0.67 +/- 0.23 mm; P < or = 0.019) levels, and had a higher prevalence of carotid intima-media thickening (49% versus 11% of controls; P < or = 0.001). The patient subset with high carotid IMT showed an increased prevalence of leukopenia and circulating anti-SSA antibodies; interestingly, the number of leukocytes was inversely correlated with the level of arterial IMT in patients with SS. Multivariate analysis demonstrated that anti-SSA antibodies were independent predictors of carotid artery thickening, while leukopenia was a predictor of both carotid and femoral artery thickening. CONCLUSION: Subclinical ATS was evident in about one-half of the patients with SS. Its association with some features typical of connective tissue diseases, such as the presence of anti-SSA and leukopenia, suggests that the immune dysregulation characterizing this autoimmune disorder may play a key role in inducing early ATS.

Tzioufas AG, Wassmuth R, Dafni UG, Guialis A, Haga HJ, Isenberg DA, Jonsson R, Kalden JR, Kiener H, Sakarellos C, Smolen JS, Sutcliffe N, Vitali C, Yiannaki E, Moutsopoulos HM. · Department of Pathophysiology, School of Medicine, University of Athens, Greece. · Ann Rheum Dis. · Pubmed #11959762 links to  free full text

Abstract: OBJECTIVES: To investigate the clinical and immunogenetic aspects of antibody formation against Ro/SSA and La/SSB as well as their linear B cell epitopes in patients with primary Sjögren's syndrome (pSS) from different European countries. PATIENTS AND METHODS: Ninety patients with pSS from six European centres were studied. Serum samples from all patients were tested in a control laboratory for anti-Ro/SSA and anti-La/SSB autoantibodies by RNA precipitation assay and autoantibodies to the previously reported B cell linear epitopes of Ro 60 kDa (p169-190aa and p211-232aa) and La/SSB (p147-154aa, p291-302aa, p301-318aa, and p349-364aa). DNA from 88 patients was used for the determination of HLA-DRB1, -DQA1, and -DQB1 genotypes. Analysis of the results was performed in the 88 patients who were genotyped and tested also for antipeptide antibodies. RESULTS: Antibodies to B cell epitopes of Ro 60 kDa were detected at a low frequency (range 10-37%). In contrast, B cell epitopes of La/SSB were detected frequently (range 58-86%) among the anti-La/SSB positive sera. Autoantibodies to the La/SSB epitope, p349-364aa, were significantly positively associated with longer disease duration (p<0.05), recurrent or permanent parotid gland enlargement (p<0.005), and a higher proportion of non-exocrine manifestations (p<0.005), compared with patients without autoantibodies. The presence of anti-Ro/SSA and anti-La/SSB autoantibodies was significantly associated with the presence of HLA-DRB1*03 and DQB1*02 (p=0.038 and p=0.034, respectively). This association was even more prominent and extended to HLA-DQA1*0501 when patients were stratified according the presence of autoantibodies to discrete La/SSB B cell epitopes in comparison with autoantibody negative patients (p<0.01). They were found also to be highly associated with the alleles HLA-DQB1*02 and HLA-DQA1*0501 as well as the presence of a shared amino acid motif in the region 59-69aa of DQB1 first domain (p<0.01, respectively). CONCLUSIONS: Autoantibodies against La/SSB, binding to four synthetic peptides, derived from the sequence of the La protein were identified with increased frequency in sera of patients with pSS. The formation of autoantibodies against B cell epitope analogues of La/SSB in European patients with pSS may be dependent on the presence of a permissive HLA-DQ heterodimer, most prominently represented by the HLA-DQA1*0501/DQB1*0201 heterodimer, suggesting that a model of HLA restricted presentation of La/SSB peptide determinants is crucial for the autoimmune response against La/SSB.

Tavoni A, Vitali C, Cirigliano G, Frigelli S, Stampacchia G, Bombardieri S. · University of Pisa, Italy. · Arthritis Rheum. · Pubmed #10524701 links to  free full text

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Aragona P, Magazzù G, Macchia G, Bartolone S, Di Pasquale G, Vitali C, Ferreri G. · Institute of Ophthalmology, Institute of Paediatrics and Department of Internal Medicine, University of Messina, Italy. · J Rheumatol. · Pubmed #10381048 No free full text.

Abstract: OBJECTIVE: Helicobacter pylori infection elicits a local and systemic immune response against bacterial antigens, including a heat-shock protein of 60 kDa (HSP60). The homology between microbial and human HSP suggests that the immune response to bacterial HSP may play a role in the pathogenesis of autoimmune disorders. Since gastric involvement and H. pylori have been reported in Sjögren's syndrome (SS), we investigated the prevalence of antibodies against H. pylori and its specific HSP60 in sera from patients with SS. METHODS: Four groups of patients were studied. Group 1, 34 patients with primary SS (pSS); Group 2.19 patients with secondary SS; Group 3, 22 patients with various autoimmune diseases and Group 4, 43 healthy controls. Serum IgG levels against HSP60 were determined by an ELISA using recombinant full length HSP60 expressed in Escherichia coli, as the antigen. To confirm the H. pylori infection, a commercial ELISA was used. RESULTS: Out of 34 patients in Group 1, 27 (79.4%) and 30 (88.2%) had antibodies against H. pylori and its HSP60, respectively. The prevalence was significantly higher than that found in Group 3 (18.2%, p < 0.0001 and 27.3%, p < 0.0001) and in Group 4 (48.8%, p < 0.005 and 37.2%, p < 0.0001) but not than that of Group 2 (48.8% and 37.2%). If the prevalence of patients either positive or negative for both antibodies was considered, a statistically significant difference was found between Group I and respectively Groups 3 and 4. CONCLUSION: The hypothetical role of HSP60 in the development of the immune response both in pSS and secondary SS seems strictly linked to the prevalence rate of H. pylori infection.

Gerli R, Bartoloni Bocci E, Vaudo G, Marchesi S, Vitali C, Shoenfeld Y. · No affiliation provided · Rheumatology (Oxford). · Pubmed #17043043 links to  free full text

This publication has no abstract.

Vitali C. · No affiliation provided · Ann Rheum Dis. · Pubmed #12480687 links to  free full text

This publication has no abstract.