Rheumatoid Arthritis: Delle Monache F

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A digest of articles written 1999 and later, on the topic "Arthritis, Rheumatoid," originating from Planet Earth —» Delle Monache F.  Display:  All Citations ·  All Abstracts
1 Review [Recent views on the pathogenesis of cardiovascular damage associated with rheumatoid arthritis] 2005

Bocci EB, Delle Monache F, Angrisani MC, Gerli R. · Sezione di Medicina Interna e Scienze Oncologiche, Centro per lo Studio delle Malattie Reumatiche, Dipartimento di Medicina Clinica e Sperimentale, Università degli Studi, Perugia. · Recenti Prog Med. · Pubmed #15844764 No free full text.

Abstract: Cardiovascular disease is the commonest cause of premature mortality in rheumatoid arthritis and several data have shown that rheumatoid arthritis is an independent risk factor for the development of atherosclerotic disease. In last years it has become evident that atherosclerosis is an immune-mediated inflammatory disorder sharing a number of pathogenic features with rheumatoid arthritis. It is conceivable, therefore, that chronically raised concentrations of proinflammatory cytokines and pathological immune response characterizing rheumatoid arthritis may play a key role in inducing acceleration of atherosclerotic processes and, consequently, in the development of cardiovascular disease in these patients.

2 Article Precocious intima-media thickening in patients with primary Sjögren's syndrome. free! 2005

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.

3 Article [Subclinical atherosclerosis in young patients with rheumatoid arthritis and low disease activity] free! 2005

Bartoloni Bocci E, Marchesi S, Delle Monache F, Vaudo G, Giordano A, Ragni Alunni F, Angrisani C, Mannarino E, Shoenfeld Y, Gerli R. · Centro per lo Studio delle Malattie Reumatiche, Sez. di Medicina Interna e Scienze Oncologiche, Policlinico di Monteluce, 06122 Perugia. · Reumatismo. · Pubmed #15776142 links to  free full text

Abstract: BACKGROUND: There is an increasing body of evidence suggesting that subjects with rheumatoid arthritis (RA) are characterized by acceleration of atherosclerotic process of arterial wall. However, all investigations performed so far to evaluate subclinical atherosclerosis in RA included subjects without selection for age and degree of disease activity that may represent confounding factors in such an evaluation. OBJECTIVES: To verify signs of accelerated subclinical atherosclerosis in young subject suffering from RA but with low disease activity. METHODS: Thirty-two patients with RA and 28 age- and sex-matched control subjects with non-inflammatory rheumatic diseases were enrolled. Inclusion criteria were age less than 60 and low disease activity with score < or =3.2 according to DAS28, while subjects with traditional risk factors for and/or overt cardiovascular disease were ruled out from the study. Both patients and controls underwent evaluation of carotid and femoral artery intima-media thickness by ultrasounds. RESULTS: Patients had higher intima-media thickness than controls of all the sites evaluated at carotid artery level, whereas there were no differences at the comparison of the superficial and common femoral artery wall. At the univariate analysis, a positive correlation between LDL cholesterol levels and intima-media thickness at the carotid bifurcation was found. CONCLUSIONS: Young patients with RA and low disease activity have acceleration of atherosclerosis development as shown by increased intima-media thickness of carotid artery with respect to subjects without inflammatory rheumatic disease. It is conceivable that the organic damage of arterial wall could be the result of persistent endothelial dysfunction induced by chronic inflammation and immune dysregulation which characterize RA.