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1.
Osteoporos Int ; 29(8): 1897-1903, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29951868

RESUMO

This is the first study that has found that rehabilitation services (RS) intervention, following the onset of rheumatoid arthritis (RA), may significantly reduce the risk of osteoporosis in RA patients. Those patients who received more than five sessions of RS had the greatest benefit for the prevention of osteoporosis. INTRODUCTION: People with rheumatoid arthritis have increased risk of developing osteoporosis (OP). It remains unclear whether use of rehabilitation services can reduce the risk of developing OP. We conducted a longitudinal cohort study to compare the effect of RS on the risk of OP in Taiwanese individuals with RA. METHODS: A national health insurance database was used to identify 2693 newly diagnosed RA patients, 20-70 years old, between 1998 and 2007. Among them, 808 received RS after the onset of RA (RS users) and 1885 patients did not receive RS (non-RS users). All enrollees were followed until the end of 2012 to record incident cases of OP. A Cox proportional hazards regression model was used to compute adjusted hazard ratios (aHRs) for the relationship of use of RS with OP. RESULTS: During the 15-year follow-up, 358 RS users and 1238 non-RS users developed OP, corresponding to incidence rates of 87.24 and 129.27 per 1000 person-years, respectively. Use of RS was significantly associated with a lower risk of OP (aHR 0.62; 95% confidence interval [CI] = 0.56-0.71). Those who received more than five sessions of RS had the greatest benefit (aHR 0.47; 95% CI = 0.38-0.56). CONCLUSIONS: The integration of RS into the clinical management of patients with RA may decrease their risk of developing OP.


Assuntos
Artrite Reumatoide/reabilitação , Osteoporose/prevenção & controle , Adulto , Idoso , Artrite Reumatoide/complicações , Artrite Reumatoide/epidemiologia , Estudos de Coortes , Comorbidade , Bases de Dados Factuais , Feminino , Humanos , Incidência , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Osteoporose/epidemiologia , Osteoporose/etiologia , Medição de Risco/métodos , Taiwan/epidemiologia , Adulto Jovem
2.
Clin Exp Immunol ; 151(3): 383-90, 2008 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-18190609

RESUMO

Decoy receptor 3 (DcR3/TR6) is a decoy receptor for the Fas ligand (FasL) and can inhibit FasL-induced apoptosis. It has been reported recently that DcR3 can induce T cell activation via co-stimulation of T cells, suggesting that DcR3 may be involved in the pathophysiology of autoimmune diseases. This study aims to analyse the serum DcR3 in patients with systemic lupus erythematosus (SLE) and to investigate the role of DcR3 in the pathogenesis of SLE. Significantly elevated serum DcR3 was observed in SLE patients, and the mean serum DcR3 level was significantly higher for those with active disease [SLE disease activity index (SLEDAI) >/= 10] compared with that in patients with inactive disease (SLEDAI < 10). In addition to reducing activation-induced cell death in activated T cells via neutralization of the FasL, soluble DcR3-Fc enhanced T cell proliferation and increased interleukin-2 and interferon-gamma production via co-stimulation of T cells. Moreover, enhanced T cell reactivity to DcR3-induced co-stimulation was demonstrated in lymphocytes from patients with SLE, suggesting the elevated serum DcR3 may associate with enhanced T cell activation in vivo. These findings are the first to demonstrate that serum DcR3 concentrations are increased in SLE patients, and this may imply a possible role of DcR3 in the pathogenesis of SLE via enhanced T cell hyperreactivity and reduced apoptosis in activated T cells.


Assuntos
Lúpus Eritematoso Sistêmico/imunologia , Ativação Linfocitária/imunologia , Membro 6b de Receptores do Fator de Necrose Tumoral/sangue , Linfócitos T/imunologia , Adulto , Apoptose/imunologia , Proliferação de Células , Células Cultivadas , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Índice de Gravidade de Doença
3.
Phys Rev C Nucl Phys ; 51(6): 3427-3434, 1995 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-9970447
5.
Phys Rev C Nucl Phys ; 44(2): 738-746, 1991 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-9967458
6.
Phys Rev C Nucl Phys ; 43(3): R935-R938, 1991 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-9967200
8.
Phys Rev C Nucl Phys ; 41(6): 2940-2942, 1990 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-9966680
11.
Phys Rev Lett ; 59(20): 2384, 1987 Nov 16.
Artigo em Inglês | MEDLINE | ID: mdl-10035533
12.
13.
Phys Rev C Nucl Phys ; 35(5): 1844-1850, 1987 May.
Artigo em Inglês | MEDLINE | ID: mdl-9953970
15.
Phys Rev C Nucl Phys ; 34(6): 2351-2352, 1986 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-9953724
16.
Phys Rev C Nucl Phys ; 34(5): 1845-1854, 1986 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-9953649
17.
Phys Rev Lett ; 57(8): 968-971, 1986 Aug 25.
Artigo em Inglês | MEDLINE | ID: mdl-10034212
19.
20.
Phys Rev C Nucl Phys ; 31(2): 510-514, 1985 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-9952547
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