High prevalence of metabolic syndrome in antisynthetase syndrome
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Citações na Scopus
18
Tipo de produção
article
Data de publicação
2018
Título da Revista
ISSN da Revista
Título do Volume
Editora
CLINICAL & EXPER RHEUMATOLOGY
Citação
CLINICAL AND EXPERIMENTAL RHEUMATOLOGY, v.36, n.2, p.241-247, 2018
Resumo
Objective A high frequency of metabolic syndrome (MetS) has been recently described in different idiopathic inflammatory myopathies, but not in antisynthetase syndrome (ASS). Therefore, the aim of the present study was to determine the prevalence of MetS in ASS and also its possible association with cardiovascular the risk factors and ASS-related disease characteristics. Methods A cross-sectional single centre study of 42 consecutive ASS patients was conducted from 2012 to 2015 and compared to 84 healthy individuals matched for gender, age, ethnicity and body mass index-matched (control group). MetS was defined according to the 2009 Join Interim Statement. Clinical and laboratory data were assessed according to a standardised protocol. Results ASS patients had a median age of 41.1 years with a predominance of female gender and white race. ASS patients had a higher frequency of MetS (42.9% vs. 13.1%; p<0.001) as well as of insulin resistance than controls. Moreover, ASS patients had higher resistin, lower leptin and similar adiponectin levels in serum than controls. Further analysis of ASS patients with (n=18) and without (n=24) MetS revealed that older age at disease onset (48.7 vs. 35.4 years; p<0.001) was identified in those with the syndrome but were similar regarding disease duration, disease status, treatment, insulin resistance and serum adipocytokine levels. Conclusion The prevalence of MetS was high in ASS patients that also had serum resistin and low leptin levels. As also identified in other idiopathic inflammatory myopathies, MetS in ASS is more prevalent in older patients.
Palavras-chave
antisynthetase syndrome, cardiovascular diseases, idiopathic inflammatory myopathies, metabolic syndrome, myosins
Referências
- Abella V, 2017, NAT REV RHEUMATOL, V13, P100, DOI 10.1038/nrrheum.2016.209
- Alberti KGMM, 2009, CIRCULATION, V120, P1640, DOI 10.1161/CIRCULATIONAHA.109.192644
- BOHAN A, 1975, NEW ENGL J MED, V292, P344, DOI 10.1056/NEJM197502132920706
- Bruce Bonnie, 2003, Health Qual Life Outcomes, V1, P20, DOI 10.1186/1477-7525-1-20
- de Souza FHC, 2013, REV BRAS REUMATOL, V53, P352, DOI 10.1590/S0482-50042013000400007
- Craig CL, 2003, MED SCI SPORT EXER, V35, P1381, DOI 10.1249/01.MSS.0000078924.61453.FB
- de Moraes MT, 2013, ARTHRIT CARE RES, V65, P793, DOI 10.1002/acr.21879
- de Souza FHC, 2014, CLIN EXP RHEUMATOL, V32, P82
- Delaigle AM, 2004, ENDOCRINOLOGY, V145, P5589, DOI 10.1210/en.2004-0503
- Filkova M, 2012, ARTHRITIS RES THER, V14, DOI 10.1186/ar3836
- Ghirardello A, 2017, CLIN EXP RHEUMATOL, V35, P176
- Harris-Love MO, 2009, RHEUMATOLOGY, V48, P134, DOI 10.1093/rheumatology/ken441
- Hosseini Z, 2016, NUTR RES REV, V29, P152, DOI 10.1017/S095442241600007X
- Kaur J, 2014, CARDIOL RES PRACT, DOI 10.1155/2014/943162
- Le Clanche S, 2016, BIOCHIMIE, V121, P238, DOI 10.1016/j.biochi.2015.12.008
- Lega JC, 2014, AUTOIMMUN REV, V13, P883, DOI 10.1016/j.autrev.2014.03.004
- LOVE LA, 1991, MEDICINE, V70, P360, DOI 10.1097/00005792-199111000-00002
- MATTHEWS DR, 1985, DIABETOLOGIA, V28, P412, DOI 10.1007/BF00280883
- Mika A, 2017, OBES REV, V18, P247, DOI 10.1111/obr.12475
- Miller FW, 2001, RHEUMATOLOGY, V40, P1262, DOI 10.1093/rheumatology/40.11.1262
- Nolan JJ, 2012, DIABETOLOGIA, V55, P2863, DOI 10.1007/s00125-012-2684-0
- Orlandi M, 2016, CLIN EXP RHEUMATOL, V34, P966
- Popa C, 2005, ANN RHEUM DIS, V64, P1195, DOI 10.1136/ard.2004.032243
- Rider LG, 1997, ARTHRITIS RHEUM, V40, P1976, DOI 10.1002/art.1780401109
- Rider Lisa G., 2003, Journal of Rheumatology, V30, P603
- Sada KE, 2006, J RHEUMATOL, V33, P1545
- Shinjo SK, 2010, REV BRAS REUMATOL, V50, P496
- Silva MG, 2016, CLINICS, V71, P709, DOI 10.6061/clinics/2016(12)06