Please use this identifier to cite or link to this item:
|標題:||Serum insulin-like growth factor-axis and matrix metalloproteinases in patients with rheumatic arthritis or rheumatic heart disease||作者:||Lee, S.D.
|關鍵字:||endocrine system;GH-IGF-axis;MMPs;rheumatic heart disease;factor-i;igf-i;interleukin-10;hormone;failure;cytokines;fever;association;expression;therapy||Project:||Clinica Chimica Acta||期刊/報告no：:||Clinica Chimica Acta, Volume 367, Issue 1-2, Page(s) 62-68.||摘要:||
Background: Insulin-like growth factor (IGF)-I plays an important role for maintaining cardiac functions. We clarified the unknown role of IGF-axis in rheumatic heart disease (RHD). Method: Interleukin (IL)-10, growth hormone (GH), IGF, IGF binding protein (IGFBP)-3 and matrix metalloproteinase (MMP) were measured by ELISA and zymography in 30 age range-matched normal subjects (control), 36 patients with acute phase of rheumatoid arthritis (RA) with positive rheumatoid factor (RF) and C-reactive protein (CRP), and in 43 patients with RHD with negative RF and CRP. Result: Compared with normal subjects, increased IL-10 level and decreased GH were found in RA group whereas unchanged IL-10 and decreased GH were found in RHD group. Compared with age range-matched normal subjects, decreased IGFBP-3, MMP-9 levels, unchanged IGF-I were found in RA group whereas decreased IGF-I levels, unchanged IGFBP3 and increased MMP-9 at age > 30 years were found in RHD group. IGF-II was not changed in RA and RHD groups. Conclusion: These findings may imply that during inflammatory phase, the levels of anti-inflammation was high and total lGF-I and IGF bioavailability were maintained in patients with RA. Our findings in RHD may speculate that the long-term reduction of GH and lGF-I as well as the compensating effects of upregulated MMP-9 activity may be partially involved in the long-term pathogenesis from RHD to heart failure. Decreased GH, decreased IGF-I and increased MMP-9 activities may be possible diagnostic markers in RHD for developing heart failure. (c) 2005 Elsevier B.V. All rights reserved.
|Appears in Collections:||獸醫病理生物學所|
Show full item record
TAIR Related Article
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.