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Association between plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphism and circulating PAI-1 level in systemic lupus erythematosus and rheumatoid arthritis A meta-analysisopen accessZusammenhang zwischen PAI-1(Plasminogenaktivator-Inhibitor)-4G/5G-Polymorphismus und zirkulierendem PAI-1 bei systemischem Lupus erythematosus und rheumatoider Arthritis: Eine Metaanalyse

Other Titles
Zusammenhang zwischen PAI-1(Plasminogenaktivator-Inhibitor)-4G/5G-Polymorphismus und zirkulierendem PAI-1 bei systemischem Lupus erythematosus und rheumatoider Arthritis: Eine Metaanalyse
Authors
Bae, Sang CheolLee, Young Ho
Issue Date
Apr-2020
Publisher
SPRINGER HEIDELBERG
Keywords
Matrix metalloproteinases; Serine proteinase inhibitors; Polymorphism; genetic; Autoimmune diseases; Case-control studies
Citation
ZEITSCHRIFT FUR RHEUMATOLOGIE, v.79, no.3, pp.312 - 318
Indexed
SCIE
SCOPUS
Journal Title
ZEITSCHRIFT FUR RHEUMATOLOGIE
Volume
79
Number
3
Start Page
312
End Page
318
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/9902
DOI
10.1007/s00393-019-00689-y
ISSN
0340-1855
Abstract
Objective: This study systemically reviewed the evidence regarding the association between plasminogen activator inhibitor‑1 (PAI‑1) 4G/5G polymorphism and susceptibility to systemic lupus erythematous (SLE)/lupus nephritis (LN) and rheumatoid arthritis (RA) and the relationship between circulating PAI‑1 levels and SLE/LN and RA. Methods: We conducted a meta-analysis on the association between the PAI‑1 4G/5G polymorphism and SLE/LN or RA risk and serum/plasma PAI‑1 levels in patients with SLE/LN and RA and healthy controls. Results: Nine articles including 657 patients with SLE and 668 controls and 567 patients with RA and 772 controls were included. No association was revealed between SLE and PAI‑1 4G allele in all study subjects (odds ratio [OR] = 0.944, 95% confidence interval [CI] = 0.808–1.102, p = 0.463). Ethnicity-based stratification showed no association between the PAI‑1 4G allele and SLE among Europeans and Asians. No association was detected between LN and RA and the PAI‑1 4G allele (OR = 0.886, 95% CI = 0.713–1.102, p = 0.278; OR = 0.8736, 95% CI = 0.747–1.020, p = 0.088, respectively) or between SLE/LN and RA and the PAI‑1 4G/5G polymorphism using the recessive and dominant models and homozygote contrast. The circulating PAI‑1 level was significantly higher in the SLE group than in the control group (standardized mean difference [SMD] = 0.337, 95% CI = 0.057–0.619, p = 0.019). However, serum/plasma PAI‑1 level showed no significant difference between RA and control group (SMD = 0.333, 95% CI = −0.6989–1.35, p = 0.527). Conclusions: There was no association between the PAI‑1 4G/5G polymorphism and SLE/LN and RA development and significantly higher levels of circulating PAI‑1 were observed in patients with SLE but not in those with RA.
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