Zusammenhang zwischen PAI-1(Plasminogenaktivator-Inhibitor)-4G/5G-Polymorphismus und zirkulierendem PAI-1 bei systemischem Lupus erythematosus und rheumatoider Arthritis: Eine Metaanalyse

Translated title of the contribution: 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-analysis

S. C. Bae, Young Ho Lee

Research output: Contribution to journalArticle

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.

Original languageGerman
JournalZeitschrift fur Rheumatologie
DOIs
Publication statusAccepted/In press - 2019 Jan 1

Fingerprint

Plasminogen Activators
Systemic Lupus Erythematosus
Rheumatoid Arthritis
Lupus Nephritis
Confidence Intervals
Alleles
Odds Ratio
Control Groups
Homozygote
Serum

Keywords

  • Autoimmune diseases
  • Case-control studies
  • Matrix metalloproteinases
  • Polymorphism, genetic
  • Serine proteinase inhibitors

ASJC Scopus subject areas

  • Rheumatology

Cite this

@article{f4b44141efcb45af9f8cb6779368159f,
title = "Zusammenhang zwischen PAI-1(Plasminogenaktivator-Inhibitor)-4G/5G-Polymorphismus und zirkulierendem PAI-1 bei systemischem Lupus erythematosus und rheumatoider Arthritis: Eine Metaanalyse",
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.",
keywords = "Autoimmune diseases, Case-control studies, Matrix metalloproteinases, Polymorphism, genetic, Serine proteinase inhibitors",
author = "Bae, {S. C.} and Lee, {Young Ho}",
year = "2019",
month = "1",
day = "1",
doi = "10.1007/s00393-019-00689-y",
language = "German",
journal = "Zeitschrift fur Rheumatologie",
issn = "0340-1855",
publisher = "D. Steinkopff-Verlag",

}

TY - JOUR

T1 - Zusammenhang zwischen PAI-1(Plasminogenaktivator-Inhibitor)-4G/5G-Polymorphismus und zirkulierendem PAI-1 bei systemischem Lupus erythematosus und rheumatoider Arthritis

T2 - Eine Metaanalyse

AU - Bae, S. C.

AU - Lee, Young Ho

PY - 2019/1/1

Y1 - 2019/1/1

N2 - 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.

AB - 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.

KW - Autoimmune diseases

KW - Case-control studies

KW - Matrix metalloproteinases

KW - Polymorphism, genetic

KW - Serine proteinase inhibitors

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U2 - 10.1007/s00393-019-00689-y

DO - 10.1007/s00393-019-00689-y

M3 - Article

AN - SCOPUS:85070816779

JO - Zeitschrift fur Rheumatologie

JF - Zeitschrift fur Rheumatologie

SN - 0340-1855

ER -