title: PAI-1 4G/5G insertion/deletion promoter polymorphism and microvascular complications in type 2 diabetes mellitus.
abstract: BACKGROUND
  Plasminogen activator inhibitor-1 (PAI-1) plays an important role in the regulation of fibrinolysis and extracellular matrix turnover. PAI-1 4G/5G insertion/deletion polymorphism in the PAI-1 promoter region has been shown to modulate PAI-1 plasma levels. We investigated the relationship between this polymorphism and the prevalence of diabetic nephropathy and retinopathy in patients with type 2 diabetes in the Austrian population.
  
  
  METHODS
  147 consecutive patients with type 2 diabetes mellitus (96 men, 51 women; median age, 65 years; IQR, 59-71) were analyzed for the PAI-1 4G/5G genotype.
  
  
  RESULTS
  The genotype distribution in the individuals tested was as follows: 17% (n = 25) 5G/5G, 54% (n = 80) 4G/5G, and 29% (n = 42) 4G/4G. Patients homozygous for allele 4G had a significantly higher risk of diabetic proliferative retinopathy than patients without signs of diabetic retinopathy or nonproliferative retinopathy (OR, 7.3; 95% CI, 1.4-38.8; P = 0.02). No significant associations were observed between the PAI-1 genotype and the presence of albuminuria.
  
  
  CONCLUSIONS
  According to our results, diabetic proliferative retinopathy might be associated with the prevalence of PAI-1 genotype 4G/4G.
authors.affiliation: Department of Medical and Chemical Laboratory Diagnostics, University of Vienna Medical School, Vienna, Austria.
authors.forename: Marion
authors.initials: M
authors.lastname: Funk
authors.forename: Georg
authors.initials: G
authors.lastname: Endler
authors.forename: Markus
authors.initials: M
authors.lastname: Exner
authors.forename: Rodrig
authors.initials: R
authors.lastname: Marculescu
authors.forename: Lukas
authors.initials: L
authors.lastname: Endler
authors.forename: Heidemarie
authors.initials: H
authors.lastname: Abrahamian
authors.forename: Harald
authors.initials: H
authors.lastname: Mauler
authors.forename: Angelika
authors.initials: A
authors.lastname: Grimm
authors.forename: Marianne
authors.initials: M
authors.lastname: Raith
authors.forename: Christine
authors.initials: C
authors.lastname: Mannhalter
authors.forename: Rudolf
authors.initials: R
authors.lastname: Prager
authors.forename: Karl
authors.initials: K
authors.lastname: Irsigler
authors.forename: Oswald F
authors.initials: OF
authors.lastname: Wagner
mesh_terms: D000368:Aged; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics*; D001317:Austria / Q000453:epidemiology; D014408:Biomarkers, Tumor / Q000235:genetics; D004252:DNA Mutational Analysis / Q000379:methods; D004251:DNA Transposable Elements / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics*; D003930:Diabetic Retinopathy / Q000097:blood / Q000235:genetics*; D005260:Female; D017353:Gene Deletion; D020022:Genetic Predisposition to Disease / Q000453:epidemiology* / Q000235:genetics; D005820:Genetic Testing / Q000379:methods; D006579:Heterozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics; D018570:Risk Assessment / Q000379:methods; D012307:Risk Factors
chemical_list: D014408:Biomarkers, Tumor; D004251:DNA Transposable Elements; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D001189:Aryl Hydrocarbon Hydroxylases; C414206:CYP2A13 protein, human