Tissue Plasminogen Activator and Plasminogen Activator Inhibitor Type 1 Gene Polymorphism in Patients with Gastric Ulcer Complicated with Bleeding.
10.3346/jkms.2003.18.1.58
- Author:
Hong Soo KIM
1
;
Kyu Yoon HWANG
;
Il Kwon CHUNG
;
Sang Heum PARK
;
Moon Ho LEE
;
Sun Joo KIM
;
Sae Yong HONG
Author Information
1. Department of Internal Medicine, Soonchunhyang University Chunan Hospital, Soonchunhyang University, Chonan, Korea. syhong@schch.co.kr
- Publication Type:Original Article
- Keywords:
Tissue Plasminogen Activator;
Plasminogen Activator Inhibitor 1;
Peptic Ulcer;
Fibrinolysis;
Hemostasis
- MeSH:
Adult;
Aged;
Alu Elements/genetics;
DNA Mutational Analysis;
Duodenal Ulcer/complications;
Duodenal Ulcer/genetics*;
Female;
Gene Frequency;
Genetic Predisposition to Disease;
Genotype;
Human;
Male;
Middle Aged;
Mutagenesis, Insertional;
Peptic Ulcer Hemorrhage/etiology;
Peptic Ulcer Hemorrhage/genetics*;
Plasminogen Activator Inhibitor 1/genetics*;
Polymorphism (Genetics)*;
Promoter Regions (Genetics)/genetics;
Recurrence;
Sequence Deletion;
Stomach Ulcer/complications;
Stomach Ulcer/genetics*;
Tissue Plasminogen Activator/genetics*
- From:Journal of Korean Medical Science
2003;18(1):58-64
- CountryRepublic of Korea
- Language:English
-
Abstract:
Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) may be involved in the pathogenesis of peptic ulcers through suppression of fibrinolysis. This study was designed to investigate associations of t-PA and PAI-1 genes with clinical features of the patients with bleeding gastric ulcers. Eighty-four patients with peptic ulcers and 100 controls were studied between January 1998 and April 2000. We used polymerase chain reaction and endonuclease digestion to genotype for 4G/5G polymorphism in the promoter region of the PAI-1 gene and the Alurepeat insertion/deletion (I/D) polymorphism in intron h of the t-PA gene. Various clinical features, including lesion site, bleeding event, recurrence of ulcer, and rebleeding, were assessed using a multiple logistic regression model. The genotype distributions of both the t-PA and PAI-1 genes did not differ between the patient and control groups. The occurrence of the I/D or D/D genotype of t-PA was significantly higher in cases of duodenal ulcer (adjusted OR=4.39, 95% CI=1.12-17.21). When a dominant effect (i.e., 4G/4G or 4G/5G versus 5G/5G) of the 4G allele was assumed, the PAI-1 4G/4G genotype was independently associated with rebleeding after hemostasis (adjusted OR=5.07, 95% CI=1.03-24.87). Our data suggest that t-PA gene polymorphism is associated with duodenal ulcers, and that the PAI-1 gene may be a risk factor leading to recurrent bleeding after initial hemostasis.
