ID 112143
Title Alternative
高Lp(a)血症におけるaspirinの効果
Effect of aspirin treatment on serum levels of lipoprotein (a) : analysis from the apolipoprotein (a) isoforms
Author
Azuma, Hiroyuki The University of Tokushima
Kagawa, Ayako The University of Tokushima
Kanagawa, Yasuhiko The University of Tokushima
Matsuyama, Madoka The University of Tokushima
Iuchi, Takahiko The University of Tokushima
Takamori, Nobuyuki The University of Tokushima
Yoshida, Tomonori The University of Tokushima
Matsumoto, Kazuya National Sanatorium Tokushima Hospital
Hayashi, Ikuro Tokushima Prefectural Central Hospital
Tamura, Katsuya Health Insurance Naruto Hospital
Nishiuchi, Takeshi Kawashima Cardiovascular Clinic
Keywords
lipoprotein (a)
apolipoprotein (a)
aspirin
apo(a) isoform
Lp(a) phenotype
Content Type
Journal Article
Description
We have found that aspirin lowers elevated serum lipoprotein(a) [Lp(a)] levels via reduction of the transcriptional activity of apolipoprotein(a) [apo(a)] gene with suppression of apo(a) mRNA expression. In the present study, we evaluated the effect of aspirin treatment on serum Lp(a) level and analyzed its relation to type of apo(a) isoform. Serum levels of Lp(a) were measured by turbidimetric immunoassay before and after the oral administration of aspirin therapy (81 mg/day) in 57 patients with coronary artery disease or cerebral infarction. Apo(a) isoforms were determined by immunoblotting method. In patients with high serum Lp(a) levels (more than 30 mg/dl), aspirin reduced serum Lp(a) levels to approximately 80 % of the baseline after one month. Their levels sustained significantly low even after six months. The effect of aspirin in reducing elevated serum Lp(a) levels were stronger in patients with smaller-sized type or double-band type of apo(a) isoforms. The transcriptional efficiency of apo(a) gene is thought to be increased in patients with these apo(a) isoforms. Therefore, these findings suggest that aspirin reduces apo(a) gene transcription preferentialy in patients with high transcriptional efficiency of this gene.
Journal Title
Shikoku Acta Medica
ISSN
00373699
NCID
AN00102041
Publisher
徳島医学会
Volume
55
Issue
3
Start Page
109
End Page
114
Sort Key
109
Published Date
1999-06-25
EDB ID
FullText File
language
jpn
TextVersion
Publisher
departments
Medical Sciences
Institute of Advanced Medical Sciences