Is epsilon 4 allele of apolipoprotein E associated with more severe end-organ damage in essential hypertension?

Citation
F. Yilmaz et al., Is epsilon 4 allele of apolipoprotein E associated with more severe end-organ damage in essential hypertension?, CELL BIOC F, 19(3), 2001, pp. 191-195
Citations number
19
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL BIOCHEMISTRY AND FUNCTION
ISSN journal
02636484 → ACNP
Volume
19
Issue
3
Year of publication
2001
Pages
191 - 195
Database
ISI
SICI code
0263-6484(200109)19:3<191:IE4AOA>2.0.ZU;2-T
Abstract
The aim of the present study comparing patients with mild to moderate hyper tension with controls, was to explore a possible association between hypert ension-related target organ damage and evaluation found in the gene encodin g apolipoprotein E (apo E) genotype. Detailed medical history was recorded and physical examination was per-formed for all patients in the study (88 h ypertensives, 63 normotensive controls). PCR (Polymerase Chain Reaction), R FLP (Restriction Fragment Length Polymorphism), and agarose gel electrophor esis techniques were used to determine the apo E genotypes. The frequencies of apo epsilon2, apo epsilon3, and apo epsilon4 alleles were 3.97, 88.06, and 9.95%, respectively in the hypertensive group. The frequencies of apo e psilon2, apo epsilon3, and apo epsilon4 alleles were 5.5, 92.0, and 2.38%, respectively in the control group. There were about twice as many individua ls in the heterozygote hypertensive group who had apo E3/4 as compared to t he control group (7.30 vs. 2.38%) (p = 0.07). The hypertensive patients who were carriers of the apo epsilon4 had significantly higher organ damage (l eft ventricular hypertrophy (p < 0.001). dilated left atrium (p < 0.05), re tinopathy (p < 0.05)) as compared to those who were not carriers of apo eps ilon4. These results showed a trend for the epsilon4 allele to be associate d with a higher prevalence of target organ damage in patients with mild to moderate hypertension. Copyright (C) 2001 John Wiley & Sons, Ltd.