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ASSESSMENT OF A Psti POLYMORPHISM OF THE APOLIPOPROTEIN‐AI GENE IN AUSTRALIAN PATIENTS WITH CORONARY ARTERY DISEASE
Author(s) -
DOROW D. S.,
BURKE J.,
GODING J. W.
Publication year - 1989
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1989.tb00332.x
Subject(s) - medicine , psti , apolipoprotein b , coronary artery disease , allele , restriction enzyme , polymorphism (computer science) , genetics , gastroenterology , population , gene , biology , cholesterol , environmental health
In 1986 Ordovas et al. , 1 reported that a polymorphism in the 3' flanking region of the apolipoprotein Al gene was strongly associated with premature coronary artery disease. This polymorphism affects a restriction site for the endonuclease Pstl, resulting in the identification of a 3.3 kb band, rather than the more common 2.2 kb band, when genomic blots of Pstl digested human DNA are probed with an apolipoprotein Al gene probe. In a study population of 88 patients with severe coronary artery disease before the age of 60, 28 (32%) carried the 3.3 kb allele, which was found in only five (4%) of 123 randomly chosen control subjects. In the present study, we have assessed the prevalence of this polymorphism in coronary artery disease patients and outpatients with abnormal lipid levels at the Alfred Hospital, Melbourne, and in normal volunteers. The 3.3 kb allele was present in 7–12% of subjects in these populations, and showed no association with coronary artery disease.