This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

ERNST P. BOAS, M.D.; DAVID ADLERSBERG, M.D.

AMA Arch Intern Med. 1952;90(3):347-354.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

E VIDENCE has accumulated that an error of lipid metabolism is closely related to the process of atherogenesis in man and experimental animals.¹ Many attempts have been made to characterize this disturbance of lipid metabolism. Elevation of the serum cholesterol level,² alteration of the cholesterol-phospholipid ratio,^1f-h higher concentrations of giant lipoprotein molecules,^1i,j and abnormal shifts from alpha to beta lipoprotein^1m have been studied. The precise role of each of these factors is still under investigation; each represents a different facet of the faulty lipid metabolism. Our previous studies on patients with coronary artery disease whose symptoms began before the age of 50, as well as on their siblings,³ and on families with xanthomatosis⁴ led to the conclusion that the common factor for patients with coronary atherosclerosis may be a genetically transmitted fault of lipid metabolism manifesting itself as hypercholesteremia.⁴ Familial xanthomatosis is the severest form of this inherited disturbance. Many . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the First Medical Service and The Division of Chemistry of the Mount Sinai Hospital.

Footnotes
This study was supported in part by a research grant from the Division of Research Grants and Fellowships of the National Institutes of Health, United States Public Health Service.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?