This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on Web of Science (5)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Thomas A. Wilson, MD; Bennett A. Alford, MD; Leon Morris, MD

Arch Neurol. 1982;39(11):733.

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

Lipodystrophy is characterized by a partial or complete absence of body fat in association with a propensity to develop insulin-resistant, nonketotic diabetes mellitus. At least three clinical entities share this phenotype: (1) total congenital lipodystrophy, (2) total acquired lipodystrophy, and (3) partial acquired lipodystrophy. The first is inherited as an autosomal recessive trait, while the latter two forms occur sporadically.^1,2

Although the etiology of lipodystrophy is unknown, the presence of a lipolytic factor of pituitary or hypothalamic origin has been suspected.^2-6 The clinical similarities between lipodystrophy and the diencephalic syndrome, which is also characterized by decreased adipose tissue and is usually associated with a CNS tumor located in the diencephalon,⁷ suggest the possibility that a structural hypothalamic lesion may be involved. In the initial report of congenital generalized lipodystrophy, pneumonencephalograms showed dilated venticles and enlarged basal cisterns in three patients.⁸ A postmortem examination on another . . . [Full Text PDF of this Article]

Author Affiliations
From the Departments of Pediatrics (Dr Wilson) and Radiology (Drs Alford and Morris), University of Virginia Medical Center, Charlottesville.

Footnotes
Accepted for publication Feb 9, 1982.

Reprints not available.

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