Skip Navigation

European Heart Journal 2003 24(22):1995-1996; doi:10.1016/S0195-668X(03)00391-9
Copyright © 2003 by the European Society of Cardiology.
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in EHJ
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by McCully, K. S
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McCully, K. S
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Editorial

Homocysteine, Marfan Syndrome and arteriosclerosis

Kilmer S McCully*

Pathology and Laboratory Medicine Service, Veterans Affairs Medical Center, Boston Healthcare System, 1400 Veterans of Foreign Wars Parkway, West Roxbury MA 02132, USA

* Tel.: 617-363-5618; fax: 617-363-5623
E-mail address: kilmer.mccully@med.va.gov

Received 30 June 2003; accepted 4 July 2003

The first 10% of the full text of this article appears below.

See doi:10.1016/j.ehj.2003.08.020for the article to which this editorial refers

Homocystinuria is an inherited disease of homocysteine metabolism most commonly caused by deficiency of the pyridoxal phosphate-dependent enzyme, cystathionine synthase. The disease is manifested in many cases by accelerated growth in childhood, dislocated ocular lenses, skeletal abnormalities, retarded mental development, and propensity to thrombosis with increasedmortality from vascular disease.1Before the discovery of homocystinuria in 1962, many of these subjects were considered to have Marfan Syndrome, because of accelerated growth, dislocated ocular lenses, and vascular disease. Subsequent screening of the urine for homocysteine revealed a number of cases of homocystinuria that were originally attributed to MarfanSyndrome.2

Review of an archival case of homocystinuria originally reported in 1933 disclosed generalized arteriosclerosis and death from carotid thrombosis and stroke . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related articles in EHJ:

Phenotypic variability of cardiovascular manifestations in Marfan Syndrome: Possible role of hyperhomocysteinemia and C677T MTHFR gene polymorphism
Betti Giusti, Maria Cristina Porciani, Tamara Brunelli, Lucia Evangelisti, Sandra Fedi, Gian Franco Gensini, Rosanna Abbate, Guido Sani, Magdi Yacoub, and Guglielmina Pepe
EHJ 2003 24: 2038-2045. [Abstract] [Full Text]