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European Heart Journal 2003 24(22):1995-1996; doi:10.1016/S0195-668X(03)00391-9
Copyright © 2003 by the European Society of Cardiology.
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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]


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