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A correction has been published: N Engl J Med 1998;339(7):477.

Review Article
Mechanisms of Disease
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Volume 338:1042-1050 April 9, 1998 Number 15
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Homocysteine and Atherothrombosis
George N. Welch, M.D., and Joseph Loscalzo, M.D., Ph.D.

Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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 by Lawson, M. F.
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In 1969, McCully made the clinical observation linking elevated plasma homocyst(e)ine concentrations with vascular disease.1 He reported autopsy evidence of extensive arterial thrombosis and atherosclerosis in two children with elevated plasma homocyst(e)ine concentrations and homocystinuria. On the basis of this observation, he proposed that elevated plasma homocyst(e)ine (hyperhomocyst(e)inemia) can cause atherosclerotic vascular disease. The term "homocyst(e)ine" is used to define the combined pool of homocysteine, homocystine, mixed disulfides involving homocysteine, and homocysteine thiolactone found in the plasma of patients with hyperhomocyst(e)inemia.

Subsequent investigations have confirmed McCully's hypothesis, and it has recently become clear that hyperhomocyst(e)inemia is an independent risk factor . . . [Full Text of this Article]

Homocyst(e)ine Metabolism

Measurement of Plasma Homocyst(e)ine

Genetic Defects in Homocyst(e)ine Metabolism

Nutritional Deficiencies Causing Hyperhomocyst(e)inemia

Other Causes of Hyperhomocyst(e)inemia

Association between Hyperhomocyst(e)inemia and Atherosclerosis

Treatment of Hyperhomocyst(e)inemia

Pathophysiologic Mechanisms of Hyperhomocyst(e)inemia

Conclusions


Source Information

From the Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 715 Albany St., W-507, Boston, MA 02118, where reprint requests should be addressed to Dr. Loscalzo.

References


Related Letters:

Homocyst(e)ine and Atherothrombosis
Lawson M. F., van Guldener C., Donker A. J.M., Stehouwer C. D.A., Nath K. A., Welch G. N., Loscalzo J.
Extract | Full Text  
N Engl J Med 1998; 339:477-479, Aug 13, 1998. Correspondence

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