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A correction has been published: N Engl J Med 1995;332(20):1381.

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Volume 331:1559-1562 December 8, 1994 Number 23
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Variability of Thrombosis among Homozygous Siblings with Resistance to Activated Protein C Due to an Arg-to-Gln Mutation in the Gene for Factor V
Judith S. Greengard, Sabine Eichinger, John H. Griffin, and Kenneth A. Bauer

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 Hopmeier, P.
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The most frequent laboratory abnormality in patients with idiopathic deep-vein thrombosis is resistance to activated protein C1. Depending on the selection criteria, in vitro resistance to activated protein C can be identified in 20 to 50 percent of patients2,3,4,5,6. Protein C, a key element in the regulation of coagulation, circulates in plasma as an inactive precursor. On contact with thrombin bound to the thrombomodulin receptors on vascular endothelial cells, protein C rapidly becomes activated. Activated protein C enzymatically lyses two cofactors of the coagulation cascade, factor VIIIa and factor Va. It is thus a natural anticoagulant that controls . . . [Full Text of this Article]

Methods

Collection of Blood Samples

Assay for Resistance to Activated Protein C

Coagulation Measures

Sequencing of Genomic DNA

Factor V Complementary DNA Sequence

Results

Discussion


Source Information

From the Departments of Molecular and Experimental Medicine and Vascular Biology, the Scripps Research Institute, La Jolla, Calif. (J.S.G., J.H.G.); and the Department of Medicine, Brockton-West Roxbury Veterans Affairs Medical Center, and Beth Israel Hospital, Harvard Medical School, Boston (S.E., K.A.B.).

Address reprint requests to Dr. Bauer at the Veterans Affairs Medical Center, 1400 VFW Pky., West Roxbury, MA 02132.

References


Related Letters:

Factor V Leiden and Thrombophilia
Hopmeier P., Krugluger W., Simioni P., Scudeller A., Girolami A., Kalafatis M., Mann K. G., Belliveau R. R., Bauer K. A., Griffin J. H., Hajjar K. A.
Extract | Full Text  
N Engl J Med 1995; 332:1381-1384, May 18, 1995. Correspondence

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