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Case Report and Review of the Literature

PAUL DIDISHEIM, M.D.

Arch Intern Med. 1962;110(2):170-177.

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

Among the congenital disorders of blood clotting, Hageman factor deficiency (HF deficiency, Hageman trait), described by Ratnoff and Colopy in 1955,¹ is unique: affected individuals have a profound abnormality of clotting, yet they are not bleeders. They come to the attention of a physician not because of a tendency to bleed or bruise excessively, but usually because a routine clotting time is fortuitously found to be prolonged. From this it is evident that HF is not essential for normal hemostasis, although it is essential for the normal clotting of blood in a test tube.

The role of HF in blood clotting may be demonstrated in the following manner. Normal plasma exposed to glass markedly accelerates the clotting of normal "intact" plasma, i.e. plasma not previously exposed to glass. This clot-accelerating activity generated in plasma by glass contact has been called Activation Product.² Plasma from subjects with HF deficiency, . . . [Full Text PDF of this Article]

Author Affiliations
SALT LAKE CITY

Instructor, Department of Medicine, University of Utah College of Medicine.; Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah.

Footnotes
Submitted for publication Nov. 13, 1961.

This work was supported by a U.S. Public Health Service research grant (A-4489).

Part of this work has been previously presented: The Activation of Hageman Factor by Silicic Acid, Fed. Proc. 18:1868 (March) 1959.39

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