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JAMES S. McLESTER, M.D.; MARION T. DAVIDSON, M.D.; BLANCHE FRAZIER

Arch Intern Med. 1925;35(2):177-183.

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

Foster and Whipple¹ have devised a relatively simple method for the clinical estimation of fibrinogen. In their experiments on animals, these investigators have found that fibrinogen, in direct contrast to the other blood proteins, varies widely in amount, and that the production of this labile protein is stimulated in different degrees by different diseases. Whipple concludes that the liver is the chief, if not the sole, source of fibrinogen, and finds that those diseases which stimulate or depress liver function in like manner and in equal degree stimulate or depress fibrinogen production.

This suggested to us the possible clinical value of a more comprehensive knowledge of the fibrin content of the blood in disease, especially in disease of the liver, and led us to undertake a series of fibrin estimations on the blood of patients and of normal people. These first observations were reported elsewhere.² Our fibrin studies have been . . . [Full Text PDF of this Article]

Author Affiliations
BIRMINGHAM, ALA.

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