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GARNETT CHENEY, M.D.; FREDERICK NIEMAND, M.D.

Arch Intern Med. 1932;49(6):925-933.

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

As a result of the investigations of Whipple, Minot, Castle and others, the present conception of Addison-Biermer anemia is that it is a deficiency disease of a distinct type. An insufficient amount of some protein derivative is available for normal red blood corpuscle maturation, finally resulting in megaloblastic, macrocytic, hyperchromic anemia and hyperbilirubinemia. This lack of necessary protein derivative may be dependent in part on an inadequate intake of readily available protein, such as that contained in liver and stomach, and in part on inadequate digestion of less available protein-containing substances, such as beef. It has been contended by Castle and his co-workers¹ that the lack of normal protein digestion resulting in anemia is in some way due to the gastric achylia, although Castle has been unable to show what the necessary missing factor is. He has shown by feeding experiments that it is not hydrochloric acid and not . . . [Full Text PDF of this Article]

Author Affiliations
SAN FRANCISCO

From the Stanford University Medical School Service at the Laguna Honda Home and the San Francisco County Hospital.

Footnotes
Submitted for publication, Sept. 8, 1931.

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