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ROBERT C. GRIGGS, M.D.; JOHN W. HARRIS, M.D.

AMA Arch Intern Med. 1956;97(3):315-326.

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

Previous studies have demonstrated that the unique behavior of hemoglobin S with respect to polymerization, molecular orientation,¹ and decreased solubility consequent upon deoxygenation* is responsible for the sickling phenomenon and that blood from patients with sickle-cell disease shows increased number of sickled cells, increased erythrocyte mechanical fragility, and increased whole blood viscosity at reduced oxygen tensions.⁴ The erythrocytes of sickle-cell anemia contain hemoglobin S in sufficient concentration to allow these changes to occur within the physiologic range of oxygen tensions; the erythrocytes of sickle-cell trait contain a concentration of hemoglobin S insufficient to show these changes except upon extreme reduction of the oxygen tension, to levels usually considered nonphysiologic. The relationship of these effects of dexoygenation to the mechanism of production of the hematologic abnormalities and circulatory alterations clinically seen in patients with sickle-cell disease has been discussed by Harris and his associates.⁴

The identification and description of patients in . . . [Full Text PDF of this Article]

Author Affiliations
Cleveland

Footnotes
Submitted for publication Sept. 30, 1955.

This is one of a series of three articles concerning the hemolytic anemias, appearing in the A. M. A. Archives of Internal Medicine.

Western Reserve University School of Medicine and the Department of Medicine, City Hospital. Scholar in Medical Science, John and Mary R. Markle Foundation (Dr. Harris).

This investigation was supported in part by research grant A-745 from the National Institute of Arthritis and Metabolic Diseases of the National Institutes of Health, Public Health Services, and by a grant in support of Hematology Research by Eli Lilly & Company, Indianapolis.

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