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Clinical Diagnosis of Sickle-C Disease
CAPT. WILLIAM F. DENNY, MC;
THOMAS O. FINN, M.D.;
ROBERT M. BIRD, M.D.
AMA Arch Intern Med. 1957;99(2):214-217.
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In 1949, Pauling reported that the hemoglobin molecule in sickle-cell anemia differed from normal adult hemoglobin.1 Subsequently, a number of abnormal hemoglobins have been described. Numerically, the most important of these abnormal hemoglobins are S- and C-hemoglobin. When the two are present in the same person, a characteristic syndrome may occur, which is designated as sickle-C disease. The C-hemoglobin is said to occur in 2% of the American Negro population, either alone or in combination with other hemoglobin types.2 Thus it is not rare, and an area which has a large Negro population may expect to see disorders arising therefrom. Until recently, the pathogenic significance of the heterozygous combination of S- and C-hemoglobins was not recognized, and the sickle trait was regarded as a completely benign, inherited abnormality of the erythrocyte. Through the work of Pauling 3 and others it became possible to identify other abnormal hemoglobins in
. . . [Full Text PDF of this Article]
Author Affiliations
U.S.A.F.; Oklahoma City
From the Departments of Medicine and Pediatrics, University of Oklahoma School of Medicine and University Hospitals. Present address: University of Oklahoma School of Medicine and University Hospitals (Dr. Denny).
Footnotes
Received for publication April 26, 1956.
Presented in part before the Southern Section, American Federation for Clinical Research, New Orleans, Jan. 20, 1956.
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