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Infection and Immunity in Chronic Lymphocytic Leukemia
RICHARD K. SHAW, M.D.;
CLARENCE SZWED;
DANE R. BOGGS, M.D.;
JOHN L. FAHEY, M.D;
EMIL FREI III, M.D.;
ELEANOR MORRISON;
JOHN P. UTZ, M.D.
Arch Intern Med. 1960;106(4):467-478.
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Bacterial infections are responsible for considerable morbidity and mortality in patients with chronic lymphocytic leukemia.1-6 The nature of the defects in host resistance to bacterial infections in this disease have not been clearly defined. In our experience, absolute granulocyte counts are normal or only slightly decreased throughout most of the course of chronic lymphocytic leukemia. The polymorphonuclear response to inflammation in chronic lymphocytic leukemia is usually normal,7,8 and the phagocytic function of the polymorphonuclear cells is normal.9,10 Thus it appears that the majority of infectious complications result from factors other than qualitative or quantitative abnormalities of the polymorphonuclear leukocytes.
Since the introduction of serum protein electrophoresis, several investigators have noted hypogammaglobulinemia, often of a severe degree, in patients with chronic lymphocytic leukemia.11-25 Creyssel et al.19 have reported a good correlation between bacterial infections and hypogammaglobulinemia in this disease. A decreased or absent circulating antibody response following antigenic stimulation has also
. . . [Full Text PDF of this Article]
Author Affiliations
Bethesda, Md.
From the National Cancer Institute (Dr. Shaw, Dr. Boggs, Dr. Fahey, Dr. Frei); the National Institute of Allergy and Infectious Diseases (Mr. Szwed, Dr. Utz), and the Division of Biological Standards (Miss Morrison), National Institutes of Health.
Footnotes
Submitted for publication Jan. 18, 1960.
Requests for reprints should be sent to Dr. Frei. Present Address: Department of Medicine, University of Washington Medical School, Seattle, Wash. (Dr. Shaw); Department of Medicine, University of Utah Medical School, Salt Lake City, Utah (Dr. Boggs).
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