Charles D. West
Kettering University
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Annals of the New York Academy of Sciences | 1955
Olof H. Pearson; Min C. Li; John P. Maclean; M. B. Lipsett; Charles D. West
Cortisone and ACTH will induce suppression of growth and regression of several types of human neoplasms.. These hormones are useful for the palliative treatment of chronic lymphatic leukemia, acute leukemia, breast carcinoma, lympliosircoma, multiple myeloma, prostatic carcinoma, and Hodgkins disease. Hormone-induced remissions are transient, and relapse usually occurs promptly when the hormone is withdrawn. Sustained remissions require continuous hormone treatment although, with most neoplasms, refractoriness to the effects of the hormone develops and treatment is no longer effective. Pharmacological doses of hormone are usually required to induce remissions. Prolonged administ ration of large doses of cortisone produces (ushings syndrome, but most patients tolerate this condition well, even when treatment is continued for several years. Most Ilatients with chronic lymphatic leukemia respond to cortisone or hydrocortisone as evidenced by marked shrinkage of enlarged lymph nodes, liver, antl spleen. liegrowth of lymphoid tumor masses usually occurs within a few weeks if the hormone is stopped. Iieadministration of the hormone will again produce marked shrinkage of the lymphoid tumors. Refractoriness to the effects of cortisone does not appear to develop, even after periods as long as four years. Continuous administration of cortisone in doses 100 to 300 mg. per day is necessary to sustain suppression of the lymphoid tumor growth. Most patients w i l l obtain improvement in the hematological picture during hormone treatment. There is a rise in the reticulocyte count, followed by better maintenance of hemoglobin levels and, sometimes, a spontaneous rise in hemoglobin to normal levels. Patients with frank heniolyt ic anemia respond tlramatically to cortisone with a prompt remission of the hemolytic phenomenon. I he total leukocyte count rises initially, reaching a peak after about two weeks of treatment, after which the white cell count recedes gradually to below the initial level. There is no signilicant change i n the differential leukocyte count during the first few weeks of treatment. Vitl i prolonged treatment, a few patients have shown a return to normal of the total leukocyte count and of the differential white-cell count antl a disappearance of the lymphoid infiltration of the bone marrow. With most patients, however, some lymphoid infiltration remains in the bone marrow and in the peripheral blootl. Hemorrhagic manifestations sometimes subside I,romptly wi th hormone administration, even though the platelet count does not rise immediately. A rise in platelet count may occur with prolonged therapy. Chroriic lymphatic leukemia.
JAMA | 1954
Olof H. Pearson; Charles D. West; Vincent P. Hollander; Norman Treves
JAMA Internal Medicine | 1955
Olof H. Pearson; Charles D. West; Min Chiu Li; John P. Maclean; Norman Treves
JAMA | 1956
Olof H. Pearson; Bronson S. Ray; Charles C. Harrold; Charles D. West; Min C. Li; John P. Maclean; Mortimer B. Lipsett
Journal of Clinical Investigation | 1958
T. F. Gallagher; Attallah Kappas; Leon Hellman; M. B. Lipsett; Olof H. Pearson; Charles D. West
The Journal of Clinical Endocrinology and Metabolism | 1956
Attallah Kappas; Olof H. Pearson; Charles D. West; T. F. Gallagher
Cancer | 1952
Charles D. West; Vincent P. Hollander; Willet F. Whitmore; Henry T. Randall; Olof H. Pearson
JAMA | 1955
Olof H. Pearson; Min C. Li; John P. Maclean; Mortimer B. Lipsett; Charles D. West
JAMA | 1956
W. P. Laird Myers; Charles D. West; Olof H. Pearson; David A. Karnofsky
The American Journal of Medicine | 1955
Charles D. West; Allyn B. Ley; Olof H. Pearson