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Leukemia of Large Granular Lymphocytes: Association with Clonal Chromosomal Abnormalities and Autoimmune Neutropenia, Thrombocytopenia, and Hemolytic Anemia

THOMAS P. LOUGHRAN Jr., M.D.; MARSHALL E. KADIN, M.D.; GORDON STARKEBAUM, M.D.; JANIS L. ABKOWITZ, M.D.; EDWARD A. CLARK, Ph.D.; CHRISTINE DISTECHE, Ph.D.; LAWRENCE G. LUM, M.D.; and SHERRILL J. SLICHTER, M.D.
[+] Article and Author Information

Grant support: by grants CA 34199 and CA 31615 from the National Cancer Institute; CH 254 from the American Cancer Society; HL 31641 from National Heart, Lung, and Blood Institute; and GM 15253 from the National Institute of Health; and the Veterans Administration. Dr. Loughran is a recipient of a Clinical Fellowship from the American Cancer Society. Dr. Abkowitz is a Fellow of the Leukemia Society of America.

▸Requests for reprints should be addressed to Thomas P. Loughran, Jr., M.D.; Fred Hutchinson Cancer Research Center, 1124 Columbia Street; Seattle, WA 98104.


Seattle, Washington


© 1985 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1985;102(2):169-175. doi:10.7326/0003-4819-102-2-169
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Three patients had leukocytosis of large granular lymphocytes and chronic neutropenia. Clonal chromosomal abnormalities (trisomy 8 and trisomy 14) and lymphocytic infiltration of splenic red pulp, hepatic sinusoids, and bone marrow indicated the neoplastic nature of the large granular lymphocytes. Demonstration of a T3 + , T8+y HNK-I + phenotype and low natural killer cell activity that was augmented by interferon treatment showed the leukemic cells to be immature natural killer cells. Multiple autoantibodies were present and included rheumatoid factor and antinuclear, antineutrophil, antiplatelet, and antierythrocyte antibodies, suggesting a defect of B-cell immunoregulation. In addition, in-vitro studies showed impaired suppression of immunoglobulin biosynthesis by abnormal cells from one patient. Antineutrophil antibodies and absence of direct cell-mediated inhibition of granulocyte-macrophage colony formation supported a humoral immune mechanism for the neutropenia. In these patients the syndrome of splenomegaly, multiple autoantibodies with neutropenia, and lymphocytosis of large granular lymphocytes is due to a neoplastic proliferation of immature natural killer cells.

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