Autoimmune Hematologic Complications in Malignant Lymphoproliferative Disorders

Abstract

The interpretation of cytopenia in patients with malignant lymphoproliferative disorders can be perplexing. Several mechanisms, acting singly or in concert, may operate. Of these, reduced marrow cellular production, due to either marrow infiltration by neoplastic cells or therapy-induced hypoplasia, and increased sequestration of circulating cells in a spleen enlarged by the underlying neoplastic disorder (hypersplenism), are the commonest. Other explanations, such as autoimmune hemolytic anemia and immune-thrombocytopenia should not, however, be over- looked. A compromised bone marrow, hypersplenism, or both generally result in a reduction in all three formed elements; a disproportionate fall in the count of one element, usually the red blood cells or platelets, strongly suggests an alternative cause and, in this context, an immune-mediated mechanism must be considered. Coombs positive, autoimmune hemolytic anemia (AIHA) is the commonest immune-mediated hematologic complication in these patients, occurring in 10% to 20% with chronic lymphocytic leukemia (CLL)1,2and 2%