Chapter 70: Monocytosis and Monocytopenia

SUMMARY

The blood monocyte is in transit between the marrow and tissues where it transforms (matures) into a macrophage. In tissues, the monocyte develops a phenotype characteristic of the specific tissue of residence (e.g., Kupffer cells of liver, microglia of brain, osteoclasts of bone). Because the monocyte participates in virtually all inflammatory and immune reactions, its concentration in the blood may be increased in many such conditions, including autoimmune diseases, gastrointestinal disorders, sarcoidosis, and several viral and bacterial infections. Monocytosis, an increase in the blood absolute monocyte count to more than 800/μL (0.8 × 10⁹/L), may occur in some patients with cancer and several unrelated conditions, such as postsplenectomy states, inflammatory bowel disease, and some chronic infections (e.g., bacterial endocarditis, tuberculosis, and brucellosis). The inconsistency and unpredictability in the blood monocyte concentration among patients with the same disease is a function of its relatively small blood pool size, the damping effect of a large tissue pool, its relatively long life span, the number and complexity of effectors in the relevant cytokine network that can influence the response, and the ability to expand macrophage numbers by local mitosis in tissues. The most striking increase in blood monocyte concentration occurs with hematopoietic malignancies, especially clonal monocytosis, and monocytic or myelomonocytic leukemia. Depression, myocardial infarction, parturition, thermal injuries, and marathon competition are closely associated with monocytosis. Table 70–1 is a comprehensive list of causes of monocytosis. Monocytopenia is notable in patients with aplastic anemia or hairy cell leukemia as a feature of pancytopenia. Although other cytopenias accompany the monocytopenia, the latter contributes significantly to the predisposition to infection and in hairy cell leukemia is an aid to diagnosis because of its constancy. The MonoMAC syndrome, the result of GATA2 mutations, is associated with extreme monocytopenia and amonocytosis.