Neutropenia pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Daniel A. Gerber, M.D. [2]

Overview

Neutropenia may develop as a result of one of the three mechanisms: impaired granulocyte production, margination, and peripheral destruction. Genes involved in the pathogenesis of neutropenia include ELA2, HAX1, and CXCR4.

Pathophysiology

Pathogenesis

Neutropenia may develop as a result of one of the three mechanisms:^[1]

Impaired granulocyte production
- Hematologic malignancy with bone marrow infiltration
- Myelosuppressive chemotherapy or other medications that are toxic to the bone marrow
- Nutritional deficiencies
Margination (process where free flowing blood cells exit circulation)
- Splenic sequestration
- Adherence to the vascular endothelium
Peripheral destruction
- Autoimmune hemolysis
- Drug-induced hemolysis

Genetics

Genes involved in the pathogenesis of neutropenia include ELA2, HAX1, and CXCR4.

References

↑ Schwartzberg LS. (2006). “Neutropenia: etiology and pathogenesis”. Clin Cornerstone. 8 (5): 5–11. Text “pmid 17379162” ignored (help)

[PMID17379162-1] Schwartzberg LS. (2006). “Neutropenia: etiology and pathogenesis”. Clin Cornerstone. 8 (5): 5–11. Text “pmid 17379162” ignored (help)

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