Neutropenia pathophysiology: Difference between revisions
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==Overview== | ==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]]''. | [[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== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
Neutropenia may develop as a result of one of the three mechanisms:<ref name="PMID17379162">{{cite journal |author=Schwartzberg LS. |title=Neutropenia: etiology and pathogenesis.|journal=Clin Cornerstone. |volume=8|issue=5 |pages=5-11|year=2006|pmid 17379162|doi=|url=https://www.ncbi.nlm.nih.gov/pubmed/17379162}}</ref> | Neutropenia may develop as a result of one of the three mechanisms:<ref name="PMID17379162">{{cite journal |author=Schwartzberg LS. |title=Neutropenia: etiology and pathogenesis.|journal=Clin Cornerstone. |volume=8|issue=5 |pages=5-11|year=2006|pmid 17379162|doi=|url=https://www.ncbi.nlm.nih.gov/pubmed/17379162}}</ref> | ||
'''1) Impaired [[granulocyte]] production''' | '''1) Impaired [[granulocyte]] production''' | ||
*[[Hematologic]] [[malignancy]] with [[bone marrow]] infiltration | *[[Hematologic]] [[malignancy]] with [[bone marrow]] infiltration | ||
*Myelosuppressive chemotherapy or other medications that are toxic to the bone marrow | *Myelosuppressive [[chemotherapy]] or other medications that are toxic to the bone marrow | ||
*Nutritional deficiencies | *Nutritional deficiencies | ||
'''2) Margination''' (process where free flowing blood cells exit circulation) | '''2) Margination''' (process where free flowing blood cells exit circulation) | ||
*Splenic sequestration | *Splenic sequestration | ||
*Adherence to the [[vascular]] [[endothelium]] | *Adherence to the [[vascular]] [[endothelium]] | ||
'''3) Peripheral destruction''' | '''3) Peripheral destruction''' | ||
*Autoimmune [[hemolysis]] | *[[Autoimmune]] [[hemolysis]] | ||
*Drug-induced [[hemolysis]] | *Drug-induced [[hemolysis]] | ||
Revision as of 23:49, 16 November 2016
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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] 1) Impaired granulocyte production
- Hematologic malignancy with bone marrow infiltration
- Myelosuppressive chemotherapy or other medications that are toxic to the bone marrow
- Nutritional deficiencies
2) Margination (process where free flowing blood cells exit circulation)
- Splenic sequestration
- Adherence to the vascular endothelium
3) 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)