Neutropenia pathophysiology: Difference between revisions
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===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><br/> | 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><br/> | ||
#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 | ||
#Margination''' (process where free flowing blood cells exit circulation) | |||
*Splenic sequestration | #*Splenic sequestration | ||
*Adherence to the [[vascular]] [[endothelium]] | #*Adherence to the [[vascular]] [[endothelium]] | ||
#Peripheral destruction''' | |||
*[[Autoimmune]] [[hemolysis]] | #*[[Autoimmune]] [[hemolysis]] | ||
*Drug-induced [[hemolysis]] | #*Drug-induced [[hemolysis]] | ||
===Genetics=== | ===Genetics=== |
Latest revision as of 23:43, 21 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]
- 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)