Febrile neutropenia pathophysiology: Difference between revisions
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Latest revision as of 21:44, 29 July 2020
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Febrile Neutropenia Microchapters |
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Febrile neutropenia pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: F and N; fever and neutropenia; FN; hot and low; hot leuk; neutropenic fever; neutropenic fever syndrome; neutropenic sepsis
Overview
Factors contributing to neutropenia fever entail absolute or functional leukopenia, altered microbiota, breaches of natural barriers, immune defects associated with specific primary malignancies, hyposplenism, and lymphotoxicity.
Pathophysiology
A number of factors pose an increased risk for infections in cancer patients:
- Absolute or functional leukopenia
- Leukocytes, particularly neutrophils, constitute one of the front-line defense mechanisms against invading microorganisms. Chemotherapy is associated with both qualitative and quantitative deficits in circulating neutrophils by lowering neutrophil counts and impairing chemotaxis and phagocytosis, respectively.
- Altered microbiota
- Microbiota that inhabit the skin, respiratory tract, and digestive tract may be altered by cancer and its treatment or the use of antibiotics.[1]
- Breaches of natural barriers
- Mucositis may occur as a direct adverse effect of chemotherapy or radiotherapy and disrupt the barrier function of the endothelial lining. Indwelling catheters and implanted devices allow access of skin commensals into blood or subcutaneous tissues or serve as a biofilm which bacteria can colonize. Solid tumors that overgrow their blood supply may undergo necrosis and form a nidus for infection.
- Immune defects associated with specific primary malignancies
- Patients with leukemias, non-Hodgkin's lymphoma, or myelodysplastic syndrome may be leukopenic due to malignant infiltration or marrow dysfunction. Absolute or functional hypogammaglobulinemia predisposes patients with chronic lymphocytic leukemia or multiple myeloma to recurrent sinopulmonary infections and septicemia caused by encapsulated pathogens such as Streptococcus pneumoniae and Haemophilus influenza.[2][3] An increased risk of infection has also been observed in patients with Hodgkin's lymphoma as a result of defective cell-mediated immunity.
- Hyposplenism
- Production of opsonizing antibodies takes place in the spleen. Hyposplenism, either as a complication of graft-versus-host disease or irradiation, may contribute to overwhelming infection with encapsulated bacteria.
- Lymphotoxicity
- High-dose corticosteroids affect the distribution and function of lymphocytes as well as other immunocytes. Fludarabine, an adenosine analogue, depletes CD4+ lymphocytes and increases the risk of listeriosis, mycobacterial infections, and opportunistic infections.[4] Therapy with alemtuzumab, a humanized monoclonal antibody targeting CD52 on lymphocytes, heightened the risk for a wide variety of infections.[5][6][7] In addition, the use of anti-CD20 monoclonal antibodies such as rituximab and ofatumumab has been associated with an escalated risk for hepatitis B virus reactivation.[8]
References
- ↑ Bennett, Charles L. (2013-03-21). "Colony-stimulating factors for febrile neutropenia during cancer therapy". The New England Journal of Medicine. 368 (12): 1131–1139. doi:10.1056/NEJMct1210890. ISSN 1533-4406. PMC 3947590. PMID 23514290. Unknown parameter
|coauthors=ignored (help) - ↑ Griffiths, H. (1992-09). "Predictors of infection in chronic lymphocytic leukaemia (CLL)". Clinical and Experimental Immunology. 89 (3): 374–377. ISSN 0009-9104. PMC 1554487. PMID 1516254. Unknown parameter
|coauthors=ignored (help); Check date values in:|date=(help) - ↑ Savage, D. G. (1982-01). "Biphasic pattern of bacterial infection in multiple myeloma". Annals of Internal Medicine. 96 (1): 47–50. ISSN 0003-4819. PMID 6976144. Unknown parameter
|coauthors=ignored (help); Check date values in:|date=(help) - ↑ Anaissie, E. J. (1998-10-01). "Infections in patients with chronic lymphocytic leukemia treated with fludarabine". Annals of Internal Medicine. 129 (7): 559–566. ISSN 0003-4819. PMID 9758577. Unknown parameter
|coauthors=ignored (help) - ↑ Moreton, Paul (2005-05-01). "Eradication of minimal residual disease in B-cell chronic lymphocytic leukemia after alemtuzumab therapy is associated with prolonged survival". Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology. 23 (13): 2971–2979. doi:10.1200/JCO.2005.04.021. ISSN 0732-183X. PMID 15738539. Unknown parameter
|coauthors=ignored (help) - ↑ Thursky, Karin A. (2006-01). "Spectrum of infection, risk and recommendations for prophylaxis and screening among patients with lymphoproliferative disorders treated with alemtuzumab*". British Journal of Haematology. 132 (1): 3–12. doi:10.1111/j.1365-2141.2005.05789.x. ISSN 0007-1048. PMID 16371014. Unknown parameter
|coauthors=ignored (help); Check date values in:|date=(help) - ↑ Keating, Michael J. (2002-05-15). "Therapeutic role of alemtuzumab (Campath-1H) in patients who have failed fludarabine: results of a large international study". Blood. 99 (10): 3554–3561. ISSN 0006-4971. PMID 11986207. Unknown parameter
|coauthors=ignored (help) - ↑ "Drug Safety and Availability - FDA Drug Safety Communication: Boxed Warning and new recommendations to decrease risk of hepatitis B reactivation with the immune-suppressing and anti-cancer drugs Arzerra (ofatumumab) and Rituxan (rituximab)" (WebContent).