The risk of developing chemotherapy-induced febrile neutropenia (FN), a life-threatening adverse effect of myelosuppressive chemotherapy, was explored in a study published in the Journal of the National Comprehensive Cancer Network.

Previously identified pathologic mechanisms contributing to FN include bone marrow suppression, impaired neutrophil function, or disturbances of barrier function. In this study, the authors investigated if clinical characteristics, such as surgery, radiation therapy, selected dermatologic/mucosal conditions, and use of antibiotics and corticosteroids, which may be associated with these pathologic mechanisms, may also be an indication of increased FN risk.

The study included 15,971 patients with non-Hodgkin lymphoma or breast, lung, colorectal, ovarian, or gastric cancer between 2000 and 2009 at Kaiser Permanente Southern California who were treated with myelosuppressive chemotherapy. Patients who received prophylactic granulocyte colony-stimulating factor (G-CSF) or antibiotics were excluded. Electronic medical records were used to evaluate association between risk factors and the development of FN in the first chemotherapy cycle.

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During the first chemotherapy cycle 4.3% of patients developed FN. The use of corticosteroids was significantly associated with increased risk of FN; while dermatologic/mucosal conditions and intravenous antibiotic use were only minimally associated with increased FN risk. Increased FN risk was not significantly associated with surgery, radiation therapy, and oral antibiotic use.

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“Dermatologic or mucosal conditions that might affect barrier integrity and use of corticosteroids and intravenous antibiotics prior to chemotherapy may increase risk of FN and should be considered in prophylaxis use and FN prediction modeling,” advised the study authors.


Family L, Li Y, Chen LH, Page JH, Klippel ZK, Chao C. A study of novel febrile neutropenia risk factors related to bone marrow or immune suppression, barrier function, and bacterial flora. J Natl Compr Canc Netw. 2018;16(10):1201-120816:10.