Growth factors: G-CSF and febrile neutropenia prevention
Injections of filgrastim or its long-acting form pegfilgrastim after chemotherapy make white cells recover faster, cutting the risk of life-threatening infections and allowing chemotherapy on schedule.
Filgrastim (1991) and pegfilgrastim (2002) reduce febrile neutropenia incidence by ~50% and infection-related mortality; guidelines (ASCO, EORTC, NCCN) recommend primary prophylaxis when regimen risk of febrile neutropenia is >20% or 10-20% with patient risk factors, and secondary prophylaxis after an episode. Biosimilars (since 2015 in the US) cut cost; on-body injectors and same-day dosing trials address logistics. Efbemalenograstim and eflapegrastim (2022) are newer long-acting forms; trilaciclib (CDK4/6 inhibitor, 2021) protects marrow in SCLC; plinabulin failed. Febrile neutropenia itself is managed by risk score (MASCC, CISNE) with outpatient oral antibiotics for low risk. G-CSF also mobilises stem cells (with plerixafor) and is contraindicated during concurrent chemoradiation to the chest.
How it works
Recombinant granulocyte colony-stimulating factor accelerates neutrophil precursor proliferation and release, shortening the neutropenic nadir after myelosuppressive chemotherapy.
- Halves febrile neutropenia; maintains dose intensity
- Biosimilars widely available
- Enables dose-dense regimens (e.g. every-2-week AC-T)
- Bone pain in ~30%
- Cost drove over- and under-use
- Rare splenic rupture; theoretical MDS/AML risk debated
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