Erythropoiesis-stimulating agents (ESAs) are recommended to manage chemotherapy-induced anemia (CIA). Intravenous (IV) iron supplementation improves the response to ESAs, particularly in cases of iron deficiency, but is underused. SYNERGY evaluated the impact of epoetin alfa biosimilar and IV iron on CIA in current practice.
This observational, longitudinal, prospective, multicenter study was conducted in France, from a representative, random sample of oncologists and hematologists. The primary objective was response to epoetin alfa biosimilar (achieving target Hb level with increase of ≥1 g/dL versus baseline or increase of ≥2 g/dL in the absence of a transfusion in the 3 previous weeks). Data on patient characteristics, iron use, anemia and iron status assessment were collected on enrollment. Iron deficiency was classed as absolute (transferrin saturation coefficient (TSC) <20%, ferritin (FT) <100 Âµg/mL) or absolute (TSC <20%, FT ≥100 Âµg/mL). Patients aged ≥18 years with CIA, with solid tumors, lymphoma or myeloma, and prescribed epoetin alfa biosimilar were included, with follow-up at 12–16 weeks.
Oncologists and hematologists (n = 195) enrolled 2167 patients between June 2012–December 2014; 2076 patients (49.4% male) were analyzed (see Table for patient characteristics). In 76.5% of patients with an iron assessment, TSC, FT and serum iron levels were determined according to ESMO recommendations. The mean Hb level was 9.6 g/dL.
|Iron status assessment||51.7|
|Epoetin alfa biosimilar + iron prescribed for:|
|No iron deficiency||18.6|
At follow-up, 71.9% of patients had a maximum Hb level >11 g/dL. IV iron did not affect response rates in patients with no iron deficiency (71.4% vs 72.3% without iron), or functional iron deficiency (68.3% vs 67.8% without iron) but improved the response in patients with absolute iron deficiency (75.8% vs 67.4% without iron).
This study demonstrates an increase in use of iron status assessment compared with previous French cohorts, and confirms the importance of IV iron supplementation in ESA treatment of CIA.
Clinical trial identification
F. ScottÃ©, K. Laribi, D. Spaeth: grant and/or research support from Hospira SAS. I. Ray-Coquard: grant and/or research support from Hospira SAS, consultancy fees from Amgen, PharmaMar, Roche, and paid instructor for Amgen, PharmaMar, and Roche. E. Kasdaghli, H. Albrand: employee of Hospira. E. Leutenegger: employee of GECEM. All other authors have declared no conflicts of interest.