Imatinib front-line therapy is safe and effective in patients with chronic myelogenous leukemia with pre-existing liver and/or renal dysfunction
✍ Scribed by Wei-Gang Tong; Hagop Kantarjian; Susan O'Brien; Stefan Faderl; Farhad Ravandi; Gautam Borthakur; Jianqin Shan; Sherry Pierce; Mary Beth Rios; Jorge Cortes
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 198 KB
- Volume
- 116
- Category
- Article
- ISSN
- 0008-543X
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
BACKGROUND:
Imatinib 400 mg daily is the standard treatment for patients with chronic myelogenous leukemia (CML). The safety and efficacy of imatinib in CML patients with pre‐existing liver and/or renal dysfunction has not been analyzed.
METHODS:
The authors analyzed the outcome of 259 patients with early chronic phase CML treated with imatinib (starting dose 400 mg in 50, 800 mg in 209). Pre‐existing liver and/or renal dysfunction was seen in 38 (15%) and 11 (4%) patients, respectively.
RESULTS:
Dose reductions were required in 91 (43%) of 210 patients with normal organ function, compared with 8 (73%) of 11 (P = .065) with renal dysfunction, and 19 (50%) of 38 (P = .271) with liver dysfunction. Grade 3‐4 hematologic toxicities including anemia (29%, 10%, and 7% of patients with renal dysfunction, liver dysfunction, and normal organ function, respectively), neutropenia (57%, 30%, and 30%), and thrombocytopenia (43%, 30%, and 26%) were more frequent in patients with pre‐existing renal dysfunction treated with high‐dose imatinib. Grade 3‐4 nonhematologic toxicities were observed at similar frequencies. Complete cytogenetic response rates, event‐free survival, and overall survival were similar in all groups.
CONCLUSIONS:
Although patients with pre‐existing liver and/or renal dysfunction might have a higher rate of hematologic toxicity and require more frequent dose reductions, most patients can be adequately managed, resulting in response rates and survival similar to those without pre‐existing organ dysfunction. Cancer 2010. © 2010 American Cancer Society.