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Introduction: New tyrosine kinase inhibitor treatments for chronic myeloid leukemia based on nilotinib, dasatinib and imatinib have improved patient quality of life and have turned chronic myeloid leukemia from a fatal disease into a chronic disease. Objective: To evaluate the cost-effectiveness of nilotinib, 600 mg, and dasatinib, 100 mg, each compared to imatinib, 400 mg, as first-line therapy in chronic myeloid leukemia in Colombia from a third-party payer's perspective. Materials and methods: A cost-effectiveness analysis was performed using a Markov model to evaluate a hypothetical cohort of one hundred 55 year-old patients with newly diagnosed chronic myeloid leukemia in the chronic phase, and the time horizon for the baseline case was established as being until the end of life. Progression-free life-years saved were considered the primary outcome. Transition probabilities for major molecular response, disease progression to accelerated phase or blast crisis, and chronic myeloid leukemia related deaths were analyzed in the model for each arm. A 3% discount rate was applied to all costs and patient outcomes. Model robustness was evaluated using both univariate and multivariate Montecarlo sensitivity analysis. Results: Nilotinib was higher in expected progression-free life-years saved (15.21 vs. 12.64 for imatinib), followed by dasatinib (14.91 vs. 14.54 for imatinib). Imatinib had lower total lifetime costs.

7042 Background: Imatinib is the standard first line treatment for CML. Imatinib penetrates the CSF poorly. We examined the incidence and outcome of CNS disease in pts with CML treated with imatinib at our institution. Methods: The clinical data for pts with early or late chronic phase and accelerated phase CML treated with imatinib between 1999 and 2006 were reviewed. Pts who were started on imatinib elsewhere and progressed to blast phase were also included. CNS disease was defined as a pathologically proven enhancing lesion (leptomeningeal or parenchymal) or presence of CSF leukemic cells. Results: Nine hundred and ten pts with chronic or accelerated phase CML were treated with imatinib. Fifty five developed blast crisis while on imatinib; another 28 pts had blast transformation while receiving imatinib elsewhere, making up a total of 83 pts. At diagnosis, their median age was 51 yrs, median Hgb, WBC and PLT counts were 10.6 g/dl, 59.7×109/L and 307×109/L, respectively. Median time from diagnosis to starting imatinib was 45.4 mts and the median duration of imatinib therapy was 17.9 mts. Fifteen pts had achieved a complete cytogenetic response and 47 had a complete hematologic response before progressing to blast phase. Their median overall survival from diagnosis was 73.2 mts. Thirty pts developed extramedullary disease; they had similar baseline characteristics as the rest with a median survival of 68.3 mts. Fifteen pts developed CNS disease (5 leptomenigeal, 5 CSF, 3 parenchymal, and 2 spinal cord); 14 had concomitant medullary blast crisis. They had a statistically significant younger age at diagnosis (41.9 vs 52.4 yrs), lower platelet counts (186 vs 334×109/L), and shorter overall survival (66.7 vs 73.2 mts) compared to the other pts with blast phase. Conclusions: CNS disease occurs infrequently in pts receiving imatinib for CML but should be suspected in pts with relevant symptoms. Pts developing CNS leukemia had a worse prognosis; this may be secondary to an inherently worse disease, poor CSF penetration of imatinib, and subsequent difficulty in eradicating CNS disease using available therapies. More potent tyrosine kinase inhibitors, such as nilotinib and dasatinib, and new agents with the ability to cross the blood-brain barrier should be evaluated in this setting. No significant financial relationships to disclose.