Chronic Myeloid Leukemia. 15-Years Experience at a Single Institution in Mexico City

Chronic myeloid leukemia (CML) is a malignant disease of the hematopoietic stem cell caused by the t(9;22)(q13;q11). The disfunctional hybrid-protein (PBCR-ABL) produced has a tyrosin kinase activity leading to a factor-independent myeloid proliferation and leukemic transformation. Imatinib mesilate (IM), a competitive inhibitor of PBCR-ABL, is now considered the treatment of choice for patients (pts) with CML. The primary goal of the treatment is to reach a complete cytogenetic response (CCgR) which is achieved in 48% of previously-treated chronic phase (CP)-CML pts and 87% with front-line IM. We retrospectively analyzed and compared the demographics, clinical data and outcome of all CML patients with at least 3-months of follow-up referred to our Institution (INCMNSZ) from January 1992 to April 2007. RESULTS: Ninety-nine medical charts were evaluated and divided in IM-treated group and a historical group. Median age was 37-y (12–79), 52.5% pts were male, 29.2% were asymptomatic, 64.4% had anemia, 37.4% had bleeding, and 46.5% pts had fever at diagnosis. Hepatomegaly, splenomegaly and lymphadenopathy were present in 20/92 (21.7%), 54/93 (58.1%), and 22/96 (22.9%) respectively. At diagnosis 85 (86%) pts were in CP; 7 (7%) in accelerated phase (AP), and 7 (7%) in blastic phase (BP). Hasford risk was low in 49 (49.5%), intermediate in 34 (34.3%) and high in16 (16.2%) of the pts. Table 1 summarizes demographics and clinical variables by groups. Table 1. Characteristics by group Variable Imatinib (n=57) Historical (n=42) Male 26 (45.6%) 26 (61.9%) Median age 33 (12–79) 41 (15–75) Asymtomatic 7 (12.3%) 13 (31%) Anemia 34 (59.6%) 30 (71.4%) Bleeding 19 (33.3%) 18 (42.9%) Fever 26 (45.6%) 20 (47.6%) Hepatomegaly 14/50 (28%) 6/42 (14.3%) Splenomegaly 35/51 (68.6%) 19/42 (45.2%) lymphadenopathy 16/54 (29.6%) 6/42 (14.3%) CML-CP 51 (89.5%) 34 (81%) CML-AP 2 (3.5%) 5 (7.1%) CML-BP 4 (7%) 3 (7.1%) Hasford Low-Risk 31 (54.4%) 18 (42.9%) Hasford Intermediate-Risk 17 (29.8%) 17 (40.5%) Hasford High-Risk 9 (15.8%) 7 (16.7%) Fifty-seven patients were treated with IM, of them 31/57 (54.4%) received IM as front-line therapy and 26/57 (45.6%) were previously treated. Interferon alfa (IFNa) was given to 17/26 (65.3%) of the pts in IM group. Responses by group of therapy are listed in Table 2. Table 2. Response by groups Variable Imatinib (n=57) Historical (n=42) * 5 pts too early for Cg evaluation; ** BMT pts CHR 52 (91.2%) 17 (40.5%) CgR 42/52* (80.8%) 2** (4.8%) CCgR 37/42 (88.1%) 2 (4.8%) Alive in CCgR @ last F-U 25/57 (43.9%) 1 (2.4%) Progress to BP @ last F-U 7/57 (12.3%) 14 (33.3%) Patients exposed to IFNa prior to receive IM had a CCgR of 58.8% compared to patients in whom IFNa was not given before IM, 77.8%. At a median follow-up of 26.2 mo, 54/57 (94.7%) pts in the group of IM were still alive; 25/57 (43.9%) pts are in CCgR, 3/57 (5.3%) with partial CgR. Eight of fifty-seven (14%) pts progressed to AC or BP and 3 pts died in BP-CML. In the historical group there is 1/42 (2.4%) alive in CCgR and 40/42 (95.2%) have progressed to AC or BP-CML. This is the first Mexican series reported comparing CML pts treated with IM and historical controls. The number of pts is representative of our Institution and the data are in accordance with the literature.