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Anagrelide Is Effective in Treating Patients with Hydroxyurea-Resistant Thrombocytosis in Patients with Chronic Myeloid Leukemia

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Anagrelide Is Effective in Treating Patients with Hydroxyurea-Resistant Thrombocytosis in Patients with Chronic Myeloid Leukemia Leukemia (2005) 19, 39–43 & 2005 Nature Publishing Group All rights reserved 0887-6924/05 $30.00 www.nature.com/leu Anagrelide is effective in treating patients with hydroxyurea-resistant thrombocytosis in patients with chronic myeloid leukemia RT Silver1 1The Leukemia and Myeloproliferative Disease Center, Division of Hematology-Oncology, Weill Medical College of Cornell University, New York, NY, USA We report phase II trial results of the use of oral anagrelide median platelet count was approximately 2.0 million/ml; seven hydrochloride for treating 38 patients with hydroxyurea (HU)- patients had thrombohemorrhagic complications. All patients resistant thrombocytosis accompanying chronic myeloid leu- kemia (CML). Anagrelide’s efficacy was well established during responded to anagrelide. The median platelet count after a phase II study of more than 400 patients with one of the four treatment was 343 000/ml; thrombohemorrhagic complications myeloproliferative disorders: essential thrombocythemia, poly- disappeared or did not recur in all patients previously affected. cythemia, idiopathic myelofibrosis, and CML. In the last As part of a large phase II efficacy and safety trial of anagrelide subgroup, there were 114 CML patients with significant in treating patients with elevated platelet counts in the thrombocytosis treated with anagrelide. Out of these patients, myeloproliferative diseases, the Anagrelide Study Group studied 38 had symptoms of thrombosis or hemorrhage and had a group of 114 patients with CML and thrombocytosis thrombocytosis resistant to HU. They were then treated with 2,12 anagrelide at an initial dose of 2.0 mg/day, followed by (Figure 1). The majority of the patients had been given modifications based upon response and toxicity. In all, 71% anagrelide solely because the platelet count was elevated of these patients responded with platelet reductions of more according to study criteria. However, within this group, we than 50% in a median time of approximately 4 weeks. The subsequently identified a subset of 38 patients who had been response rate was not influenced by age, gender, or prior given HU prior to anagrelide specifically for the thrombohemor- thrombosis or hemorrhage. Importantly, the response rate to anagrelide in patients refractory to prior HU was essentially the rhagic complications accompanying thrombocytosis. same as that of the other 76 CML patients. Treatment with This report emphasizes the rare complications associated with anagrelide was well tolerated and without undue toxicity. thrombocytosis in CML and its treatment with anagrelide, Reduction of excessive platelet counts by anagrelide some- especially in patients not satisfactorily treated with HU that times occurring in CML may lead to the prevention of had been given for increased blood platelets. As in other thrombohemorrhagic complications occurring in this clinical myeloproliferative diseases, it suggests that aggressive platelet setting and is relevant even in those patients in whom imatinib mesylate is primary therapy. control aimed at reducing the number of excess blood platelets Leukemia (2005) 19, 39–43. doi:10.1038/sj.leu.2403556 with anagrelide is a treatment objective for CML patients. Published online 28 October 2004 Keywords: CML; thrombocytosis; anagrelide Materials and methods The diagnosis of CML required the typical phenotypic clinical and hematologic picture and demonstration of the Philadelphia Introduction chromosome in the bone marrow in all cases. Molecular studies for rearrangement of the BCR–ABL oncogene and fluorescent in Chronic myeloid leukemia (CML) is uniquely distinguished from situ hybridization studies were not routinely performed in all the three other common myeloproliferative disorders, essential patients at the time of the initiation of this study. Other criteria thrombocythemia (ET), polycythemia vera (PV), and idiopathic included a white blood cell count of X60 000/ml, granulocytic myelofibrosis (IMF), by the Philadelphia chromosome and/or by hyperplasia of the marrow, and decreased or absent leukocyte the molecular rearrangement yielding the chimeric BCR-ABL alkaline phosphatase score. Patients were 18 years or older and 1,2 oncogene. Thrombocytosis is often seen in CML patients, but gave written informed consent. Children were treated as part of 2 thrombohemorrhagic complications are rarely reported. Re- a compassionate-use program. Women of childbearing age had duction in levels of the white blood cell and platelet counts in to have a negative pregnancy test. Failure of a prior therapy was patients treated with interferon has been implemented by using not required. HU and, less commonly, busulfan. Even in the imatinib era, HU The 114 patients with CML eligible to receive anagrelide were has been routinely used when thrombocytosis has been required to have a platelet count of at least 900 000/ml on two 2 excessive. separate occasions at least 1 month apart or a count of at least It is well known that increased platelet counts are associated 650 000/ml on two successive determinations and documenta- 3–5 with an increased risk of microvascular occlusion, thrombo- tion of symptoms attributable to thrombocytosis. 6–9 10 sis, and bleeding. In only one study in CML has anagrelide Not all of the 114 patients were given routine prophylactic been reported to control the thrombocytosis and thrombohe- aspirin. Detailed coagulation studies for hypercoagulable states 11 morrhagic complications. Of the 12 patients in this study, the were not systematically performed. During the analysis of this group, we noted a number of patients who had been treated Correspondence: Professor RT Silver, Division of Hematology- with HU specifically for platelet control because of thrombo- Oncology, New York Presbyterian Hospital-Weill Medical College hemorrhagic symptoms or signs. In these 38 patients, the use of of Cornell University, Box 581, 525 East 68th Street, New York, NY HU was not successful for this purpose; because of excessive 10021, USA; Fax: þ 1 212 746 8246; E-mail: [email protected] thrombocytosis, anagrelide had been substituted. We therefore Received 22 December 2003; accepted 13 September 2004; reviewed the data pertaining to this subgroup to determine the Published online 28 October 2004 nature of the complications and the usefulness of anagrelide in Anagrelide treats thrombocytosis RT Silver 40 577 Chronic myeloproliferative disorders 335 114 68 60 Essential thrombocythemia Chronic myeloid leukemia Polycythemia vera Undifferentiated disease 38 Hydroxyurea-resistant 19 19 Definitely refractory to hydroxyurea Probably refractory to hydroxyurea Figure 1 Patients in the original Phase II study for thrombocythemic states of the Anagrelide Study Group. Table 1 Grouping of 38 patients based on their refractory response Time to platelet response was computed as the time from day to hydroxyurea 1 of anagrelide therapy until a response was first noted. Treatment time was determined from the first dosing date to 1. Refractory to hydroxyurea (HU): 19 the end of therapy or the last follow-up of patients still receiving 1.1 Leukopenia with thrombocytosis (platelets treatment. Observations were censored at the time of the last X600 000/ml) after 3 months of HU therapy, or dosing date of the patients still being treated.12 Note that the end 1.2 Platelet count X900 000/ml despite a dose of at least point was neither hematologic nor cytogenetic response of CML, 2 g/day for at least 2 months, or 1.3 Platelet count X2 000 000/ml after at least 2 months but rather reduction of platelet counts and associated symptoms of HU at any dose and signs contemporaneous with administration of anagrelide. 2. Probably, but not definitely, refractory to HU: 19 X Platelet count 600 000/ml for at least 2 months with any Results dose of HU and documented symptoms and signs attributed to thrombocytosis During the phase II study, 114 patients with CML with elevated platelet counts were treated with anagrelide. For their leukemia, the patients had been previously treated with HU, interferon, this particular situation. In the majority of cases, HU had been busulfan, 32P, chlorambucil, thiotepa, cytosine arabinoside, given as a single agent; in the minority, it supplemented another nitrogen mustard, and/or alkeran as antileukemic therapy. drug used for treating the leukemia. Overall, more than 70% of the 114 patients in chronic phase For the purpose of analysis, this subset of HU-resistant disease had received HU. As they had thrombocytosis as patients was divided into two groups (Table 1). The first group defined in the major study, they were given anagrelide as part of (n ¼ 19) consisted of those whose thrombocytosis was consid- the single-arm, open-label trial, together with antileukemic ered refractory to HU, defined as one of the following three: (1) therapy. We identified 38 patients who had been specifically leukopenia with thrombocytosis (WBC p3000/ml; platelets given HU to treat thrombocytosis, prior to starting anagrelide. X600 000/ml) after 3 months of HU therapy; or (2) a platelet The use of anagrelide to treat the thrombocytosis after HU was count X900 000/ml despite a dose of at least 2 g of HU for at the result of an inability to control the platelet count, an adverse least 2 months; or (3) a platelet count X2 000 000/ml for at least event accompanying HU, or both. 2 months of HU treatment at any dose. The second group The entire group of 114 CML patients, including the subgroup (n ¼ 19) consisted of patients who were considered probably, of 38 HU-resistant patients, had the age, sex, and race but not definitely refractory to HU, defined as a platelet count distribution typical of a CML cohort (Table 2). For the 38 median of 600 000/ml for at least 2 months with any dose of HU patients, the median age was 54.5 years; only one patient was and documented symptoms and signs attributed to thrombocy- African American. More than 90% were Caucasian, 53% were tosis. For the most part, these patients had had a temporary women. The mean baseline body weight was 70 kg (range 41– suspension of other antileukemic therapy before institution of 128 kg).
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