Hydroxyurea in the Treatment of Polycythemia Vera: A Prospective Study of 100 Patients Over a 20-Year Period

West, Wilk O.

doi:10.1097/00007611-198703000-00012

Cited by 55 publications

(25 citation statements)

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“…In concert with other studies, 6,8-11 we failed to identify hydroxyurea therapy as an independent risk factor for AML transformation in MF although it was found to be a factor associated with shorter OS. The critical role of chromosomal abnormalities in AML transformation has been highlighted in studies from the Mayo Clinic.…”

Section: Resultssupporting

confidence: 44%

Prognostic Model to Identify Patients With Myelofibrosis at the Highest Risk of Transformation to Acute Myeloid Leukemia

Quintás‐Cardama

Kantarjian

Pierce

et al. 2013

Clinical Lymphoma Myeloma and Leukemia

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A fraction of patients with myelofibrosis (MF) will progress to acute myeloid leukemia (AML) but no current tools are available to identify such patients. By multivariate analysis of 649 patients with MF, we have identified several independent prognostic factors for death. Among those factors, the presence of bone marrow blasts >10% and high risk karyotype were identified as independent risk factors for transformation from MF to AML. Background Some patients with myelofibrosis (MF) progress to acute myeloid leukemia (AML). Current prognostic tools were not devised to assess risk of AML transformation. Methods Multivariate analysis in 649 patients followed for a median of 19 months (range, 1-180 months). Results We identified age > 60 (P = .004; hazard ratio [HR], 1.63), platelets <100 × 109/L (P < .001; HR, 1.62), bone marrow blast > 10% (P = .002; HR, 2.18), high-risk karyotype (P < .001; HR, 2.44), transfusion dependency (P < .001; HR, 2.64), performance status > 1 (P = .003; HR, 1.47), lactate dehydrogenase > 2000 U/L (P < .001; HR, 1.62), previous hydroxyurea (P < .001; HR, 1.69), and male sex (P = .005; HR, 1.41) as independent poor prognostic factors for survival. Using the same baseline variables we identified bone marrow blasts >10% and worst karyotype as independent risk factors for AML transformation. Patients with 1 or both of these risk factors (n = 80; 12%) had a median survival of 10 months and a 1-year AML transformation rate of 13% (2% if none of those factors, P = .001). Conclusion We have identified risk factors that predict high risk of transformation from MF to AML.

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Section: Resultssupporting

confidence: 44%

Prognostic Model to Identify Patients With Myelofibrosis at the Highest Risk of Transformation to Acute Myeloid Leukemia

Quintás‐Cardama

Kantarjian

Pierce

et al. 2013

Clinical Lymphoma Myeloma and Leukemia

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“…Similarly, the incidence of AML in patients treated with hydroxyurea, compared to a historical control treated with either chlorambucil or radiophosphorus, was significantly lower (5.9 % vs. 10.6% vs. 8.3%, respectively, in the first 11 years of treatment) [105]. Other studies have confirmed the low incidence of AML in PV patients treated with hydroxyurea (1-5.6%) [106][107][108].…”

Section: Annual Clinical Updates In Hematological Malignanciesmentioning

confidence: 99%

Polycythemia vera and essential thrombocythemia: 2015 update on diagnosis, risk‐stratification and management

2015

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Disease overview: Polycythemia vera (PV) and essential thrombocythemia (ET) are myeloproliferative neoplasms, respectively characterized by erythrocytosis and thrombocytosis. Other disease features include leukocytosis, splenomegaly, thrombosis, bleeding, microcirculatory symptoms, pruritus, and risk of leukemic or fibrotic transformation. Diagnosis: PV is defined by a JAK2 mutation, whose absence, combined with normal or increased serum erythropoietin level, makes the diagnosis unlikely. Differential diagnosis in ET includes reactive thrombocytosis, chronic myeloid leukemia, and prefibrotic myelofibrosis. Janus kinase 2 (JAK2), calreticulin (CALR), or myeloproliferative leukemia virus oncogene (MPL) mutations occur in approximately 55%, 25%, and 3% of ET patients, respectively. The same molecular markers are also present in prefibrotic myelofibrosis, which needs to be morphologically distinguished from ET. Survival and leukemic/fibrotic transformation: Median survivals are ∼14 years for PV and 20 years for ET; the corresponding values for younger patients are 24 and 33 years. Life‐expectancy in ET is inferior to the control population. JAK2/CALR mutational status does not affect survival in ET. Risk factors for survival in ET and PV include advanced age, leukocytosis, and thrombosis. Leukemic transformation rates at 20 years are estimated at <10% for PV and 5% for ET; fibrotic transformation rates are slightly higher. Thrombosis risk stratification: Current risk stratification in PV and ET is designed to estimate the likelihood of recurrent thrombosis: high‐risk is defined by the presence of age >60 years or presence of thrombosis history; low‐risk is defined by the absence of both of these two risk factors. Recent data consider JAK2V617F and cardiovascular risk factors as additional risk factors. Presence of extreme thrombocytosis might be associated with acquired von Willebrand syndrome (AvWS) and, therefore, risk of bleeding. Risk‐adapted therapy: The main goal of therapy in PV and ET is to prevent thrombohemorrhagic complications. In low risk patients, this is accomplished by the use of low‐dose aspirin and phlebotomy (hematocrit target <45%) in PV. In high risk (for thrombosis) patients, treatment with hydroxyurea is additionally recommended. Treatment with busulfan or interferon‐α is usually effective in hydroxyurea failures and the additional value of JAK inhibitor therapy in such cases is limited. Screening for AvWS is recommended before administrating aspirin, in the presence of extreme thrombocytosis. Am. J. Hematol. 90:163–173, 2015. © 2014 Wiley Periodicals, Inc.

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“…In PV patients treated with HU alone, the incidence of AML has been reported to be about 1-3% in two larger studies each encompassing about 100 patients who have been followed over a median of 5 years [1,6]. Two more recent PV studies have documented a much higher incidence of AML after treatment with HU when the patients are followed for longer periods (5.9% at 8.5 years and 8% at 12 years, respectively) [31,32].…”

Section: Discussionmentioning

confidence: 99%

Acute leukemia and myelodysplasia in patients with a Philadelphia chromosome negative chronic myeloproliferative disorder treated with hydroxyurea alone or with hydroxyurea after busulphan

Nielsen¹,

Hasselbalch²

2003

American J Hematol

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Hydroxyurea in the Treatment of Polycythemia Vera: A Prospective Study of 100 Patients Over a 20-Year Period

Cited by 55 publications

References 0 publications

Prognostic Model to Identify Patients With Myelofibrosis at the Highest Risk of Transformation to Acute Myeloid Leukemia

Prognostic Model to Identify Patients With Myelofibrosis at the Highest Risk of Transformation to Acute Myeloid Leukemia

Polycythemia vera and essential thrombocythemia: 2015 update on diagnosis, risk‐stratification and management

Acute leukemia and myelodysplasia in patients with a Philadelphia chromosome negative chronic myeloproliferative disorder treated with hydroxyurea alone or with hydroxyurea after busulphan

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