Efficacy and safety of low-dose aspirin in polycythemia vera

Landolfi, Raffaele; Marcholi, R.; Kutti, Jack

doi:10.1016/j.accreview.2004.03.074

Cited by 136 publications

(207 citation statements)

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“…This statement is based on the ECLAP double blind placebo controlled randomised clinical trial, in which a benefit of 100 mg ASA in reducing major thrombosis in PV was demonstrated. 37 In this trial, after a follow-up of about 3 years, there was a statistically significant 59% reduction of major thrombosis (both arterial and venous) without a significant increase in hemorrhagic complications in the ASA group.…”

Section: How To Manage Childrenmentioning

confidence: 67%

How to manage children and young adults with myeloproliferative neoplasms

Barbui

2012

Leukemia

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On the basis of my personal clinical and research experience and validated by the current literature, my approach to the management of pediatric (age o18 years) and young patients (age o40 years) with classic myeloproliferative neoplasms is presented by focusing on diagnosis, patient communication, risk stratification and therapy. The WHO-2008 diagnostic criteria are recommended, even though in children suspected with essential thrombocythemia (ET), a specific set of diagnostic features may be required. Patient communication includes information on natural history, genetic abnormalities and counseling in all women of child-bearing age. The main challenge in children and young adults with ET and polycythemia vera (PV) is to avoid recurrence of major thrombosis by selecting those patients who ultimately can benefit from cytotoxic and antithrombotic therapy without increasing the incidence of drug-induced side effects. In asymptomatic low-risk patients no therapy is prescribed while in high-risk low-dose aspirin, hydroxyurea and interferon-alpha are my first line drugs. My first decision when considering treatment of a young patient with primary myelofibrosis (PMF) or post-PV or post ET-myelofibrosis, is whether he/she qualifies for bone marrow allotransplantation. In the remaining young PMF patients palliative therapy or experimental drugs are considered.Leukemia ( Keywords: myeloproliferative neoplasms; treatment; young people INTRODUCTION Polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) are currently classified among the bcr/abl-negative, 'classic' myeloproliferative neoplasms (MPNs) and represent a stem cell-derived clonal myeloproliferation. Hematopoietic progenitors derived from patients with MPNs are hypersensitive to the stimulation of physiological growth factors such as thrombopoietin or erythropoietin (EPO). 1 Since 2005, the pathophysiology of these diseases has advanced considerably with the discovery of an acquired mutation of JAK2 V617F in a vast majority of PV patients and in almost half of those with ET and PMF. 2 The mutation, located within the negative regulatory pseudokinase, or Janus homology 2 domain, causes cytokine-independent activation of several biochemical pathways implicated in EPO receptor signaling. Subsequently, mutations in MPL were reported in B4% of patients with ET or PMF. The significance of JAK2 and MPL mutations for the evolution of the MPNs and their relative roles in determining disease phenotype as well as progression to myelofibrosis and leukemic transformation are unclear at present.In this context, it should be underscored that most of the information in terms of diagnosis, prognosis and therapy focuses on the 'average' MPN patients of whom median age ranges between 60 and 65 years. On the other hand, less consistent data are available in the groups of MPN patients who are presenting below this median age such as pediatric and young adults (20% of MPN patients). This issue is now becoming more and more important, because with the ad...

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Section: How To Manage Childrenmentioning

confidence: 67%

How to manage children and young adults with myeloproliferative neoplasms

Barbui

2012

Leukemia

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“…A similar effort was carried out in Europe by Tiziano Barbui (b. 1938), an Italian physician scientist, through the Italian group for hematological diseases in adults (GIMEMA) [83][84][85]. Historically, treatment in MPN was documented more in PV and included skeletal radiation therapy (1917) [86], acetylphenylhydrazine (1918) [87], potassium arsenite (1933) [88], P-32 (1940) [89], lead acetate (1942) [90], nitrogen mustard (1950) [91], triethylene melamine (1952) [92], pyrimethamine (1954) [93], busulfan (1958) [94], 6-mercaptopurine (1962) [95], pipobroman (1962) [96], uracil mustard (1964) [97], chlorambucil (1965) [98], and dapsone (1966) [99].…”

Section: Background Information On Treatment In Myeloproliferative Nementioning

confidence: 88%

“…The utilization of aspirin therapy in PV is supported by controlled evidence [83], which has also been used as a rationale to treat ET patients with arterial risk factors [112]. In terms of cytoreductive therapy, there is controlled evidence of value for chlorambucil or radiophosphorus in PV [113], and hydroxyurea in high risk ET [85].…”

Section: Polycythemia Vera and Essential Thrombocythemiamentioning

confidence: 99%

Myeloproliferative neoplasms: A decade of discoveries and treatment advances

2015

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Myeloproliferative neoplasms (MPN) are clonal stem cell diseases, first conceptualized in 1951 by William Dameshek, and historically included chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). In 1960, Nowell and Hungerford discovered an invariable association between the Philadelphia chromosome (subsequently shown to harbor the causal BCR‐ABL1 mutation) and CML; accordingly, the term MPN is primarily reserved for PV, ET, and PMF, although it includes other related clinicopathologic entities, according to the World Health Organization (WHO) classification system. In 2005, William Vainchenker and others described a Janus kinase 2 mutation (JAK2V617F) in MPN and this was followed by a series of additional descriptions of mutations that directly or indirectly activate JAK‐STAT: JAK2 exon 12, myeloproliferative leukemia virus oncogene (MPL) and calreticulin (CALR) mutations. The discovery of these, mostly mutually exclusive, “driver” mutations has contributed to revisions of the WHO diagnostic criteria and risk stratification in MPN. Mutations other than JAK2, CALR and MPL have also been described in MPN and shown to provide additional prognostic information. From the standpoint of treatment, over the last 50 years, Louis Wasserman from the Unites States and Tiziano Barbui from Italy had skillfully organized and led a number of important clinical trials, whose results form the basis for current treatment strategies in MPN. More recently, allogeneic stem cell transplant, as a potentially curative treatment modality, and JAK inhibitors, as palliative drugs, have been added to the overall therapeutic armamentarium in myelofibrosis. In the current review, I will summarize the important advances made in the last 10 years regarding the science and practice of MPN. Am. J. Hematol. 91:50–58, 2016. © 2015 Wiley Periodicals, Inc.

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“…Although primary prevention with aspirin in patients with PV has been proven to reduce the risk of death from cardiovascular causes [6], the role of antiplatelet therapy in patients with ET without cardiovascular risk factors is unclear [7]. This is a relevant issue because coronary ischemia in young patients with ET without cardiovascular risk factors has been consistently reported [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Coronary microvascular dysfunction due to essential thrombocythemia and policythemia vera: The missing piece in the puzzle of their increased cardiovascular risk?

Vianello¹,

Cella

Osto³

et al. 2014

American J Hematol

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Myeloproliferative neoplasms are most commonly associated with venous thrombosis. Up to 60% of patients experience a thrombotic event in their lifetimes, including stroke or myocardial infarction. It is unclear whether pathogenetic factors linking essential thrombocythemia (ET) and polycythemia vera (PV) to thrombotic complications do play a role in the risk of coronary artery disease (CAD). We aimed to assess coronary flow reserve (CFR) as a marker of coronary microvascular function in asymptomatic patients with ET and PV. Fifty-two patients with ET (M/F 13/39, age 61 ± 7 years) and 22 patients with PV (M/F 13/9, age 60.4 ± 13 years) without clinical evidence of heart disease, and 50 controls matched for age and gender were studied. None had CAD. All control subjects were asymptomatic with no history of heart disease. CFR in the left anterior descending coronary artery was detected by transthoracic Doppler echocardiography, at rest, and during adenosine infusion. In patients with ET and PV, CFR was lower than in controls (2.9 ± 0.94 and 2.2 ± 0.7 vs. 3.8 ± 0.7, P < 0.004 and P < 0.0001 respectively). The prevalence of CFR ≤ 2.5 was higher in patients with ET (20 cases, 38.5%) and PV (15 cases, 68.2%) compared with controls (4.1%) (P < 0.0001). Severe CFR (CFR < 2) impairment was found in eight patients with ET (15.4%), in nine patients with PV (40.9%), and in none of control subjects. The mutation of JAK2 gene was associated with abnormal CFR. Asymptomatic patients with ET and PV have coronary microvascular dysfunction in the absence of clinical conditions suggesting CAD

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Efficacy and safety of low-dose aspirin in polycythemia vera

Cited by 136 publications

References 0 publications

How to manage children and young adults with myeloproliferative neoplasms

How to manage children and young adults with myeloproliferative neoplasms

Myeloproliferative neoplasms: A decade of discoveries and treatment advances

Coronary microvascular dysfunction due to essential thrombocythemia and policythemia vera: The missing piece in the puzzle of their increased cardiovascular risk?

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