scholarly journals What’s in a Number? Examining the Prognostic and Predictive Importance of Platelet Count in Patients With Essential Thrombocythemia

2020 ◽  
Vol 18 (9) ◽  
pp. 1279-1284
Author(s):  
Andrew T. Kuykendall ◽  
Rami Komrokji
Keyword(s):  
Platelet Count ◽  
Essential Thrombocythemia ◽  
Myeloproliferative Neoplasm ◽  
Consensus Guidelines ◽  
Thrombotic Risk ◽  
Increased Risk ◽  
Hemorrhagic Events ◽  
Platelet Number ◽  
Mutation Age ◽  
Shed Light

Essential thrombocythemia (ET) is a myeloproliferative neoplasm characterized by clonal overproduction of platelets and an increased risk of thrombohemorrhagic complications. Patients are risk stratified by driver mutation, age, and thrombotic history and treated to reduce the risk of thrombotic and hemorrhagic events. The significance of platelet number as a risk factor or treatment goal is unclear. Despite the preponderance of data failing to demonstrate an association, there exists a pervasive belief that higher platelet counts correlate with an increased thrombotic risk. In fact, the association between thrombocytosis and bleeding is more clearly supported. Variability in regional consensus guidelines contributes to the uncertainty. This article reviews the data that shed light on the importance of platelet count in patients with ET.

Procoagulant Platelet-Derived Microparticles Are Lower in Calreticulin-Than in-JAK2-Mutated Essential Thrombocythemia

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 110-110 ◽  
Author(s):  
Agnes Charpentier ◽  
Nathalie Cambier ◽  
Anne Bauters ◽  
Nathalie Trillot ◽  
Matthieu Wemeau ◽  
...  
Keyword(s):  
Essential Thrombocythemia ◽  
Lower Risk ◽  
Conflicts Of Interest ◽  
Myeloproliferative Neoplasm ◽  
Jak2 V617f ◽  
Procoagulant Activity ◽  
P Value ◽  
Thrombotic Risk ◽  
Testing Procedures ◽  
Increased Risk

Abstract Rationale: Essential Thrombocythemia (ET) is a Philadelphia-negative myeloproliferative neoplasm characterized by an increased risk of thrombosis. Previous reports suggest a role for microparticles (MP) in the pathogenesis of thrombosis in ET. MPs are small plasma membrane vesicles bearing potent procoagulant proteins and phospholipids. They are released into the circulation by various blood and endothelial cells after cellular activation and/or apoptosis. The recently described somatic calreticulin (CALR) exon 9 mutations in almost 20% of ET defines a lower-risk thrombosis ET subtype. We extensively studied phenotype and procoagulant activity of plasma MPs in order to assess MP contribution to the thrombotic risk in CALR versus JAK2 (V617F) mutated ET patients. Patients and methods: We analyzed MP count, phenotype and procoagulant activity in 45 JAK2 V617F+ and 15 CALR+ consecutive and newly diagnosed ET patients in accordance to WHO criteria recruited between november 2010 and april 2013. After given informed consent, blood samples were obtained in all patients before initiating any cytoreductive therapy. Pre-analytical and testing procedures complied with the recommendations of the ISTH Standardization Sub-Committee and each test was performed in duplicate . Using flow cytometry (FC500 flow-cytometer, Beckman-Coulter™), MPs were characterized and measured in platelet-free plasma samples. MPs were characterized by their size and co-expression of bound Annexin V and the following cell-specific monoclonal antibodies: CD41 (Platelet-MP, PMP), CD235a (Red cell-MP, RMP), CD14 (Monocytes-MP, MoMP), CD11b (Granulocytes-MP, GMP), CD144 (Endothelial-MP, EMP), CD62P and CD41 (P-Selectin+ PMP), CD142 and CD41 (Tissue Factor (TF)+ PMP, TF+PMP). MP-associated procoagulant activity was also measured using a-thrombin generation assay (Zymuphen™ MP-activity). Statistical analysis was performed with SPSS software. Results are expressed as median [interquartile range]. Results: Patients characteristics: The platelet count (109/L) was higher in CALR+ than in JAK2+ patients (866 [666 – 918], 659 [571 – 807] respectively, p= 0.049), and all other clinical and hematological characteristics were also distributed in agreement with previous reports. Furthermore, CALR+ patients were preferentially distributed in the lower risk categories of the IPSET-thrombosis and IPSET-survival scores than in JAK2+ patients (p<0.00001 and p= 0.04 respectively). The main results are summarized in table 1. MP count and MP/Platelets ratio were significantly lower in CALR+ than in JAK2+ patients. PMP count, PMP percentage of all MPs and PMP/Platelets ratio were lower in CALR+ than in JAK2+ patients. Furthermore, CALR+ patients had lower PMP surface P-Selectin. MP-associated procoagulant activity/Platelets ratio was significantly lower in CALR+ than in JAK2+ patients. There were no significant differences in TF-carrying PMP or in other cell-derived MP (RMP, MoMP, GMP, EMP). Conclusion: Our results demonstrate a decreased in circulating procoagulant PMP in CALR+ ET-patients compared to JAK2+ patients and lower platelet activation in CALR+ ET patients as measured by P-Selectin expression on PMP. Thus, as CALR+ patients have lower thrombotic-risk according to the literature and the IPSET-survival and IPSET-thrombosis scores observed in our study, the lower level of procoagulant PMP could account, at least in part, for a lower thrombotic risk of CALR+ ET patients. Table 1 main results CALR + JAK2 V617F + p value MP (/µL) 3289 [1662-4240] 4961 [2697-6687] 0.04 MP/Platelets 3.6 [2.8-5.3] 6.9 [4.7-9.6] 0.01 PMP (/µL) 3100 [2068–3887] 5702 [3423-10257] 0.004 PMP/Platelets 3.38 [2.97–6.33] 7.55 [5.12–12.66] 0.002 % PMP 90 [84–92] 93 [90–96] 0.03 MP-activity(nM)/platelet 0.015 [0.008–0.028] 0.029 [0.019–0.041] 0.05 P-Selectin+ PMP (/µL) 195 [152-219] 747 [383-965] 0.001 RMP (/µL) 4 [1.7–8.2] 4 [2.5–9.7] ns MoMP (/µL) 43 [27–52] 74.5 [22–135] ns GMP (/µL) 31.5 [24–48] 30 [11–55] ns EMP (/µL) 99.4 [32–110] 95.6 [51–140] ns TF+ PMP (/µL) 22.3 [9.8–115] 27.1 [20.8–94.4] ns Disclosures No relevant conflicts of interest to declare.

Increased Thromboxane Biosynthesis in Essential Thrombocythemia

1995 ◽  
Vol 74 (05) ◽  
pp. 1225-1230 ◽  
Author(s):  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Raffaele Tartaglione ◽  
Sergio Cortelazzo ◽  
Tiziano Barbui ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Essential Thrombocythemia ◽  
Therapeutic Strategy ◽  
Low Dose ◽  
Thrombotic Risk ◽  
Dose Aspirin ◽  
Gender And Age ◽  
Low Dose Aspirin

SummaryIn order to investigate the in vivo thromboxane (TX) biosynthesis in essential thromboeythemia (ET), we measured the urinary exeretion of the major enzymatic metabolites of TXB2, 11-dehydro-TXB2 and 2,3-dinor-TXB2 in 40 ET patients as well as in 26 gender- and age-matched controls. Urinary 11-dehydro-TXB2 was significantly higher (p <0.001) in thrombocythemic patients (4,063 ± 3,408 pg/mg creatinine; mean ± SD) than in controls (504 ± 267 pg/mg creatinine), with 34 patients (85%) having 11-dehydro-TXB2 >2 SD above the control mean. Patients with platelet number <1,000 × 109/1 (n = 25) had significantly higher (p <0.05) 11 -dehydro-TXB2 excretion than patients with higher platelet count (4,765 ± 3,870 pg/mg creatinine, n = 25, versus 2,279 ± 1,874 pg/mg creatinine, n = 15). Average excretion values of patients aging >55 was significantly higher than in the younger group (4,784 ± 3,948 pg/mg creatinine, n = 24, versus 2,405 ± 1,885 pg/mg creatinine, n = 16, p <0.05). Low-dose aspirin (50 mg/d for 7 days) largely suppressed 11-dehydro-TXB2 excretion in 7 thrombocythemic patients, thus suggesting that platelets were the main source of enhanced TXA2 biosynthesis. The platelet count-corrected 11-dehydro-TXB2 excretion was positively correlated with age (r = 0.325, n = 40, p <0.05) and inversely correlated with platelet count (r = -0.381, n = 40, p <0.05). In addition 11 out of 13 (85%) patients having increased count-corrected 11-dehydro-TXB2 excretion, belonged to the subgroup with age >55 and platelet count <1,000 × 1099/1. We conclude that in essential thrombocythemia: 1) enhanced 11-dehydro-TXB2 excretion largely reflects platelet activation in vivo;2) age as well as platelet count appear to influence the determinants of platelet activation in this setting, and can help in assessing the thrombotic risk and therapeutic strategy in individual patients.

Oxidative Stress Levels, JAK2V617F Mutational Status and Thrombotic Complications in Patients with Essential Thrombocythemia

2019 ◽  
Vol 70 (8) ◽  
pp. 2822-2825 ◽  
Author(s):  
Cornel Moisa ◽  
Mihnea Alexandru Gaman ◽  
Camelia Cristina Diaconu ◽  
Amelia Maria Gaman
Keyword(s):  
Oxidative Stress ◽  
Essential Thrombocythemia ◽  
Myeloproliferative Neoplasm ◽  
Oxygen Species ◽  
Mutational Status ◽  
Increased Risk ◽  
Stress Levels ◽  
Total Antioxidant ◽  
Thrombotic Complications ◽  
The Relationship

Essential thrombocythemia (ET) is a BCR-ABL1-negative myeloproliferative neoplasm associated with thrombotic and haemorrhagic complications. Reactive oxygen species (ROS) overexpression induces a growth advantage to JAK2V617F-positive clones and, in association with a higher number of immature platelets, leukocytosis, and additional cardiovascular risk factors, leads to an increased risk for thrombotic events. We evaluated oxidative stress by measuring ROS levels and the total antioxidant capacity (TAC) in 62 ET patients and investigated the relationship between oxidative stress, JAK2V617F mutational status and the development of thrombotic events. We found higher oxidative stress levels in JAK2V617F-positive vs. JAK2V617F-negative ET cases with no significant differences between homozygous and heterozygous genotypes. Increased ROS levels and thrombotic events were more frequent in ET patients with old age at diagnosis, higher haematocrit levels or leukocytosis.

scholarly journals Correlation of blood counts with vascular complications in essential thrombocythemia: analysis of the prospective PT1 cohort

Blood ◽  
2012 ◽  
Vol 120 (7) ◽  
pp. 1409-1411 ◽  
Author(s):  
Peter J. Campbell ◽  
Cathy MacLean ◽  
Philip A. Beer ◽  
Georgina Buck ◽  
Keith Wheatley ◽  
...  
Keyword(s):  
Platelet Count ◽  
Essential Thrombocythemia ◽  
Myeloproliferative Neoplasm ◽  
Vascular Complications ◽  
Complication Rates ◽  
Normal Range ◽  
Major Hemorrhage ◽  
Confounding Variables ◽  
Wbc Count

Abstract Essential thrombocythemia, a myeloproliferative neoplasm, is associated with increased platelet count and risk of thrombosis or hemorrhage. Cytoreductive therapy aims to normalize platelet counts despite there being only a minimal association between platelet count and complication rates. Evidence is increasing for a correlation between WBC count and thrombosis, but prospective data are lacking. In the present study, we investigated the relationship between vascular complications and 21 887 longitudinal blood counts in a prospective, multicenter cohort of 776 essential thrombocythemia patients. After correction for confounding variables, no association was seen between blood counts at diagnosis and future complications. However, platelet count outside of the normal range during follow-up was associated with an immediate risk of major hemorrhage (P = .0005) but not thrombosis (P = .7). Elevated WBC count during follow-up was correlated with thrombosis (P = .05) and major hemorrhage (P = .01). These data imply that the aim of cytoreduction in essential thrombocythemia should be to keep the platelet count, and arguably the WBC count, within the normal range. This study is registered at the International Standard Randomized Controlled Trials Number Registry (www.isrctn.org) as number 72251782.

scholarly journals Thrombocytosis: Diagnostic Evaluation, Thrombotic Risk Stratification, and Risk-Based Management Strategies

Thrombosis ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-16 ◽  
Author(s):  
Jonathan S. Bleeker ◽  
William J. Hogan
Keyword(s):  
Polycythemia Vera ◽  
Essential Thrombocythemia ◽  
Myeloproliferative Neoplasms ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Diagnostic Evaluation ◽  
Diagnostic Process ◽  
Special Focus ◽  
Thrombotic Risk ◽  
Increased Risk

Thrombocytosis is a commonly encountered clinical scenario, with a large proportion of cases discovered incidentally. The differential diagnosis for thrombocytosis is broad and the diagnostic process can be challenging. Thrombocytosis can be spurious, attributed to a reactive process or due to clonal disorder. This distinction is important as it carries implications for evaluation, prognosis, and treatment. Clonal thrombocytosis associated with the myeloproliferative neoplasms, especially essential thrombocythemia and polycythemia vera, carries a unique prognostic profile, with a markedly increased risk of thrombosis. This risk is the driving factor behind treatment strategies in these disorders. Clinical trials utilizing targeted therapies in thrombocytosis are ongoing with new therapeutic targets waiting to be explored. This paper will outline the mechanisms underlying thrombocytosis, the diagnostic evaluation of thrombocytosis, complications of thrombocytosis with a special focus on thrombotic risk as well as treatment options for clonal processes leading to thrombocytosis, including essential thrombocythemia and polycythemia vera.

New Advances in the Pathogenesis and Therapy of Essential Thrombocythemia

Hematology ◽  
2008 ◽  
Vol 2008 (1) ◽  
pp. 76-82 ◽  
Author(s):  
Ross L. Levine ◽  
Mark Heaney
Keyword(s):  
Essential Thrombocythemia ◽  
Myeloid Leukemia ◽  
Significant Proportion ◽  
Myeloproliferative Neoplasm ◽  
Primary Myelofibrosis ◽  
Clinical Syndrome ◽  
Activating Mutations ◽  
Thrombopoietin Receptor ◽  
Increased Risk

Abstract Essential thrombocythemia (ET) is a hematopoietic disorder that manifests clinically as thrombocytosis, and patients with ET are at increased risk for developing thrombosis, myelofibrosis, and transformation to acute myeloid leukemia. Although ET was recognized as a distinct clinical syndrome more than 6 decades ago and was classified as a myeloproliferative neoplasm (MPN) by William Dameshek in 1951, the molecular pathogenesis of ET remained unknown until 2005, when activating mutations in the JAK2 tyrosine kinase (JAK2V617F) were identified in a significant proportion of patients with ET, polycythemia vera (PV) and primary myelofibrosis (PMF). In addition, subsequent studies have identified gain-of-function mutations in the thrombopoietin receptor (MPL) in a subset of patients with JAK2V617F-negative ET, suggesting that JAK2 activation by distinct mechanisms contributes to the pathogenesis of ET. Despite these important observations, important questions remain regarding the role of JAK2/MPL mutations in ET pathogenesis, the etiology of JAK2/MPL negative ET, the factors that distinguish ET from other MPNs with the JAK2V617F mutation, and the role of JAK2-targeted therapies for the treatment of these MPNs.

scholarly journals PB2192 GLOBAL COAGULATION CAPACITY OF ESSENTIAL THROMBOCYTHEMIA PATIENTS BY ROTEM ANALYSIS ADJUSTED FOR PLATELET COUNT CORRELATES WITH THROMBOTIC RISK CLASS

HemaSphere ◽  
2019 ◽  
Vol 3 (S1) ◽  
pp. 983
Author(s):  
C. Giaccherini ◽  
M. Marchetti ◽  
C. Verzeroli ◽  
S. Gamba ◽  
L. Russo ◽  
...  
Keyword(s):  
Platelet Count ◽  
Essential Thrombocythemia ◽  
Thrombotic Risk ◽  
Risk Class

The Use of the PFA-100® and Thromboelastograph in Assessing Haemostasis and Drug Efficacy in Essential Thrombocythemia.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4959-4959
Author(s):  
Betty Y.Y. Cheung ◽  
Kiran Parmar ◽  
Ghasem Yadegarfar ◽  
Beverley J. Hunt ◽  
Claire N. Harrison
Keyword(s):  
Platelet Count ◽  
Retinal Vein Occlusion ◽  
Essential Thrombocythemia ◽  
Central Retinal Vein Occlusion ◽  
Clot Strength ◽  
Vein Occlusion ◽  
Increased Risk ◽  
History Of ◽  
Digital Ischaemia ◽  
Central Retinal Vein

Abstract Introduction. Essential thrombocythemia (ET) is associated with an increased risk of thrombosis. Many patients are treated with anti-platelet agents and/or cytoreductive therapy in order to minimise the risk but some still develop thrombotic events. The PFA-100® is an effective near-patient platelet function analyser and the Thromboelastograph (TEG®) Haemostasis Analyser assesses global haemostasis in whole blood. The usefulness of these technologies has not been fully evaluated in ET. Patients and Methods. We compared results from the PFA-100® and TEG® in 25 ET patients and 19 controls. Overall the ET patients comprised 18 females and 7 males, their median age was 55 yrs, median platelet count 423x109/l. Twenty-two were on anti-platelet therapy (21 on 75mg aspirin, 1 on aspirin and clopidogrel). Seventeen patients were receiving cytoreductive therapy (10 hydroxyurea, 2 a-interferon, 4 busulphan and 1 busulphan with anagrelide). Eight patients had previous thrombosis (4 transient ischaemic attacks, 1 stroke, 1 central retinal vein occlusion, 2 multiple events [1 stroke, erythromelalgia and digital ischaemia; 1 central retinal vein occlusion and digital ischaemia]) and 2 had haemorrhagic events. Results. All had normal INR, APTT and fibrinogen levels. Using the PFA-100®, Collagen/ADP closure times were prolonged in 15 (60%) patients compared to normal controls, suggesting platelet dysfunction, which included both patients with previous bleeding episodes. Twenty (91%) patients on aspirin had prolonged Collagen/Epinephrine closure times but for 2 (9%) patients these were within the normal range indicating aspirin-resistance. Both these patients had a history of thrombosis whilst on aspirin alone. Using TEG®, ET patients when compared to controls, took longer to initiate and to reach maximal clot strength (significantly longer R and K times, p=0.001, p=0.012 respectively and smaller angle, p=0.01) but the developed clot had a higher tensile strength (larger MA, p=0.024). There was a positive correlation between fibrinogen levels and MA (r=0.54, p=0.006) as well as APTT with R time (r=0.437, p= 0.029). There was no correlation between platelet count or prior history of thrombosis with any PFA-100® or TEG® variables. Conclusion. Low-dose aspirin had biochemical efficacy as assessed by PFA-100® Collagen/Epinephrine closure times in most but not all ET patients. Further studies are necessary to assess whether Collagen/ADP times can identify those at risk of bleeding. In ET, the TEG® demonstrates slower formation but a higher tensile clot strength than controls. Larger studies are needed to fully evaluate these findings and their clinical relevance.

Long-Term Evaluation of 205 Patients with Essential Thrombocythemia: Clinical Outcome, Efficacy and Safety with Respect to Different Therapies.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4941-4941
Author(s):  
Nicola Vianelli ◽  
Antonio deVivo ◽  
Mauro Fiacchini ◽  
Alessandro Lucchesi ◽  
Benedetta Giannini ◽  
...  
Keyword(s):  
Essential Thrombocythemia ◽  
Normal Population ◽  
Alkylating Agents ◽  
Thrombotic Event ◽  
Age At Diagnosis ◽  
Thrombotic Risk ◽  
Blastic Transformation ◽  
Solid Malignancy ◽  
Hemorrhagic Events

Abstract Essential Thrombocythemia (ET) is a myeloproliferative disorder associated with persistent thrombocytosis. The main clinical features are recurrent thrombotic and/or hemorrhagic events, involving both the arterial and venous systems. Data concerning the role of platelet-lowering agents to prevent thrombotic and hemorrhagic events are not conclusive, despite the risk associated to the use of some of them as hydroxyurea (HU) or alkylating agents like busulfan (BU), to induce a leukemic transformation or solid malignancy. We report here our experience, on 205 (M 78, F 127) consecutive ET patients (pts) referred to our Institute between January 1977 and December 2003, with a median follow-up of 76 months (4–318). Median age at diagnosis was 66 (15–91) years; median platelet (PLT) number was 780 (465–3700) x109/L. One hundred and ninety-five pts (95%) were considered at high risk for thrombosis. One hundred and eighty of them (92.3%) were treated with platelet-lowering agents: HU (82 pts), BU (39 pts), HU+BU (37 pts), IFNa (6 pts), HU+IFNa (10 pts), BU+IFNa (2 pts) or HU+BU+IFNa (4 pts). In 30/180 (16.7%) and 124/180 (68.9%) pts the treatments were able to maintain the PLT number <400x109/L (Complete remission) and 400–600x109/L (Partial remission), respectively, for at least 2/3 of their follow-up. Only three pts withdrawn HU or BU for toxicity. A total of 192 (93.6%) pts received antiplatelet agents (121 Aspirin, 34 Ticlopidine, 37 others) for a median period of 53(1–318) months; in 42 pts this therapy was withdrawn, in most cases after gaining control of the platelet count (PLT <600x109/L). During follow-up we registered 33 thrombotic events in 21 (10.2%) pts, and 22 hemorrhagic events in 20 (9.8%) pts, while dizziness, headache and other symptoms due to microvascular disturbance were present in 88 pts. Patients who received both HU and BU consecutively developed a significantly higher number of thrombotic events, compared to pts who received a single drug (p=0.004); this could be explained by the difficult control of the disease in this subgroup of pts. Previous thrombotic event, age and platelet number at diagnosis, thrombocytosis control during follow-up and presence of one or more common cardiovascular risk factors were evaluated in order to establish any correlation with thrombotic risk. Only the first two factors resulted significant. Blastic tranformations, myelofibrosis evolution and solid malignancy occurred in 2(1.0%), 4(1.9%) and 8(3.9%) pts, respectively. The two pts who showed blastic transformation were treated with a particularly high total dose of HU (3039500mg) if compared to the median dose administered (462000mg) or with the sequential association of HU and BU. No strict correlation was observed between the 8 pts who developed a solid malignancy and the therapy administered. The overall survival expressed by the Kaplan-Meier curve was approximately 85% at 12 years after diagnosis, that is similar to the life expectancy of normal population. In conclusion, in our experience HU and BU resulted effective with neglegible toxicity in controlling thrombocytosis in ET pts. Only previous thrombosis and older age at diagnosis significantly increase the risk of thrombotic event during follow-up. The ET blastic transformation seems to be related to the HU+BU association or to a higher total HU dose administered.

The expression pattern of c-mpl in megakaryocytes correlates with thrombotic risk in essential thrombocythemia

Blood ◽  
2002 ◽  
Vol 100 (2) ◽  
pp. 714-717 ◽  
Author(s):  
Luciana Teofili ◽  
Francesco Pierconti ◽  
Annalaura Di Febo ◽  
Nicola Maggiano ◽  
Nicola Vianelli ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Expression Pattern ◽  
Essential Thrombocythemia ◽  
Staining Intensity ◽  
Thrombotic Risk ◽  
Significant Percentage ◽  
Increased Risk ◽  
Significant Difference ◽  
Thrombotic Complications ◽  
Strong Staining

Abstract Using immunohistochemistry, we investigated the expression of c-mpl in bone marrow megakaryocytes of 88 patients with essential thrombocythemia (ET), 6 patients with secondary thrombocytosis (ST), and 20 patients with lymphoma (controls). Considering both the pattern of expression and the staining intensity, we identified a uniform and a heterogeneous pattern of c-mplexpression. The uniform pattern was found in all the controls, all the patients with ST, and 28 of the patients with ET, with a strong staining intensity observed in most megakaryocytes (&gt; 80%). In contrast, c-mpl expression was heterogeneous in 60 patients with ET, 18 of whom (30%) presented with thrombosis at diagnosis, a significant difference from patients with a uniform c-mpl pattern (2 of 28; 7%; P = .026). In particular, the overrepresentation of thrombotic complications in patients with a heterogeneous c-mpl expression pattern was found mainly among patients with a significant percentage (10% to 40%) of weakly stained or c-mpl–negative megakaryocytes (heterogeneous-weak pattern; 13 of 30; 43%;P = .002). Accordingly, this pattern was associated with a 6.1-fold increased risk of thrombosis compared with that of patients with a uniform c-mpl pattern. In conclusion, the presence of a heterogeneous pattern of c-mpl distribution in bone marrow megakaryocytes could be a useful diagnostic criterion in the differential diagnosis of thrombocytosis. Furthermore, detection of a significant percentage of weakly stained or c-mpl–negative megakaryocytes can identify patients with a higher risk of thrombosis.

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