TextbookHaematologyEssential Thrombocythaemia

Essential Thrombocythaemia

Myeloproliferative neoplasm characterised by sustained thrombocytosis with risk of thrombotic and haemorrhagic complications, driven by JAK2, CALR, or MPL mutations.

Key Facts

Essential thrombocythaemia (ET) is a chronic MPN defined by sustained platelet count ≥450 × 10⁹/L with clonal mutation Driver mutations: JAK2 V617F (~60%), CALR (~25%), MPL (~5%); ~10% are triple-negative CALR-mutated ET has the best prognosis and lowest thrombotic risk; JAK2-mutated has highest thrombotic risk Risk of thrombosis: 10-25% at 10 years; risk of major haemorrhage: 5-10% First-line cytoreduction for high-risk patients: hydroxycarbamide 500mg-1g OD (PT-1 trial) Anagrelide 0.5mg BD is second-line (lowers platelets via megakaryocyte inhibition) Median survival exceeds 20 years; risk of transformation to myelofibrosis or AML is relatively low

Overview

Key Facts

Essential thrombocythaemia is a myeloproliferative neoplasm characterised by megakaryocyte proliferation leading to persistent thrombocytosis. The main clinical consequences are thrombosis and haemorrhage.

Epidemiology

  • Incidence: 1-2.5 per 100,000/year in the UK
  • Median age at diagnosis: 55-60 years (bimodal: peak at 30 and 55)
  • Slight female predominance
  • Most common MPN at presentation

Aetiology

  • JAK2 V617F: ~60% (shared with PV and PMF)
  • CALR mutations (calreticulin): ~25% (type 1 and type 2)
  • MPL mutations (thrombopoietin receptor): ~5%
  • Triple-negative: ~10% (no known driver mutation)

Pathophysiology

  • Driver mutations cause cytokine-independent megakaryocyte proliferation
  • Increased platelet production → sustained thrombocytosis
  • Abnormal platelet function → paradoxical thrombosis AND bleeding
  • Extreme thrombocytosis (>1500 × 10⁹/L) → acquired von Willebrand disease (consumption of large vWF multimers) → bleeding risk
  • Leukoerythroblastic change and fibrosis suggest transformation to myelofibrosis

Clinical Presentation

Common Presentations

  • Incidental finding of raised platelet count on FBC (~50%)
  • Microvascular symptoms: erythromelalgia, headache, dizziness, visual disturbance, acral paraesthesiae
  • Thrombotic events: stroke, TIA, MI, DVT/PE, splanchnic vein thrombosis
  • Haemorrhagic events: mucosal bleeding, bruising (especially with very high platelets)
  • Splenomegaly (mild, in ~40%)

Red Flags

  • Splanchnic vein thrombosis in a young patient → screen for MPNs
  • Platelets >1500 × 10⁹/L with bleeding → acquired von Willebrand disease
  • Rapidly rising platelets with constitutional symptoms → consider transformation
  • Leukoerythroblastic blood film → myelofibrotic transformation

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Reactive thrombocytosisInfection, iron deficiency, post-splenectomy, malignancyCRP, ferritin, clinical context
Polycythaemia veraPredominant erythrocytosis, JAK2+Hb/Hct, EPO, bone marrow
Primary myelofibrosis (prefibrotic)Anaemia, splenomegaly, leukoerythroblastic filmBone marrow (fibrosis)
CMLLeucocytosis, basophilia, BCR-ABL positiveBCR-ABL (Philadelphia chromosome)
MDS with ring sideroblasts and thrombocytosisAnaemia, ring sideroblasts, SF3B1 mutationBone marrow
Iron deficiencyMicrocytosis, low ferritin, reactive plateletsFerritin, iron studies

Diagnosis / Investigation

Bedside

  • Examination for splenomegaly, evidence of thrombosis or bleeding

Bloods

  • FBC: sustained platelets ≥450 × 10⁹/L on two occasions at least 1 month apart
  • Blood film: large platelets, platelet clumps; exclude leukoerythroblastic features
  • JAK2 V617F: first-line molecular test
  • CALR mutation: if JAK2 negative
  • MPL mutation: if JAK2 and CALR negative
  • BCR-ABL: to exclude CML (mandatory)
  • Iron studies, CRP, ESR: exclude reactive causes
  • LDH: raised in MPNs
  • vWF activity/antigen and ristocetin cofactor: if platelets >1000 and bleeding

Imaging

  • Abdominal ultrasound: splenomegaly assessment

Special Tests

  • Bone marrow biopsy: proliferation of large mature megakaryocytes with hyperlobulated nuclei; no significant fibrosis (reticulin grade 0-1); mandatory for diagnosis
  • Cytogenetics: exclude MDS, CML

Management

Non-pharmacological

  • Cardiovascular risk factor modification: smoking cessation, weight management
  • Low-risk patients may require observation only

Pharmacological

Low-risk (age <60, no prior thrombosis):

  • Aspirin 75mg OD (if microvascular symptoms or cardiovascular risk factors)
  • Some very low-risk patients (CALR-mutated, young) may not need aspirin

High-risk (age ≥60 OR prior thrombosis):

  • Hydroxycarbamide 500mg-1g OD – first-line cytoreductive therapy (PT-1 trial)
  • Target platelet count <400 × 10⁹/L
  • Plus aspirin 75mg OD

Hydroxycarbamide-intolerant/resistant:

  • Anagrelide 0.5mg BD (titrate to response, max 10mg/day) – PT-1 trial showed non-inferiority but more arterial thrombosis and fibrosis
  • Interferon alfa (pegylated): preferred in younger patients and pregnancy
  • Busulfan: elderly patients, short course

Very high platelets (>1500 × 10⁹/L):

  • Withhold aspirin (acquired vWD risk → bleeding)
  • Check vWF activity: restore aspirin when platelets reduced and vWF normalised

Referral Criteria

  • All patients with sustained thrombocytosis >450 → haematology
  • Thrombotic or haemorrhagic events → urgent haematology

Prognosis

  • Median survival: >20 years (near-normal life expectancy for low-risk)
  • Thrombosis risk: 10-25% at 10 years (higher in JAK2-positive)
  • Transformation to myelofibrosis: 3-10% at 10 years
  • Transformation to AML: 1-3% at 10 years
  • CALR-mutated ET has best prognosis and lowest thrombotic risk
  • IPSET-thrombosis score guides risk stratification: age, JAK2 status, prior thrombosis, cardiovascular risk factors

Other Relevant Information

IPSET-Thrombosis Risk Stratification

RiskCriteriaManagement
Very lowAge <60, no thrombosis, CALR+/JAK2-Observation or aspirin
LowAge <60, no thrombosis, JAK2+Aspirin 75mg OD
IntermediateAge ≥60, no thrombosis, CALR+/JAK2-Aspirin or cytoreduction
HighAge ≥60 with JAK2+ OR prior thrombosisCytoreduction + aspirin

Driver Mutation Comparison

MutationFrequencyThrombosis RiskSurvival
JAK2 V617F~60%HighestIntermediate
CALR~25%LowestBest
MPL~5%IntermediateIntermediate
Triple-negative~10%VariableVariable