π¬ Aetiology of Thrombocytosis
Overview: Four Main Categories
THROMBOCYTOSIS (Platelets >450Γ10βΉ/L)
β
Reactive (>80%)
Clonal Myeloid
Clonal Haematopoiesis
Hereditary
1. Reactive (Secondary) Thrombocytosis
Pathophysiology
Thrombopoietin (TPO) is the primary regulator:
Produced by the liver
Cleared via receptors (TPOR/MPL) on megakaryocytes and platelets
Plasma TPO regulated by platelet mass
Acute phase reactants (IL-6) increase hepatic TPO production
Category
Common Causes
Deficiency/Loss
Iron deficiency, bleeding
Inflammation
Infection, autoimmune disease, malignancy
Tissue Damage
Trauma, surgery, burns
Splenic
Hyposplenism, splenectomy
Metabolic
Obesity, metabolic syndrome
Drug-Related
TPO agonists, ESAs, chemotherapy recovery
2. Clonal Myeloid Disorders
Classical MPNs - Driver Mutations
JAK2 V617F: 50-60% of ET
CALR exon 9 frameshift: 25-35% of ET
MPL exon 10 variants: 5-10% of ET
Triple-negative ET: 10-15% of ET
Triple-Negative ET Characteristics
β Predominantly young females
β Most lack definitive clonal evidence
β Lower myelofibrotic transformation risk
β Lower thrombosis risk
β Highly favourable survival
3. Clonal Haematopoiesis (CH)
Definition: Presence of clonal blood cell populations in otherwise healthy individuals
Common genes: DNMT3A, TET2, ASXL1
Prevalence:
~10% of individuals >70 years (conventional sequencing)
>66% with sensitive sequencing (VAF <1%)
Clinical significance: May indicate emergent haematological malignancy, especially if:
High VAF (>10%)
Multiple pathogenic variants
Younger individuals
Additional cytopenias
4. Hereditary Thrombocytosis
Gene
Key Features
Clinical Implications
JAK2 germline
Various variants (V617I, R564Q/L, etc.)
Variable thrombotic risk
MPL germline
S505N, P106L, R170H, etc.
S505N: high thrombotic risk, fibrosis progression
THPO
Various regulatory variants
May associate with distal limb defects
SH2B3
Biallelic variants
Autoimmune features, hepatosplenomegaly
β Previous
Next: Investigation β
π Investigation Approach
β οΈ Critical First Principle
Over 80% of thrombocytosis is REACTIVE - thorough exclusion of secondary causes is fundamental!
Stage 1: Initial Clinical Assessment & Testing
Clinical History & Examination
Symptoms: Headaches, erythromelalgia, microvascular disturbances
Risk Factors: Cardiovascular risks, thrombotic/haemorrhagic history
Family History: Thrombocytosis, MPN, malignancy
Examination: BMI, splenomegaly, signs of systemic disease
First-Line Investigations
Test
Purpose
Blood Film
Spurious thrombocytosis, other myeloid features
Iron Studies
Exclude iron deficiency
CRP
Inflammatory markers
CXR (age >40)
Malignancy screening
Abdominal US
If splenomegaly suspected
JAK2, CALR, MPL
MPN driver mutations (peripheral blood)
BCR::ABL1
If triple-negative (exclude CML)
β οΈ Important Note
Serum TPO levels do NOT distinguish reactive from clonal thrombocytosis and are NOT routinely recommended .
Stage 2: When to Perform Comprehensive Investigations
β
GRADE 1C - Strong Recommendation
Perform BM biopsy + NGS-MGP +/- cytogenetics if:
Age >60 years, OR
Age 40-60 with significant cardiovascular risk factors*, OR
Prior vascular event(s), OR
Platelets >1500Γ10βΉ/L
*Hypertension, diabetes, hypercholesterolaemia on therapy, or high QRISK3 score
π€ GRADE 2C - Consider Offering
May offer BM biopsy + NGS-MGP +/- cytogenetics if:
Age <60 years without significant vascular risk, BUT
Platelets 600-1500Γ10βΉ/L AND/OR
Unexplained pertinent symptoms (headaches, erythromelalgia)
β NOT Required
BM biopsy and additional genomics NOT needed if:
Age <60 years
No previous vascular events
No cardiovascular risk factors or symptoms
Mild thrombocytosis (<600Γ10βΉ/L)
BUT: Secondary causes MUST be fully excluded!
Bone Marrow Histology
Key Features of ET:
Megakaryocyte proliferation
Increased enlarged, mature megakaryocytes
Hyperlobated nuclei (characteristic finding)
Limitations:
Subjective interpretation (18% diagnosis changes after expert review)
Borderline features common in triple-negative cases
Inter-observer variability exists
π‘ Best Practice
All BM histology should undergo expert haematopathologist review within a multidisciplinary team (MDT) setting, integrating molecular and clinical features.
Next-Generation Sequencing (NGS) Myeloid Gene Panel
NHS England Minimum Panel Includes:
ASXL1, CALR, CBL, CSF3R, CUX1, DNMT3A, EZH2, HRAS, IDH1, IDH2, IKZF1, JAK2, KIT, KRAS, MPL, NFE2, NRAS, RUNX1, SETBP1, SF3B1, SH2B3, SRSF2, TET2, TP53, U2AF1, ZRSR2
Findings in Triple-Negative Thrombocytosis:
70-85% negative
Non-canonical JAK2/MPL variants (minority)
Putative pathogenic germline variants
Variants in CH-associated genes
Paediatric Considerations
πΆ Special Considerations for Children
>50% of paediatric ET is triple-negative
Low complication rates
Higher platelet thresholds:
650Γ10βΉ/L at 2 months
Decreasing to 450Γ10βΉ/L by 6 years
Additional tests: Parental blood counts, inherited thrombocytosis panel
Higher BM threshold: Consider 800-1000Γ10βΉ/L in asymptomatic children
β Previous
Next: Diagnostic Terms β
π Novel Diagnostic Terminology
π― Why New Terms?
Current WHO/ICC classifications have limitations for triple-negative cases:
Histological interpretation is subjective
Triple-negative ET has distinctive natural history vs. mutation-positive ET
No category exists for thrombocytosis without reactive cause OR typical ET morphology
Patient counselling challenging when extrapolating from mutation-positive data
Four New Diagnostic Categories
NO Clonal Marker
Normal Megakaryocytes
β
ITUS
Atypical Megakaryocytes
β
ITAM
Clonal Marker Present
Normal Megakaryocytes
β
CTUS
Atypical Megakaryocytes
β
Triple-negative ET with clonal marker(s)
1. ITUS - Idiopathic Thrombocytosis of Undetermined Significance
Diagnostic Criteria:
β Persistent* thrombocytosis >450Γ10βΉ/L, no reactive cause
β Negative broad genomic analysis (NGS-MGP)
β Histology: normal or increased megakaryocytes WITHOUT significant morphological atypia
Clinical Implications:
No evidence of clonal process
Uncertain aetiology
Likely indolent course
Management:
NO routine antiplatelet therapy
Annual FBC surveillance
Re-evaluate if significant change in counts, new vascular events, or at age 60
2. ITAM - Idiopathic Thrombocytosis with Atypical Megakaryocytes
Diagnostic Criteria:
β Persistent* thrombocytosis >450Γ10βΉ/L, no reactive cause
β Negative broad genomic analysis (NGS-MGP) and cytogenetics
β Histology: increased megakaryocytes with large forms showing hyperlobated nuclei
Alternative term: "Triple-negative ET without clonal markers" (aligns with WHO terminology)
Management:
Consider aspirin if age >60 or cardiovascular risk factors
Consider cytoreduction if:
Age >60
Vascular event where thrombocytosis implicated
Platelets >1500Γ10βΉ/L
Refractory symptoms
Multiple cardiovascular risk factors
Preferred agent: Interferon-alpha (no DNA-damaging mechanism)
3. CTUS - Clonal Thrombocytosis of Undetermined Significance
Diagnostic Criteria:
β Persistent* thrombocytosis >450Γ10βΉ/L, no reactive cause
β Positive for somatic mutations in CH driver genes (NOT JAK2/CALR/MPL)
VAF β₯2% (β₯4% for X-linked in males)
OR clonal cytogenetic abnormality
β Histology: normal or increased megakaryocytes WITHOUT ET-like atypia
β No features of other myeloid neoplasm
Clinical Implications:
Evidence of clonal haematopoiesis
Falls outside current WHO/ICC classifications
Uncertain natural history and vascular risk
Unknown progression risk to classical ET
Management:
Conservative cytoreduction threshold - only if pronounced thrombocytosis contributing to symptoms or unexplained vascular event
Cardiovascular risk optimization crucial (especially smoking cessation)
Could consider aspirin if age >60 or cardiovascular risks
Counsel patients that benefits of therapy are uncertain
4. Triple-Negative ET with Clonal Marker(s)
Diagnostic Criteria:
β Persistent* thrombocytosis >450Γ10βΉ/L, no reactive cause
β Positive for mutations in CH driver genes (NOT JAK2/CALR/MPL), VAF β₯2%
OR clonal cytogenetic abnormality
β Histology: increased megakaryocytes with large forms showing hyperlobated nuclei
β No features of other myeloid neoplasm
Clinical Implications:
Clonal marker supports ET diagnosis (WHO minor criterion)
Subcategorization distinguishes from cases without clonal markers
Management:
Follow ITAM guidance
Low threshold for repeat BM/genomic assessment if atypical features develop
β οΈ Important Notes
*Persistence: Thrombocytosis must be persistent for at least 3 months before confirming diagnosis. Longer surveillance may be preferable for mild/variable thrombocytosis.
Minimum VAF threshold: 2% for autosomal genes, 4% for X-linked genes in males (aligns with clonal cytopenia of undetermined significance criteria)
Special Consideration: Very Low VAF JAK2 V617F
If JAK2 V617F detected at VAF <1%:
May not meet criteria for ET
Consider CTUS-type management if histology non-diagnostic
Repeat mutational testing (with VAF) if platelet count rises
Could repeat every 2-3 years if stable
β Previous
Next: Management β
π Management Strategies
1. Reactive Thrombocytosis
Primary Strategy: Treat the Underlying Cause
β No routine antiplatelet/anticoagulant therapy unless other indications (GRADE 1C)
β Standard thromboprophylaxis for hospitalized patients per local guidelines
β Monitor FBC to ensure resolution
β Special consideration: Iron deficiency with normal Hct - repeat FBC after iron replacement to exclude PV
2. Hereditary Thrombocytosis
Essential Steps (GRADE 1C):
MDT discussion (may include genomics tumor advisory board, clinical genetics)
Clinical monitoring for thrombosis, bleeding, myelofibrotic progression
Cardiovascular risk factor optimization
FBC and blood film monitoring
Aspirin (GRADE 2C) - Consider if:
Other cardiovascular risks present
Family member with same variant had unexplained thrombotic episode
Particular variant associated with high thrombosis incidence
Cytoreduction (GRADE 2C):
NOT routine
Consider for severe intractable symptoms or recurrent thrombosis
Thrombosis Management (GRADE 1C):
Unexplained venous thrombosis: standard anticoagulation protocols
Expectation of long-term anticoagulation (if acceptable bleeding risks)
3. ITUS Management
Conservative Approach
β No routine antiplatelet therapy unless other standard indications (GRADE 1C)
β Annual FBC surveillance appropriate for most with stable counts (GRADE 2C)
β Community-based intermittent monitoring acceptable
β Pregnancy: standard obstetric VTE prevention guidelines
Re-evaluation Triggers (GRADE 2C):
Significant change in blood counts
Age 60 years (for younger patients)
New unprovoked vascular event
Development of MPN-suggestive features
4. ITAM / Triple-Negative ET Management
Risk-Stratified Approach
Aspirin (GRADE 2C) - Consider for:
Age >60 years
Additional cardiovascular risk factors (hypertension, diabetes, hypercholesterolaemia, smoking)
Refractory symptoms
Cytoreduction (GRADE 2B) - Consider for:
Age >60 years
Thrombotic/haemorrhagic event where thrombocytosis implicated
Persistent platelets >1500Γ10βΉ/L
Refractory symptoms
Multiple cardiovascular risk factors
Agent Selection:
Interferon-alpha may be favoured (no DNA-damaging mechanism) if no contraindications
No evidence favouring any particular agent otherwise
Platelet Count Targets (GRADE 1C)
Should reflect treatment indication:
Symptoms: Aim for resolution
Extreme thrombocytosis: <1500Γ10βΉ/L
Age/vascular risk without events: <600Γ10βΉ/L
Otherwise unexplained vascular events: Normal range
Surgery Considerations (GRADE 2C)
Consider temporary cytoreduction if:
Marked thrombocytosis (>1000Γ10βΉ/L)
Reduced von Willebrand factor activity levels
5. CTUS Management
More Conservative Than ITAM
Cytoreduction (GRADE 2D):
Only if pronounced thrombocytosis thought contributing to:
Refractory symptoms, OR
Otherwise unexplained vascular event
Cardiovascular Risk Factors:
Especially important given CH associations
Smoking cessation critical (smoking increases CH risk)
Could consider aspirin based on other indications (cardiovascular disease, risk score)
Patient Counselling:
Benefits of aspirin/cytoreduction are uncertain
Shared decision-making essential
6. Triple-Negative ET with Clonal Marker(s)
Follow ITAM Guidance
Low threshold for repeat BM/genomic assessment if atypical features develop:
Unexplained/disproportionate cytopenias on cytoreduction
New monocytosis
General Principles Across All Categories
Key Management Principles
Optimize cardiovascular risk factors in all patients (GRADE 1B)
Expert haematopathologist review essential (GRADE 2B for ITAM)
Low threshold for interval repeat assessment if starting therapy
Consider re-evaluation if original assessment >5 years ago
Individualize decisions based on patient preferences and clinical context
β Previous
Next: Algorithm β
πΊοΈ Interactive Diagnostic Algorithm
π‘ How to Use This Algorithm
Click on each decision node to reveal the next steps. This mirrors the clinical decision-making process.
STEP 1: Persistent Isolated Thrombocytosis >450Γ10βΉ/L
Click to expand
β
Clinical History & Examination
Blood film, iron studies, CRP
Consider: CXR (age >40), abdominal US, targeted imaging
Click to continue
β
Secondary cause identified?
YES
β Reactive Thrombocytosis
β Treat underlying cause
β Monitor FBC for resolution
NO
β Proceed to mutation screening
Click to continue
β
Peripheral Blood Screening
JAK2, CALR, MPL
If negative: BCR::ABL1
β
JAK2/CALR/MPL POSITIVE
β Likely ET/PV/PMF
β Consider BM biopsy
β Follow MPN guidelines
TRIPLE-NEGATIVE
β Assess need for comprehensive investigation
Click to continue
β
Risk Stratification for Comprehensive Testing
β
Age <60, No CV Risk
Platelets <600
β No additional investigations
β Annual FBC monitoring
β Re-evaluate at age 60
Age <60, No CV Risk
Platelets 600-1500
OR unexplained symptoms
Click for options
Age >60 OR
CV Risk/Prior Events OR
Platelets >1500
Click to continue
β
GRADE 2C: May Offer
BM biopsy + NGS-MGP +/- cytogenetics
β Proceed to histology interpretation
β
GRADE 1C: Perform
BM biopsy + NGS-MGP +/- cytogenetics
β
Integrate Results
Histology + Genomics + Clinical
Click to see diagnostic outcomes
β
NO Clonal Marker
Normal Megakaryocytes
β ITUS
β Conservative management
Atypical Megakaryocytes
β ITAM
β Consider aspirin/cytoreduction
Clonal Marker Present
Normal Megakaryocytes
β CTUS
β CV risk optimization
Atypical Megakaryocytes
β Triple-neg ET with clonal markers
β Manage as ITAM
β οΈ Important Reminders
All BM histology should undergo expert haematopathologist review in MDT setting
Consider family history and parental blood counts, especially in children
Germline testing if pathogenic variant identified on BM NGS-MGP
Threshold for comprehensive testing may be higher in children (e.g., 800-1000Γ10βΉ/L)
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Next: Case Scenarios β