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Systemic Mastocytosis (SM)
CD2+, CD25+ Mast Cells
KIT D816V mutation in >90% patient (or other exon 17)
WHO 2021 diagnostic Criteria (1 major + 1 minor, or 3 minor)
Major
Multifocal, dense infiltrates (>15 mast cells in aggregates) in marrow or extracutaneous organs.
Minor
>25% mast cells with spindled / atypical morphology
KIT point mutation at codon 816 (KIT D816V), or at other critical regions of KIT
CD25, CD2 and/or CD30 expression in mast cells
Serum tryptase >20 ng/ml, unless there is an associated clonal myeloid disorder
WHO-HAEM5 Classification of Systemic Mastocytosis
Bone marrow mastocytosis
Indolent systemic mastocytosis
Smouldering systemic mastocytosis
Aggressive systemic mastocytosis
Systemic mastocytosis with an associated haematologic neoplasm
Mast cell leukaemia
(WDSM - Well-differentiated systemic mastocytosis - is a morphological subtype occurring in any SM subtype. Most of these cases are CD25-, CD2-, CD30+ and are KITD816V negative)
Clinical Presentation
Features of mast cell degranulation (‘mediator’ symptoms)
Anaphylaxis, flushing, itch, N&V, diarrhoea, lightheadedness, severe hypotension, bone paine, neuropsychiatric distrubance
Often no identifiable triggers
Staging Work-Up
Serum total tryptase
BM Biopsy
Relevant organ biopsy
KITD816V mutation (or other exon 17)
CD2 / CD25 Mast cell expression
If eosinophilia, screen for FIP1L1-PDGFRA
Indolent / Smouldering / Advanced (as per who)
Indolent
No B or C findings
Smouldering = 2 or more B Findings
(B = Burden of disease)
BM >30% mast cells and/or Tryptase >200 ng/ml and/or KITD816V mutation with a variant allele frequency (VAF) of >10%
Signs of dysplasia or myeloproliferation without frank AHN, & normal FBC
Hepatomegaly without liver dysfunction and/or splenomegaly without hypersplenism and/or palpable lymphadenopathy >2cm
Advanced (ASM, MCL, SM-AHN with organ damage) = C Findings, ie organ damage
(C = Cytoreduction-requiring)
One or more cytopenias (Hb <100, Plt <100, Neut <1.0)
Hepatomegaly with liver dysfunction
Osteolytic lesions or fractures
Splenomegaly with symptomatic hypersplenism
Malabsorption with weight loss due to GI infiltration
Management
Avoidance of triggers
Treatment of mediator symptoms
EpiPen
H1 anti-histamines (Cetirizine, Fexofenadine, Hydroxyzine)
H2 antagonists (Ranitidine, Cimetidine)
Leukotriene antagonists (Montelukast)
Bisphosphonates for osteoporosis / bone pain / fractures
Mast cell stabilisers (ketotifen, cromolyn)
PUVA light therapy
NSAID - Aspirin
Cytoreductive Therapy
Steroids
PEG Interferon alpha - Variable outcomes reported in small case series. Low median treatment duration due to poor tolerance of side effects.
Cladribine - Approx. 50% response rate. Presence of KIT mutation predicts response. 30% cytopenias.
Multi-agent chemotherapy
Allogeneic Transplant - All patient 3yr OS 57% retrospective studies (74% for SM-AHN)
Targeted Therapies / Trials (Presence of KIT D816V confers resistance against many TKI’s)
Midostaurin (KIT inhibitor)
60% ORR
SE: Gastrointestinal, Cytopenias, QT interval prolongation
Avapritinib (KIT + PDGFRA kinase inhibitor)
75% ORR in PATHFINDER 2021
Large number or patients dose reduced or discontinued due to adverse events
SE: Gastrointestinal, Oedema, Cytopenias, Cognitive impairment (hair colour change in 20%!)
Dasatinib / Nilotinib
Mastinib
Imatinib
Everolimus
Mabs – Daclizumab, Omalizumab
Other Mabs to consider based on pt’s immunophenotype – CD30, CD33, CD52, CD123
Mast Cell Activation Syndrome (MCAS)
Meeting only 1 or 2 of the minor diagnostic criteria
Lack the characteristic BM mast cell aggregates
Episodic symptoms of mast cell degranulation