Aplastic Anaemia (bsh 2024)
Pancytopenia with a hypocellular marrow & no abnormal infiltrate or fibrosis
Camitta Criteria requires 2 or more of: Hb <100, Plt <50, Neut <1.5
Intro
2-3 cases per million per year in Europe (higher incidence in East Asia)
70-80% Idiopathic
Two peaks at 10-25 yo and >60 yo
Assessing Severity: Modified Camitta Criteria
Severe Aplastic Anaemia (SAA)
<25% BM cellularity (or 25-50% with <30% haematopoeitic cells)
2 or more of:
Neut <0.5
Plt <20
Reticulocytes <60 (by an automated count)
Very Severe Aplastic Anaemia (VSAA)
As for SAA but Neutrophils <0.2
Non-Severe Aplastic Anaemia (NSAA)
Not meeting criteria for SAA or VSAA
Clinical Presentation
Anaemia and thrombocytopenia symptoms more common than infections at the start
Organomegaly/Lymphadenopathy usually absent
Precipitants:
Preceding history of jaundice --> ?Post-Hepatic AA – rare. Occurs 2-3 months after illness
SLE – pancytopenia in SLE may be due to AI, fibrosis or more rarely AA
Drugs – Chloramphenicol, Carbamazepine, Phenytoin, Quinine
Occupation History – Benzenes, Radiation
Family History – see later for congenital syndromes
work-up of aplastic anaemia
Differential Dx of pancytopenia with a hypocellular marrow
Aplastic Anaemia
PNH
Hypoplastic MDS
Hypoplastic AML
Lymphoma – e.g. Hairy Cell
Myelofibrosis
Anorexia / Starvation
Drug Induced
Inherited BM Failure Syndromes
Mycobacterial Infection
Inherited BM Failure Syndromes (IBMFS)
Fanconi Anaemia (FA)
Short stature, skin hypo/hyperpigmentation, Skeletal abnormalities (e.g. thumb)
90% pts have BM failure (AA)
Increased risk of malignancy
DEB Test for chromosomal breakage analysis
Dyskeratosis Congenita (DC)
Triad: Nail dystrophy + Oral Leukoplakia + Skin reticular pigmentation
80% pts have BM failure (AA)
Increased risk of malignancy
Telomere length by FISH / PCR
Schwachman-Diamond Syndrome (SDS)
SBDS gene mutations
Pancreatic insufficiency with cytopenias and recurrent infection
~20% have BM failure (AA)
Increased risk of malignancy
Diamond-Blackfan Anaemia (DBA)
RSP19 gene mutation (Autosomal dominant)
Red cell aplasia in the neonate/infant
Associated features: Craniofacial, Skeletal, Cardiac, Urogenital tract
Increased risk of malignancy
Mx: Steroids, Transfusion, Chelation, BM Transplant
Congenital Dyserythropoietic Anaemia (CDA)
Dyserythropoiesis
Extra-haematopoietic features are rare
Congenital Amegakaryocytic Thrombocytopenia and Syndromic Thrombocytopenia (CAMT)
MPL gene mutations
Isolated severe thrombocytopenia from birth, BM failure later in childhood
Increased risk of malignancy
Severe Congenital Neutropenia (SCN)
Neutropenia
Extra-haematopoietic features are rare
Increased risk of malignancy
GATA2 Deficiency Syndromes
GATA2 mutation with lymphedema, immunodeficiency, sensorineural deafness, lung disease
Emberger Syndrome = GATA2 mutation with lymphoedema
MonoMAC = GATA2 mutation with monocytopenia +/- mycobacterial infection
TAR (Thrombocytopenia with Absent Radii)
Other bones of forearm also affected. Asscoiated with cow’s milk intolerance
Investigations
AA is a diagnosis of exclusion, tests listed aimed at ruling out other causes.
FBC – Lymphocyte count often normal. If monocytopenia, think Hairy Cell / GATA2
Reticulocyte count
Film – Small platelets, macrocytosis, anisopoikilocytosis, neut toxic granulation, may exclude other causes
HbF% - Prognostic indicator in children. May be elevated in IBMFS
B12/Folate
LFT - to detect hepatitis
Viral Serology – Hep A/B/C/E, EBV, CMV, Parvovirus B19, HIV. Note even in posthepatitis AA, virology for known viruses is often negative.
Autoantibodies – ANA, Anti-dsDNA
PNH Screen - Flow for GPI-anchored proteins
Chromosomal breakage analysis - Diepoxybutane (DEB) test. Performed on peripheral blood, consider screening all transplant candidates and siblings of FA patients.
Leucocyte Telomere length - performed on peripheral blood. Classic finding in DC but can be seen in other rare cases
CXR - screen for infection
Skeletal XR’s - for suspected IBMFS
HRCT Chest - to assess for lung fibrosis in suspected IBMFS
Abdo USS – splenomegaly, displaced kidneys (Fanconi)
Echo
HLA Tissue Typing – pre-transplant
Genetic Tests - e.g. NGS panels to help distinguish AA from hypocellular MDS. Note however that somatic mutations present in 20-30% of AA patients.
BM Features of AA
Aspirate
Hypocellular trails with prominent fat spaces
Dysplastic red cells are common and can be marked
Megakaryocytes and Granulocytes reduced, but not dysplastic
Haemophagocytosis & increased macrophage numbers seen in early disease
Eosinophilic background staining
Trephine
Hypocellular
Focal hyperplasia of erythroid or granulocytic cells all at same stage of maturation
Cytogenetics/FISH/SNP array
Cytogenetic abnormalities present in up to 12% of cases
(del)13q, Trisomy 8, Monosomy 7
management of aplastic anaemia
Supportive Care
Red Cell Transfusion
Rh and Kell-matched products preferred
Irradiated if ATG, Campath or HSCT
No specific transfusion threshold, individual plans should be made
Alloimmunisation and Iron overload significant problems
Platelet Transfusions
Irradiated if ATG, Campath or HSCT
Not indicated for asymptomatic patients with chronic thrombocytopenia
Keep >10 if stable and currently on active therapy
Keep >20 during ATG treatment
Keep >20 in sepsis
HLA alloimunisation —> platelet refractoriness and increased graft rejection post HSCT
Iron Chelation
Patient-by-patient decision
Desferrioxamine and Deferasirox (Exjade) are licensed
Venesect after successful recovery of counts
See also iron chelator details
Infection Prevention in Severe Neutropenia
Nurse in isolation
Quinolone (eg Ciprofloxacin) prophylaxis
Itraconazole / posaconazole prophylaxis
Aciclovir prophylaxis if on immunosuppression
Epo & GCSF are ineffective. GCSF does not improve longterm outcomes
Vaccination
Case reports of vaccination triggering primary episodes and relapses of AA
Benefit likely to outweigh risk so discuss with patient
Wait 6 months after ATG before vaccination due to reduced responses
Psychological Support
Aplastic Anaemia Trust patient support group
Consider referral to formal counselling or psychology services
PNH Clones in Aplastic Anaemia
See also: PNH Page
Principles
PNH clone present in 50-60% of AA cases
Presence of a large PNH clone makes a diagnosis of IBMFS unlikely
Presence of a PNH clone does not directly influence treatment of the AA but additional anti-complement therapy may be required if thrombosis or haemolysis develops
All UK pts should be referred to national PNH centre
Monitoring
If positive, test every 3 months for one year, then annually if clone stable
If negative, test in 6 months and then annually
First line treatment of Severe / Very Severe AA
Age <40:
HLA-identical sibling allograft
If no sibling donor, consider matched unrelated allograft for children (or for case-by-case adults requiring urgent correction of neutropenia)
Alternative, ATG + Ciclosporin +/- Eltrombopag
Age >40:
ATG + Ciclosporin +/- Eltrombopag
If no response, matched unrelated allograft vs non-transplant options
Age >60:
Requires careful assessment of fitness to proceed with ATG
Higher rates of dysrhythmias, MI and heart failure
Immunosuppression Therapy (IST)
Horse Anti-Thymocyte Globulin (ATG)
40mg/kg/day for four days
Must be given into a central vein
Give test dose due to risk of anaphylaxis
Methylprednisolone + Piriton prior to each dose
Keep platelets >20 prior to each dose (consider increment studies prior to treatment)
SE: Fever, rash, rigors, hypo/hypertension, oedema, ARDS, anaphylaxis, serum sickness
Long-term SE: 8-25% MDS/AML at 10 years
Prospective and meta-analysis data found superiority over rabbit ATG
Ciclosporin
5mg/kg/day, aiming for trough levels of 150-200 ug/l
Continue for minimum 12 months and then consider slow weaning
Interaction with posaconazole requires pre-emptive dose adjustments
Protocol
Give ATG for four days
Start Ciclosporin on Day 1
4 weeks prednisolone to prevent serum sickness
Infection prevention as per section above
GCSF not required
Serum Sickness
Most common 7-14 days after ATG
Arthralgia, myalgia, rash, fever
Treat with QDS hydrocortisone
Assessing Response (SAA)
None – still meets severe disease category
Partial – transfusion independent, no longer in severe category
Complete – normal Hb, Neut >1.5, Plt >150
Outcomes
Response is delayed - at least 3-4 months on average
SAA 6 months response rate 50-70%, VSAA 23%
Late events occur in 50% of pts - 35% relapse, 8-25% MDS/AML, 10% haemorrhagic PNH
5 year OS
<20 yo: 100%
>60 yo: 56%
Factors predicting a good outcome
Young age, less severe disease
Retic >25, Lymph >1.0
Trisomy 8 or del(13q)
Presence of PNH clone
Eltrombopag
Small molecule, oral thrombopoeitin receptor agonist
150mg daily from Day 14 until 6 months (or 3 months if achieve a CR)
Improves outcomes when added to ATG + Ciclosporin
Not currently approved in UK for first line use (as of early 2024)
Concern about long term risk of clonal evolution - avoid in pts with monosomy 7, consider BM surveillance.
1st line ATG + Ciclosporin with or without Eltrombopag
6 mo overall response benefit (68% vs 41%)
No difference in 2 yr overall survival
Alternative IST to ATG+Ciclo?
Alemtuzumab?
Seek expert advice
Response rate 35-55% in R/R patients
Do NOT use:
Mycophenolate, Sirolimus, Corticosteroids and Cyclophosphamide
Stem Cell Transplant (HSCT)
Indications
1st line for SAA <40 yo, with an HLA-matched sibling donor (40-50yo = grey zone)
2nd line if no response to IST, with an HLA-matched, unrelated donor
Syngeneic donor – consider at any age as long term OS = >90%
Pre-transplant work-up
Repeat BM biopsy and PNH flow
Assess co-morbidities
Select donor, conditioning regimen and stem cell dose
Address fertility issues
Offer psychological support
Conditioning Regimens
Beyond scope of Haembase. See guideline
Outcomes
OS 70-90% in ages 30-50
Specific Scenarios
Non-Severe AA
Poorly defined treatment recommendations
Many patients do not require any treatment
Consider if: transfusion dependent, progress to severe AA, lifestyle factors
If treating, prefer ATG + Ciclosporin (Eltrombopag is not approved)
Elderly (>60 yo)
Outcomes worse, tolerability of treatment is poor
Consider QoL issues and patients wishes
ATG + Ciclosporin if fit
Alternatives: Ciclosporin alone, Danazol, Alemtuzumab
(NB Danazol has been discontinued in the UK)
Pregnancy
1st presentation may occur in pregnancy, and may spon. Remit post delivery
Relapse post-IST is common in pregnancy
50% of pregnancies in patients post-IST involve a maternal complication
Ciclosporin is safe in pregnancy
Keep platelets >20
Focus is on supportive care