Approach

Treatment is guided by the patient’s ability to tolerate intensive chemotherapy (e.g., based on age, fitness/performance status, comorbidities), risk stratification (e.g., based on genetic abnormalities), disease biology/subtype, measurable (minimal) residual disease (MRD) assessment, and patient preference/goals.

​​​Patients unsuitable for intensive chemotherapy should be considered for lower-intensity therapy.

Enrolment in a clinical trial should be considered for all patients, where possible, particularly those who are older, are unable to tolerate chemotherapy, who have unfavourable disease (e.g., those with TP53 mutations or 17p deletion), or have relapsed/refractory disease.[45][70][71]​​​​​

Treatment goals

The early goals of treatment are to achieve complete remission and reduce the risk of relapse. See Criteria for treatment response criteria.

The long-term goal is to improve disease-free survival and overall survival, with minimal long-term adverse effects. For fit younger patients (<60 years of age) who are treated with intensive chemotherapy, the overall goal is disease cure. In older patients, the goal is usually to achieve complete remission that extends survival and quality of life; cure may be possible for a subset of fit older patients.

The goals of treatment should be discussed with the patient in the context of their disease, fitness, and preferences, and this should inform decision-making and treatment planning throughout the course of treatment.

Management of AML: suitable for intensive chemotherapy

Patients with acute myeloid leukaemia (AML) who are fit and able to tolerate intensive therapy should undergo treatment with dose-intense chemotherapy regimens in two main phases: induction and consolidation.[27][45]

Intensive induction therapy for AML

The aim of induction therapy is to achieve complete remission with low or undetectable MRD.[27][45]

The standard chemotherapy backbone for intensive induction therapy is cytarabine plus an anthracycline, which is associated with a complete remission rate of 70% to 80% in patients <60 years of age.[72][73][74][75]​​​​ In patients ≥60 years of age, the complete remission rate is lower (60% to 70%).[76][77]​​​​ However, complete remission rate varies significantly depending on disease biology.

Targeted therapies can be added to intensive chemotherapy regimens for patients with certain AML subtypes, biological markers, or genetic abnormalities.[27][45]

The recommended treatment approach for patients eligible for intensive induction therapy is premised on European LeukemiaNet (ELN) risk stratification risk groups. The ELN risk stratification is based on genetic abnormalities; other risk factors include therapy-related AML (tAML) or antecedent myelodysplastic syndrome (MDS)/chronic myelomonocytic leukaemia (CMML).[45] See Criteria for European LeukemiaNet risk stratification by genetic abnormalities.

The following regimens are recommended for patients eligible for intensive induction therapy who have favourable-risk disease according to cytogenetic abnormalities (i.e., RUNX1::RUNX1T1 or CBFB::MYH11 associated with core binding factor [CBF]-AML):[45]

  • Cytarabine for 7 days plus an anthracycline (e.g., daunorubicin or idarubicin) for 3 days (standard 7+3 [daunorubicin or idarubicin])

  • Cytarabine for 7 days plus mitoxantrone for 3 days (standard 7+3 [mitoxantrone]), for patients ≥60 years of age

  • Standard 7+3 (daunorubicin or idarubicin) plus gemtuzumab ozogamicin (an anti-CD33 monoclonal antibody conjugated with the cytotoxic agent calicheamicin), for CD33-positive AML

  • Fludarabine plus cytarabine plus granulocyte colony-stimulating factor (G-CSF) plus idarubicin (i.e., FLAG-IDA) plus gemtuzumab ozogamicin, for CD33-positive AML (use with caution in patients >60 years of age)

The following regimens are recommended for patients eligible for intensive induction therapy who have favourable-risk disease according to genetic mutations (i.e., mutated NPM1 without FLT3-ITD; or basic leucine zipper [bZIP] in-frame mutated CEBPA), or intermediate-risk disease:[45]

  • Standard 7+3 (daunorubicin or idarubicin)

  • Standard 7+3 (mitoxantrone), for patients ≥60 years of age

  • FLAG-IDA (use with caution in patients >60 years of age)

  • Cladribine plus cytarabine plus G-CSF plus mitoxantrone (CLAG-M)

  • Standard 7+3 (daunorubicin or idarubicin) plus gemtuzumab ozogamicin, for CD33-positive AML

  • FLAG-IDA plus gemtuzumab ozogamicin, for CD33-positive AML (use with caution in patients >60 years of age)

  • Standard 7+3 (daunorubicin or idarubicin) plus midostaurin (a tyrosine kinase inhibitor), for FLT3-ITD mutated or FLT3-TKD mutated AML

  • Standard 7+3 (daunorubicin or idarubicin) plus quizartinib (a tyrosine kinase inhibitor available in the US only through a restricted Risk Evaluation and Mitigation Strategy [REMS] program), for FLT3-ITD mutated AML only

The following regimens are recommended for patients eligible for intensive induction therapy who have therapy-related AML (tAML) other than CBF-AML, or antecedent MDS/CMML, or cytogenetic changes consistent with MDS (previously classified as AML with myelodysplasia-related changes [AML-MRC]):[45]

  • Liposomal daunorubicin/cytarabine (a liposome-encapsulated fixed-dose combination of daunorubicin plus cytarabine), preferred for patients ≥60 years of age

  • Standard 7+3 (daunorubicin or idarubicin), preferred for patients <60 years of age

  • A hypomethylating agent (decitabine or azacitidine) plus venetoclax (a BCL2 inhibitor)

A clinical trial (preferred) or the following regimens are recommended for patients eligible for intensive induction therapy who have poor/adverse-risk disease without TP53 mutation or 17p deletion:[45]

  • Standard 7+3 (daunorubicin or idarubicin)

  • Liposomal daunorubicin/cytarabine

  • FLAG-IDA (use with caution in patients >60 years of age)

  • A hypomethylating agent (decitabine or azacitidine) plus venetoclax (a lower-intensity therapy)

  • CLAG-M

A clinical trial is recommended for patients with TP53 mutation or 17p deletion as these patients respond poorly to standard induction chemotherapy and have an especially poor prognosis.[45][78]​ If a clinical trial is not available, less intensive therapy (e.g., decitabine plus venetoclax) is preferred.[45][79]​ 

Patients who achieve complete remission with induction therapy should proceed to consolidation therapy. Those who do not achieve complete remission following induction therapy are considered to have refractory disease.

Consolidation therapy for AML

The aim of consolidation therapy is to maintain complete remission and reduce the risk of relapse following intensive induction therapy.

Consolidation therapy is guided by risk factors for relapse (e.g., genetic abnormalities, white blood cell [WBC] count at presentation, MRD).

Consolidation regimens usually consist of up to 4 cycles of intermediate-dose or high-dose cytarabine (IDAC or HiDAC) alone or in combination with other chemotherapy drugs (e.g., idarubicin, daunorubicin, mitoxantrone) and/or targeted therapy (e.g., gemtuzumab ozogamicin, midostaurin, or quizartinib) if the targeted therapy was used during intensive induction therapy.[27][45]

Patients who received liposomal daunorubicin/cytarabine for intensive induction therapy (e.g., those with tAML [other than core binding factor-AML]) can also receive this regimen for consolidation therapy.[45][80][81][82]

Patients with poor/adverse-risk disease (according to genetic abnormalities) who received the FLAG-IDA regimen or a hypomethylating agent (decitabine or azacitidine) plus venetoclax regimen for induction therapy can receive these regimens for consolidation therapy.[27][45]

Allogeneic stem cell transplantation (SCT) may be considered for consolidation therapy in certain patients (see below).

Measurable (minimal) residual disease (MRD) assessment in AML

MRD assessment (e.g., using polymerase chain reaction [PCR] or flow cytometry assays) should be performed during and after treatment to assess treatment response (i.e., the presence of leukaemic cells in the peripheral blood and/or bone marrow).[27][83]​​ MRD should also be assessed at the time of, and following, allogeneic SCT.[45]

MRD assessment can inform prognosis and treatment planning when combined with standard morphology-based assessment of treatment response. Leukaemic cells may persist in patients who achieve morphological complete remission following treatment; therefore, MRD assessment can determine deeper remission status and improve prognostication and risk stratification.

The European LeukemiaNet has published recommendations for assessing MRD (including frequency and timing) in AML patients.​​​​​​​[27][83]

Stem cell transplantation (SCT) for AML

Patients with intermediate-risk disease and particularly those with poor/adverse-risk disease (including those with tAML [other than CBF-AML], or antecedent MDS/CMML, or cytogenetic changes consistent with MDS) may be considered for allogeneic SCT (with reduced-intensity conditioning for older patients) at first complete remission (i.e., in lieu of consolidation chemotherapy) if they are fit and able to tolerate SCT, and a suitable donor is available.[27][45]​​[84][85]​​​​​​ 

Patients with favourable-risk disease may be considered for allogeneic SCT at first complete remission if they are unable to complete consolidation therapy or they have persistent MRD, and a suitable donor is available.[27][45]

Autologous SCT is not commonly performed, but may be an alternative to allogeneic SCT in select patients (e.g., those with intermediate-risk disease who are MRD negative) if a donor is not available.[27][70]​​​[86][87]​​​​

Maintenance therapy for AML

Maintenance therapy may be considered after induction/consolidation chemotherapy or allogeneic SCT in patients with certain AML subtypes, genetic mutations, and high-risk features.

Non-CBF-AML: maintenance therapy post-induction chemotherapy

Patients with non-CBF-AML who are in complete remission after intensive induction chemotherapy may be considered for oral azacitidine maintenance therapy (until progression or unacceptable toxicity) if no consolidation therapy or some consolidation therapy has been completed and no allogeneic SCT is planned.[45][88] Oral azacitidine maintenance therapy should not replace consolidation therapy.​

FLT3-mutated AML: maintenance therapy post-consolidation chemotherapy

Patients with FLT3-mutated AML who previously received midostaurin or quizartinib (in combination with standard induction and consolidation chemotherapy) may continue these agents as monotherapy post-consolidation chemotherapy, if no allogeneic SCT is planned.[45][89][90][91]

FLT3-mutated AML: maintenance therapy post-allogeneic SCT

Several oral tyrosine kinase inhibitors can be considered for maintenance therapy in patients with FLT3-mutated AML who are in complete remission post-allogeneic SCT. These include:[45][90][91]​​​​[92][93][94]​​​​​​

  • Gilteritinib (FLT3-ITD-mutated or FLT3-TKD-mutated)

  • Sorafenib (FLT3-ITD-mutated only)

  • Midostaurin (FLT3-ITD-mutated or FLT3-TKD-mutated)

  • Quizartinib (FLT3-ITD-mutated only)

Gilteritinib is preferred for post-allogeneic SCT maintenance therapy in patients with FLT3-ITD-mutated AML who were MRD-positive at first complete remission before transplant.[45]

AML with high-risk features: maintenance therapy post-allogeneic SCT

Patients with AML with high-risk features (e.g., poor/adverse risk genetic abnormalities, secondary AML) who are in complete remission post-allogeneic SCT may be considered for maintenance therapy with low-dose decitabine plus G-CSF.[45][95]

Management of AML: not suitable for intensive chemotherapy

Lower-intensity therapy should be considered for newly diagnosed patients who are not suitable for intensive chemotherapy (e.g., due to age, frailty, comorbidities).

​The following lower-intensity regimens are recommended for AML patients with an IDH1 mutation who are ineligible for intensive induction therapy:[45]

  • Azacitidine plus venetoclax

  • Azacitidine plus ivosidenib (an IDH1 inhibitor)

  • Decitabine plus venetoclax

  • Ivosidenib monotherapy

The following lower-intensity regimens are recommended for AML patients without an IDH1 mutation who are ineligible for intensive induction therapy:[45]

  • Azacitidine plus venetoclax

  • Decitabine plus venetoclax

  • Cladribine plus low-dose cytarabine (LDAC) plus venetoclax

Other lower-intensity regimens that can be considered for AML patients ineligible for intensive induction therapy include:[45]

  • LDAC plus venetoclax, for those with prior exposure to azacitidine or decitabine

  • LDAC plus glasdegib (a Hedgehog pathway inhibitor)

  • Gilteritinib with or without azacitidine, for FLT3-ITD-mutated or FLT3-TKD-mutated AML

  • Enasidenib (an IDH2 inhibitor) with or without azacitidine, for IDH2-mutated AML

  • Gemtuzumab ozogamicin, for CD33-positive AML

Decisions relating to prescribing of other lower-intensity regimens will be informed by IDH1 mutation status.

Targeted therapies may be associated with serious complications. Tumour lysis syndrome (TLS) is an oncological emergency that has been uncommonly reported in patients with AML treated with venetoclax.[96] Differentiation syndrome has been reported in patients treated with ivosidenib, enasidenib, and gilteritinib, which can be life-threatening if not treated.[97][98][99][100]​​ See 'Supportive care for AML and APL' section (below) for guidance on managing these complications.

Patients responding to lower-intensity regimens may continue these regimens until disease progression or intolerance.[27][45][71]

Allogeneic SCT may be an option in select patients who respond to lower-intensity therapy.[45] If eligible and a suitable donor is available, patients should undergo allogeneic SCT (with reduced-intensity conditioning) at first remission.[45][70]

Relapsed or refractory AML

Patients with relapsed or refractory disease have a poor prognosis.[101]

There is no standard salvage regimen for relapsed or refractory disease. Where possible, patients should be offered enrollment in a clinical trial.

At relapse, all patients should undergo molecular re-evaluation to identify targets (actionable genes) for salvage therapy, which may have emerged since diagnosis (due to clonal evolution) or were not detected at diagnosis.[27][45]

Important predictors of response to salvage therapy are age, genetic abnormalities, duration of first remission, and history of previous SCT.[102][103][104]

Relapsed or refractory AML: suitable for intensive salvage chemotherapy

Relapse after first complete remission occurs in approximately 50% of patients who received intensive induction therapy, usually in the first year following treatment.[105]​ Approximately 40% to 60% of relapsed patients achieve a second complete remission with intensive salvage chemotherapy (e.g., IDAC or HiDAC with or without an anthracycline or mitoxantrone), although duration of remission is usually limited.[102][105]​​[106]​​

Patients who achieve a second complete remission with intensive salvage therapy should be considered for allogeneic SCT (if eligible and a suitable donor is available) to reduce the risk of relapse.[45][74]​​​[101]

Relapsed or refractory AML: not suitable for intensive salvage chemotherapy

Patients unsuitable for intensive salvage chemotherapy can be considered for lower-intensity salvage therapy, which should be followed by allogeneic SCT (if eligible and a suitable donor is available) or continued until disease progression or intolerance. Options include:[45]

  • Venetoclax plus a hypomethylating agent (azacitidine or decitabine) or LDAC

  • Gilteritinib for FLT3-ITD-mutated or FLT3-TKD-mutated AML

  • Ivosidenib for IDH1-mutated AML. In Europe, ivosidenib is not approved for use in patients with relapsed or refractory AML

  • Olutasidenib (an IDH1 inhibitor) for IDH1-mutated AML.​​ Olutasidenib has been associated with differentiation syndrome

  • Enasidenib for IDH2-mutated AML.

  • Gemtuzumab ozogamicin for CD33-positive AML (off-label use in Europe)

  • Revumenib (an oral menin inhibitor) for KMT2A-rearranged AML

Patients who are unable to tolerate intensive or lower-intensity salvage therapy, or who decline further treatment, should be offered best supportive care and/or palliative care.[45]

Reinduction therapy (with chemotherapy) may be considered for patients with relapse following long remission (i.e., ≥12 months) after intensive chemotherapy.[45][70]​​​​

Management of acute promyelocytic leukaemia (APL)

APL is a subtype of AML (characterised by the presence of the PML::RARA fusion gene) that requires urgent treatment to prevent very early death caused by coagulopathy.[45][70][107]​​​ Treatment should commence as soon as APL is suspected (i.e., before confirmation by genetic testing).

Patients with APL are managed in three treatment phases: induction, consolidation, and maintenance.

Treatment is based on whether patients are non-high risk (defined as WBC count ≤10 × 10⁹/L [≤10,000/microlitre] at presentation) or high risk (defined as WBC count >10 × 10⁹/L [>10,000/microlitre] at presentation).[45][70][107]

Once a treatment regimen and protocol have been decided, it should be adhered to in its entirety from induction to consolidation and maintenance (barring major complication or inadequate response).[45]

Induction therapy for APL

Induction regimens for non-high-risk APL include:[45][107]

  • All-trans-retinoic acid (ATRA; also known as tretinoin) plus arsenic trioxide (standard of care)

  • ATRA plus idarubicin or gemtuzumab ozogamicin; considered only if arsenic trioxide is not available or contraindicated

Induction regimens for high-risk APL include:[45][107]

  • ATRA plus arsenic trioxide plus idarubicin

  • ATRA plus arsenic trioxide plus gemtuzumab ozogamicin (single dose)

  • ATRA plus anthracycline-based chemotherapy (e.g., idarubicin; or daunorubicin plus cytarabine)

ATRA and arsenic trioxide can cause differentiation syndrome, which can be life-threatening if not treated promptly. Arsenic trioxide can also prolong QT interval and cause electrolyte abnormalities. See 'Supportive care for AML and APL' section (below) for guidance on managing these complications.

Induction therapy should continue until complete remission is achieved, after which consolidation therapy should be given.[45][107] Complete remission following ATRA-based induction therapy is achieved in most (>90%) patients.[108]

Consolidation therapy for APL

Consolidation regimens for APL are usually similar to induction regimens (e.g., ATRA plus arsenic trioxide [for non-high-risk APL]; ATRA plus arsenic trioxide plus chemotherapy [for high-risk APL]).[45][107]

Maintenance therapy for APL

Maintenance therapy may be considered for patients with high-risk APL who achieve molecular remission after consolidation therapy, but it is not required for non-high-risk patients.​[70][107]

Maintenance regimens for APL vary depending on the treatment protocol, but usually consist of ATRA plus mercaptopurine and methotrexate for 1-2 years.[109][110][111]​

With close MRD monitoring post-consolidation, the role of maintenance therapy is now being challenged.[108][112][113]​​​​​ In some countries, such as the UK, maintenance therapy for APL is no longer used.

Measurable (minimal) residual disease (MRD) assessment in APL

MRD assessment (PCR testing to detect the PML::RARA fusion transcript) should be carried out following consolidation therapy to evaluate treatment response (i.e., molecular remission) and guide subsequent treatment.[70][107]

Patients with high-risk APL should undergo long-term MRD monitoring (e.g., every 3 months for 2 years following treatment) due to the increased risk of relapse.[45][70][107]​​ Long-term MRD monitoring is not required for non-high-risk patients in molecular remission following consolidation therapy.

Relapsed or refractory APL

Patients with relapsed or refractory APL should be considered for salvage therapy to achieve molecular remission (i.e., MRD negativity).

Salvage therapy for relapsed APL should be based on previous treatment and whether relapse occurs early or late (definitions vary, but most relapses occur <2 years).[45][70][107]​​​

Patients who relapse early following treatment comprising ATRA plus arsenic trioxide can be treated with ATRA plus chemotherapy, or single-agent gemtuzumab ozogamicin.[45][107]​​ Patients who relapse early following treatment with ATRA plus chemotherapy (without arsenic trioxide) can be treated with arsenic trioxide-containing regimens (e.g., ATRA plus arsenic trioxide).[45][107]​​​ Retreatment with the previous regimen may be considered if relapse occurs late.

Patients with relapsed or refractory disease should be referred to a transplant centre. An autologous SCT should be arranged if remission and MRD negativity are achieved after salvage therapy.[45][107]​ An allogeneic SCT should be arranged if there is no remission (i.e., refractory disease) or there is detectable MRD after salvage therapy.[45][107]​

Patients not eligible for SCT may be continued on salvage therapy or enrolled in a clinical trial (if available).

Central nervous system (CNS) involvement in AML and APL

CNS imaging and diagnostic lumbar puncture should be carried out in patients with neurological signs and symptoms suggesting CNS involvement.[27][45]

If CNS disease is confirmed on diagnostic lumbar puncture, intrathecal cytarabine or intrathecal methotrexate (or a combination of these drugs) should be given two times per week until the cerebrospinal fluid is clear, and weekly thereafter for a further 4-6 weeks.[45]

Occult CNS involvement at first remission

A screening lumbar puncture (in patients without neurological signs and symptoms) should be considered to detect occult CNS involvement at first remission before first intensive consolidation therapy in patients at high-risk for CNS disease (e.g., patients with AML with FLT3 mutation; patients with high-risk APL).[45]

If occult CNS disease is confirmed on screening lumbar puncture, intrathecal cytarabine or intrathecal methotrexate (or a combination of these drugs) should be given two times per week until the cerebrospinal fluid is clear.[45]​ Alternatively, if the patient is to receive consolidation therapy containing doses of cytarabine that can cross the blood-brain barrier (i.e., ≥2 g/square metre of body surface area), then clearance of CNS disease should be documented on lumbar puncture after the first cycle of consolidation.[45]

Supportive care for AML and APL

Consider supportive care measures for all patients, at all stages of treatment, to prevent or manage complications.

Patients with AML who are unsuitable for or decline intensive- or lower-intensity therapy should be offered best supportive care.[45]​​

Electrolyte abnormalities

  • Correction of electrolyte abnormalities is important before and during treatment (particularly for patients treated with venetoclax, and those with APL who are treated with arsenic trioxide).

  • Patients should be commenced on hydration (e.g., intravenous fluids).

Tumour lysis syndrome (TLS)

  • An oncological emergency. TLS is characterised by hyperkalaemia, hyperphosphataemia, hyperuricaemia, hypocalcaemia, and/or elevated serum lactate dehydrogenase, which can occur following treatment (including chemotherapy and targeted agents e.g., venetoclax). Spontaneous TLS is rare; elevated WBC count (tumour burden) is a risk factor.

  • TLS can lead to cardiac arrhythmias, seizures, acute kidney injury, and death, if untreated.​ Vigorous hydration (with intravenous fluids), phosphate-binding agents, and hypouricaemic agents (e.g., allopurinol or rasburicase) should be used to prevent or treat TLS. See Tumour lysis syndrome.

  • TLS associated with venetoclax may occur as early as 6-8 hours following the first dose in patients with AML.[96] TLS risk assessment should be carried out before administering venetoclax, and​ guidance on TLS prophylaxis, laboratory monitoring, dose titration, and drug interactions should be strictly adhered to during treatment with venetoclax.[45][96]

Differentiation syndrome

  • Treatments for AML (e.g., ivosidenib, enasidenib, olutasidenib, gilteritinib) and APL (e.g., ATRA, arsenic trioxide) can cause differentiation syndrome, which can be life-threatening if not treated promptly.[97][98][99][100]​​[114][115]​​​ 

  • Differentiation syndrome has been reported as early as 10 days, and up to 5 months, after starting enasidenib.

  • Differentiation syndrome is characterised by fever, fluid retention, respiratory distress, pulmonary infiltrates, pulmonary or pericardial effusion, and an elevated WBC count (>10 × 10⁹/L [>10,000/microlitre]). Patients should be monitored for hypoxia, pulmonary infiltrates, and pleural effusion. Patients with differentiation syndrome should be promptly treated with dexamethasone.[107]​ In severe cases, the treatment causing differentiation syndrome may be temporarily discontinued until symptoms resolve.[107]

Hyperleukocytosis

  • Generally defined as a WBC count >100 × 10⁹/L (>100,000/microlitre) and is considered a poor prognostic factor.

  • In AML patients with hyperleukocytosis, hydroxycarbamide is recommended for leukoreduction.[27][45] Lower WBC count to <25 × 10⁹/L (<25,000/microlitre) before initiating treatment (particularly if hypomethylating agents and venetoclax are to be used).[27][45]​​​​​

  • In APL patients with low-risk disease, hydroxycarbamide should be considered to manage high WBC count during treatment with ATRA and arsenic trioxide (particularly if differentiation syndrome occurs).​[45][107]

  • Urgent leukapheresis may be considered in patients with AML who are symptomatic and have a very high WBC count; however, this approach is not recommended in patients with APL because leukapheresis may worsen coagulopathy.[27][45][70][107]

Anaemia and thrombocytopenia

  • Red blood cell and platelet transfusions may be required depending on symptoms and blood counts.[116] During the acute phase of APL, patients are at particular risk of significant coagulopathy.

  • Packed red blood cell transfusion is recommended to keep haematocrit >25%.

  • Platelets should be transfused once platelet count is <10 × 10⁹/L (<10,000/microlitre) or with any signs of bleeding.[27][45]​​ Platelet count needs to be maintained at >50 × 10⁹/L (>50,000/microlitre) in patients with APL or those with significant bleeding.[45][107][117]​​​

  • Activated partial thromboplastin time (aPTT) and fibrinogen levels should be normalised by infusions of fresh frozen plasma and cryoprecipitate in patients with APL or those with significant bleeding.[45][107]

Infections and febrile neutropenia

  • During acute illness and chemotherapy, all patients should receive antibiotic prophylaxis (e.g., a fluoroquinolone) to reduce the risk of infection and febrile neutropenia.[118] Patients should also receive antifungal prophylaxis with a mould-active antifungal agent (e.g., posaconazole).[118]

  • Patients presenting with febrile illness need to be investigated and treated appropriately and promptly with antibiotics or anti-infective agents. See Febrile neutropenia.

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