Skip to textbook content
Doctor’s PassportTextbook
TopicsAll topics

Loading topic navigation…

Textbook navigation
TopicsAll topics

Loading topic navigation…
← Haematology and transfusion indexChapter sections
OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
Full textbook13 sectionsOpen only what you need
Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Eosinophilia and basophilia

Haematology and transfusion · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
!
Time-critical presentation

Eosinophilia with chest pain, troponin rise, heart failure, neurological deficit, hypoxaemia, pulmonary infiltrates, severe drug reaction, thrombosis or rapidly progressive organ dysfunction requires urgent haematology and organ-specialist assessment. Marked basophilia with hyperleucocytosis, splenomegaly or leukostasis symptoms requires an urgent myeloid-neoplasm pathway. Do not start non-essential corticosteroids before assessing Strongyloides risk when the patient is stable enough.

Overview

Interpret persistent eosinophilia and basophilia by absolute count, tempo and organ involvement, distinguish reactive from clonal disease and escalate eosinophilic organ injury or a myeloid-neoplasm phenotype promptly.

Eosinophils normally participate in mucosal immunity and type 2 inflammation. Blood eosinophilia can be transient, recurrent or persistent and may arise from allergy, parasitic infection, medicines, autoimmune disease, cancer, adrenal deficiency or a myeloid clone. The count should be read against symptoms and treatment: corticosteroids suppress circulating eosinophils, while tissue infiltration can be severe even after the blood count falls. A structured assessment therefore establishes magnitude and duration, searches for organ injury immediately and investigates common reactive causes before or alongside clonal disease according to risk.

Basophils are a much smaller circulating population. Mild or transient basophilia can accompany inflammation, allergy, hypothyroidism and recovery states, but persistent absolute basophilia, particularly with granulocytic left shift and splenomegaly, raises chronic myeloid leukaemia or another myeloproliferative neoplasm. Automated basophil counts can be inaccurate at low levels, so film review matters. BCR::ABL1 testing answers the CML question; JAK2, CALR, MPL or broader myeloid tests are selected from the accompanying erythrocytosis, thrombocytosis or fibrosis phenotype.

Practice

Two practice questions

Your practice draft is saved in this browser.

Question 1 of 2
0 correct
Haematology and transfusionOriginal SBA

Eosinophilia with cardiac symptoms

An adult with persistent eosinophilia develops chest pain, dyspnoea, a raised troponin and new ventricular dysfunction. What is the most appropriate immediate plan?

Choose one answer, then submit
← Rapid synopsisBack to overviewAll Haematology and transfusion topics →
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • BSH eosinophilia guidelineReactive and clonal investigation plus assessment of organ damage.
  • BSH chronic myeloid leukaemia guidelineBasophilic myeloid phenotype and BCR::ABL1 diagnosis.
  • UKHSA migrant health parasite guidanceStrongyloides exposure, testing and the risk created by immune suppression.
  • MHRA daptomycin eosinophilic pneumonia warningOfficial example of medicine-associated eosinophilic organ disease and withdrawal.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

The dangerous aspect of eosinophilia is granule-mediated organ damage. Myocarditis, endomyocardial fibrosis and thrombosis may develop with few early symptoms; pulmonary, neurological, renal, gastrointestinal and skin disease can also progress quickly. Investigation is parallel: ECG and troponin for cardiac symptoms, imaging and organ tests for the phenotype, Strongyloides assessment before immunosuppression in exposed people, and molecular or marrow evaluation for clonal features. The label hypereosinophilic syndrome requires unexplained eosinophilia with attributable organ damage after reasonable exclusions, not merely a laboratory threshold.

Key points

  • Use absolute eosinophil and basophil counts, not percentages, and confirm persistence and trajectory. A high percentage during neutropenia may represent a normal absolute population.
  • Eosinophilia is most often reactive to allergy, asthma, medicines or infection, but severity, duration, constitutional symptoms, splenomegaly and organ injury determine the need for clonal testing.
  • Take a precise medicine timeline including antibiotics, anticonvulsants, allopurinol, supplements and recent stopped drugs; systemic drug hypersensitivity can continue after the culprit is withdrawn.
  • Travel and residence history should identify helminth risk, freshwater, soil, raw food and animal exposure. Send species-directed tests with infectious-disease or microbiology advice rather than an indiscriminate parasite panel.
  • Eosinophil count does not measure organ damage. Ask about chest pain, dyspnoea, neuropathy, rash, abdominal symptoms, fever, thrombosis and weight loss and examine heart, lungs, skin, nerves, nodes and spleen.
  • Persistent basophilia is uncommon in ordinary allergy and is a strong clue to myeloid disease when accompanied by neutrophilia, left shift, thrombocytosis, splenomegaly or constitutional symptoms.
  • The first clonal branch uses film, BCR::ABL1 and phenotype-directed molecular testing, followed by marrow morphology and genetics when a myeloid neoplasm remains plausible.
  • In organ-threatening eosinophilic disease, take blood, molecular, infection and tissue samples promptly, then use specialist-directed corticosteroid or targeted treatment without waiting for every slow result.

Aetiology

01

Allergic and inflammatory stimulation

Atopy, asthma, eczema, allergic bronchopulmonary disease, eosinophilic gastrointestinal disease and vasculitis increase eosinophil production through type 2 cytokine signalling.

02

Medicines and infection

Drug hypersensitivity, helminth infection, selected fungal or parasitic disease and recovery from some infections produce reactive eosinophilia through immune stimulation.

03

Clonal myeloid disease

Chronic myeloid leukaemia, myeloproliferative neoplasms and kinase-fusion eosinophilic neoplasms expand basophil or eosinophil lineages as part of a stem-cell clone.

04

Secondary malignancy and endocrine disease

Lymphoma, solid cancer, immune deficiency and adrenal insufficiency can produce cytokine- or physiology-driven eosinophilia without a primary eosinophil clone.

Pathophysiology

  1. 1
    Cytokine-driven marrow output

    Interleukin signalling prolongs eosinophil survival and increases marrow maturation during allergic, parasitic, inflammatory or malignant immune stimulation.

  2. 2
    Tissue recruitment

    Chemokines draw eosinophils from blood into lung, skin, gut, heart and nerves, where circulating counts may underestimate tissue disease.

  3. 3
    Granule-mediated injury

    Activated eosinophils release cytotoxic proteins, lipids and oxidants that damage endothelium, epithelium and myocardium and promote thrombosis or fibrosis.

  4. 4
    Clonal signalling

    Constitutively active tyrosine-kinase or myeloid pathways drive autonomous eosinophil or basophil expansion alongside splenomegaly and other lineage abnormalities.

Clinical features and red flags

Atopic reactive pattern

Rhinitis, eczema, variable asthma or allergen exposure with otherwise normal counts supports reactive eosinophilia, provided systemic symptoms and organ injury are absent.

Severe drug reactionRed flag

Fever, widespread rash, facial oedema, lymphadenopathy, liver or kidney injury after a medicine suggests DRESS or another systemic hypersensitivity syndrome.

Parasitic exposure pattern

Travel, migration or soil and food exposure with gastrointestinal, pulmonary or skin symptoms raises helminth disease; Strongyloides risk changes corticosteroid safety.

Eosinophilic organ damageRed flag

Chest pain, heart failure, neuropathy, pulmonary infiltrates, thrombosis or progressive organ dysfunction with eosinophilia indicates a time-critical eosinophilic syndrome.

Clonal myeloid pattern

Persistent basophilia or eosinophilia with left shift, anaemia, thrombocytosis, splenomegaly, constitutional symptoms or abnormal morphology suggests a myeloid neoplasm.

Eosinophilic vasculitis patternRed flag

Adult asthma, sinus disease, pulmonary infiltrates, neuropathy, purpura or renal and cardiac involvement raises eosinophilic granulomatosis with polyangiitis.

Investigations

  1. 01
    Repeat FBC, absolute differential and blood filmFirst step
    Why
    Confirm persistence, verify basophils and identify reactive or clonal accompanying changes.
    Interpretation and limitations
    Look for left shift, blasts, dysplasia, thrombocytosis and anaemia. Percentages are insufficient; automated basophilia should be confirmed morphologically when it changes the pathway.
  2. 02
    Medicine, allergy and exposure review
    Why
    Identify common reactive causes and urgent drug hypersensitivity.
    Interpretation and limitations
    Link start and stop dates to rash, fever and organ injury. Ask about travel, residence, raw food, soil and animals; absence of gastrointestinal symptoms does not exclude Strongyloides.
  3. 03
    Renal, liver, inflammatory, troponin and cardiac tests
    Why
    Detect eosinophil-related organ injury and systemic inflammation.
    Interpretation and limitations
    Use ECG, troponin, natriuretic peptide, echocardiography or cardiac MRI when cardiac disease is plausible. Normal initial troponin does not end surveillance if symptoms evolve.
  4. 04
    Species-directed parasite testing
    Why
    Confirm infection before immunosuppression and direct antimicrobial treatment.
    Interpretation and limitations
    Use serology, stool or other tests selected with infection specialists. Strongyloides serology can be negative in immune suppression, and stool sensitivity may require repeated specialised sampling.
  5. 05
    BCR::ABL1 and myeloid molecular testing
    Why
    Identify CML or a kinase-driven eosinophilic or myeloproliferative neoplasm.
    Interpretation and limitations
    BCR::ABL1 addresses persistent basophilic granulocytosis. Fusion and mutation panels follow phenotype and haematology advice because targeted therapy depends on the exact driver.
  6. 06
    Bone marrow and tissue biopsy
    Why
    Assess clonality, mast cells, fibrosis, infiltrates and organ-specific eosinophilic injury.
    Interpretation and limitations
    Coordinate morphology, flow, cytogenetics and molecular studies. Tissue eosinophils alone do not prove causality; pathology must be integrated with exposure and systemic disease.

Differential diagnosis

01

Atopy or asthma

Compatible airway, nasal or skin disease supports reactive eosinophilia, but a high persistent count or systemic organ injury needs a broader search.

02

Drug hypersensitivity

A new medicine followed by rash, fever, facial swelling, hepatitis, nephritis or systemic illness suggests a severe drug reaction and requires urgent withdrawal and assessment.

03

Helminth infection

Travel, migration, raw food, soil or animal exposure with species-directed testing supports parasitic disease; corticosteroids can dangerously amplify occult Strongyloides infection.

04

Eosinophilic vasculitis or HES

Asthma, neuropathy, pulmonary infiltrates, skin, renal, cardiac or thrombotic disease suggests eosinophilic granulomatosis or hypereosinophilic organ damage.

05

Myeloid neoplasm

Basophilia, splenomegaly, left shift, thrombocytosis, abnormal film or constitutional symptoms raises CML or another clonal myeloid process requiring molecular testing.

Management

01Organ threatProtect heart, lungs and nervesFirst stepEosinophilia accompanies cardiac, respiratory, neurological, thrombotic or rapidly progressive systemic disease.+
  1. 1Use ABCDE and obtain urgent FBC, film, renal, liver, coagulation, troponin, ECG and phenotype-led imaging, involving haematology plus the threatened-organ specialty immediately.
  2. 2PreferredTake parasite, molecular, flow and tissue samples before treatment where feasible; preferred initial anti-inflammatory treatment is specialist-directed systemic corticosteroid when eosinophilic organ injury is strongly supported.
  3. 3EscalationIf Strongyloides exposure is credible, arrange urgent infectious-disease assessment and treatment alongside immunosuppression decisions; escalate shock, myocarditis, hypoxaemia or neurological deficit to critical care.
02ReactiveFind medicine, allergy or infectionEosinophilia is confirmed without current organ threat and no strong clonal phenotype is present.+
  1. 1Review previous counts, allergic and inflammatory disease, every medicine and supplement, travel, residence, food, soil, animals, immune status and adrenal symptoms.
  2. 2First lineAlternativeFirst-line tests are targeted to the supported cause, such as liver and renal tests for drug reaction or species-directed parasite studies; broad low-probability panels are an alternative only after specialist advice.
  3. 3EscalationRemove a suspected non-essential medicine safely, treat confirmed disease and repeat the count at a defined interval; escalate persistence, rising magnitude, systemic symptoms or organ signs to haematology.
03ClonalTest persistent basophilia or eosinophiliaCounts persist with splenomegaly, constitutional symptoms, left shift, thrombocytosis, anaemia, dysplasia or no credible reactive cause.+
  1. 1Request expert film review, LDH, urate, BCR::ABL1 and phenotype-directed myeloid testing after haematology discussion, while assessing for leukostasis or organ injury.
  2. 2PreferredDefinitiveAlternativeThe preferred definitive route is marrow morphology, flow, cytogenetics and fusion or mutation testing; an alternative peripheral molecular diagnosis is sufficient only when the disease-specific criteria allow it.
  3. 3EscalationEscalate a targetable kinase fusion, CML or evolving blast phenotype promptly because disease-specific therapy differs markedly from empirical corticosteroids alone.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Rapidly suppresses eosinophil-driven inflammation when cardiac, pulmonary, neurological, thrombotic or other organ injury is strongly supported.

Prednisolone for organ-threatening eosinophilic disease

A BSH emergency regimen is 1 mg/kg by mouth once daily under specialist supervision after urgent diagnostic samples when this causes no harmful delay; use an intravenous corticosteroid only through the acute organ-support protocol.

Assess Strongyloides exposure urgently and give infection-specialist-directed antiparasitic treatment alongside corticosteroids when risk is credible. Monitor infection, glucose, blood pressure, mood, gastric and bone risk, and do not equate a falling count with organ recovery.

Complications

01

Eosinophilic cardiac injury

Myocarditis, endomyocardial fibrosis and intracardiac thrombus can cause chest pain, heart failure, arrhythmia, embolism and sudden deterioration.

02

Pulmonary failure

Eosinophilic asthma, pneumonia, vasculitis or drug injury can cause infiltrates, severe bronchospasm and hypoxaemic respiratory failure.

03

Neurological and vascular damage

Vasculitic neuropathy, cerebral events and eosinophil-associated thrombosis can leave irreversible disability despite later control of the circulating count.

04

Progressive clonal disease

CML and other myeloid neoplasms can evolve to accelerated or blast-phase disease when the driver is not recognised and treated.

05

Unsafe empirical immunosuppression

Corticosteroids given before assessing Strongyloides or clonal disease can precipitate hyperinfection or obscure the diagnostic phenotype.

Monitoring and follow-up

  • Trend absolute eosinophil and basophil counts with symptoms, medicine changes and treatment; percentage changes alone are not reliable endpoints.
  • During possible organ injury, repeat cardiac, respiratory, renal, neurological and thrombotic assessment even if the blood eosinophil count falls after corticosteroids.
  • After removing a suspected drug, monitor rash, temperature, liver, renal and blood-count trajectory because systemic hypersensitivity can progress after withdrawal.
  • For parasite treatment, use species-specific clinical and microbiological follow-up and document corticosteroid or immune-treatment plans.
  • For clonal disease, follow the molecular marker, counts, spleen, symptoms and marrow milestones specified by the specialist service.
  • Reconsider tissue disease, hidden corticosteroid exposure and sampling timing when organ symptoms persist despite a normalised circulating count.

Special situations

Blood is only transit

Eosinophils migrate quickly into tissue. A modest or suppressed blood count can coexist with severe myocarditis, vasculitis or pulmonary disease.

Basophilia is a myeloid clue

Persistent absolute basophilia with left shift and splenomegaly is unusual in simple allergy and should trigger BCR::ABL1 reasoning.

Steroids hide and harm

Corticosteroids rapidly lower eosinophils and obscure phenotype while risking Strongyloides hyperinfection. Obtain key samples and assess exposure whenever clinically possible.

Organ damage defines urgency

A count cannot determine severity alone. Cardiac, neurological, pulmonary and thrombotic involvement makes eosinophilia a same-day specialist problem.

One clone can involve several lineages

Eosinophilia or basophilia with thrombocytosis, erythrocytosis or fibrosis may reflect a stem-cell neoplasm rather than isolated lineage disease.

Common pitfalls

  1. 01

    Interpreting eosinophil or basophil percentage without the absolute count.

  2. 02

    Calling persistent basophilia seasonal allergy despite left shift and splenomegaly.

  3. 03

    Starting corticosteroids before assessing Strongyloides exposure in a stable patient.

  4. 04

    Using eosinophil magnitude as a substitute for cardiac and neurological assessment.

  5. 05

    Ordering a generic parasite screen without an exposure-led species question.

  6. 06

    Stopping after a reactive explanation when the count and systemic symptoms continue to progress.

  7. 07

    Treating a targetable clonal eosinophilia with corticosteroid monotherapy before molecular classification.