Assessment of eosinophilia

Strongyloides species hyperinfection may result in pulmonary involvement.

Supplementary method for detecting Strongyloides species, although more sensitive than stool examination.[32]Nutman TB. Evaluation and differential diagnosis of marked, persistent eosinophilia. Immunol Allergy Clin North Am. 2007 Aug;27(3):529-49. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2099264 http://www.ncbi.nlm.nih.gov/pubmed/17868863?tool=bestpractice.com [33]Caruana SR, Kelly HA, Ngeow JY, et al. Undiagnosed and potentially lethal parasite infections among immigrants and refugees in Australia. J Travel Med. 2006 Jul-Aug;13(4):233-9. https://academic.oup.com/jtm/article/13/4/233/1801922 http://www.ncbi.nlm.nih.gov/pubmed/16884406?tool=bestpractice.com [34]Stauffer W, Walker P. Eosinophilia in refugees. Clin Infect Dis. 2006 Jun 1;42(11):1655-6. http://cid.oxfordjournals.org/content/42/11/1655.full http://www.ncbi.nlm.nih.gov/pubmed/16652328?tool=bestpractice.com

Should be performed if there has been possible exposure to parasitic infection, particularly if the patient has adult T-cell leukaemia/lymphoma and before commencing chemotherapy or immunosuppressive therapy with corticosteroids in patient with eosinophilia, because hyperinfection may otherwise occur.[35]Al Samman M, Haque S, Long JD. Strongyloidiasis colitis: a case report and review of the literature. J Clin Gastroenterol. 1999 Jan;28(1):77-80. http://www.ncbi.nlm.nih.gov/pubmed/9916676?tool=bestpractice.com Should be performed in all migrants or travellers arriving from the tropics with eosinophilia.[19]Checkley AM, Chiodini PL, Dockrell DH, et al; British Infection Society and Hospital for Tropical Diseases. Eosinophilia in returning travellers and migrants from the tropics: UK recommendations for investigation and initial management. J Infect. 2010 Jan;60(1):1-20. http://www.ncbi.nlm.nih.gov/pubmed/19931558?tool=bestpractice.com

First test to confirm intestinal parasitic infection,[32]Nutman TB. Evaluation and differential diagnosis of marked, persistent eosinophilia. Immunol Allergy Clin North Am. 2007 Aug;27(3):529-49. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2099264 http://www.ncbi.nlm.nih.gov/pubmed/17868863?tool=bestpractice.com [36]Seybolt LM, Christiansen D, Barnett ED. Diagnostic evaluation of newly arrived asymptomatic refugees with eosinophilia. Clin Infect Dis. 2006 Feb 1;42(3):363-7. http://cid.oxfordjournals.org/content/42/3/363.full http://www.ncbi.nlm.nih.gov/pubmed/16392081?tool=bestpractice.com although not useful for detecting Schistosoma haematobium.

Terminal urine sample is examined for Schistosoma species.

Principal method for detecting S haematobium.

Supplementary method for detecting Schistosoma species, although more sensitive than stool examination.[32]Nutman TB. Evaluation and differential diagnosis of marked, persistent eosinophilia. Immunol Allergy Clin North Am. 2007 Aug;27(3):529-49. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2099264 http://www.ncbi.nlm.nih.gov/pubmed/17868863?tool=bestpractice.com [33]Caruana SR, Kelly HA, Ngeow JY, et al. Undiagnosed and potentially lethal parasite infections among immigrants and refugees in Australia. J Travel Med. 2006 Jul-Aug;13(4):233-9. https://academic.oup.com/jtm/article/13/4/233/1801922 http://www.ncbi.nlm.nih.gov/pubmed/16884406?tool=bestpractice.com [34]Stauffer W, Walker P. Eosinophilia in refugees. Clin Infect Dis. 2006 Jun 1;42(11):1655-6. http://cid.oxfordjournals.org/content/42/11/1655.full http://www.ncbi.nlm.nih.gov/pubmed/16652328?tool=bestpractice.com ​ Serology is indicated, in addition to microscopy of a terminal urine sample, for Schistosoma species, in migrants and travellers returning from Africa with eosinophilia.[19]Checkley AM, Chiodini PL, Dockrell DH, et al; British Infection Society and Hospital for Tropical Diseases. Eosinophilia in returning travellers and migrants from the tropics: UK recommendations for investigation and initial management. J Infect. 2010 Jan;60(1):1-20. http://www.ncbi.nlm.nih.gov/pubmed/19931558?tool=bestpractice.com

A newly-formed blister should be biopsied, if possible, in its entirety.

Best available method of diagnostic testing. Normal, uninvolved skin adjacent to a blister should be biopsied. The specimen must be either snap-frozen or placed in Michel's medium for transportation.

Positive in up to 96% of patients.

Forced expiratory volume at 1 second (FEV₁)/forced vital capacity (FVC) ratio is the primary diagnostic test.[39]Global Initiative for Asthma. Global strategy for asthma management and prevention. May 2024 [internet publication]. https://ginasthma.org/2024-report

A bronchodilator reversibility test may be used, which can demonstrate reversibility of airflow obstruction to short-acting bronchodilator, usually defined as improvement in FEV₁ by ≥12% and 200 mL from baseline.[39]Global Initiative for Asthma. Global strategy for asthma management and prevention. May 2024 [internet publication]. https://ginasthma.org/2024-report [40]Louis R, Satia I, Ojanguren I, et al. European respiratory society guidelines for the diagnosis of asthma in adults. Eur Respir J. 2022 Feb 15:2101585. https://erj.ersjournals.com/content/60/3/2101585.long http://www.ncbi.nlm.nih.gov/pubmed/35169025?tool=bestpractice.com [41]National Institute for Health and Care Excellence. Asthma: diagnosis, monitoring and chronic asthma management (BTS, NICE, SIGN). NICE guideline NG245. Nov 2024 [internet publication]. https://www.nice.org.uk/guidance/ng245 ​​ ​ ​​

Eosinophilia is usually mild (i.e., <1.5 × 10⁹/L [1500/microlitre]; if eosinophil count is higher, allergic bronchopulmonary aspergillosis or eosinophilic granulomatosis with polyangiitis is possible.

Not routinely performed if diagnosis is clear on grounds of history and examination.

Testing for food allergy in patients with eczema should not be considered before intervention with patient education and optimal skin care, including topical corticosteroids, has been initiated.

High sensitivity and low specificity of skin-prick testing for food allergy can yield false positive results, which may lead to elimination diets that are potentially harmful to patients with eczema.

Not routinely performed if diagnosis is clear on grounds of history and examination.

Testing for food allergy in patients with eczema should not be considered before intervention with patient education and optimal skin care, including topical corticosteroids, has been initiated.

High sensitivity and low specificity of IgE testing for food allergy can yield false positive results, which may lead to elimination diets that are potentially harmful to patients with eczema.

Eosinophilia is usually mild (i.e., <1.5 × 10⁹/L [1500/microlitre]); if the eosinophil count is higher, eosinophilic granulomatosis with polyangiitis is possible.

Supplementary method for detecting flukes.

Supplementary method for diagnosis of fascioliasis.

Supplementary method for detecting Opisthorchis species.

Laboratory will distinguish pathogenic microfilariae from non-pathogenic.

It may be necessary to take blood samples during the evening for Wuchereria bancrofti and Brugia malayi because the microfilariae usually appear at night. 

Supplementary method for detecting filariasis if blood film is not successful.

Should be sought in endemic areas (e.g., parts of Queensland, Australia)[37]Walker NI, Croese J, Clouston AD, et al. Eosinophilic enteritis in northeastern Australia: pathology, association with Ancylostoma caninum, and implications. Am J Surg Pathol. 1995 Mar;19(3):328-37. http://www.ncbi.nlm.nih.gov/pubmed/7872431?tool=bestpractice.com

Precipitin test and complement fixation test detect IgM and IgG antibodies. Enzyme immunoassay is highly sensitive but lacks specificity.

More than one diagnostic test is recommended in patients with suspected coccidioidomycosis (including direct visualisation and culture of sputum, bronchoalveolar lavage (BAL), or other biopsy material; urine and serum antigen testing; and serology [serum antibody testing]) because current evidence does not support a single best test.[21]Hage CA, Carmona EM, Epelbaum O, et al. Microbiological laboratory testing in the diagnosis of fungal infections in pulmonary and critical care practice. An official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2019 Sep 1;200(5):535-50. https://www.atsjournals.org/doi/10.1164/rccm.201906-1185ST http://www.ncbi.nlm.nih.gov/pubmed/31469325?tool=bestpractice.com

More than one diagnostic test is recommended in patients with suspected coccidioidomycosis (including direct visualisation and culture of sputum, BAL, or other biopsy material; urine and serum antigen testing; and serology [serum antibody testing]) because current evidence does not support a single best test.[21]Hage CA, Carmona EM, Epelbaum O, et al. Microbiological laboratory testing in the diagnosis of fungal infections in pulmonary and critical care practice. An official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2019 Sep 1;200(5):535-50. https://www.atsjournals.org/doi/10.1164/rccm.201906-1185ST http://www.ncbi.nlm.nih.gov/pubmed/31469325?tool=bestpractice.com

A positive culture gives a definitive diagnosis of coccidioidomycosis, because there is no colonised state. However, sputum for culture can be difficult to obtain because patients’ coughs are often non-productive.[38]Centers for Disease Control and Prevention. Clinical overview of valley fever (coccidioidomycosis). Apr 2024 [internet publication]. https://www.cdc.gov/fungal/diseases/coccidioidomycosis/health-professionals.html Processing and manipulation of cultures should be done in a biosafety level 3 laboratory.

More than one diagnostic test is recommended in patients with suspected coccidioidomycosis (including direct visualisation and culture of sputum, BAL, or other biopsy material; urine and serum antigen testing; and serology [serum antibody testing]) because current evidence does not support a single best test.[21]Hage CA, Carmona EM, Epelbaum O, et al. Microbiological laboratory testing in the diagnosis of fungal infections in pulmonary and critical care practice. An official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2019 Sep 1;200(5):535-50. https://www.atsjournals.org/doi/10.1164/rccm.201906-1185ST http://www.ncbi.nlm.nih.gov/pubmed/31469325?tool=bestpractice.com

Urinary antigen detection is not widely used, but may have some utility in diagnosing coccidioidomycosis in immunocompromised patients with severe forms of the disease.[38]Centers for Disease Control and Prevention. Clinical overview of valley fever (coccidioidomycosis). Apr 2024 [internet publication]. https://www.cdc.gov/fungal/diseases/coccidioidomycosis/health-professionals.html

More than one diagnostic test is recommended in patients with suspected coccidioidomycosis (including direct visualisation and culture of sputum, BAL, or other biopsy material; urine and serum antigen testing; and serology [serum antibody testing]) because current evidence does not support a single best test.[21]Hage CA, Carmona EM, Epelbaum O, et al. Microbiological laboratory testing in the diagnosis of fungal infections in pulmonary and critical care practice. An official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2019 Sep 1;200(5):535-50. https://www.atsjournals.org/doi/10.1164/rccm.201906-1185ST http://www.ncbi.nlm.nih.gov/pubmed/31469325?tool=bestpractice.com

Non-specific test.

There may be isolated eosinophilia or also other reactive changes (e.g., atypical lymphocytes).

Also used to monitor follow-up.[27]Agarwal R, Sehgal IS, Muthu V, et al. Revised ISHAM-ABPA working group clinical practice guidelines for diagnosing, classifying and treating allergic bronchopulmonary aspergillosis/mycoses. Eur Respir J. 2024 Apr 4;63(4):2400061. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10991853 http://www.ncbi.nlm.nih.gov/pubmed/38423624?tool=bestpractice.com

A type III reaction may be noted after 6 hours.

Allergic bronchopulmonary aspergillosis can be categorised as occurring either with or without central bronchiectasis.[27]Agarwal R, Sehgal IS, Muthu V, et al. Revised ISHAM-ABPA working group clinical practice guidelines for diagnosing, classifying and treating allergic bronchopulmonary aspergillosis/mycoses. Eur Respir J. 2024 Apr 4;63(4):2400061. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10991853 http://www.ncbi.nlm.nih.gov/pubmed/38423624?tool=bestpractice.com

Non-specific and may be seen in many other causes of eosinophilia.

Non-specific and may be seen in many other causes of eosinophilia.

May also be seen with other causes of eosinophilia, such as drug hypersensitivity or lymphocytic variant of hypereosinophilic syndrome. Less likely to be present in eosinophilic leukaemia than in reactive eosinophilia.

A strong pointer to this diagnosis in a patient with eosinophilia.[29]Emmi G, Bettiol A, Gelain E, et al. Evidence-based guideline for the diagnosis and management of eosinophilic granulomatosis with polyangiitis. Nat Rev Rheumatol. 2023 Jun;19(6):378-93. https://www.nature.com/articles/s41584-023-00958-w http://www.ncbi.nlm.nih.gov/pubmed/37161084?tool=bestpractice.com [42]Hagen EC, Daha MR, Hermans J, et al; EC/BCR Project for ANCA Assay Standardization. Diagnostic value of standardized assays for anti-neutrophil cytoplasmic antibodies in idiopathic systemic vasculitis. Kidney Int. 1998 Mar;53(3):743-53. https://www.kidney-international.org/article/S0085-2538(15)60452-5/pdf http://www.ncbi.nlm.nih.gov/pubmed/9507222?tool=bestpractice.com

Not specific.

Multiple biopsy samples should be taken to increase diagnostic sensitivity.[43]Aceves SS, Alexander JA, Baron TH, et al. Endoscopic approach to eosinophilic esophagitis: American Society for Gastrointestinal Endoscopy consensus conference. Gastrointest Endosc. 2022 Oct;96(4):576-92. https://www.giejournal.org/article/S0016-5107(22)01725-4/fulltext http://www.ncbi.nlm.nih.gov/pubmed/35965102?tool=bestpractice.com

Blast cells ≥2% of circulating cells. Eosinophils may be cytologically abnormal, but this is not specific for eosinophilic leukaemia. Presence of blast cells plus eosinophilia could also be due to acute lymphoblastic leukaemia with reactive eosinophilia.[24]Shomali W, Gotlib J. World Health Organization-defined eosinophilic disorders: 2022 update on diagnosis, risk stratification, and management. Am J Hematol. 2022 Jan 1;97(1):129-48. https://onlinelibrary.wiley.com/doi/10.1002/ajh.26352 http://www.ncbi.nlm.nih.gov/pubmed/34533850?tool=bestpractice.com [31]Arber DA, Orazi A, Hasserjian RP, et al. International consensus classification of myeloid neoplasms and acute leukemias: integrating morphologic, clinical, and genomic data. Blood. 2022 Sep 15;140(11):1200-28. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9479031 http://www.ncbi.nlm.nih.gov/pubmed/35767897?tool=bestpractice.com [44]Li W. The 5th edition of the World Health Organization classification of hematolymphoid tumors. In: Li W, ed. Leukemia. 5th ed. Brisbane: Exon Publications; 2022.​​​

Detection of this fusion gene confirms that eosinophilia is the result of eosinophilic leukaemia.

These are highly specialised tests performed in a reference laboratory. Detecting the FIP1L1::PDGFRA fusion gene is important because the condition is sensitive to imatinib therapy and, in the absence of effective treatment, can be fatal.​[24]Shomali W, Gotlib J. World Health Organization-defined eosinophilic disorders: 2022 update on diagnosis, risk stratification, and management. Am J Hematol. 2022 Jan 1;97(1):129-48. https://onlinelibrary.wiley.com/doi/10.1002/ajh.26352 http://www.ncbi.nlm.nih.gov/pubmed/34533850?tool=bestpractice.com ​​[45]Cools J, DeAngelo DJ, Gotlib J, et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med. 2003 Mar 27;348(13):1201-14. https://www.nejm.org/doi/full/10.1056/NEJMoa025217 http://www.ncbi.nlm.nih.gov/pubmed/12660384?tool=bestpractice.com [46]Bain BJ, Fletcher SH. Chronic eosinophilic leukemias and the myeloproliferative variant of the hypereosinophilic syndrome. Immunol Allergy Clin North Am. 2007 Aug;27(3):377-88. http://www.ncbi.nlm.nih.gov/pubmed/17868855?tool=bestpractice.com [47]Helbig G. Advances in the diagnosis and treatment of eosinophilia. Curr Opin Hematol. 2014 Jan;21(1):3-7. http://www.ncbi.nlm.nih.gov/pubmed/24322486?tool=bestpractice.com

5% to 19% bone marrow blast cells is a criterion for diagnosis of chronic eosinophilic leukaemia.

Specific cytogenetic abnormalities are strongly correlated with eosinophilic leukaemia, specifically t(5;12)(q32;p13.2) and other translocations that lead to rearrangement of the PDGFRB gene, and t(8;13)(p11.2;q12.1) and other translocations that lead to rearrangement of the FGFR1 gene. Chromosomal rearrangements that can lead to rearrangement of the PDGFRB gene are important because the condition, which can otherwise be fatal, is sensitive to imatinib therapy.[23]Khoury JD, Solary E, Abla O, et al. The 5th edition of the World Health Organization classification of haematolymphoid tumours: myeloid and histiocytic/dendritic neoplasms. Leukemia. 2022 Jul;36(7):1703-19. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9252913 http://www.ncbi.nlm.nih.gov/pubmed/35732831?tool=bestpractice.com [24]Shomali W, Gotlib J. World Health Organization-defined eosinophilic disorders: 2022 update on diagnosis, risk stratification, and management. Am J Hematol. 2022 Jan 1;97(1):129-48. https://onlinelibrary.wiley.com/doi/10.1002/ajh.26352 http://www.ncbi.nlm.nih.gov/pubmed/34533850?tool=bestpractice.com ​​​​​

The recognition of chronic eosinophilic leukaemia related to t(8;9)(p22;p24.1) and PCM1::JAK2 is also important since response to ruxolitinib may occur.[17]Butt NM, Lambert J, Ali S, et al; British Society for Haematology. Guideline for the investigation and management of eosinophilia. Br J Haematol. 2017 Feb;176(4):553-72. https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.14488 http://www.ncbi.nlm.nih.gov/pubmed/28112388?tool=bestpractice.com ​​[48]Bain BJ, Ahmad S. Should myeloid and lymphoid neoplasms with PCM1-JAK2 and other rearrangements of JAK2 be recognized as specific entities? Br J Haematol. 2014 Sep;166(6):809-17. http://www.ncbi.nlm.nih.gov/pubmed/24913195?tool=bestpractice.com

Similarly, the presence of t(12;13)(p13;q12) leading to ETV6::FLT3 fusion should be recognised because of the possibility of response to FLT3 inhibitors such as sorafenib and sunitinib.[49]Walz C, Erben P, Ritter M, et al. Response of ETV6-FLT3-positive myeloid/lymphoid neoplasm with eosinophilia to inhibitors of FMS-like tyrosine kinase 3. Blood. 2011 Aug 25;118(8):2239-42. http://www.bloodjournal.org/content/118/8/2239.long?sso-checked=true http://www.ncbi.nlm.nih.gov/pubmed/21705501?tool=bestpractice.com Cases with t(9;12)(q34;p13) and ETV6::ABL1 should be recognised because of their responsiveness to imatinib.

Increase in eosinophils and their precursors is not specific for eosinophilic leukaemia. Increase in mast cells favours a diagnosis of either systemic mastocytosis or chronic eosinophilic leukaemia associated with FIP1L1::PDGFRA or with a translocation such as t(5;12)(q31-33;q24), leading to PDGFRB rearrangement. Presence of increased cytologically abnormal mast cells does not exclude a diagnosis of eosinophilic leukaemia.

Trephine biopsy is important to exclude systemic mastocytosis and lymphoma as a cause of eosinophilia.

Concentration >20 nanograms/mL is a criterion for diagnosis of systemic mastocytosis (which can cause eosinophilia) but can also be seen in patients with chronic eosinophilic leukaemia associated with FIP1L1::PDGFRA. The higher the level, the more likely the diagnosis of systemic mastocytosis rather than chronic eosinophilic leukaemia.

Blast cells suggest an acute leukaemia. Rarely acute myeloid leukaemia associated with t(8;21)(q22;q22.1) presents with a very high eosinophil count with the blast cell count being only moderately elevated.[50]Stussi G, Tichelli A, Schanz U, et al. Hypereosinophilia with a low blast count as the initial manifestation of acute myeloid leukaemia with RUNX1-RUNX1T1. Br J Haematol. 2009 Aug;146(4):346. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2009.07676.x/full http://www.ncbi.nlm.nih.gov/pubmed/19388941?tool=bestpractice.com ​​ Basophilia and thrombocytosis may occur in the myeloproliferative neoplasms.

Any increase of blast cells above the normal proportion of >5% suggests malignancy. Demonstration of clonality by cytogenetic analysis confirms the diagnosis of a haematological malignancy in the correct clinical context.

Full excision biopsy is the preferred diagnostic procedure, as preserving lymph node architecture is crucial for proper diagnosis, especially when malignant aetiology such as lymphoma is suspected. Although fine needle aspiration is safe and inexpensive, it can sometimes be difficult to differentiate between malignant and benign aetiology using this technique.

Hypoproliferative anaemia can be secondary to inflammation or bone marrow replacement, and often presents with normochromic, normocytic indices. Alternatively, anaemia can result from autoimmune haemolysis (Coombs' test positive) associated with an underlying lymphoma.

Full excision biopsy is the preferred diagnostic procedure, as preserving lymph node architecture is crucial for proper diagnosis, especially when malignant aetiology such as lymphoma is suspected. Fine needle aspiration is not suitable for diagnosing Hodgkin’s lymphoma.

Eosinophilia can be seen in Hodgkin's lymphoma and is thought to be secondary to abnormal cytokine production. Haemoglobin concentration white blood cell count, and lymphocyte count are an important part of the international prognostic score for patients with advanced Hodgkin's lymphoma. There may be anaemia of chronic disease, characterised by either normocytic normochromic or hypochromic microcytic red cells with a low serum iron and increased serum ferritin.

Anaemia of chronic disease can occur with any malignant disease, but iron-deficiency anaemia suggests a possible gastrointestinal tumour with chronic blood loss.

First-line test if clinical features suggest malignancy but there are no indications of the likely site.

Non-specific finding but supports reactive eosinophilia rather than eosinophilic leukaemia.

More sensitive than bone marrow aspiration for detecting metastatic tumour.

Phenotypes reported including CD3-CD4+; CD3+CD4-CD8-; CD3+CD4+CD7-[51]Roufosse F. Hypereosinophilic syndrome variants: diagnostic and therapeutic considerations. Haematologica. 2009 Sep;94(9):1188-93. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738708 http://www.ncbi.nlm.nih.gov/pubmed/19734412?tool=bestpractice.com

T-cell receptor gene rearrangement alone is insufficient to make the diagnosis of lymphocytic variant of hypereosinophilic syndrome in the absence of phenotypically abnormal T cells.[17]Butt NM, Lambert J, Ali S, et al; British Society for Haematology. Guideline for the investigation and management of eosinophilia. Br J Haematol. 2017 Feb;176(4):553-72. https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.14488 http://www.ncbi.nlm.nih.gov/pubmed/28112388?tool=bestpractice.com

Idiopathic hypereosinophilic syndrome should not be diagnosed until all identifiable causes have been excluded. Investigation should include lymphocyte immunophenotyping and analysis for clonal rearrangement of T-cell receptor genes to exclude lymphocyte-driven eosinophilia. If marked eosinophilia (e.g., ≥1.5 × 10⁹/L [1500/microlitre]) gives rise to tissue damage and common causes of eosinophilia have been excluded, excluding all rare causes becomes relevant because some of these are life-threatening and require specific treatment. Serum troponin and echocardiography can provide evidence of cardiac damage, which is an indication for prompt treatment.[52]Klion AD. How I treat hypereosinophilic syndromes. Blood. 2015 Aug 27;126(9):1069-77. http://www.bloodjournal.org/content/126/9/1069.long?sso-checked=true http://www.ncbi.nlm.nih.gov/pubmed/25964669?tool=bestpractice.com

Specialised tests only available at selected centres.