Documents from the SIAIP Commissions

Issue 1 - 2026

The role of eosinophils in the diagnosis of allergic diseases

Authors

Serena Gracci , Davide Caimmi , Stefani Arasi , Fernanda Chiera , Giulio Dinardo , Arianna Giannetti , Carla Mastrorilli , Luca Pecoraro , Gian Luigi Marseglia , Michele Miraglia Del Giudice , Roberto Bernardini

Keywords: eosinophils, allergy diagnosis, drug allergy, food allergy, respiratory allergy, skin allergy
DOI: 10.53151/2531-3916/2026-1744
Publication Date: 2026-03-27

Summary

Eosinophilic granulocytes are hematopoietic effector cells involved in allergy, infection, chronic inflammation, and some malignancies. Produced in bone marrow, they circulate in blood before migrating to tissues where they release mediators that regulate immune responses and promote inflammation and remodeling. Normally representing about 1% of peripheral leukocytes, eosinophils reflect the balance between bone marrow production, tissue recruitment, and apoptosis. Elevated counts in blood or tissues are associated with diverse conditions. In allergic diseases, eosinophils are key biomarkers. In asthma, blood and airway eosinophilia characterize T2 inflammation, guide therapy, and predict exacerbations, although correlations between blood and tissue levels vary. Eosinophilia is also relevant in chronic rhinosinusitis, food allergies, and eosinophilic gastrointestinal disorders (EGIDs), where tissue-based criteria are essential for diagnosis, especially in eosinophilic esophagitis. In atopic dermatitis, eosinophils correlate with severity, while in urticaria and drug reactions their significance is variable. Drug-induced eosinophilia ranges from benign to severe systemic conditions such as drug reaction with eosinophilia and systemic symptoms. Overall, eosinophilia is a frequent but nonspecific finding, serving as a marker of atopy, disease severity, or treatment response. Tissue eosinophilia, however, is indispensable for diagnosing specific disorders, notably EGIDs and hypereosinophilic syndromes

1. INTRODUCTION

Eosinophilic granulocytes are hematopoietic effector cells with bilobed nuclei and large acidophilic cytoplasmic granules 1. They take part in many processes, including allergies, infections, and chronic inflammatory diseases, as well as hematological malignances 2. They grow and develop in bone marrow, and, under homeostatic conditions, they are mainly found in the gastrointestinal tract. Stimulated by cytokines, chemokines, and other mediators, they migrate into the blood and then reach tissues. There, they can be activated and release effectors that act on tissues promoting inflammation and remodeling 1. Their mediators play a crucial role on the activation and modulation of several different cells of both the innate and adaptive immune systems 3 (Fig. 1). Hence, blood eosinophils represent approximately 1% of peripheral blood leukocytes and reflect the balance between their production in bone marrow, trafficking from bone marrow into tissues and undergoing apoptosis. The finding of elevated tissue or blood eosinophils may be associated with a wide range of clinical conditions, even if very different from each other 4 (Tab. I).

2. BLOOD AND TISSUE EOSINOPHILS

The evaluation of blood eosinophils through a complete blood count is a very simple and economical test. Eosinophilia can be defined as absolute when the absolute eosinophil count (AEC) is greater than 500 cells/μL, relative when they represent more than 6% of blood cells, or combined when both are present. It can be mild if AEC is between 500 and 1490 cells/μL, moderate if between 1500 and 5000 cells/μL, and severe if above 5000 cells/μL. Hypereosinophilia (HE) is defined as moderate to severe and persistent eosinophilia, detected on at least two occasions at least four weeks apart, or marked tissue eosinophilia 4. However, “normal” AEC is influenced by numerous conditions, such as age, sex, environmental exposure, BMI, drugs, comorbidities 6,7. It is highest in childhood and adolescence, independent of age in adults and has higher levels in males in all age groups 7. AEC has considerable variability over time 8 and may also be influenced by technical factors, such as storage conditions and the time between collection and analysis 9. Moreover, eosinophil count, both in peripheral blood and in sputum, shows a wide range of variation through the day 10. For this reason, it is recommended to repeat the evaluation of blood eosinophils over time. HE can therefore be distinguished into transient, episodic (recurrent), or persistent if it is confirmed after at least 2 weeks 5.

Mild and transient eosinophilia is frequent in pediatric age and often has no clinical relevance, but may be associated with various conditions, such as atopy, asthma, drug hypersensitivity, and helminthic infections 11. HE, however, is relatively rare and can cause organ manifestations that characterize hypereosinophilic syndromes (HES) 5. Primary HE is caused by myeloid and stem cell neoplasms, which result in clonal expansion of eosinophils in the bone marrow. Secondary or reactive HE, which is much more frequent, results from the polyclonal expansion of eosinophils, which can be supported by many different conditions: atopic diseases, helminthic, fungal or viral infections, drugs, gastrointestinal disorders, hematologic diseases, immunodeficiencies, rheumatologic diseases, adrenal insufficiency, graft versus host disease, and solid organ transplant rejection 12. Allergic disorders, especially in children, are often associated with HE, whenever the increase in blood eosinophilia is severe, other causes should always be excluded.

The assessment of tissue eosinophils, through techniques such as immunohistochemistry and flow cytometry, provides more precise information on the presence and activation of eosinophils at the inflammatory site. Tissue eosinophilia is defined by the presence of at least one of the following criteria: eosinophils > 20% of nucleated cells in the bone marrow section; massive tissue infiltration of eosinophils; extensive extracellular deposits of eosinophil granule proteins upon immunostaining 5. When blood HE is associated with tissue HE, the infiltration and activation of eosinophils in tissues may cause organ damage, leading to HES. The diagnosis of HES requires the finding of blood and/or tissue HE, associated with organ damage (fibrosis, thrombosis, skin, lung, gastrointestinal, neurological involvement, eosinophilic vasculitis and other rarer manifestations), excluding other possible causes. Generally, tissue eosinophilia is associated with blood eosinophilia, but there are conditions in which it is isolated, called “tissue-restricted HES” or “organ-restricted HES” 5.

3. EOSINOPHILS AND ALLERGIES

In the diagnostic framework of allergic diseases, various degrees of blood or tissue eosinophilia or an increase in their markers are frequently found, with different meanings depending on the clinical context.

3.1. Respiratory diseases

Asthma is the most common respiratory disease associated with peripheral eosinophilia, which is generally mild to moderate 13. The evaluation of eosinophils and their markers is not a necessary test for the diagnosis of asthma, but it may be helpful to understand the patient’s phenotype, establish the risk of exacerbations and future evolution, and to propose an adapted treatment, especially in severe forms 5. Various studies have evaluated the relationship between peripheral and airway eosinophilia, highlighting important discordances 14,15, and also confirmed in a few pediatric studies 16,17. Universally accepted criteria do not yet exist in the definition of asthma phenotypes. “T2 inflammation” (previously referred to also as “Th2-high phenotype/endotype”) may be found in both allergic and non-allergic patients and is characterized by the presence of eosinophilic inflammation of the airways. Blood eosinophils (≥ 150/mm3), together with those in sputum (≥ 2%), fractional exhaled nitric oxide (FeNO, ≥ 20 ppb), serum periostin, and circulating IgE, are considered as markers of T2 inflammation in asthmatic patients 18-21. Childhood-onset atopic asthma is usually associated with T2 inflammation, in which eosinophilia in blood and sputum is a consequence of stimulation by IL-5, produced following an allergic immune response, thereby identifying a subset of T2 asthma, defined as allergic or atopic asthma, covering approximately 80% of asthmatic children 17,22. This differs from adult-onset eosinophilic asthma, which is often poorly responsive to therapy with inhaled corticosteroids, as it is difficult to control and often leads to remodeling and obstruction of the airways, without a very frequent allergic origin 18. Non-T2 asthma is less frequent in children, but often more severe and poorly responsive to steroids 22. In adults, blood eosinophilia and elevated FeNO levels have been associated with a greater risk of exacerbations, while sputum and blood eosinophilia have been identified as risk factors for developing persistent airflow limitation 21. Also, in the pediatric population, elevated AEC and FeNO identify patients at high risk of severe exacerbations 23.

In preschool children, recurrent wheezing is a manifestation of many different conditions, with different outcomes 24. The finding of a T2 phenotype in this age group has been associated with an increased risk of exacerbations and persistence of wheezing, especially when, in addition to elevated blood eosinophils, there is a sensitization to aeroallergens 25-27. Higher AECs are found in children with recent hospitalizations due to wheezing, history of eczema, allergic sensitizations, and higher levels of total serum IgE 25. Even in preschool age, the correlation between eosinophils in the airways and those in the blood is debated 28,29. Elevated blood eosinophils are a marker of good response to inhaled steroid therapy in children with wheezing, even in those presenting without allergic sensitization 30. Relative eosinophilia ≥ 4% is also part of the Asthma Predictive Index (API) and the subsequent modified API (mAPI), widespread clinical scores that allow the identification of children with recurrent wheezing at risk of developing asthma 27,31.

Concerning the upper airways, while in allergic rhinitis (AR) eosinophilia is generally mild, in chronic rhinosinusitis significant eosinophilic inflammation may occur, sometimes associated with nasal polyposis and asthma 32. In the diagnostic pathway of chronic rhinosinusitis, especially if it does not respond to steroid therapy, in addition to performing a nasal endoscopy to highlight the possible presence of polyposis, it is important to evaluate blood eosinophils. If they are >0.24 cells/μL or >4.3% 33, they indicate the presence of T2 inflammation. The combination of these two investigations therefore allows to identify the different phenotypes of chronic rhinosinusitis, which require different therapeutic strategies 34. The presence of tissue eosinophilia may be readily assessed through nasal cytology; however, it is not specific to AR, as it may also be detected in non-allergic rhinitis (NAR), such as NAR with eosinophilic infiltration (NARES) and NAR with eosinophils and mast cells (NARESMA) 35. In AR, tissue and blood eosinophil levels are influenced by seasons and/or allergen exposure, and their levels are higher in patients presenting with more severe symptoms or comorbidities, such as asthma and allergic conjunctivitis 36.

3.2. Food allergies and eosinophilic gastrointestinal diseases

Eosinophils are normally present throughout the gastrointestinal tract 37 and are widely involved in food allergies, particularly in some non-IgE-mediated clinical pictures, which include food protein induced allergic proctocolitis (FPIAP), food protein induced enteropathy (FPE), food protein induced enterocolitis syndrome (FPIES) and food protein induced motility disorders (FPIMD), and mixed, including eosinophilic esophagitis (EoE) and eosinophilic gastrointestinal disorders beyond eosinophilic esophagitis (non-EoE EGIDs). Eosinophilia is generally localized in tissues and therefore only found on biopsies, but it can sometimes also involve peripheral blood.

In patients suffering from FPIAP, the diagnosis is usually clinical but, as a nonspecific sign of atopic state, blood eosinophilia (44% of patients) or tissue eosinophilia in the colon (89% of patients) 38 and eosinophilic granules on stool smear may be found. The latter are higher in patients with FPIAP than in those with nonspecific colitis, but they do not allow to distinguish these children from those presenting with food protein-induced enterocolitis 40,41. Histologically, in FPIAP, tissue lesions have a patchy distribution and endoscopy may vary, showing normal patterns, or nonspecific features, or even a granulomatous aspect 41,42. An eosinophil cut-off of 60 cells/HPF in the lamina propria and the presence of an eosinophilic infiltrate in the epithelium or muscular mucosa is suggestive of FPIAP 43.

In FPE there is generally no blood eosinophilia and, even in tissues, eosinophilic infiltration is poor 44.

In acute FPIES, alterations of blood leukocytes occur 45 with an increase in neutrophils, but also a reduction in eosinophils, basophils and lymphocytes, while monocytes undergo a reduction at the beginning of the reaction and increase hours later. Therefore, the finding of neutrophilia, associated with reduction of eosinophils, basophils, and lymphocytes, may support a diagnosis of acute FPIES during acute episodes or oral food challenges 46, even though the diagnosis remains mainly a clinical one. In chronic FPIES, however, it is possible to find neutrophilia, eosinophilia, thrombocytosis, and anemia, as well as neutrophils and eosinophils in the stool.

In the diagnosis of EoE it is essential to demonstrate tissue eosinophilia through the finding of at least 1 positive esophageal biopsy (≥15 eosinophils/hpf), without eosinophilic infiltration of the stomach or duodenum, in association with symptoms compatible with EoE 47. The distribution of the infiltration may not be homogeneous; for this reason, it is recommended to perform multiple biopsies (at least 6) at both the proximal and distal esophagus level. Histologically, eosinophils may stratify on the surface, form microabscesses, and show signs of degranulation. Eosinophilic infiltration, however, is not exclusive to EoE and other causes, such as HIES, inflammatory bowel disease, celiac disease, gastroesophageal reflux disease, achalasia, infections, connective tissue disorders, drug hypersensitivity reactions, and extraesophageal eosinophilic gastrointestinal disorders, must be excluded before reaching a firm diagnosis, although they generally show different clinical characteristics. The density of the eosinophilic infiltration also represents a parameter of severity, but it is not the only determinant. In fact, a histological severity score index (EoEHSS) has been developed, which considers other criteria in addition to the density of the eosinophils, such as hyperplasia of the basal zone, eosinophilic abscesses, superficial stratification of eosinophils, dilated intercellular spaces (DIS), superficial epithelial change, dyskeratotic epithelial cells, and fibrosis of the lamina propria 48. The presence of blood eosinophilia is common in EoE, but, although some studies demonstrate a higher AEC in subjects with EoE compared to healthy controls, such a difference is not found when comparing EoE patients with atopic subjects 49.

Non-EoE EGIDs are classified based on the anatomic site of eosinophilic inflammation, including eosinophilic gastritis (EoG), eosinophilic duodenitis (EoD), eosinophilic enteritis (EoN), and eosinophilic colitis (EdC). In the presence of clinical symptoms, the diagnosis is based on the finding of eosinophilic infiltration in these sites, after excluding secondary causes of eosinophilic inflammation 50. Conditions that fall within the differential diagnosis for intestinal eosinophilia include hypersensitivity reactions to drugs or foods, malignant tumors, inflammatory bowel disease, infections, drug-induced diseases, primary immunodeficiencies and HES 51. Unlike the esophagus, which, in physiological conditions, does not contain eosinophils, the rest of the gastrointestinal tract contains resident eosinophils, in variable proportions in the different parts. Therefore, different cut-offs have been suggested for the diagnosis of various forms of non-EoE EGID: 30 eosinophils/hpf for the stomach, 50 eosinophils/hpf for the duodenum, 60 eosinophils/hpf for the terminal ileum, 100 eosinophils/hpf for cecum and ascending colon, 80 eosinophils/hpf for transverse and descending colon, 60 eosinophils/hpf for sigmoid colon and rectum 50. Additionally, it is worth underlining that some patients may show eosinophilic infiltration of more than one segment of the gastrointestinal tract, especially in pediatrics 52. Blood eosinophilia is possible in patients with non-EoE EGID 53, but this parameter is neither sensitive nor specific, and is not related to the severity of the disease 50.

3.3. Skin diseases

Eosinophilic inflammation is a characteristic of many skin diseases, not only of allergic ones, but also of infectious, hematological, autoimmune, vascular, or even idiopathic conditions 19. Eosinophils are widely involved in the pathogenesis of atopic dermatitis (AD) 54, and tissue eosinophilia is a typical feature of this condition 55. Furthermore, AD may be associated with generally mild peripheral eosinophilia, which is considered a biomarker of clinical severity 56. Serum and urinary levels of eosinophil secretion products are also elevated in AD patients 57. The importance of the role of eosinophils in AD is confirmed by the effectiveness of anti-IL-5 and anti-IL-5R biological therapies, which act on a fundamental growth and survival factor for eosinophils 58. However, elevated levels of T2 inflammatory biomarkers, including AEC, are also found in patients with Staphylococcus aureus colonization 59 and some studies found higher AECs in patients with atopic comorbidities 60. Under physiological conditions, eosinophils should not be present in the skin, which are instead found in many skin diseases. Therefore, when the clinical picture is not so clearly suggestive of AD and peripheral or tissue eosinophilia is found, alternative diagnoses should be ruled out, including cutaneous hematological malignancies, para-neoplasia or autoimmune blistering diseases, myeloid or stem cell neoplasm 61,62.

Although IgE mediated activation is the main immunological pathway in acute and chronic urticaria, autoimmune mechanisms are also involved and eosinophils also participate in the mechanism and contribute to tissue damage 63. However, children with acute and chronic urticaria generally have normal blood eosinophils, and the percentage of eosinophils does not differentiate between acute or chronic urticaria and healthy controls 64-66. In chronic spontaneous urticaria (CSU), eosinopenia, meant as AEC <50 cells/μL, is found in approximately 10% of patients 67, with a clinical significance that is still unclear, although it has been associated with greater disease activity, longer duration, poor response to treatment with both second-generation antihistamines and omalizumab, and type IIb autoimmune CSU 67-70.

Angioedema may be associated with eosinophilia and is classified into two types, episodic (EAE) and non-episodic (NEAE), both of which are rare in pediatric age 71. NEAE has a good spontaneous prognosis, generally without recurrence. EAE is part of HES and is characterized by blood HE that tends to increase during attacks and may disappear between exacerbations, associated with high IgM levels. Histologically, eosinophilic infiltrate and deposition of eosinophilic granule proteins are present. Despite being a rare disease, if a child presents recurrent attacks of HE-associated angioedema, in-depth extensive investigations must be considered and carried out 72.

3.4. Drug reactions

In areas with a low incidence of helminthic infections, drugs are the leading cause of persistent eosinophilia 73. Although an increase in blood eosinophil counts may be induced by any drug, antibiotics, particularly penicillins and sulphonamides, are the two classes most often responsible for such a finding 74. Reactions range from eosinophilia without clinical consequences, association with skin rashes, involvement of other single organs, to systemic reactions. However, peripheral and tissue eosinophilia characterize drug reactions with low sensitivity and specificity and, even if the association between eosinophilia and skin drug reactions is frequent, one study found that only 18% of patients with hospital drug rashes had peripheral eosinophilia, thus reducing the clinical value of eosinophilia to associate the appearance of the cutaneous manifestation to drug exposure 75. Eosinophilia, in drug hypersensitivity reactions, is mainly mediated by type IV reactions which determine a Th2-mediated response with consequent production of eosinophils activating cytokines 76. The most common skin rashes are maculopapular or morbilliform, for which it is possible to find a local eosinophilic infiltrate and blood eosinophilia in 50% of patients 77. Nevertheless, even when this infiltrate is detected, it remains impossible to differentiate a drug-induced reaction from a viral manifestation 78. Skin reactions with eosinophilic infiltration and possible blood eosinophilia may also present as acute generalized exanthematous pustulosis, eosinophilic pustular folliculitis, psoriasis-like reactions, drug-induced pseudo-lymphoma, and Wells syndrome 79.

In drug reactions with eosinophilia and systemic symptoms (DRESS), a serious adverse drug reaction with systemic involvement, peripheral eosinophilia is present in 30-90% of patients 79 and occurs approximately 2 weeks after mainly persistent exposure to the drug. Eosinophilia is not only detected in peripheral blood, but also in skin and involved organs. The most commonly drugs possibly responsible for this syndrome are anticonvulsants and antibiotics 80, leading to a T cell-mediated delayed-type hypersensitivity reaction with production of drug-specific T cells, polarizing a Th2-mediated response and subsequent hypereosinophilia 81,82. There is no biological test that allows to reach a diagnosis of DRESS, but it is possible to use the European Registry of Serious Skin Adverse Reactions (RegiSCAR) score, that includes, among several other parameters evocative of DRESS, the presence of blood eosinophilia, considered as AEC >700 cells/μL or eosinophils >10% of white blood cells 82. Eosinophils are also involved in drug-induced lung diseases, such as eosinophilic lung disease, diagnosed in the presence of eosinophilia in the BAL or on lung biopsy, and eosinophilic pleural effusions, with eosinophilia in the pleural fluid 83. The respiratory disease exacerbated by aspirin, which is a drug hypersensitivity reaction, but not an allergic one, is also characterized by activation of eosinophils, with eosinophilia in blood, induced sputum and nasal lavage 84. Drug-induced acute interstitial nephritis, which is characterized by the triad of fever, rash and eosinophilia, often incomplete, may be associated with eosinophiluria 79. Hypersensitivity myocarditis is a hypersensitivity reaction with delayed onset, which can also occur isolated as well as part of a DRESS and differs from viral myocarditis by a predominant eosinophilic infiltration and minor myocyte necrosis 79. Finally, drug-induced eosinophilic meningitis is characterized by the presence of >10 eosinophils/mm3 in cerebrospinal fluid or eosinophilia >10% of the total leukocyte count in cerebrospinal fluid 85.

4. CONCLUSIONS

Eosinophilia is frequent in conditions that may be found in patients suffering from different allergic manifestations. However, in some patients, it may require further evaluations to reach specific diagnosis. In most allergic diseases, blood eosinophilia represents a generic marker of atopy, which does not necessarily reflect the presence of eosinophilic infiltration of affected organs. Nevertheless, it may provide important information in the assessment of the specific patient, being a marker of clinical severity, prognosis, and response to available therapies. In other conditions, however, especially in non-IgE mediated and mixed food allergies, the identification of tissue eosinophilic infiltration is of fundamental importance, with specific cut-offs that allow their diagnosis.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Conflicts of interest statement

With regards to the present work, the Authors have no conflict of interest to declare.

Authors’ contributions

Conceptualization: RB, SG, DC. Original draft, and investigation: SG, DC. Writing-Review & Editing: SA, FC, GD, AG, CM, LP. Supervision: RB, MMDG, GLM.

History

Received: October 14, 2025

Published: March 27, 2026

Figures and tables

FIGURE 1. Eosinophils and their mediators on different innate and adaptive immune system cells (from Varricchi et al., 2017, adapted) 3.

Allergic diseases Asthma, AD, food allergy, allergic rhinitis, drug allergy, urticaria, angioedema
Primary immunodeficiency Combined immunodeficiency, congenital neutropenia, SCID, HIES, Netherton syndrome, CVID, MSMD, X-linked agammaglobulinemia, selective IgA deficiency, chronic granulomatous disease, ataxia telangiectasia, hyper immunoglobulin M syndrome, SCID-GVHD, Wiskott-Aldrich syndrome, IPEX, Di-George syndrome, cartilage hair hypoplasia, innate immune system dysfunction
Infectious disease Secondary infection of AD lesion, parasitic infection, cellulitis, lymphadenitis, HIV, sepsis, osteomyelitis, neutropenic fever
Rheumatic diseases FMF, PFAPA, PAN+FMF, systemic lupus erythematosus, urticaria vasculitis, Kawasaki syndrome
Malignancy Acute lymphoblastic leukemia, Hodgkin lymphoma, non-Hodgkin lymphoma, rhabdomyosarcoma, Wilms’ tumor, Kaposi sarcoma
Idiopathic hyper-eosinophilic syndrome
AD: atopic dermatitis; FMF: familial mediterranean fever; GVHD: graft versus host disease; HIES: hyper immunoglobulin E syndromes; IPEX: immunodysregulation polyendocrinopathy enteropathy X-linked; MSMD: Mendelian susceptibility to mycobacterial disease; PAN: polyarteritis nodosa; PFAPA: periodic fever, aphthous stomatitis, pharyngitis and cervical adenitis; SCID: severe combined immunodeficiency
TABLE I. Conditions associated with peripheral blood eosinophilia.

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Authors

Serena Gracci - Pediatrics and Neonatology Unit, Maternal and Child Department, San Giuseppe Hospital, Empoli, Azienda USL Toscana Centro, Italy

Davide Caimmi - Allergy Unit, CHU de Montpellier, Montpellier, France; IDESP, UMR 1318, INSERM, University of Montpellier, Montpellier, France

Stefani Arasi - Area of Translational Research in Pediatric Specialities, Allergy Unit, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy

Fernanda Chiera - Department of Pediatrics, Giovanni Paolo II Hospital, Lamezia Terme, ASP Catanzaro, Italy

Giulio Dinardo - Department of Woman, Child and General and Specialized Surgery, University of Campania “Luigi Vanvitelli’” Naples, Italy

Arianna Giannetti - Pediatric Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy

Carla Mastrorilli - Department of Pediatrics, University Hospital Consortium Corporation Polyclinic of Bari, Pediatric Hospital Giovanni XXIII, Bari, Italy

Luca Pecoraro - Pediatric Unit, Ospedale Vito Fazzi, ASL Lecce, Lecce, Italy

Gian Luigi Marseglia - Pediatric Unit, Department of Clinical, Surgical, Diagnostic, and Pediatric Sciences, University of Pavia, Pavia, Italy

Michele Miraglia Del Giudice - Department of Woman, Child and General and Specialized Surgery, University of Campania “Luigi Vanvitelli’” Naples, Italy

Roberto Bernardini - Pediatrics and Neonatology Unit, Maternal and Child Department, San Giuseppe Hospital, Empoli, Azienda USL Toscana Centro, Italy

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Gracci, S., Caimmi, D., Arasi, S., Chiera, F., Dinardo, G., Giannetti, A., Mastrorilli, C., Pecoraro, L., Marseglia, G. L., Miraglia Del Giudice, M., & Bernardini, R. (2026). The role of eosinophils in the diagnosis of allergic diseases. Italian Journal of Pediatric Allergy and Immunology, 40(1), 44–51. https://doi.org/10.53151/2531-3916/2026-1744
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