Eosinophilia is defined as an increase in the peripheral blood eosinophil count. The upper limit of normal is usually taken as about 600/microliter, but it is lower (about 400/microliter) if people with minor allergies are excluded. There is no ethnic variation in the normal eosinophil count and no physiologic cause of an increased count.
Causes of eosinophilia
The most common cause of eosinophilia depends on socioeconomic and geographic factors. In the developing world the most common cause is parasitic infection (and parasitic infections result in the greatest number of cases worldwide), whereas in the developed world it is allergy. Uncommon and rare causes are important because eosinophilia may be the result of a serious underlying condition.
The terms eosinophilia and hypereosinophilia do not have precise definitions. Nevertheless, the higher the eosinophil count, the more urgent it is to determine the cause, first because the underlying disease may need treatment in its own right, and second because hypereosinophilia can lead to tissue damage, which can be life-threatening. If eosinophils are extensively degranulated, tissue damage is more likely because of the enzymes, cytotoxic proteins, and cytokines released.
Investigation of eosinophilia
Follows the traditional model of clinical history, physical exam, and laboratory and other investigations, taking into account the likely causes in the individual patient.
- Ancylostoma caninum infestation
- Herpes gestationis
- Drug hypersensitivity
- Allergic bronchopulmonary aspergillosis
- Eosinophilic granulomatosis with polyangiitis
- Eosinophilic esophagitis
- Eosinophilic gastroenteritis
- Eosinophilic cellulitis (Wells syndrome)
- Chronic eosinophilic leukemia
- Other leukemias
- Non-Hodgkin lymphoma
- Hodgkin lymphoma
- Nonhematologic malignancy-associated hypereosinophilia
- Lymphocytic variant of hypereosinophilic syndrome
- Idiopathic hypereosinophilic syndrome
- Wiskott-Aldrich syndrome
- Job syndrome
- Hyperimmunoglobulin E syndrome
- Severe combined immune deficiency due to adenosine deaminase deficiency
- Omenn syndrome
- immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome
- Autoimmune lymphoproliferative syndrome (ALPS)
- Loeys-Dietz syndrome
- Comel-Netherton syndrome
- Severe dermatitis, multiple allergies, and metabolic wasting (SAM) syndrome
- Muscular sarcocystosis
- Cystoisospora belli (formerly Isospora belli) infection
Barbara J. Bain, MBBS, FRACP, FRCPath
Professor of Diagnostic Haematology
St Mary's Hospital Campus
Imperial College London
BJB is an author of a number of references cited in this topic.
James Uprichard, MBBS, BSc, PhD, FRCP, FRCPath
Department of Haematology
St George's University Hospitals NHS Foundation Trust
JU is on Bayer, Vifor Pharma, and Octapharma scientific advisory boards; Bayer, Octapharma, Shire, Vifor Pharma, and Daiichi-Sankyo speaker bureaus; is involved in clinical trials associated with Portola, Bayer, Boehringer-Ingelheim, and Daiichi-Sankyo; and has received travel support from Bayer.
Jonathan Bernstein, MD
Professor of Medicine
Department of Internal Medicine
Division of Immunology/Allergy Section
University of Cincinnati
JB is the editor of the Joint Task Force Practice Parameters on Urticaria.
Jan Cools, PhD
Department of Molecular and Developmental Genetics
Katholieke Universiteit Leuven
JC is an author of a reference cited in this topic.
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