a. Eosinophils, a type of white blood cell (WBC), are a normal component of peripheral blood and certain tissues. However, their presence in other tissues is often a sign of a pathologic process.
1. Defend the body against multicellular, helminthic parasites
2. Elaborate mediators that promote mucus secretion and alter vascular permeability in allergic diseases
3. Induce mast cells and basophils to release allergic mediators
b. Eosinophil count. The normal range of eosinophils in the blood is 0–400 cells/μL (0%–4%), and counts greater than 500 cells/μL are abnormal. However, counts may vary based on numerous factors including age, environmental factors, and time of day (owing to the diurnal variation of cortisol production).
i. Eosinopenia can be seen in acute bacterial or viral infections, exogenous corticosteroid use, and epinephrine use.
ii. Eosinophilia is associated with many diseases (as described later in the chapter).
B. Causes of Eosinophilia.
a. One way of remembering the various causes of eosinophilia is to use the following mnemonic:
MNEMONIC: PHILIA CAN ACT FAST with “FAST” falling under “H” and “ACT” under “I”.
Schistosomiasis or Strongyloides infection
Allergic bronchopulmonary aspergillosis
Tuberculosis (especially chronic)
Cutaneous disorder and cholesterol emboli
b. Pulmonary diseases. Primary lung disorders can lead to eosinophilia, including Löffler’s syndrome, eosinophilic pneumonia, bronchiectasis, and cystic fibrosis. Asthma can also be associated with eosinophilia.
c. Helminthic infections. The level of eosinophilia may reflect the burden of the helminthic infection, but the absence of eosinophilia does not rule out this type of infection. Common helminthic infections that lead to peripheral eosinophilia include:
Disseminated strongyloides sometimes does not cause eosinophilia because of the superimposed bacterial infection that may accompany parasitic dissemination.
d. Other infections
i. Allergic bronchopulmonary aspergillosis (ABPA)
Invasive aspergillosis does not cause eosinophilia.
iii. Tuberculosis, especially chronic tuberculosis
iv. HIV. The eosinophilia in HIV may be from the virus itself, secondary infections common to HIV, or special antiretroviral therapies.
e. Contaminated l-tryptophan can cause eosinophilia-myalgia syndrome.
f. Immunologic disorders (e.g., vasculitis [especially Churg-Strauss syndrome], severe rheumatoid arthritis, eosinophilic fasciitis, hyper–immunoglobulin E [hyper-IgE] syndrome)
g. Addison’s disease
h. Cutaneous disorders (e.g., bullous pemphigoid, scabies, eosinophilic cellulitis)
i. Allergic disorders (e.g., asthma, allergic rhinitis, atopic dermatitis, drug reactions, acute urticaria)
j. Cholesterol embolization
k. Neoplasms. Solid tumors, lymphoma, leukemia, hypereosinophilic syndrome, and mastocytosis can all lead to eosinophilia.
i. Hypereosinophilic syndrome (absolute eosinophil count >1500 cells/μL) is associated with a peripheral eosinophilia as well as tissue deposition of eosinophils into the lungs, heart, kidneys, and gastrointestinal (GI) tract. Specific testing for tissue involvement is required. Assessment for chromosomal abnormalities, such as chromosome 4q12 deletion (resulting in the FIP1L1-PDGFR alpha fusion) is important as it directs treatment. When clonality is present, the condition may be best characterized as a chronic eosinophilic leukemia.
ii. Mast cell disorders, including cutaneous and systemic mastocytosis, can be associated with an eosinophilia.Diagnosis is based on either a tissue or bone marrow biopsy demonstrating an accumulation of an abnormal population of mast cells.
a. History and physical examination
i. Ask for new exposures, including dietary changes and new medications.
ii. Obtain a travel history, including international travel, travel to the southwestern United States, and exposure to unpurified water. Risks for specific infections may be tied to geographic boundaries and may direct the diagnostic testing. Asking whether companions developed similar symptoms may help focus the evaluation on possible infectious causes.
iii. Focal symptoms, including rash, cough, shortness of breath, fever, connective tissue complaints, and GI symptoms, may help clinically focus the evaluation.
b. Laboratory examination
i. Stool examination, including an examination for ova and parasites on several occasions, may be required. Consideration for specific parasitic serologies (i.e., Strongyloides IgG) or molecular testing (i.e., Coccidioides polymerase chain reaction) may be helpful.
ii. Radiographic imaging and pulmonary testing including bronchoscopy may be required to evaluate for pulmonary involvement of the eosinophilia as well as to establish the diagnosis of ABPA.
iii. Peripheral blood smear may help identify specific pathogens (e.g., microfilariae) or may identify an acute or chronic leukemia associated with eosinophilia.
iv. Other laboratory assessments to consider are complete blood count, serum immunoglobulins (including IgE), serum tryptase, and bone marrow biopsy.
a. Treatment of the underlying cause of eosinophilia is key. If hypereosinophilic syndrome is present and a FIP1L1-PDGFR-α is found, imatinib should be considered.
Suggested Further Readings
Klion AD. How I treat hypereosinophilic syndromes. Blood 2015;126:1069.Find this resource:
Rothenberg ME. Eosinophilia. N Engl J Med 1998;338:1592–600. (Classic Article.)Find this resource: