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INTRODUCTION — Peripheral blood eosinophilia

can be caused by numerous allergic, infectious,

and neoplastic disorders, which require a variety

of different treatments. A major goal of the initial

evaluation is to identify disorders that require

specific treatments (eg, parasitic infection, drug

hypersensitivity, leukemia, non-hematologic

cancer).

The peripheral blood eosinophil count does not

accurately predict the risk of organ damage in all

patients. Although complications of eosinophilia

are more common in patients with higher

eosinophil counts (eg, >1500 eosinophils/microL),

a patient with mild peripheral blood eosinophilia

may have significant organ involvement by

eosinophils. Thus, it is also important to consider

the clinical status of the patient and to determine

whether there is evidence of end-organ

involvement.

This topic presents our approach to determining

the underlying cause of unexplained peripheral

blood eosinophilia. Disorders with eosinophilic

involvement of specific organs are presented

separately.

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MLT-Hematologist

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14:09

TERMINOLOGY — We use the following terms:

PATHOPHYSIOLOGY — Eosinophils are primarily

tissue-dwelling cells; they are several hundredfold

more abundant in tissues than in blood.

Importantly, the degree of peripheral blood

eosinophilia does not always accurately predict

the risk of organ damage. Thus, organ

involvement and end-organ damage cannot be

predicted by a high eosinophil count, nor can they

be excluded by a low eosinophil count.

Target organs — Common target organs of

eosinophils in disease include the skin, lung, and

gastrointestinal tract. However, cardiac and

nervous system damage can also occur, and can

be more concerning and potentially life-

threatening.

Eosinophil biology in health and disease is

reviewed elsewhere. (See "Eosinophil biology and

causes of eosinophilia", section on 'Eosinophil

biology' .)

MAJOR CAUSES OF

EOSINOPHILIA — Eosinophilia can be caused by a

number of conditions ( table 1). The degree of

eosinophilia is rarely helpful for identifying the

cause, except at extremes of eosinophil counts

(eg, very mild eosinophilia may be associated

with asthma or allergic rhinitis; very severe

eosinophilia [ie, ≥20,000 eosinophils/microL] is

more likely to be caused by a myeloproliferative

neoplasm). The disorders that can cause

eosinophilia are best distinguished by the

patient's history, clinical presentation, and

specific laboratory testing. A more detailed

discussion of the causes of eosinophilia is found

separately. (See "Eosinophil biology and causes of

eosinophilia", section on 'Major causes of

eosinophilia' .)

OVERVIEW OF OUR APPROACH — The most

important steps in evaluating an individual with

eosinophilia are assessing the presence and

degree of tissue/organ involvement, which

determines the urgency of the evaluation; and

determining the etiology, which has major

implications for treatment.

Acutely ill patient or extremely high eosinophil

count — An acutely ill patient with eosinophilia, or

an individual with an extremely high eosinophil

count (eg, ≥100,000 eosinophils/microL), requires

hospitalization and urgent evaluation for the

cause of the eosinophilia; these cases are rare.

(See "Hypereosinophilic syndromes: Clinical

manifestations, pathophysiology, and diagnosis" .)

If the acute illness appears to be due to organ

dysfunction (possibly caused by tissue eosinophil

infiltration), or if an appropriate alternate therapy

is not identified, urgent therapy directed at

reducing eosinophilia (eg, high dose

glucocorticoids) should be initiated. Ideally,

baseline laboratory testing to determine the

potential cause of the eosinophilia is sent before

initiating urgent therapy, because therapy may

obscure the underlying cause. However, urgent

therapy should not be delayed while attempting to

obtain, or awaiting results of, this testing. (See

'Initial testing' below and "Hypereosinophilic

syndromes: Treatment", section on 'Immediate

treatment for severe disease' .)

The risk of dissemination of strongyloides in the

setting of glucocorticoid therapy necessitates that

individuals with potential exposure to

strongyloides infection be treated empirically for

strongyloides with ivermectin (200 mcg/kg daily

for two days). This applies to all individuals with

potential exposure, even if the serology is

negative, because the reliability of serologic

testing is variable. (See "Strongyloidiasis", section

on 'Epidemiology' and "Strongyloidiasis", section

on 'Treatment' .)

Outpatient with signs of organ

involvement — Peripheral blood eosinophilia does

not correlate well with the extent of tissue

damage except at the extremes of absolute

eosinophil counts. Thus, signs of organ

dysfunction should be addressed promptly,

regardless of the level of blood eosinophilia.

Helminth infections are among the most common

causes worldwide. In the developed world,

allergies and asthma predominate overall, and

drug hypersensitivity is common in those with

eosinophils counts >1500/microL.

For a patient with signs of organ involvement who

is not acutely ill or hospitalized, the pace of the

evaluation and the need for specialist refe

14:09

rral

depends on the specific organ involved and the

degree of organ dysfunction. In many cases, initial

testing can be done in the outpatient setting. (See

'Laboratory evaluation and other testing' below

and 'When to refer' below.)

Incidental finding, healthy

individual — Eosinophilia discovered as an

incidental finding on a complete blood count in an

otherwise healthy individual can be evaluated on

an outpatient basis. The initial evaluation should

include a complete history, physical examination,

and baseline laboratory testing. (See 'Laboratory

evaluation and other testing' below.)

If signs of organ involvement are found on the

initial evaluation or develop during this evaluation,

the patient may need to be seen more urgently by

a physician experienced in evaluating eosinophilic

disorders and/or admitted to the hospital. (See

'When to refer' below.)

The patient with no signs of organ involvement

should undergo periodic monitoring for the

development of organ involvement at six month

intervals. (See 'Initial testing' below.)

In some cases, eosinophilia resolves without

treatment. Potential explanations for resolution of

eosinophilia include removal of an offending agent

(ie, transient exposure); clearance of an infection;

and downregulation of host responses (as has

been reported in the setting of chronic helminth

infection). The expected time course of resolution

of eosinophilia after a transient exposure is

unknown, although in the case of drug

hypersensitivity and removal of the offending

agent, resolution can take many months.

The optimal evaluation of the asymptomatic

traveler or immigrant with eosinophilia is

uncertain. Up to 50 percent of such patients never

have a cause of their eosinophilia identified

despite exhaustive evaluation [10 ].

Children — The likely causes of eosinophilia in

children and our approach to the evaluation of

children are identical to that in adults with a few

exceptions. Asthma and atopic disease remain

the most common causes of mild to moderate

eosinophilia in children; however, close attention

should be paid to the frequency and etiology of

infections, since immunodeficiency syndromes

typically present in childhood and can be

associated with atopic disease and peripheral

blood and tissue eosinophilia. (See "Primary

humoral immunodeficiencies: An overview" and

"Combined immunodeficiencies" and "Approach to

the child with recurrent infections" .)

Food allergy and eosinophilic esophagitis are also

more common causes of eosinophilia in the

pediatric age group and can be missed if an

appropriate history is not elicited; the only clue to

the diagnosis of eosinophilic esophagitis in a child

may be occasional vomiting. (See "Clinical

manifestations of food allergy: An overview" and

"History and physical examination in the patient

with possible food allergy" and "Clinical

manifestations and diagnosis of eosinophilic

esophagitis" .)

Since helminth infections require appropriate

exposure, some infections are more or less

prevalent in children. As an example, visceral

larva migrans, which requires ingestion of eggs

from soil contaminated with animal feces, is seen

almost exclusively in young children; whereas

filariasis, which requires repeated exposure to the

bites of infected insect vectors, increases with age

and is rare in children under four years of age.

(See "Toxocariasis: Visceral and ocular larva

migrans" .)

Some forms of leukemia and lymphoma (eg, pre-

B cell acute lymphoblastic leukemia [ALL]) are

more common in childhood and can present with

asymptomatic eosinophilia, sometimes several

years before the malignancy is detected. In

contrast, solid tumors are rarely the cause of

eosinophilia in children. Although definitive data

are lacking, the prevalence of other rare causes of

eosinophilia, including FIP1L1/PDGFRA-positive

myeloproliferative neoplasms, eosinophilic

granulomatosis and polyangiitis, and episodic

angioedema and eosinophilia, appear to be

comparable in children and adults.

HISTORY — All patients should have a thorough

history that addresses symptoms of organ

involvement, me

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dical conditions, exposures

(medications, foods, over-the-counter remedies,

travel, and occupational and recreational

exposures), and prior eosinophil counts. Family

history may also be helpful in rare cases of

familial hematologic syndromes. (See 'Family

history' below.)

Symptoms — Symptoms of specific organ system

involvement may suggest a potential cause of

eosinophilia and/or the consequences of

eosinophil-induced tissue damage. We assess the

following:

We also ask about medical conditions that may

be associated with eosinophilia (eg, asthma,

rheumatologic conditions, malignancy) and

whether there has been a recent change in

disease symptoms that could represent disease

progression or a new diagnosis.

Exposures — Exposure history should include

occupational and recreational activities,

medications and supplements, foods, and travel.

Occupational/recreational exposures — Some

occupations and/or recreational activities are

associated with specific exposure risks. Examples

include a risk for strongyloides infection in miners,

a risk for ascariasis in slaughterhouse workers,

and a risk for schistosomiasis in river rafters.

Medications and over the counter

remedies — Eosinophilia can be caused by almost

any prescription or nonprescription drug, herbal

remedy, or dietary supplement ( table 2). Thus, a

detailed review of past, current, and over-the-

counter medications and remedies should be

elicited. The temporal relationship between

administration of the medication or herbal remedy

may be helpful, but the time course of

eosinophilia does not always follow a consistent

pattern. Although drug-induced eosinophilia is

often accompanied by fever, rash, or other clinical

manifestations, signs and symptoms may be

absent.

In a prospective cohort study of 824 patients

receiving prolonged intravenous antibiotic therapy

as outpatients, 25 percent developed eosinophilia

(peak absolute eosinophil count ranging from 500

to 8610/mL, median 726/mL) after a median of

15 days of therapy [11 ]. Patients with eosinophilia

had a significantly higher likelihood of rash (15

versus 6 percent; adjusted hazard ratio [HR],

4.16) or renal injury (15 versus 10 percent;

adjusted HR, 2.13), compared with patients

without eosinophilia. Liver injury was comparable

between the two groups. DRESS (drug rash with

eosinophilia and systemic symptoms) syndrome

or possible DRESS, occurred in seven patients,

four of whom were receiving vancomycin .

Medication-associated eosinophilia per se does

not mandate cessation of medication

administration but rather requires careful

consideration of the following questions: a) are

there clinical manifestations in association with

the eosinophilia that would dictate changing the

medication, b) are there alternative medications

(eg, antibiotics, seizure meds) that could be

substituted, or is the likely medication the

preferred or required therapy. It is also important

to realize that eosinophilia may not resolve for

weeks to months after discontinuation of the

offending agent.

Foods — Dietary history should ascertain the

ingestion of raw or undercooked meat because

incompletely cooked pork containing encysted

larvae is a source of trichinellosis. Ingestion of

soil or vegetables contaminated by excrement

from infected dogs or cats can cause toxocariasis,

and undercooked or raw crab or crayfish can

transmit paragonimiasis. (See "Trichinellosis" and

"Toxocariasis: Visceral and ocular larva migrans"

and "Paragonimiasis" .)

Travel — A history of residence in or recent

travel to a parasite-endemic area may be helpful

in suggesting a parasitic etiology of eosinophilia.

However, a lack of recent travel should not

eliminate parasitic infection as a potential cause

of eosinophilia, especially for helminths with a

worldwide distribution and/or a long latency

period. As an example, foreign military service,

even decades earlier, could be a source of

strongyloides infection, which occurs via

penetration of the skin upon contact with soil or

water contaminated by human feces. This history

may be omitted unless it is specifically queried.

(

14:09

See "Eosinophil biology and causes of

eosinophilia", section on 'Parasites and other

infections' .)

Since some helminth parasites have a limited

geographic distribution, a detailed travel history is

especially important. As an example, Loa loa

infection is endemic only in Central and West

Africa, whereas gnathostomiasis has a worldwide

distribution ( table 3). Consequently, a patient

presenting with migratory angioedema without a

history of travel to Africa should be evaluated for

some causes of migratory angioedema (eg,

gnathostomiasis), but not for loiasis (eg, such an

individual does not require a midday blood smear

or filarial serology). (See "Skin lesions in the

returning traveler" and "Loiasis (Loa loa

infection)" .)

In contrast to helminthic parasites, most

pathogens responsible for travelers' diarrhea,

including bacteria and protozoan parasites (eg,

Giardia , Entamoeba ), generally do not cause

eosinophilia. Exceptions are Dientamoeba fragilis ,

Isospora belli , and Sarcocystis species, which can

cause eosinophilia. These organisms have a

worldwide distribution, with geographic

concentrations (eg, I. belli in tropical/subtropical

areas and India). (See "Dientamoeba fragilis" and

"Epidemiology, clinical manifestations, and

diagnosis of Cystoisospora infections" and

"Sarcocystosis" .)

Prior eosinophil counts — New onset of

eosinophilia suggests a new diagnosis, although it

does not help narrow the diagnosis. Persistent

eosinophilia without symptoms is reassuring and

suggests that the evaluation can be done less

urgently.

Waxing and waning eosinophilia can result from

the following:

Family history — Cases of familial clustering of

eosinophilic syndromes have been described (eg,

eosinophilic esophagitis), but familial clustering is

uncommon in most cases of eosinophilia [13 ].

Familial hypereosinophilia is rare, but has been

described. (See "Hypereosinophilic syndromes:

Clinical manifestations, pathophysiology, and

diagnosis", section on 'Diagnosis of familial

HES' .).

PHYSICAL EXAMINATION — The physical

examination should focus on identifying lesions

that suggest a possible cause of eosinophilia, and

on determining the presence of organ

involvement. We specifically assess the skin, eyes,

nose, lymph nodes, gastrointestinal, cardiac,

respiratory, and neurologic systems, and the

presence of splenomegaly.

LABORATORY EVALUATION AND OTHER TESTING

Whom to test — The initial tests for etiology and

organ involvement listed below should be

performed in the following patients:

Patients not in these categories (eg,

asymptomatic, no concerning travel history, mild

eosinophilia [absolute eosinophil count

<1500/microL]) may be observed. The eosinophil

count may be repeated to determine if it is

increasing.

An increasing eosinophil count or development of

new signs or symptoms should prompt

reevaluation.

Initial testing — In the patient groups listed

above, we suggest the following initial tests for

possible causes of eosinophilia and signs of organ

involvement ( table 4) (see 'Whom to test' above):

Evidence of organ dysfunction should prompt

initiation of therapy in order to reduce the risk of

permanent and/or life-threatening organ damage

in most patients. This is discussed in detail

separately. (See "Hypereosinophilic syndromes:

Treatment" and "Eosinophil biology and causes of

eosinophilia", section on 'Disorders with

eosinophilic involvement of specific organs' .)

For those without signs of organ involvement, we

periodically repeat this testing, along with

complete blood count and differential (eg, at six

month intervals). Any temporal relationships with

exposures or illnesses should be noted. Of note,

intermittent administration of steroids can

produce a false appearance of episodic

eosinophilia. (See 'Prior eosinophil counts'

above.)

Additional testing in selected patients — The

following may be also appropriate in selected

patients, depending on individual patient

characteristics and the results of the initial

evaluation ( table 4 ):

Testing for other parasites and infections — In

addition to serologies for Strongyloides sp

👍 1

14:09

ecies,

which should be performed in all patients,

additional testing for parasitic or other infections

may be indicated depending on the exposure

history ( table 4). (See 'Exposures' above and

"Strongyloidiasis", section on 'Whom to test' .)

TRIAL OF DRUG DISCONTINUATION — If a drug-

induced cause of eosinophilia is suspected based

on an implicated medication and lack of other

explanation, a trial of drug discontinuation (and

substitution of an alternative if necessary) may be

helpful. The most likely drug(s) can be

discontinued first if the patient is not acutely ill; if

the cause remains undetermined or the patient

becomes acutely ill, discontinuation of all non-

essential medications is appropriate.

WHEN TO REFER

Specialist referral — Referral to a specialist is

appropriate for clinical evaluation and biopsy of a

potentially affected tissue. As examples,

pulmonary evaluation is appropriate for

individuals with evidence of lung involvement (eg,

symptoms, radiographic findings); allergy testing

is appropriate for those with suspected

eosinophilic esophagitis. (See "Causes of

pulmonary eosinophilia" and "Allergy testing in

eosinophilic esophagitis" .)

Referral to a clinician who specializes in

eosinophilia is appropriate if a thorough

evaluation has been conducted and the cause of

persistent eosinophilia is not found. This may be

an infectious diseases expert, hematologist, or

allergist, depending on the institution. Individuals

with expertise in tropical diseases should be

consulted rather than attempting empiric

antihelminthic therapy, which may delay

appropriate diagnostic testing and lead to

complications of a therapy that was not indicated

or that was used incorrectly.

Bone marrow examination — Hematologic

evaluation with bone marrow examination

(aspiration and biopsy) is appropriate for any

individual with a potential primary hematologic

cause of eosinophilia. Examples include the

following:

Bone marrow morphology should be evaluated for

abnormalities of eosinophilic precursors ( picture

1), with special stains for reticulin and/or mast

cells if indicated. Detection of mast cells in the

bone marrow is discussed separately. (See

"Mastocytosis (cutaneous and systemic):

Evaluation and diagnosis in adults", section on

'Bone marrow examination' .)

Bone marrow should undergo cytogenetic and/or

specific molecular testing for hematologic

neoplasms associated with eosinophilia, including

the following:

Depending upon the clinical presentation and the

urgency for initiating therapy, investigations may

be performed sequentially, starting with those

that appear more likely to be informative. For

example, if a patient presents with splenomegaly,

mucosal ulcers of the oral cavity, and signs of

heart failure, testing for the FIP1L1/PDGFRA

fusion indicative of myeloproliferative

hypereosinophilic syndrome (HES) is indicated.

Ideally, diagnostic testing for myeloproliferative or

lymphocytic etiologies for HES should be

performed prior to initiating therapies that might

suppress clonal cell populations.

SUMMARY AND RECOMMENDATIONS

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REFERENCES

1. Tefferi A. Blood eosinophilia: a new

paradigm in disease classification,

diagnosis, and treatment. Mayo Clin Proc

2005; 80:75.

2. Roufosse F, Weller PF. Practical approach to

the patient with hypereosinophilia. J Allergy

Clin Immunol 2010; 126:39.

3. Chen YY, Khoury P, Ware JM, et al. Marked

and persistent eosinophilia in the absence of

clinical manifestations. J Allergy Clin

Immunol 2014; 133:1195.

4. Klion AD, Bochner BS, Gleich GJ, et al.

Approaches to the treatment of

hypereosinophilic syndromes: a workshop

summary report. J Allergy Clin Immunol

2006; 117:1292.

5. Simon HU, Rothenberg ME, Bochner BS, et

al. Refining the definition of

hypereosinophilic syndrome. J Allergy Clin

Immunol 2010; 126:45.

6. Valent P, Klion AD, Rosenwasser LJ, et al.

ICON: Eosinophil Disorders. World Allergy

Organ J 2012; 5:174.

7. Helbig G, Hus M, Francuz T, et al.

Characteristics and clinical outcome of

patients with hypereosinophilia of

und

14:09

etermined significance. Med Oncol 2014;

31:815.

8. Valent P, Klion AD, Horny HP, et al.

Contemporary consensus proposal on

criteria and classification of eosinophilic

disorders and related syndromes. J Allergy

Clin Immunol 2012; 130:607.

9. Gotlib J. World Health Organization-defined

eosinophilic disorders: 2012 update on

diagnosis, risk stratification, and

management. Am J Hematol 2012; 87:903.

10. Libman MD, MacLean JD, Gyorkos TW.

Screening for schistosomiasis, filariasis, and

strongyloidiasis among expatriates returning

from the tropics. Clin Infect Dis 1993;

17:353.

11. Blumenthal KG, Youngster I, Rabideau DJ, et

al. Peripheral blood eosinophilia and

hypersensitivity reactions among patients

receiving outpatient parenteral antibiotics. J

Allergy Clin Immunol 2015; 136:1288.

12. Georgiou S, Maroulis J, Monastirli A, et al.

Anaphylactic shock as the only clinical

manifestation of hepatic hydatid disease. Int

J Dermatol 2005; 44:233.

13. Klion A. Hypereosinophilic syndrome: current

approach to diagnosis and treatment. Annu

Rev Med 2009; 60:293.

14. Esposito DH, Stich A, Epelboin L, et al. Acute

muscular sarcocystosis: an international

investigation among ill travelers returning

from Tioman Island, Malaysia, 2011-2012.

Clin Infect Dis 2014; 59:1401.

Topic: 5691 Version: 18.0

Release: 24.1 - C24.54

Previous Topic New Search

Absolute eosinophil count – The absolute

eosinophil count refers to the number of

circulating eosinophils in the peripheral blood

(in cells/microL). It is determined by

multiplying the total white blood cell (WBC)

count by the percentage of eosinophils. Some

laboratories report this calculated number

directly, while others require the clinician to

make the calculation.

●

Eosinophilia – Eosinophilia refers to an

absolute eosinophil count in the peripheral

blood of ≥500 eosinophils/microL; this is

considered abnormal in most laboratories

[ 1,2 ]. The degree of eosinophilia can also be

categorized as mild (500 to 1500

eosinophils/microL), moderate (1500 to 5000

eosinophils/microL), or severe (>5000

eosinophils/microL).

●

The typical percentage of eosinophils in an

individual without eosinophilia is less than 5

percent, but the presence of eosinophilia

cannot be determined based on the

eosinophil percentage alone, because this

percentage is a relative number that varies

with the total WBC count and the relative

percentages of other WBCs (eg, neutrophils,

lymphocytes).

Hypereosinophilia (HE) – Hypereosinophilia

(HE) is defined as moderate to severe

eosinophilia (ie, ≥1500 eosinophils/microL).

End-organ manifestations may be present,

but are not required for the HE designation.

When the cause of the eosinophilia is

unknown and clinical manifestations are

absent, patients with hypereosinophilia are

considered to have hypereosinophilia of

unknown significance (HE US )

MLT-H

.

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م

14:47

مختبرات طبــ🔬ــية

Hypereosinophilic syndrome (HES) –

Hypereosinophilic syndrome (HES) is used to

describe a group of heterogeneous clinical

syndromes; it does not necessarily imply a

primary hematologic or neoplastic disorder.

Only the following two features are required

[ 4-6 ]:

●

Hypereosinophilia (ie, absolute

eosinophil count ≥1500/microL) on at

least two occasions

•

Signs of organ dysfunction attributable

to the eosinophilia

14:51

Historically, the terms "HES" and "idiopathic

HES" have been used to describe eosinophilia

≥1500/microL associated with end organ

dysfunction attributable to the eosinophilia in

which the cause is unknown. From a

practical standpoint, however, it is important

to recognize that 1) end organ manifestations

of eosinophilia can be identical irrespective of

the cause; 2) the etiology of the eosinophilia

may not be evident at presentation but may

be determined later; and 3) some individuals

with moderate to severe eosinophilia remain

asymptomatic or develop signs of organ

dysfunction many years after the eosinophilia

is first noted [3,7 ]. Furthermore, with the

availability of new diagnostic tests and

targeted therapies, the ability to identify

specific etiologies of HES continues to grow.

(See "Hypereosinophilic syndromes: Clinical

manifestations, pathophysiology, and

diagnosis", section on 'Definitions' .)

In view of the clinical heterogeneity of HE and

HES, there have been many attempts to

develop a classification system in order to

better direct clinical management [4-6,8,9 ].

For example, some experts subdivide HES

into myeloproliferative syndrome-type HES

(M-HES), in which clinical features point

towards a myeloproliferative disorder; and

lymphoid HES (L-HES), in which T cell

production of cytokines, such as IL-5, leads

to overproduction of eosinophils [2].

However, none of the available classification

systems is perfect, and the majority of

patients with HES (eg, up to two-thirds) do

not fit neatly into a specific category.

From the perspective of patient management,

a more important distinction is whether the

treatment should be directed at the

eosinophilia or at another condition that is

stimulating eosinophil production (eg,

parasitic infection, drug hypersensitivity, non-

hematologic cancer). (See 'Overview of our

approach' below.)

Primary (or neoplastic) hypereosinophilic

syndrome (HES) – Primary (neoplastic) HES

refers to a myeloproliferative neoplasm that

produces a predominance of mature

eosinophils.

..

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14:53

PATHOPHYSIOLOGY — Eosinophils are primarily

tissue-dwelling cells; they are several hundredfold

more abundant in tissues than in blood.

Importantly, the degree of peripheral blood

eosinophilia does not always accurately predict

the risk of organ damage. Thus, organ

involvement and end-organ damage cannot be

predicted by a high eosinophil count, nor can they

be excluded by a low eosinophil count.

.

MLT-AMGED

15:00

MAJOR CAUSES OF

EOSINOPHILIA — Eosinophilia can be caused by a

number of conditions .The degree of

eosinophilia is rarely helpful for identifying the

cause, except at extremes of eosinophil counts

(eg, very mild eosinophilia may be associated

with asthma or allergic rhinitis; very severe

eosinophilia [ie, ≥20,000 eosinophils/microL] is

more likely to be caused by a myeloproliferative

neoplasm). The disorders that can cause

eosinophilia are best distinguished by the

patient's history, clinical presentation, and

specific laboratory testing. A more detailed

discussion of the causes of eosinophilia is found

separately.

.

.

Amged

.

.

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15:06

Acutely ill patient or extremely high eosinophil

count — An acutely ill patient with eosinophilia, or

an individual with an extremely high eosinophil

count (eg, ≥100,000 eosinophils/microL), requires

hospitalization and urgent evaluation for the

cause of the eosinophilia; these cases are rare.

(See "Hypereosinophilic syndromes: Clinical

manifestations, pathophysiology, and diagnosis" .)

If the acute illness appears to be due to organ

dysfunction (possibly caused by tissue eosinophil

infiltration), or if an appropriate alternate therapy

is not identified, urgent therapy directed at

reducing eosinophilia (eg, high dose

glucocorticoids) should be initiated. Ideally,

baseline laboratory testing to determine the

potential cause of the eosinophilia is sent before

initiating urgent therapy, because therapy may

obscure the underlying cause. However, urgent

therapy should not be delayed while attempting to

obtain, or awaiting results of, this testing. (See

'Initial testing' below and "Hypereosinophilic

syndromes: Treatment", section on 'Immediate

treatment for severe disease' .)

The risk of dissemination of strongyloides in the

setting of glucocorticoid therapy necessitates that

individuals with potential exposure to

strongyloides infection be treated empirically for

strongyloides with ivermectin (200 mcg/kg daily

for two days). This applies to all individuals with

potential exposure, even if the serology is

negative, because the reliability of serologic

testing is variable.

.

.

💊🔬 مختبرات طبيه🔬🔭 @laboratory1

15:07

Outpatient with signs of organ

involvement — Peripheral blood eosinophilia does

not correlate well with the extent of tissue

damage except at the extremes of absolute

eosinophil counts. Thus, signs of organ

dysfunction should be addressed promptly,

regardless of the level of blood eosinophilia.

Helminth infections are among the most common

causes worldwide. In the developed world,

allergies and asthma predominate overall, and

drug hypersensitivity is common in those with

eosinophils counts >1500/microL.

For a patient with signs of organ involvement who

is not acutely ill or hospitalized, the pace of the

evaluation and the need for specialist referral

depends on the specific organ involved and the

degree of organ dysfunction. In many cases, initial

testing can be done in the outpatient setting.

.

.

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15:09

Incidental finding, healthy

individual — Eosinophilia discovered as an

incidental finding on a complete blood count in an

otherwise healthy individual can be evaluated on

an outpatient basis. The initial evaluation should

include a complete history, physical examination,

and baseline laboratory testing. (See 'Laboratory

evaluation and other testing' below.)

If signs of organ involvement are found on the

initial evaluation or develop during this evaluation,

the patient may need to be seen more urgently by

a physician experienced in evaluating eosinophilic

disorders and/or admitted to the hospital. (See

'When to refer' below.)

The patient with no signs of organ involvement

should undergo periodic monitoring for the

development of organ involvement at six month

intervals. (See 'Initial testing' below.)

In some cases, eosinophilia resolves without

treatment. Potential explanations for resolution of

eosinophilia include removal of an offending agent

(ie, transient exposure); clearance of an infection;

and downregulation of host responses (as has

been reported in the setting of chronic helminth

infection). The expected time course of resolution

of eosinophilia after a transient exposure is

unknown, although in the case of drug

hypersensitivity and removal of the offending

agent, resolution can take many months.

The optimal evaluation of the asymptomatic

traveler or immigrant with eosinophilia is

uncertain. Up to 50 percent of such patients never

have a cause of their eosinophilia identified

despite exhaustive evaluation.

.

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15:12

Children — The likely causes of eosinophilia in

children and our approach to the evaluation of

children are identical to that in adults with a few

exceptions. Asthma and atopic disease remain

the most common causes of mild to moderate

eosinophilia in children; however, close attention

should be paid to the frequency and etiology of

infections, since immunodeficiency syndromes

typically present in childhood and can be

associated with atopic disease and peripheral

blood and tissue eosinophilia. (See "Primary

humoral immunodeficiencies: An overview" and

"Combined immunodeficiencies" and "Approach to

the child with recurrent infections" .)

Food allergy and eosinophilic esophagitis are also

more common causes of eosinophilia in the

pediatric age group and can be missed if an

appropriate history is not elicited; the only clue to

the diagnosis of eosinophilic esophagitis in a child

may be occasional vomiting. (See "Clinical

manifestations of food allergy: An overview" and

"History and physical examination in the patient

with possible food allergy" and "Clinical

manifestations and diagnosis of eosinophilic

esophagitis" .)

.

.

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21:15

مختبرات طبــ🔬ــية

أعزائي دكاتره قناة انتظرونا غدا في قسم الكيمياء الحيوية و السريرية و أن شاءالله راح نأخذ الكربوهيدرات ❤️👍وأول تحليل معنا جلوكوز ...

📖 انتطرونا ياروع دكاتره قناة

Dr Anwar salim

1 April 2016

م

07:37

مختبرات طبــ🔬ــية

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