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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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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
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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.
(
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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
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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
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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.
.
.
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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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م
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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