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Diagnostic Complexities of Eosinophilia

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Diagnostic Complexities of Eosinophilia Review Articles Diagnostic Complexities of Eosinophilia Nathan D. Montgomery, MD, PhD; Cherie H. Dunphy, MD; Micah Mooberry, MD; Andrew Laramore, MD; Matthew C. Foster, MD; Steven I. Park, MD; Yuri D. Fedoriw, MD Context.—The advent of molecular tools capable of previously defined as hypereosinophilic syndrome. Most subclassifying eosinophilia has changed the diagnostic and notably, chromosomal rearrangements, such as FIP1L1- clinical approach to what was classically called hyper- PDGFRA fusions caused by internal deletions in chromo- eosinophilic syndrome. some 4, are now known to be associated with many Objectives.—To review the etiologies of eosinophilia chronic eosinophilic leukemias. When present, these and to describe the current diagnostic approach to this specific molecular abnormalities predict response to abnormality. directed therapies. Although an improved molecular Data Sources.—Literature review. understanding is revolutionizing the treatment of patients Conclusions.—Eosinophilia is a common, hematologic with rare causes of eosinophilia, it has also complicated abnormality with diverse etiologies. The underlying causes the approach to evaluating and treating eosinophilia. Here, can be broadly divided into reactive, clonal, and idiopath- we review causes of eosinophilia and present a framework ic. Classically, many cases of eosinophilia were grouped by which the practicing pathologist may approach this together into the umbrella category of hypereosinophilic diagnostic dilemma. Finally, we consider recent cases as syndrome, a clinical diagnosis of exclusion. In recent years, clinical examples of eosinophilia from a single institution, an improved mechanistic understanding of many eosino- demonstrating the diversity of etiologies that must be philias has revolutionized the way these disorders are considered. understood, diagnosed, and treated. As a result, specific (Arch Pathol Lab Med. 2013;137:259–269; doi: 10.5858/ diagnoses can now be assigned in many cases that were arpa.2011-0597-RA) osinophilia in the peripheral blood and in bone marrow characterization of eosinophilia is critical because treatment E biopsies is encountered frequently by practicing hema- is dependent on the underlying etiology. tologists and hematopathologists. The clinical presentation Classically, hypereosinophilic syndrome (HES) represent- and underlying etiologies are quite varied. In some cases, ed a diagnosis of exclusion for patients who met certain eosinophilia may be an incidental finding and prove benign clinical criteria. Specifically, HES required persistent eosin- ophilia, defined as an absolute eosinophil count (AEC) of at and transient. However, in other cases, chronic eosinophil- least 1500/lL (1.5 3 109/L) for 6 months or longer. These ias may cause damage to a variety of organ systems.1,2 patients must have no identifiable parasitic, allergic, or other In broad terms, eosinophilias can be divided into reactive known cause of eosinophilia. The diagnosis also requires and clonal processes. In reactive eosinophilias, there is a signs of organ involvement, most prominently the heart, polyclonal increase in the maturation and proliferation of which may develop valvular dysfunction leading to conges- eosinophils. Such cases may be triggered by allergy, tive heart failure.2 infection, various medical conditions, or neoplasms. How- During the past several years, improved molecular ever, by definition, eosinophils cannot be part of a understanding has allowed more specific classification of malignant clone in reactive eosinophilias. Conversely, clonal many cases that would once have been labeled within the eosinophilias represent neoplasms in which eosinophils or broader umbrella of HES. In light of this increasingly their precursors are part of the malignant clone. Correct complicated diagnostic picture, we review the diagnosis and treatment of eosinophilia and offer a framework by which the practicing pathologist may approach this diagnostic dilemma. Accepted for publication April 27, 2012. From the Departments of Pathology and Laboratory Medicine, Division of Hematopathology (Drs Montgomery, Dunphy, Laramore, CLASSIFICATION AND DIAGNOSIS OF EOSINOPHILIAS and Fedoriw); and Medicine, Division of Hematology and Oncology Reactive Eosinophilias (Drs Mooberry, Foster, and Park), University of North Carolina School of Medicine, Chapel Hill. Most eosinophilias are reactive, polyclonal processes. In The authors have no relevant financial interest in the products or all these reactive processes, the increase in AEC appears to companies described in this article. be mediated by cytokines, principally interleukin (IL) 5, Reprints: Yuri D. Fedoriw, MD, Department of Pathology and Laboratory Medicine, Division of Hematopathology, University of which promotes proliferation of eosinophils and their 3 North Carolina School of Medicine, CB7525, Chapel Hill, NC precursors. However, the underlying pathologic processes 27599-7525 (e-mail: [email protected]). promoting increased cytokine production are varied, rang- Arch Pathol Lab Med—Vol 137, February 2013 Diagnostic Complexities of Eosinophilia––Montgomery et al 259 ing from allergic responses to clonal expansion of IL-5 Table 1. Nonmalignant Medical Conditions expressing cells. Reactive eosinophilias may also involve Associated With Reactive Eosinophilia overproduction of additional cytokines, such as IL-3 and IL- 4, which can lead to concomitant elevation of immuno- Allergic reactions 4 Drug reactions globulin (Ig) E in reactive eosinophilias. Asthma Eosinophilia Due to Allergic Reactions.—Among the Parasitic infections reactive eosinophilias in the developed world, allergic Strongyloidiasis reactions are most common, comprising approximately Schistosomiasis 80% of cases.5 The mechanism underlying allergic eosino- Filariasis Toxocariasis philias, as with many reactive eosinophilias, involves an Metabolic abnormalities imbalance between helper T-cell subtypes, with increased Adrenal insufficiency production of IL-5 by T-helper 2 cells. Given its prevalence, Humoral immunodeficiency clinicians and pathologists should rule out allergic etiolo- Hyperimmunoglobulin E syndrome (Job syndrome) gies, such as drug reactions, before proceeding to costly Wiskott-Aldrich syndrome Hyperimmunoglobulin M syndrome molecular tests for rare, molecularly defined eosinophilias Immunoglobulin A deficiency (see below). Eosinophilia is an isolated hematologic finding Pulmonary eosinophilias in allergic reactions, although other cell counts may be Eosinophilic granulomatosis with polyangiitis (formerly abnormal in rare cases.3 Although the clinical history will Churg-Strauss syndrome) typically be informative, symptoms secondary to eosino- Allergic bronchopulmonary aspergillosis philia can themselves resemble allergic reactions, making Chronic and acute idiopathic eosinophilic pneumonias Autoimmune blistering skin diseases the diagnosis more complicated. As such, confirmation with Dermatitis herpetiformis allergen skin testing or radioallergosorbent testing may Bullous pemphigoid prove helpful. Eosinophilia Due to Parasitic Infections.—Parasitic infections represent the second most-common cause of Given the inverse relationship between glucocorticoid levels eosinophilia in developed nations, comprising 8% of and eosinophil count, the standard evaluation of eosino- eosinophilias in one large European cohort.5 Generally, philia should include attention to clinical signs of adrenal the causative organism is a helminth, such as Strongyloides insufficiency (orthostatic hypotension, skin discoloration); stercoralis. Less often, the culprit may be a single-celled routine chemistries, which may be abnormal in Addison protozoan. A thorough travel history can increase the disease; and, in some cases, morning cortisol levels. clinical suspicion of these infections because many parasites Eosinophilia is also observed in certain immunodeficiency are endemic in tropical and subtropical climates.6 However, syndromes, including hyperimmunoglobulin E syndrome, Strongyloides stercoralis may also be found in temperate formerly known as Job syndrome. Both autosomal-domi- climates, including in the southeastern United States.6,7 nant and autosomal-recessive forms of hyperimmunoglo- The diagnosis of parasitic eosinophilia ultimately requires bulin E syndrome exist. Whereas autosomal-dominant identification of an infectious trigger, either directly by hyperimmunoglobulin E syndrome is caused by mutations identifying ova or parasites or indirectly by appropriate in STAT3, DOCK8 and TYK2 mutations are implicated in the serologies, which may vary dependent on travel history. At a comparatively rare autosomal-recessive forms of the dis- minimum, the evaluation should consider strongyloidiasis, ease.16–18 Clinically, hyperimmunoglobulin E syndrome is schistosomiasis, and filariasis.8 In children, toxocariasis defined by staphylococcal skin abscesses, recurrent pneu- should also be considered. Strongyloides stercoralis can cause monias, and serum IgE levels greater than 10 times the eosinophilia years after the initial infection because the upper reference limit.18 Additional features of the autoso- organism is capable of autoinfection inside its host.6 IgG mal-dominant form include retention of primary teeth, serologies are appropriate diagnostic tests when stool skeletal abnormalities, and a characteristic facial appear- studies are not revealing. Finally, when parasites are ance.19 Ninety-three percent of patients in one series had implicated, the
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