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Hypereosinophilic Syndrome In the light of recent advances: eosinophil, eosinophilia and idiopathic hypereosinophilic syndrome Aliflan YILDIRAN1, Aydan ‹K‹NC‹O⁄ULLARI1 1 Department of Pediatric Immunology and Allergy, Ankara University School of Medicine, Ankara, TURKEY Turk J Haematol 2005;22(3): 107-116 INTRODUCTION infiltration of multiple organs leading to se- vere organ dysfunction[3]. Recently, with the Eosinophil is a different cell containing discovery of different well-characterized un- highly toxic substances the functions of derlying molecular defects that ultimately le- which are still incompletely understood. Eo- ad to eosinophil expansion in some patients, sinophilia is a condition where the eosinophil the term “idiopathic” has become outdated in concentrations in the blood and some tissu- many cases[1]. es increase to unusual high levels in some abnormal conditions and disease states. Be- In the light of recent advances, we made ing a common finding in clinical practice, in an attempt to review the eosinophil, eosinop- the majority of cases, it can be ascribed to an hilia, IHES and the evaluation and manage- underlying disease[1]. The role of interleukin- ment of the latter. 5 (IL-5) in the induction of hypereosinophilia THE EOSINOPHIL in allergic diseases and parasitosis has been established recently[2]. It is an important task The eosinophil was first recognized 125 for clinicians to distinguish these conditions years ago as a distinct cellular element thro- from the very rare, but more serious idiopat- ugh the pioneering work of Paul Erlich. The hic hypereosinophilic syndrome (IHES), cha- ruddy dye, eosin, was named after the Greek racterized by persistent eosinophilia in perip- goddess of the morning sun, for use in histo- heral blood, bone marrow and eosinophilic logic staining by Erlich[4]. Eosinophils are derived from myeloid progenitors (GEMM-CFU) in bone mar- Yeni geliflmelerin ›fl›¤›nda: eozinofil, eozinofili row[1]. Eosinophil production, maturation ve idiyopatik hipereozinofilik sendrom and survival are under the control of some Anahtar Kelimeler: Eozinofili, Hipereozinofilik sendrom. cytokines and growth factors, including IL-2, Key Words: Eosinophilia, Hypereosinophilic syndrome. IL-3, IL-5, IL-13 and granulocyte macropha- 107 In the light of recent advances: eosinophil, eosinophilia and Y›ld›ran A, ‹kincio¤ullar› A. idiopathic hypereosinophilic syndrome ge colony stimulating factor (GM-CSF)[5]. IL-5 level of 500 to 1500/µL is considered as is the major growth factor for eosinophils. mild; 1500 to 5000/µL as moderate; and > Morphologically, eosinophils in the periphe- 5000/µL as severe eosinophilia. Eosinophils ral blood are approximately the same size are cells that mainly reside in tissues. For as polymorphonuclear leukocytes (PMNLs), every one blood eosinophil, there are 100 [9] 12 to 15 µm in diameter, having mostly bilo- tissue eosinophils . In the normal indivi- bed nuclei. The cytoplasm is normally filled dual, a circadian rhythm can be noted in with approximately 200 large, eosin-staining peripheral blood absolute eosinophil count unique granules containing a central crystal- due to normal fluctuation in glucocorticoids loid core and high concentrations of hydrola- seen during the day. Besides, relative eosi- ses, cationic and basic proteins. There are al- nophilia is often noted during the convales- so several smaller, enzyme-rich non-eosinop- cent phase of a variety of systemic infecti- [4] hilic granules present in the cytoplasm. With ous processes . an appropriate stimulus, the number of spe- There is an association in children between cific granules in the average eosinophil signi- total eosinophil counts in the peripheral blood, ficantly declines, and the cell often becomes and age. Eosinophil concentrations are eleva- [4] vacuolized . They are primarily a tissue cell, ted at birth; continue to rise subsequently for with only 1-2% of them found in the circula- several weeks. Then, by 8 weeks of age, eosi- tion. They have a life span of 8 to 12 hours in nophil counts begin to decline to the levels at circulation and then remain another 1 to 2 which they are normally seen throughout the [6] weeks in destination tissues . rest of life[10]. As many as 70%, of premature Normal functions of eosinophils resemb- babies may show at least mild eosinophilia. In- le to those of other circulatory phagocytes fants with high eosinophil counts (> 700/µL) at (such as PMNLs and monocytes): chemota- 3 months of age and beyond are at risk of de- xis, chemokinesis, phagocytosis, cytotoxi- veloping atopic diseases[11]. city, antiparasitic activity, bactericidal acti- Mature eosinophils are released into the vity, effector of immediate hypersensitivity, bloodstream and rapidly migrate to periphe- modulation of inflammatory response. Un- ral tissues, namely gut and bronchial muco- like PMNLs, when stimulated, they also sa and skin, where they soon undergo apop- possess the capacity to elaborate substan- tosis and are cleared by macrophages, un- ces that are toxic to a wide variety of mul- less survival factors such as IL-3, IL-5 ticellular parasites. Eosinophils also act as and/or GM-CSF are present. Thus, overpro- immunomodulators, particularly in their duction of one or more of these cytokines is ability to dampen the host’s immediate al- sufficient to induce normal or abnormal blo- lergic response[7]. Although, it is unclear od or tissue eosinophilia, which accounts for whether they are innocent bystanders or hypereosinophilia in various disorders[12]. agents adding to tissue injury, in other di- sease states, they are involved directly with Mild and Moderate Eosinophilia critical pathologic events. Their most viru- There are many conditions associated lent effects are seen in conditions like Lo- with mild to moderate eosinophilia (500 to effler disease (eosinophilic fibroplastic en- 5000/µL) (Table 1). Moreover, a wide variety docarditis) and the IHES in which perma- of pharmaceutical agents are associated with nent deleterious tissue injuries is due to mild or moderate, sometimes profound eosi- their presence[8]. nophilia in children. EOSINOPHILIA The most common cause of eosinophilia The normal absolute eosinophil count worldwide is helminthic infection and, in in- [13,14] for both adults and children is ≤ 350/µL. A dustrialized countries, atopic disease . 108 Turk J Haematol 2005;22(3):107-116 In the light of recent advances: eosinophil, eosinophilia and idiopathic hypereosinophilic syndrome Y›ld›ran A, ‹kincio¤ullar› A. Table 1. Causes of mild to moderate eosinophilia in children[4] Nonpathologic Gastrointestinal Prematurity Milk protein allergy Neonatal rapid growth Inflammatory bowel disease Hyperalimentation Eosinophilic gastroenteritis Familial Endocrine Postadrenalectomy Dermatologic Addison’s disease Eczema Panhypopituitarism Pemphigus Dermatitis herpetiformis Cardiovascular Loeffler’s disease (fibroplastic endocarditis) Infantile eosinophilic pustular folliculitis Congenital heart disease Gleich syndrome Hypersensitivity vasculitis Eosinophilic fasciitis (Schulman syndrome) Urticaria Infectious Eosinophilic cellulitis (Well’s syndrome) Parasitic (trichinosis, strongyloidiasis, pne- Kimura disease umocystosis, cysticercosis, cutaneous and visce- ral larva migrans, echinococcosis) Pulmonary Bacterial (brucellosis, tularemia, cat-scratch dise- Allergic (rhinitis, asthma) ase, chlamydia, group A Streptococcus) Loeffler’s syndrome Hypersensitivity pneumonitis Fungal (histoplasmosis, blastomycosis, coccidi- Eosinophilic pneumonia omycosis, bronchopulmonary aspergillosis) Pulmonary interstitial eosinophilia syndromes Mycobacterial (tuberculosis, leprosy) Viral (hepatitis A, B, C, Ebstein-Barr, HIV, HTLV-II) Oncologic Neoplasm (lung, gastrointestinal, uterine) Immunologic Hodgkin’s disease IgA deficiency Leukemia Hyper IgE (Job’s) syndrome Myelofibrosis Wiscott-Aldrich syndrome Graft versus Host Disease Drugs Drug hypersensitivity Antibiotics Postirradiation Antimycobacterials Postsplenectomy In general, gastrointestinal parasites lac- sease, refers to a rather common condition king a tissue-invasive phase tend to produ- characterized by eosinophilia associated with ce only mild eosinophilia. On the other cough and transient pulmonary infiltrates. hand, tissue-invasive parasites often produ- The most common cause of the syndrome is ce severe eosinophilia like toxocara[15]. migration through the lungs of the larval sta- Nonparasitic infections capable of produ- ges of certain intestinal parasites like asca- cing a granulomatous tissue reaction such ris. Occasionally, some children may develop as mycobacterial or fungal infections (inclu- this picture without evidence of parasitic in- ding histoplasmosis, blastomycosis, and fection. One such entity is allergic broncho- coccidiomycosis) or chronic bacterial infec- pulmonary aspergillosis. Another similar tions (brucellosis, tularemia) can be associ- condition can be seen after the inhalation of [16] ated with eosinophilia . certain foreign antigens by a sensitized indi- Loeffler syndrome, in distinction to the vidual. Such antigens may be household en- fibroplastic endocarditis termed Loeffler di- vironmental substances; chemicals encoun- Turk J Haematol 2005;22(3):107-116 109 In the light of recent advances: eosinophil, eosinophilia and Y›ld›ran A, ‹kincio¤ullar› A. idiopathic hypereosinophilic syndrome tered occupationally, animal products, or Eosinophilic leukemia is exceedingly rare plant materials. The patient develops diffuse in children. The patients may develop rapid
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