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Eosinophilia information


Eosinophilia
Eosinophils in the peripheral blood of a patient with idiopathic eosinophilia
SpecialtyInfectious disease, hematology

Eosinophilia is a condition in which the eosinophil count in the peripheral blood exceeds 5×108/L (500/μL).[1] Hypereosinophilia is an elevation in an individual's circulating blood eosinophil count above 1.5 × 109/L (i.e. 1,500/μL). The hypereosinophilic syndrome is a sustained elevation in this count above 1.5 × 109/L (i.e. 1,500/μL) that is also associated with evidence of eosinophil-based tissue injury.

Eosinophils usually account for less than 7% of the circulating leukocytes.[1] A marked increase in non-blood tissue eosinophil count noticed upon histopathologic examination is diagnostic for tissue eosinophilia.[2] Several causes are known, with the most common being some form of allergic reaction or parasitic infection. Diagnosis of eosinophilia is via a complete blood count (CBC), but diagnostic procedures directed at the underlying cause vary depending on the suspected condition(s). An absolute eosinophil count is not generally needed if the CBC shows marked eosinophilia.[3] The location of the causal factor can be used to classify eosinophilia into two general types: extrinsic, in which the factor lies outside the eosinophil cell lineage; and intrinsic eosinophilia, which denotes etiologies within the eosinophil cell line.[2] Specific treatments are dictated by the causative condition, though in idiopathic eosinophilia, the disease may be controlled with corticosteroids.[3] Eosinophilia is not a disorder (rather, only a sign) unless it is idiopathic.[3]

Informally, blood eosinophil levels are often regarded as mildly elevated at counts of 500–1,500/μL, moderately elevated between 1,500 and 5,000/μL, and severely elevated when greater than 5,000/μL. Elevations in blood eosinophil counts can be transient, sustained, recurrent, or cyclical.[4][5]

Eosinophil counts in human blood normally range between 100 and 500 per/μL. Maintenance of these levels results from a balance between production of eosinophils by bone marrow eosinophil precursor cells termed CFU-Eos and the emigration of circulating eosinophils out of the blood through post-capillary venules into tissues. Eosinophils represent a small percentage of peripheral blood leucocytes (usually less than 8%), have a half-life in the circulation of only 8–18 hours, but persist in tissues for at least several weeks.[6][7]

Eosinophils are one form of terminally differentiated granulocytes; they function to neutralize invading microbes, primarily parasites and helminthes but also certain types of fungi and viruses. They also participate in transplant rejection, Graft-versus-host disease, and the killing of tumor cells. In conducting these functions, eosinophils produce and release on demand a range of toxic reactive oxygen species (e.g. hypobromite, hypobromous acid, superoxide, and peroxide) and they also release on demand a preformed armamentarium of cytokines, chemokines, growth factors, lipid mediators (e.g. leukotrienes, prostaglandins, platelet activating factor), and toxic proteins (e.g. metalloproteinases, major basic protein, eosinophil cationic protein, eosinophil peroxidase, and eosinophil-derived neurotoxin). These agents serve to orchestrate robust immune and inflammatory responses that destroy invading microbes, foreign tissue, and malignant cells. When overproduced and over-activated, which occurs in certain cases of hypereosinophilia and to a lesser extent eosinophilia, eosinophils may misdirect their reactive oxygen species and armamentarium of preformed molecules toward normal tissues. This can result in serious damage to such organs as the lung, heart, kidneys, and brain.[7][8][9]

  1. ^ a b "Eosinophilic Disorders". Merck & Co. Retrieved 2012-11-02.
  2. ^ a b Cite error: The named reference Simon was invoked but never defined (see the help page).
  3. ^ a b c Beers, Mark; Porter, Robert; Jones, Thomas (2006). "Ch. 11". The Merck Manual of Diagnosis and Therapy (18th ed.). Whitehouse Station, New Jersey: Merck Research Laboratories. pp. 1093–1096. ISBN 0-911910-18-2.
  4. ^ Butt NM, Lambert J, Ali S, Beer PA, Cross NC, Duncombe A, Ewing J, Harrison CN, Knapper S, McLornan D, Mead AJ, Radia D, Bain BJ (2017). "Guideline for the investigation and management of eosinophilia" (PDF). British Journal of Haematology. 176 (4): 553–572. doi:10.1111/bjh.14488. PMID 28112388.
  5. ^ Gotlib J (2017). "World Health Organization-defined eosinophilic disorders: 2017 update on diagnosis, risk stratification, and management". American Journal of Hematology. 92 (11): 1243–1259. doi:10.1002/ajh.24880. PMID 29044676.
  6. ^ Beeken WL, Northwood I, Beliveau C, Baigent G, Gump D (1987). "Eosinophils of human colonic mucosa: C3b and Fc gamma receptor expression and phagocytic capabilities". Clinical Immunology and Immunopathology. 43 (3): 289–300. doi:10.1016/0090-1229(87)90138-3. PMID 2953511.
  7. ^ a b Kovalszki A, Weller PF (2016). "Eosinophilia". Primary Care. 43 (4): 607–617. doi:10.1016/j.pop.2016.07.010. PMC 5293177. PMID 27866580.
  8. ^ Roufosse F (2013). "L4. Eosinophils: how they contribute to endothelial damage and dysfunction". Presse Médicale. 42 (4 Pt 2): 503–507. doi:10.1016/j.lpm.2013.01.005. PMID 23453213.
  9. ^ Long H, Liao W, Wang L, Lu Q (2016). "A Player and Coordinator: The Versatile Roles of Eosinophils in the Immune System". Transfusion Medicine and Hemotherapy. 43 (2): 96–108. doi:10.1159/000445215. PMC 4872051. PMID 27226792.

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