Eosinophilia: the eosinophil count in the peripheral blood exce

http://en.wikipedia.org/wiki/Eosinophilia

Eosinophilia is a condition in which the eosinophil count in the peripheral blood exceeds 0.45×10⁹/L (450/μl). A marked increase in non-blood tissue eosinophil count noticed upon histopathologic examination is diagnostic for tissue eosinophilia.^[1] Several causes are known, with the most common being some form of allergic reaction or parasitosis. Diagnosis of eosinophilia is via a complete blood count, but diagnostic procedures directed at the underlying cause vary depending on the suspected condition(s). An absolute eosinophil count is not generally needed if CBC shows marked eosinophilia.^[2] The location of the causal factor can be used to classify eosinophilia into two general types: extrinsic, in which the factor lies outside of the eosinophil cell lineage; and intrinsic eosinophilia, which denotes etiologies within the eosiniphil cell line.^[1] Specific treatments are dictated by the causative condition, though in idiopathic eosinophilia, the disease may be controlled with corticosteroids.^[2] Eosinophilia is not a disorder, unless it is idiopathic.^[2]

Causes

Eosinophilia can be idiopathic (primary) or, more commonly, secondary to another disease.^[2][1] In the United States, allergic or atopic diseases are the most common causes, especially those of the respiratory or integumentary systems. In the developing world, parasites are the most common cause. A parasitic infection of nearly any bodily tissue can cause eosinophilia. Diseases that feature eosinophilia as a sign include the following:

• Allergic disorders
  • Asthma^[3]
  • Hay fever^[3]
  • Drug allergies^[3]
  • Allergic skin diseases^[3]
    • Pemphigus^[3]
    • Dermatitis herpetiformis
• Parasitic infections^[3]
• Some forms of malignancy
  • Hodgkin's lymphoma^[3]
  • Some forms of Non-Hodgkin lymphoma^[3]
• Systemic autoimmune diseases^[3] (e.g. SLE)
• Some forms of vasculitis^[3] (e.g. Churg-Strauss syndrome)
• Cholesterol embolism (transiently)^[3]
• Coccidioidomycosis (Valley Fever), a fungal disease prominent in the US Southwest.^[4]
• Interstitial nephropathy

Neoplastic eosinophilia

Hodgkin lymphoma (Hodgkin’s disease) often elicits severe eosinophilia, however, non-Hodgkin lymphoma and leukemia produce less marked eosinophilia.^[2] Of solid tumor neoplasms, ovarian cancer is most likely to provoke eosinophilia, though any other cancer can cause the condition.^[2] Solid epithelial cell tumors have been shown to cause both tissue and blood eosinophilia, with some reports indicating that this may be mediated by interleukin production by tumor cells, especially IL-5 or IL-3.^[1] This has also been shown to occur Hodgkin lymphoma, in the form of IL-5 secreted by Reed-Sternberg cells.^[1] In primary cutaneous T-cell lymphoma, blood and dermal eosinophilia are often seen. Lymphoma cells have also been shown to produce IL-5 in these disorders. Other types of lymphoid malignancies have been associated with eosinophilia, as in lymphoblastic leukemia with a translocation between chromosomes 5 and 14.^[1] Patients displaying eosinophilia overexpress a gene encoding an eosinophil hematopoietin. A translocation between chromosomes 5 and 14 n patients with acute B lymphocytic leukemia resulted in the juxtaposition of the IL-3 gene and the immunoglobulin heavy-chain gene, causing overproduction production of IL-3, leading to blood and tissue eosinophilia.^[1]

Drug reactions

Drug hypersensitivity reactions (allergies) are a common cause of eosinophilia, with manifestations ranging from diffuse maculopapular rash, to severe life threatening drug reactions with eosinophilia and systemic symptoms (DRESS).^[1] Drugs that have been shown to cause DRESS are aromatic anticonvulsants and other antiepileptics, sulfonamides, allopurinol, nonsteroidal anti-inflammatory drugs (NSAIDs), and certain antibiotics. The reaction which has been shown to be T-cell mediated may also cause eosinophilia-myalgia syndrome.^[1]

Pathophysiology

IgE mediated eosinophil production is induced by compounds released by basophils and mast cells, including eosinophil chemotactic factor of anaphylaxis, leukotriene B4, complement complex (C5-C6-C7), interleukin 5, and histamine (though this has a narrow range of concentration).^[2]

Diagnosis

Diagnosis is by complete blood count (CBC). However, in some cases, a more accurate absolute eosinophil count may be needed.^[2] Medical history is taken, with emphasis on travel, allergies and drug use.^[2] Specific test for causative conditions are performed, often including chest x-ray, urinalysis, liver and kidney function tests, and serologic tests for parasitic and connective tissue diseases. The stool is often examined for traces of parasites (i.e. eggs, larvae, etc.) though a negative test does not rule out parasitic infection; for example, trichinosis requires a muscle biopsy.^[2] Elevated serum B₁₂ or low white blood cell alkaline phosphatase, or leukocytic abnormalities in a peripheral smear indicates a disorder of myleoproliferation.^[2] In cases of idiopathic eosinophilia, the patient is followed for complications. A brief trial of corticosteroids can be diagnostic for allergic causes, as the eosinophilia should resolve with suppression of the immune over response.^[2] Neoplastic disorders are diagnosed through the usual methods, such as bone marrow aspiration and biopsy for the leukemias, MRI/CT to look for solid tumors, and tests for serum LDH and other tumor markers.^[2]

Treatment

Treatment is directed toward the underlying cause.^[2] However, in primary eosinophilia, or if the eosinophil count must be lowered, corticosteroids such as prednisone may be used. However, immune suppression, the mechanism of action of corticosteroids, can be fatal in patients with parasitosis.^[1]

 

References

^{a b c d e f g h i j} Simon, Dagmar; HU Simon (16 January 2007). "Eosinophilic Disorders". Journal of Allergy and Clinical Immunology (New York: Elsevier) 119 (6): 1291–300; quiz 1301–2. doi:10.1016/j.jaci.2007.02.010. PMID 17399779. Retrieved 21 October 2010.

^ ^{a b c d e f g h i j k l m n} Beers, Mark; Porter, Robert; Jones, Thomas (2006). "11". The Merck Manual of Diagnosis and Therapy (18 ed.). Whitehouse Station, New Jersey: Merck Research Laboratories. pp. 1093–1096. ISBN [[Special:BookSources/09119010182|09119010182]].

^{a b c d e f g h i j k} Table 12-6 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.

^Saubolle, M.A., McKellar, P.P., & Sussland, D. (2007). Epidemiologic, Clinical, and Diagnostic Aspects of Coccidioidomycosis. Journal of Clinical Microbiology, 45(1), 26-30. [1]