From Wikipedia, the free encyclopedia
Eosinophilia is a condition in which the
count in the
exceeds 4.5×108/L (450/μl). Eosinophils usually account for less than 7% of the circulating leukocytes. A marked increase in non-blood tissue eosinophil count noticed upon histopathologic examination is diagnostic for tissue eosinophilia. Several causes are known, with the most common being some form of
or . Diagnosis of eosinophilia is via a
(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. 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 eos and intrinsic eosinophilia, which denotes etiologies within the eosiniphil cell line. Specific treatments are dictated by the causative condition, though in idiopathic eosinophilia, the disease may be controlled with . Eosinophilia is not a disorder, unless it is idiopathic.
Harm resulting from untreated eosinophilia potentially varies with cause. During an allergic reaction, the release of
causes vasodilation which allows
to migrate from the blood and localize in affected tissues. Accumulation of eosinophils in tissues can be significantly damaging. Eosinophils, like other , contain granules (or sacs) filled with digestive enzymes and cytotoxic proteins which under normal conditions are used to destroy parasites but in eosinophilia these agents can damage healthy tissues. In addition to these agents, the granules in eosinophils also contain inflammatory molecules and
which can recruit more eosinophils and other inflammatory cells to the area and hence amplify and perpetuate the damage. This process is generally accepted to be the major inflammatory process in the pathophysiology of atopic or allergic asthma.
When parasites enter the normal flow of blood during the second stage of cardiosphillia (small spots between the ventricles) this stage is called the serious one. Eosinophilia can be
(primary) or, more commonly, secondary to another disease. In the Western World, allergic or
diseases are the most common causes, especially those of the
systems. In the developing world,
are the most common cause. A parasitic infection of nearly any bodily
can cause eosinophilia. Diseases that feature eosinophilia as a sign include the following:
Some forms of
Some forms of
(e.g., , idiopathic eosinophilic synovitis)
Some forms of
(transiently)
(Valley fever), a fungal disease prominent in the US Southwest.
Interstitial nephropathy
, an immune disorder characterized by high levels of serum IgE
Idiopathic hypereosinophilic syndrome.
(Hodgkin’s disease) often elicits however,
produce less marked eosinophilia. Of solid tumor ,
is most likely to provoke eosinophilia, though any other cancer can cause the condition. Solid epithelial cell tumors have been shown to cause both tissue and blood eosinophilia, with some reports indicating that this may be mediated by
production by tumor cells, especially IL-5 or IL-3. This has also been shown to occur in Hodgkin lymphoma, in the form of IL-5 secreted by Reed-Sternberg cells. 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 or alterations in the genes which encode
alpha or beta. Patients displaying eosinophilia overexpress a gene encoding an eosinophil hematopoietin. A translocation between chromosomes 5 and 14 in 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.
Drug hypersensitivity reactions (allergies) are a common cause of eosinophilia, with manifestations ranging from diffuse , to severe life-threatening
(DRESS). Drugs that have been shown to cause DRESS are
and other , , ,
(NSAIDs), some antipsychotics such as risperidone, and certain antibiotics. Phenibut, an analogue of the neurotransmitter GABA, has also been implicated in high doses. The reaction which has been shown to be T-cell mediated may also cause .
IgE mediated eosinophil production is induced by compounds released by
and , including eosinophil chemotactic factor of , , complement complex (C5-C6-C7), , and histamine (though this has a narrow range of concentration).
Diagnosis is by
(CBC). However, in some cases, a more accurate absolute eosinophil count may be needed. Medical history is taken, with emphasis on travel, allergies and drug use. Specific test for causative conditions are performed, often including , ,
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 for example,
requires a . Elevated serum B12 or low white blood cell , or leukocytic abnormalities in a peripheral smear indicates a disorder of . In cases of idiopathic eosinophilia, the patient is followed for complications. A brief trial of
can be diagnostic for allergic causes, as the eosinophilia should resolve with suppression of the immune over-response. Neoplastic disorders are diagnosed through the usual methods, such as
and biopsy for the leukemias, MRI/CT to look for solid tumors, and tests for serum LDH and other .
Treatment is directed toward the underlying cause. However, in primary eosinophilia, or if the eosinophil count must be lowered,
may be used. However, immune suppression, the mechanism of action of corticosteroids, can be fatal in patients with parasitosis.
. Merck & Co.
Simon, D HU Simon (16 January 2007). . Journal of Allergy and Clinical Immunology (New York: Elsevier) 119 (6): ; quiz 1301–2. :.   2010.
Beers, M Porter, R Jones, Thomas (2006). "Ch. 11".
(18 ed.). Whitehouse Station, New Jersey: Merck Research Laboratories. pp. 1093–6.  .
Oxford Respiratory Medicine Library: Asthma, 2nd ed., ed. Graeme P. Currie and John. F. W. Baker, OUP, 2012.
Mitchell, Richard S Kumar, V Abbas, Abul K.; Fausto, Nelson. "Table 12-6". Robbins Basic Pathology (8th ed.). Philadelphia: Saunders.  .
Saubolle MA, McKellar PP, Sussland D (January 2007). . J. Clin. Microbiol. 45 (1): 26–30. :.  .  .
Fathi AT, Dec GW, Richter JM, et al. (February 2014). . N. Engl. J. Med. 370 (9): 861–72. :.  .
: Hidden categories:}