A parasitic infection, especially related to helminths, is the primary cause to raise with eosinophilia. 1 It can be associated with leukocytosis and especially to an increase in serum IgE. Eosinophilia is often significant (> 1 x 109 / L), especially when it is a parasitic impasse (accidental infestation of man by animal parasites that remain in the larval stage, example Toxocara canis). These larvae of helminths “lost” immature and erratic migration can induce local inflammatory reactions, diffuse and severe, and cause massive eosinophilia (visceral larva migrans syndrome).Eosinophilia is also very high at the stage of invasive helminths. It is then linked to the effects of mediators of the inflammatory response to subsequent larval migration phase in tissues (role of cytokines, see: To deepen 1).However, this can be moderate eosinophilia (0.5 to 1 x 109 / L) or absent, the state phase and then in the chronic phase of the infection or when a hollow organ (gut) is the ecological niche of the parasite. Apart from parasites and apart from allergic bronchopulmonary aspergillosis (ABPA), the other cases of eosinophilia postinfectious are rare, usually mild and transient. Eosinophilia associated with infection should be investigated a possible immune deficiency or a hypersensitivity reaction following antibiotic treatment.
1- Aspect of eosinophilia:
It may be fluctuating (classical “curve bow” of Lavier) with a major rise (liver fluke, roundworm, hookworm, filariasis, schistosomiasis) or moderate (pinworms), followed by a more or less rapid decay of eosinophilia with or without normalization of blood eosinophils. It can be persistent (reinfection) and massive (trichinosis, toxocariasis, eosinophil lung or tropical Weingarten’s syndrome), or cyclic and oscillating (anguillulosis: internal cycle of self-infestation).
2- ethno-geographical data:
The risk sites concepts for indigenous and stays abroad, short or old, should be considered. If the subject stayed in tropical countries, four main conditions must be mentioned: schistosomiasis, filariasis, and hookworm anguillulosis (Table I). If the subject has not left the metropolitan France, one must search in priority to high eosinophilia: liver fluke Fasciola hepatica, a ascariasis, toxocariasis, trichinosis (Table II).
It also helps guide diagnosis. It must address in particular the hygienic conditions such as contact with animals (geophagia concept in children with the example of toxocariasis; parasitosis linked to faecal peril with the example of trichuriasis) or freshwater baths (schistosomiasis); eating habits such as ingestion of contaminants plants (such as watercress, with the example of the liver fluke); the ingestion of food or water contaminated (examples of roundworm and hydatid disease); undercooked meat consumption or raw pork or horse (trichinosis), of meat undercooked beef (Taenia saginata taeniasis), or raw herring (anisakiasis).
4- respiratory events:
They may be suggestive, as Löffler’s syndrome (larvae of migration through the pulmonary parenchyma originally labile infiltrates on radiographs: examples of toxocariasis, of roundworm, hookworm of). An array of fever with poor general condition, prior lung syndrome or development endomyocardial fibrosis, evoke a tropical pulmonary eosinophilia syndrome or Weingarten. This would be linked to a state of hypersensitivity vis-à-vis microfilariae. The occurrence of chest pain with cough, sputum “rusty” linked to the presence of blood and reddish eggs, is highly suggestive of lung fluke or paragonimiasis.
5- skin or muscle Events:
The signs are suggestive to pruritus ani Vesper (pinworms), of cutaneous larva currens signs (strongyloidiasis), the “itch” with filarial nodules (onchocerciasis), pruritus with migratory edema (swelling fleeting Calabar in Loa loa) of isolated myalgia (cysticercosis) or associated with edema (trichinosis), subcutaneous swelling with externalizing the skin of a larva (myiasis), lymphangitis with elephantiasis (lymphatic filariasis).
6 Signs hépatodigestifs:
They can evoke a liver tumor (hepatomegaly of hydatid disease, with the risk of infection or cyst rupture), cholangitis (liver fluke), duodenitis (anguillulosis, hookworm), or various intestinal signs (taeniasis, bilharzia bowel, intestinal fluke, trichuriasis) or even intestinal eosinophilic granuloma (anisakiasis).
7- Signs neuromeningeal or eye:
These are signs of brain damage (hydatid disease), epilepsy (cysticercosis), eosinophilic meningitis (Angiostrongylus Angiostrongylus cantonensis), eye damage (filariasis). Faced with such events, other parasitic infections should also be sought, including toxocariasis, screwworm.
8- urogenital signs:
Before hematuria, hydronephrosis, urinary schistosomiasis is mentioned. These signs can be associated with genital involvement in LF.
In the absence of suggestive elements or to confirm the diagnosis, the following diagnostic tests are performed.The parasitic serology is often very useful, especially in the early phase of tissue invasion (antibody response, eosinophilic response) especially when it is a parasitic impasse. Delayed in time, often several weeks, repeated stool examinations, carried out at the state stage, enable the detection of eggs or larvae (retrospective diagnosis).Some more specific investigations are sometimes necessary (Tables I and II). If parasitological investigation remains unsuccessful, a deworming test, performed under surveillance (monitoring eosinophilia) can be offered. However, any blind corticosteroids should be avoided (risk of parasitic hyperinfection syndrome).
Eosinophilia and allergy:
This is eosinophilia related to a hypersensitivity reaction IgE dependent vis-à-vis different allergens (aeroallergens, food allergens, Hymenoptera venom, but some drugs).
In the allergic process, eosinophilia is often moderate (0.5 to 1 x 109 / L) or absent (disappearance during intercurrent bacterial infections). It may be associated with an elevation, inconstant and rarely important serum total IgE. The data of the anamnesis (history of atopy) and the clinical context (asthma, rhinitis, conjunctivitis, atopic dermatitis, urticaria) are often very suggestive.
Allergy testing confirms the diagnosis and guides the action to take. The interview guide the choices for achieving skin tests vis-à-vis different allergens (pollen, dust mites, mold, animal dander). These skin tests (prick tests) remain the key examination of the etiological investigation. If necessary, the total serum IgE assays and especially the specific serum IgE are requested, taking account of previous diagnostic orientation of elements. The value of additional tests assessing the release of mediators (histaminémie, of histamine release tests) is discussed.
Many drugs can induce eosinophilia (Table III): subcutaneous heparin, sulfa drugs, gold salts, but also psychotropic drugs, oral hypoglycemic agents, cytolytic and cytostatic agents, antibiotics and anti-fungal, analgesic and anti-inflammatory. Eosinophilia is variable level, often delayed compared to taking the drug. It can be of allergic origin (penicillin, sulfonamides), as we have previously mentioned. It may also depend reactions “pseudoallergic” related to a non-dependent histamine release of IgE (general anesthetics, vancomycin) or complement activation (iodinated contrast media used in radiology). Some contributing factors have been implicated (slow or fast acetylator, liver or kidney failure …). Growth factors (GM-CSF for macrophage colony stimulating factor) or cytokines (IL-2 interleukin-2) used in therapy can induce massive eosinophilia with activation of eosinophils, with sometimes severe consequences (heart disease, see: To deepen 2). Eosinophilia may also occur after peritoneal dialysis or hemodialysis after splenectomy in suites radiotherapy after chronic poisoning (copper sulphate, mercury, phosphorus, carbon sulfate, benzene …) or graft against the host.
The drug-induced blood eosinophilia is often associated with laboratory abnormalities (hepatic or renal events) or clinical signs suggestive. Cutaneous signs are frequent and varied (pruritus, rash, urticaria), isolated or associated with other events (hypersensitivity vasculitis, arthralgia, myalgia …). A drug-induced can be suspected acute or subacute respiratory syndrome (dyspnea, dry cough, radiological image more or less fleeting infiltrates), sometimes feverish. Associated signs may be found (hives, rash, arthralgia, hepatobiliary symptoms). The clinical picture can evoke a Löffler syndrome, interstitial pneumonia. The list of drugs that can be incriminated is regularly actualisée.2 The notion of intolerance to aspirin with eosinophilia, asthma, nasal polyps suggests a Widal syndrome.
In the case of drug induced eosinophilia, various additional examinations were offered: skin tests, looking for specific IgE tests for histamine release in vitro lymphoblastic transformation tests. They have limited indicative. Most often, it is the regression of signs stopping treatment, sometimes after 4 to 6 weeks, confirming the origin of the eosinophilia.
Eosinophilia and solid tumors:
Eosinophilia may announce or accompany the occurrence of cancer, with or without associated metastases.Paraneoplastic eosinophilia are often associated with abnormalities affecting other blood cells (thrombocytosis, neutrophilia). Those accompanying neoplasias are usually reaction, linked to the production of growth factors such as GM-CSF and interleukin-3, or cytokines such as interleukin 5, identified in tumor extracts or transformed cells .
Eosinophilia may be blood and (or) tissue, sometimes at a very high level. Main incriminated tumors are carcinomas, including lung large cell carcinoma (eosinophilia), or cervical cancer, in the form keratinizing large cell (tissue eosinophilia). Other primitive locations can also be incriminated: kidney, adrenal, thyroid, gallbladder, pancreas, breast.
After a rigorous clinical examination, a biological survey (inflammatory proteins, serum calcium), a chest x-ray, abdominal and pelvic ultrasound or a CT scan of the entire body may be proposed in search of the neoplastic process.
Eosinophilia and blood disorders:
It is often difficult to distinguish eosinophilia involved in the process leukemia (eosinophilic leukemia) a reaction to an associated eosinophilia hematologic malignancy. Indeed, a clonal hematological can affect a multipotent cell or a cell committed to a differentiation pathway. It can directly concern eosinophil lineage cases rarely described, or other hematopoietic lineage whose disruption sounded on the steps of the éosinopoïèse (see: To deepen 1). We will see that in some cases lymphoid lineage is particularly concerned (proliferation Th2). In other cases, it is the myeloid lineage which appears affected.
The medullary eosinophilia and (or) blood sometimes observed in hematological malignancies to nosological well defined. This is the case of eosinophilia associated with leukemias such as chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), or myeloid, including acute myelomonocytic leukemia (M4) abnormal bone marrow eosinophils, acute leukemia adult-related retrovirus HTLV-1 (Human T-cell lymphoma virus type 1). This is also the case of eosinophilia associated with lymphomas such as Hodgkin’s disease, non-Hodgkin’s malignant lymphomas, the epidermotropic lymphoma (Sezary syndrome, mycosis fungoides) or pleomorphic. In other circumstances, the eosinophilia is not part of any specific nosology. However, it is associated with an evocative picture of a lymphoproliferative or myeloproliferative or myelodysplastic syndrome (pre-leukemic condition?). Certain clinical forms of hypereosinophilic syndrome essential can evoke a “eosinophilic leukemia.” This is an exceptional situation with the appearance of immature eosinophils in the blood and bone marrow, bone marrow blasts, anemia and thrombocytopenia important, and chromosomal abnormalities. The distinction between essential and myeloproliferative disease hypereosinophilic is also difficult when eosinophilia is high, associated with myelofibrosis and abnormal karyotype.
In addition to the blood count (CBC), the médullogramme is often essential for further study because it allows the analysis of other hematopoietic lineages and used to assess the quantity and quality of spinal eosinophils (particularly in the case of leukemia acute myelomonocytic with abnormal eosinophils). The marrow biopsy in search of myelofibrosis and biological investigation – serum uric acid, lactic dehydrogenase (LDH) – may also be contributory. The study of medullary karyotype analyzes and additional cytogenetic or molecular biology (study of clonality) may be indicative as part of eosinophilia associated with hematological malignancy (case of Ph1 or Philadelphia chromosome translocation t (9, 22) chronic myeloid leukemia, inversion 16 in the acute myelomonocytic leukemia). In other circumstances, rarer, the observed cytogenetic abnormalities help explain the mechanisms of inducing eosinophilia. This is the case when the chromosomal rearrangement interested chromosome 5, which are located the genes encoding GM-CSF, interleukin 3 and 5 (see: To deepen 1). Thus, the translocation of 5q fragment, under the control of immunoglobulin genes promoters, can favor uncontrolled expression of these cytokine genes [acute lymphoblastic leukemia of the B lineage, with t (5; 14); myeloid malignancies, with t (5; 12)]. Other chromosome abnormalities observed in this context [trisomy 8, t (8; 21) …] do not bring to date, informative element of the relationship between leukemia and hypereosinophilic process, but evidence of a genetic control of eosinophilia.
Other cases of eosinophilia:
Each medical specialty knows at least one condition associated with blood eosinophilia and (or) tissue. This eosinophilia may be in the foreground, and appear as a feature of the disease (conditions related to tissue eosinophilia) or being an epiphenomenon accompanying very different conditions (contingent eosinophilia).
Eosinophilia can be integrated as part of clearly identified conditions such as vasculitis, an autoimmune disease or an immune deficiency. In polyarteritis nodosa, eosinophilia is rare. However, in vasculitis and Churg Strauss (former notion of asthma worsening, associated rhinitis, hyper-IgE serum, digestive attacks, cardiac, neurological), eosinophilia is constant and often high (> 5 x 109 / L). In autoimmune diseases, eosinophilia is rare, except bullous diseases such as pemphigoid. Eosinophilia can also be observed in various immunodeficiencies. In Wiskott-Aldrich syndrome, e.g., eosinophilia is only part of the accessory clinical and biological picture. However, the eosinophilia associated with considerable elevation of serum IgE (30 to 50 000 IU / mL) immediately orients to the hyper IgE syndrome described by Buckley. A massive eosinophilia may also be observed in Omenn syndrome, a rare immune deficiency, autosomal recessive, which appears in the first months of life. Eosinophilia may also be associated with a set of symptoms indicative of a disorder.
1- respiratory signs:
We have already mentioned the main causes of eosinophilia with pulmonary involvement that are asthma, drug causes, parasites, tumors (carcinoma, metastases, lymphangitis carcinomatosis) or allergic bronchopulmonary aspergillosis. Asthma with high and persistent eosinophilia has to look for other causes (parasitosis, allergic bronchopulmonary aspergillosis, hypereosinophilia essential), and especially systemic disease (vasculitis Churg-Strauss). Allergic bronchopulmonary aspergillosis has several signs suggestive. It occurs in a former asthma context with the notion of coughing and expectoration of “bronchial molds” (issue of mycelial plugs). Radiological images are varied: thickening of the bronchial walls, mucoid impaction, atelectasis, infiltrates and bronchiectasis especially predominant proximal to the upper lobes. We find also a marked elevation of serum IgE (> 1500 U / mL), with massive eosinophilia. It is possible to highlight specific IgE Aspergillus fumigatus. With radiological examination, assessment of the concentration of total IgE is useful for medical supervision. This rate decreases with corticosteroids is effective, while a further rise above a new push. Any cause of pleural effusion can also cause a local influx of eosinophils (pleurisy posttraumatic including eosinophils). In some circumstances, no cause is found: it is the case to some clinical pictures suggestive Löffler syndrome, especially before or chronic eosinophilic pneumonia, or Carrington.3 This disease results in various events (dyspnoea, cough) with impaired general condition (weight loss, fever, night sweats). It occurs most often in women. This is an eosinophilic alveolitis associated with eosinophilia variable level. The clinical, radiological images (multifocal alveolar opacities, sometimes migratory) are very evocative and very dramatic effectiveness of corticosteroids.
2- mucocutaneous signs:
Various cutaneous signs are part of a meaningful context in the case of vasculitis (Churg-Strauss vasculitis), hypersensitivity reactions (atopic dermatitis, urticaria, angioedema, parasitic dermatitis, drug reaction) in lymphomas (T lymphomas , mycosis fungoides, Sezary syndrome, or lymphomatoid papulosis), in the bullous dermatosis (pemphigoid, pemphigoid gestationis, Incontinentia pigmenti, dermatitis herpetiformis) in systemic mastocytosis or in hypereosinophilia associated with benign tumor proliferation (eosinophilic granuloma soft tissue or disease Kimura, the Angiolymphoid hyperplasia with eosinophilia). Itching is a common sign of alarm or accompanying eosinophilia (drug taking, allergies, parasitic disease, blood disease …). Some eosinophilic dermatoses were individualized.Among these are: pustular folliculitis Eosinophilic described by Ofuji which has certain similarities with folliculitis encountered in patients infected with HIV or with lymphoma; Wells syndrome, eosinophilic cellulitis benign evolution, which can be observed on histological examination of classic images called as “spark.” In these rare diseases, blood eosinophilia is inconstant, and data combined clinical and histologic examination is often necessary for diagnostic.4 The diagnosis is sometimes difficult to establish between certain eosinophilic dermatoses and an essential hypereosinophilia with cutaneous signs sometimes dominate the clinical picture. The angioedema with eosinophilia cyclical (weight gain with large edema of sudden onset and rapid resolution more or less associated with massive elevation of transient eosinophilia) must be differentiated essential hypereosinophilia.
3- Signs hépatodigestifs:
Furthermore parasites, there are many inflammatory conditions of the digestive tract that are accompanied by local eosinophilia (celiac disease) and (or) blood (ulcerative colitis, Whipple’s disease, Crohn’s disease). Other ailments (digestive malignancies location, vasculitis) should be investigated. The eosinophilic gastroenteritis is often seen in a context of atopy (food allergy?), Sometimes with high levels of serum IgE, especially in children. The particular arrangement of eosinophil infiltration at each of parietal intestinal structures causes various events. Thus, reaching the serous may be accompanied by a table of pseudo-peritonitis with a rich eosinophilic ascites, reaching the muscular can give a picture of subocclusion identical to that which can be observed in ‘anisakiasis (tumor-like formations). The infiltration of the mucosa is common with severe enteropathy and malabsorption. The distinction between eosinophilic gastroenteritis and eosinophilia essential to digestive localization can be difficult. Signs of liver damage with eosinophilia occur in many circumstances (parasitosis, drugs, cancer, blood diseases, primary sclerosing cholangitis, essential hypereosinophilic …).
4- muscle signs:
Apart from parasites (including trichinosis) or bacterial infections (staph myositis), a table with eosinophilia myalgia sometimes occurs in polymyositis but especially in syndrome “eosinophilia myalgia,” associated with taking L-tryptophan or rather Contaminants associated with its preparation, or in the Shulman fasciitis (eosinophilia with pain and swelling of the muscles, restricted motion and induration of subcutaneous tissues, blood disease associated).
5- cardiac signs:
Is mentioned in the first place, the essential hypereosinophilia. The heart-eosinophilia association exists in other circumstances (lymphoma, vasculitis, parasitic diseases, therapeutic use of growth factors or cytokines …).
6- Other signs focus:
Bone disorders (eosinophilic granuloma), bladder (cystitis eosinophilic sometimes drug induced) or ENT (non-allergic rhinitis or NARES) have been described. The blood eosinophilia is very fickle.
Hypereosinophilic syndrome essential:
It is a diagnosis of exclusion that should be considered only after rigorous etiological (list of diseases associated with chronic eosinophilia, see: To deepen 3). According to the criteria of Chusid, essential hypereosinophilic combines massive eosinophilia, persistent (> 1.5 x 109 / L), unexplained, lasting for at least 6 months, associated with multiple organ damage, especially heart.
There is a male predominance (80% of cases), with an age of onset typically between 20 and 50 years. The shapes of the child are rare and are more severe. The discovery of an essential eosinophilia is fortuitous (count systematic blood count) in 10% of cases, or linked to the occurrence of severe complications (heart disease, neuropathy). The warning signs are in fact with multiple general symptoms (fatigue, low grade fever), respiratory (cough, dyspnoea), skin (sweat, pruritus, rash, angioedema), muscle (myalgia), gastrointestinal (nausea, diarrhea).Hepatosplenomegaly would be observed in 50% of cases. Heart signs associated with chronic eosinophilia are very evocative of an essential hypereosinophilia. They are common (50-70% of cases), sometimes revealing (signs of cardiac failure) and diverse (cardiogenic shock, adiastolie, arrhythmias, tricuspid or mitral insufficiency). They witnessed eosinophilic myocarditis, or especially the development of endomyocardial fibrosis. Neurological signs may lead to central involvement (mental confusion, ataxia, seizures, amnesia, coma) or peripheral (sensory mononeuropathy) which seems related to vascular phenomena (vasculitis) and (or) thromboembolism. They are common and complementary tests (electroencephalogram, scanner …) can be very helpful. Eosinophilia may be insulated. As we mentioned above, it can also be associated with other hematologic signs that may be suspected a pre-leukemic condition (massive eosinophilia, damage to other lines, karyotype abnormalities) or a myeloproliferative disorder in which hepatosplenomegaly is observed , myelofibrosis, a very clear elevation of vitamin B12, the transcobalamins I and III. The prognosis is more reserved here because of frequent resistance to steroid therapy and increased risk of visceral involvement. The eosinophilia can also be associated with other signs.Cutaneous signs are frequent and varied type nodules, maculopapular or erythematous rash, angioedema or urticaria. These signs, sometimes associated with hyper-IgE serum, would be more readily met in the forms of good prognosis, sensitive to steroids. The diagnosis of essential hypereosinophilic can be discussed when the signs are focused in the lung or intestine. Whatever the form of this clinical eosinophilia, regular monitoring is required before any unexplained chronic eosinophilia due to two major risks are the possible occurrence of malignant blood disease or visceral involvement dominated by heart disease.
B- Elements of monitoring:
There are mildly symptomatic forms of essential hypereosinophilic which amount to an expression of isolated blood eosinophilia, sometimes associated with cutaneous manifestations or hepatosplenomegaly. If there are forms “stable”, the occurrence of complications, often unpredictable, which requires life-threatening:
– The systematic search for signs for a blood disease underlying (very high serum vitamin B12, variable score alkaline phosphatase, elevated serum uric acid, lowered folatémie), and indicates the chromosomal anomalies by performing a biopsy and bone marrow karyotyping of peripheral blood or cord;
– Compulsory and repeated search of cardiac involvement by necrosis, thrombosis or fibrosis (electrocardiogram renewed dimensional echocardiography every 6 months, sometimes associated with endocardial biopsy) or vascular lesions (examination of the fundus, thrombosis events of microemboli, coagulation profile, neurological evaluation).
Highlights to include:
• A blood eosinophilia is defined by a number of circulating eosinophils exceeding the figure of 0.5 x 109 / L. It can be associated with an eosinophil influx into tissues. It is important to appreciate the age and evolutionary curve over time. This is a common biological sign, often valuable to guide the etiologic investigation and enjoys the close collaboration between the clinician and the biologist. The history and the first clinical and laboratory tests can most often to diagnose and treat the cause of eosinophilia. This is often parasitic, allergic or drug.
• Eosinophilia is also associated with numerous other disorders, and its exploration can be long and difficult. It may appear in the foreground as a characteristic feature of the disease (clinical manifestations associated with tissue eosinophilia, hypereosinophilic syndrome essential), or otherwise being an epiphenomenon associated with various diseases (hypereosinophilic contingent).
• The origin of the eosinophilia sometimes remains undetermined, and its persistent nature becomes concern (risk of cardiac lesions for example).
1 / mobilization factors eosinophil lineage:
The polynuclear eosinophil is a cell bilobed nucleus, wallet, easily identified on blood smears by the dyeing properties of its granules, colored orange-pink by eosin. The specific granules, secondary granules of spherical or ellipsoidal shape, appear at the stage of promyelocyte. Their study by electron microscopy revealed the existence of a crystalline inclusion electron dense (composed of major basic protein or MBP), and a surrounding matrix (composed of the cationic eosinophil protein or ECP, of the neurotoxin derived from eosinophils or EDN and eosinophil peroxidase or EPO). Primary granules contain eosinophil lysophospholipase involved in the formation of crystals of Charcot-Leyden. The mechanisms involved in the development of eosinophilia are multiple and sometimes entangled. Eosinophilia may indicate an excess of marrow production, but also a defect elimination mature eosinophils (alteration of apoptosis). It often means increased recruitment of elements of the bone marrow reserve pool (role of chemotactic factors). Growth factors, cytokines (GM-CSF, IL-3, IL-5, whose genes are located in the 5q31-q33 region of chromosome 5), chemokines, including eotaxin family members (eotaxin, eotaxin 2), lipid factors (platelet activating factor or PAF-aceter) of anaphylatoxins (C5a) control to varying degrees and with varying degrees of selectivity, different functions of eosinophils (proliferation and differentiation in hematopoietic marrow mobilization of bone marrow reserve pool and transit in the blood transendothelial migration and domiciliation in tissues; activation – survival – apoptosis). These are interleukin 5 and eotaxin which exert the most targeted effects on elements of the eosinophil lineage. Analysis of the synthesis of cytokines by T cells profile enabled to individualize a lymphocyte subpopulation producing IFNg (Th1), and a subpopulation producing IL-4, IL-5, IL-13 (Th2), which monitor each other (Th1-Th2). Any alteration of the Th1-Th2 balance may be the source of various immunopathological process. Thus, an imbalance in favor of Th2 polarity may cause atopic state, inducing an overproduction of IgE (role of IL-4), or promoting blood eosinophilia (role of IL-5). Eotaxin is another important mediator in the recruitment process and activation of eosinophils. This chemokine can bind to a receptor called CCR3 (receptor for chemokine family, where the first two cysteines are adjacent). CCR3 is strongly represented in the eosinophil surface but also basophils and Th2 cells. Thus, this molecule has the ability to recruit a group of cells that actively participate in the development of an allergic reaction.
2 / functional potentialities of eosinophilic:
The identification of various receptors (cytokine, chemokine, lipid mediators, immunoglobulins, activated complement fractions), and adhesion molecules on the surface of eosinophils (selectins, integrins) allowed better understand the elements that control the favorable contacts migration, diapedesis, domiciliation, and intercellular communication (notable action of chemokines and cytokines). The succession of these signals results in the modulated expression of a functional program of the cell. These signals can participate in a physiological response (growth, chemotaxis cell cooperations) and (or) different pathological processes. The eosinophil is an effector cell capable of releasing cytolytic basic proteins (MBP, ECP, EDN, EPO, example of the selective process of releasing cationic proteins or pieces meal degranulation). It is also capable of releasing reactive oxygen species, toxic, such as superoxide anions. The eosinophil is an inflammatory cell, capable of producing lipid mediators (leukotrienes, prostaglandins), chemokines, pro-inflammatory cytokines (IL-1, IL-6, TNF) or immunomodulating (IL-4, IL -5). Thus, depending on the activation state of the eosinophils, celuici can induce a toxic response by release cationic protein granules, or promote amplification of inflammatory response. To assess the degree of activation of the polynuclear, we have different cellular or serum parameters. Morphological studies [hypogranulation and (or) the presence of cytoplasmic vacuoles, nuclear hypersegmentation] or analysis of cell density allows for individualized activated eosinophils (hypodenses eosinophils). These have the ability to release toxic mediators that appear to play a role in causing tissue damage. Elevated serum levels of the soluble form of the receptor for IL-2 (CD25s) were observed in severe cases of eosinophilia (hypereosinophilia essential, hematologic malignancies).
Strong Points to remember:
• The eosinophilia is observed in many diseases, but 4 major situations can be individualized.
• Most often, the blood eosinophilia fits with other clinical and laboratory manifestations, in an evocative pathological context (allergies, certain parasites, taking drugs).
• In other cases, eosinophilia is a sign of call that requires the implementation of additional investigations to establish the diagnosis (examples of parasites, cancers).
• Sometimes, the clinical manifestations are focused to an organ or tissue. The eosinophilia associated so is valuable diagnostic orientation (example of eosinophilic lung, eosinophilic gastroenteritis …).
• More rarely, eosinophilia is isolated, the etiological investigation remains unsuccessful. The situation becomes worrying when eosinophilia remains high and persistent. This may precede the development of hematologic malignancies, or announce the occurrence of visceral lesions dominated by heart disease.