EOZINOFILYYa (eosinophilia; these. a leukocytosis eosinophilic) — increase in number of eosinophils in blood in comparison with norm (the normal maintenance of eosinophils in blood at adults makes 20 — 300 cells in 1 mkl blood, or 0.5 — 5% of all leukocytes). Gilereozn-nofiliy, or big eosinophilia, call states. at to-rykh the maintenance of eosinophils in blood makes 15% and more.
usually at increase in total number of leukocytes.
Eosinophils (eosinophilic g a wound of a lotsita) count (in % to all leukocytes) in the blood smears painted by Romanovsky's method — Gimza (see Romanovsky — Gimza a method), or (with a bigger accuracy) during the definition of their absolute number in Goryaev's camera (see. To and m er to a scha of t of N y e/.
AA. arises owing to the strengthened products of eosinophils in marrow; an indicator of it is increase in absolute number of eosinophilic promyelocytes, myelocytes and metamyelocytes in marrow. AA. consider as defense reaction of an organism in response to receipt in blood of products of a foreign protein. At the same time from eosinophilic granularity (granules of eosinophils) prostaglandins E } and E2, having antihistaminic activity are released.
AA. are, as a rule, secondary. Distinguish reactive eosinophilias and
AA., arising at diseases of the hemopoietic system. Treat reactive parasitic E., observed at helminthoses, especially at fabric localization of parasites or their larval stages. Parasitic E. is also so-called tropical E., sometimes followed by leukemoid shift in blood; most often it is noted at a fascioliasis (see) and a strongyloidosis (see). Treat reactive also E. at allergic states, napr, bronchial asthma (see), a pollinosis (see), an allergic dermatosis (see the Dermatosis), a Quincke's edema (see Quincke swelled), Leffler's syndrome (see Leffler a syndrome). At allergic states emergence E. it is connected with influence of gistamnnopodobny substances, and also a special factor (eozinopoetin) allocated by lymphocytes at their antigen challenge; eozinoioetin raises products of eosinophils in marrow owing to what their receipt in blood increases. Feature E. the infectious and allergic nature increase in the phagocytal activity of eosinophils coming to phagocytal activity of neutrophils is. The hypereosinophilia in combination with other displays of an allergy or without them can arise at reception of pharmaceuticals (e.g., antibiotics. streptocides, acetilsalicylic to - you) — so-called medicinal
E. E. of not clear genesis occurs sometimes at almost healthy faces. Are known family E. the pases of a rasimpa-tichesky part of the autonomic nervous system observed preferential at persons with dominance of a tone. At nek-ry patients reduction of number of eosinophils in blood under the influence of corticosteroids is noted (in particular, Prednisolonum) that indicates a possible role of insufficiency of adrenal glands in genesis of an eosinophilia.
The hypereosinophilia is noted at a number of diseases of system of blood, napr, at a myelosis (it is frequent in combination with a basophilia — so-called eosinophilic oh - zofilnaya association), a myelofibrosis, a polycythemia (see), malignant lymphoma (see), a lymphogranulomatosis (see), sometimes at acute leukoses (see), diseases of heavy chains (see. Heavy chains of a disease). The eosinophilic hyperleukocytosis (the hyperleukocytosis connected with increase in quantity of eosinophils) meets at the so-called eosinophilic leukosis which is characterized by total substitution of marrow eosinophils of different degree of a maturity and availability of eosinophilic infiltrates in a liver, a spleen, limf, nodes, sometimes in a myocardium.
AA. it is observed at cancer went. - kish. a path, generative organs, a thyroid gland, kidneys, especially in the presence of metastasises in marrow, and also after a splenectomy (see), at diffusion option of an eosinophilic granuloma of bones (see).
AA. in blood it can be combined with a local eosinophilia, napr, in a phlegm (at the bronchitis complicated by an astmo-idny syndrome), in allocations from a nose (at allergic rhinitis), from a rectum (at mucous colic), in pleural exudate (at new growths of a pleura, a hemothorax).
At detection E. conduct a careful helmintologic research (see. Helmintologic methods of a research). According to indications at suspicion of a tumor or a disease of blood make diagnostic punctures limf, nodes, a liver, a spleen, marrow, if necessary — an intsi-zionny biopsy (see) tumorous eosinophilic infiltrates went. - kish. path, etc.
Elimination of an allergenic factor and successful treatment of a basic disease lead E.
Eozinofiliya to disappearance diagnose for children at detection of the increased quantity of eosinophils in blood in comparison. with age norm (at newborns normal the maintenance of eosinophils makes 0,5 — 8% of all leukocytes, at children of more advanced age the quantity of eosinophils usually does not exceed 5% of all leukocytes).
Distinguish reactive (secondary) eosinophilias, primary gi-pereozinofilny syndrome (a hyper-eosinophilic myeloproliferative syndrome) and a hereditary (family) eosinophilia.
Reactive E. meet at children more often others E. also proceed usually with moderated (to 12 — 15% of all leukocytes) increase in maintenance of eosinophils in blood. At newborns the reason E. there can be pre-natal infections (e.g., a toxoplasmosis), allergic reactions to pharmaceuticals (vitamin of Vkh, penicillin) or cow's milk in the presence at mother of an allergy to the same antigen (in the latter case believe that the sensitization of a fruit antigens of milk occurs vnutriutrobno). At children of more advanced age the reason E. there can be helminthoses (an ascaridosis, a strongyloidosis, a trichinosis, a fascioliasis, etc.), allergic diseases (and llergo a dermatosis, a pollinosis, a serum disease, etc.); intolerance of pharmaceuticals; malignant tumors (lymphogranulomatosis, acute leukosis, chronic myeloproliferative diseases, etc.); immunodeficient diseases, postpneumonectomy syndrome; diseases of skin of not allergic genesis, napr, herpetiform dermatitis of Dyuringa (see Dyuringa a disease); nek-ry hereditary diseases of system of blood, napr, Fankoni's anemia (see. Hypoplastic anemia); collagenoses (the nodular periarteritis is more often); viral and bacterial infections in the period of recovery (measles, chicken pox, purulent infections); mycoses (actinomycosis, aspergillosis); the diseases caused by protozoa (pneumocystosis).
Primary hyper eosinophilic syndrome occurs at children seldom and is characterized by heart failure that is caused by damage of a myocardium and (or) an endocardium, eosinophilic infiltrates in lungs, damage of a brain and a hypereosinophilia. Genesis of a syndrome is not identical. The forecast for life is more often adverse.
Carries a hereditary (family) eosinophilia of V. Mac-Kjyuzik to diseases from autosomal dominants - nym a mode of inheritance. The disease can be shown at early age in the form of attacks of the bronchitis complicated by an astmoidny syndrome, hepatomegalias, eosinophilic infiltrates in lungs, skin and muscles with the expressed eosinophilia in blood. Disease chronic. The forecast for life, as a rule, favorable.
At reactive E. special therapy is not required, it disappears in process of treatment of a basic disease. At primary gipereozino-filny syndrome, a hereditary (family) eosinophilia and dlitel-
ny reactive E. in connection with a possibility of damage of heart appoint immunodepressive substances (see) and anticoagulants (see). Bibliography: Grinshpun L. D. Big eosinophilias of blood and their clinicodiagnostic value, M., 1962;
Grinshpun JI. And Vinogradova Yu. E. Eosinophils and hypereosinophilia, Rubbed. arkh., t. 55, No. 10, page 147, 1983; Grinshpun L. D. and Pashkov V. V. O hyper eosinophilic syndrome, in the same place, t. 48, No. 8, page 102, 1976; Kassirsky I. A. and Alekseev G. A. Clinical hematology, page 389, 774, M., 1970; Kislyak N. S. A blood cell at children it is normal also of pathology, page 48, M., 1978; Lerner I. P. and Brusilovsky E. S. Allergic eosinophilic diseases, Kiev, 1961; Begemann H., R and-stetter J. u. Kabot W. Klinische Hamatologie, S. 411, Stuttgart, 1970; With h i 1 with o t e H. R. a. o. The hypereo-sinophilic syndrome and lymphoblastic leukemia with extra S-group chromosome and q14 + marker, J. Pediat., v. 101, p. 57, 1982; With h u s i d M. J. a. o. The hypereosino-philic syndrome, Medicine (Baltimore), v. 54, p. 1, 1975; About 1 s about n T. A. a. o. Cardiomyopathy in a child with hypereosi-nophilic syndrome, Pediat. Cardiol., v. 3, p. 161, 1982; Sherman M.
P. a. Cox K. L. Neonatal eosinophilic colitis, J. Pediat., v. 100, p. 587, 1982; Teb-b i of Page K. o. The role of eosinophilis in granulopoiesis, I. Eosinophilia in neutropenic patients, ibid., v. 96, p. 575, 1980; Wintrobe M. M. Clinical hematology, Philadelphia, 1981.
G. A. Alekseev, H. P. Shabalov (ped.).