Eozinofilie

HADRABOVÁ, Markéta a Michael DOUBEK. Eozinofilie. In Jiří Tomášek. Onkologie : minimum pro praxi. 1. vyd. Praha: Axonite CZ, 2015, s. 417-420. Asclepius. ISBN 978-80-88046-01-1.

Základní údaje

Originální název

Eozinofilie

Název anglicky

Eosinophilia

Autoři

HADRABOVÁ, Markéta a Michael DOUBEK

Vydání

1. vyd. Praha, Onkologie : minimum pro praxi, od s. 417-420, 4 s. Asclepius, 2015

Nakladatel

Axonite CZ

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Další údaje

Jazyk

čeština

Typ výsledku

Kapitola resp. kapitoly v odborné knize

Obor

30200 3.2 Clinical medicine

Stát vydavatele

Česká republika

Utajení

není předmětem státního či obchodního tajemství

Forma vydání

tištěná verze "print"

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/15:00085018

Organizační jednotka

Lékařská fakulta

ISBN

978-80-88046-01-1

Klíčová slova anglicky

eosinophilia; peripheral blood eosinophilic leukocytes

Štítky

EL OK

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Anotace

V originále

Eozinofilie je definována jako zvýšení periferní krve eozinofilních leukocytů na více než 700 buněk na mikrolitr krve. Důraz je kladen na počtu eosinofilů v oběhu v periferní krvi, i když nárůst eosinofilů lze pozorovat v jiných tělních tekutinách a mnoho tělesných tkání.

Anglicky

The term eosinophilia is defined as an increase in peripheral blood eosinophilic leukocytes to more than 700 cells per microliter of blood. Emphasis is placed on the number of eosinophils circulating in the peripheral blood, although an increase in eosinophils can be observed in other body fluids and many body tissues. Physiologically, eosinophils are derived from hematopoietic stem cells and their main functions include mediating parasite defense reactions, allergic response, tissue inflammation and immune modulations - which explains most of secondary or reactive hypereosinophilias - such as infections especially heminthis parasites, neoplasm, connective tissue disorders, and so on. Primary eosinophilia, on the other hand, include both clonal and idiopathic hypereosinophilic syndrome. Most cases of secondary eosinophilia are treated on the basis of their underlying causes. Allergic and connective tissue disorders may be amenable to corticosteroid treatment. Parasitic and fungal infections can be worsened or disseminated by use of steroids and should be ruled out if they are indicated by patient history. In patients with primary eosinophilia without organ involvement, no treatment may be necessary. Cardiac function should be evaluated at regular intervals, however, as peripheral eosinophilia does not necessarily correlate with organ involvement. Steroid responsiveness should be evaluated, both for prognosis (steroid-responsive patients do better) and to guide treatment when needed. Choices for systemic treatment of primary eosinophilia with organ involvement initially include corticosteroids, and interferon (IFN)-alpha for steroid-resistant disease. Other agents for steroid-resistant disease, which are usually given as long-term maintenance regimens to control organ involvement.