| Sažetak | Anafilaktičke reakcije spadaju u najozbiljniji oblik preosjetljivosti tipa I, a
karakterizirane su masovnom degranulacijom mastocita i sistemskim
otpuštanjem primarnih i sekundarnih medijatora poput histamina i
leukotriena, čije djelovanje može uzrokovati fatalan ishod u vidu
kardiovaskularnog ili respiratornog kolapsa. Okidači koji uzrokuju
anafilaktičku reakciju su razni i uključuju lijekove (uglavnom β-laktamske
antibiotike), hranu (npr. kikiriki), te otrov kukaca iz roda Hymenoptera. S
obzirom na etiologiju, anafilaksija može biti posredovana imunim
mehanizmima ili se definira kao anafilaktoidna reakcija. U slučaju
imunoloških uzroka, uglavnom je zastupljen alergijski oblik koji je ovisan o
IgE protutijelima, dok su rjeđe prisutni oblici posredovani IgG protutijelima
i aktivacijom sustava komplementa. S druge strane, anafilaktoidna reakcija
podrazumijeva nealergijsku etiologiju, čija je patogeneza slabije
razjašnjena. Neovisno o uzrocima, bolest se klinički može manifestirati u
više različitih fenotipova. Oni uključuju reakcije nalik tip I reakcijama,
reakcije nalik citokinskoj oluji, miješane reakcije te reakcije uzrokovane
komplementom. Anafilaktičku reakciju posreduju medijatori koji se dijele
na primarne i sekundarne. Primarni medijatori uključuju histamin, triptazu,
kimazu te proteoglikane, dok sekundarni uključuju čimbenik aktivacije
trombocita (PDGF), cistenil leukotriene (LTR), citokine, kemokine te faktore
rasta. Histamin je jedan od najvažnijih medijatora, a uzrokuje kliničke
simptome kao što su crvenilo kože, glavobolja, opstrukcija dišnih puteva,
hipotenzija i tahikardija putem H1 i H2 receptora. Većina drugih medijatora
uzrokuje slične simptome, i mehanizam njihovog djelovanja se također
intenzivno istražuje.
Samo liječenje anafilaktičih reakcija se najčešće izvodi administracijom
adrenalina, dok se za dugoročnu primjenu proučavaju humanizirana
monoklonalna protutijela koja se vezuju za IgE i/ili smanjuju izražaj
njegovog receptora, poput omalizumaba i ligelizumaba. |
| Sažetak (engleski) | Anaphylactic reaction is the most severe form of type I hypersensitivity
reaction. Anaphylaxis is characterized by massive degranulation of mast
cells and systemic release of primary and secondary mediators such as
histamine and leukotrienes, the effects of which can cause a fatal outcome
in the form of cardiovascular or respiratory collapse. The triggers of
anaphylactic reaction are diverse and include drugs (especially β-lactam
antibiotics), foods (e.g., peanuts), and venom from Hymenoptera insects.
In terms of etiology, anaphylaxis can be mediated by immune mechanisms,
or it can be defined as an anaphylactoid reaction. Among immunologic
causes, the allergic form, which depends on IgE antibodies, is most
prevalent, whereas forms mediated by IgG antibodies and activation of the
complement system are less common. An anaphylactoid reaction, on the
other hand, indicates a nonallergic etiology, the pathogenesis of which is
less clear. Regardless of the cause, the disease can manifest clinically in
several different phenotypes. These include Type I-like reactions, cytokine
storm-like reactions, mixed reactions, and complement-mediated reactions.
The mediators that play an important role in triggering anaphylactic
reactions are divided into primary and secondary mediators. Primary
mediators include histamine, tryptase, chymase, and proteoglycans,
whereas secondary mediators include platelet-activating factor, cysteinyl
leukotrienes, cytokines, chemokines, and growth factors. Histamine causes
clinical symptoms such as flushing, headache, airway obstruction,
hypotension, and tachycardia via H1 and H2 receptors. Most other primary
mediators cause similar symptoms, whereas secondary mediators primarily
cause an increase in endothelial permeability, vasodilation, and, in the case
of platelet-activating factors, cardiovascular collapse. Treatment of
anaphylactic reactions is usually by administration of epinephrine, while
humanized monoclonal antibodies such as omalizumab and ligelizumab,
based on the principle of binding to IgE or attenuating IgE receptor
expression, are being investigated for long-term use. |
