17.5
Alerjik Reaksiyonlar: Anafilaksi
Anafilaksi, immünoglobulin E, yani IgE, antikorları aracılığıyla gelişen, yaşamı tehdit eden şiddetli bir aşırı duyarlılık reaksiyonudur. IgE alerjenl…
Anafilaksi, IgE antikorlarının aracılığı altında anlık bir aşırı duyarlılık reaksiyonudur. Bu antikorlar alerjenlere bağlanarak alerjen–IgE antikor kompleksleri oluşturur. Yaygın alerjenler arasında polen, toz akarları, ilaçlar ve bazı gıda maddeleri bulunur.
Bu kompleksler mast hücrelerindeki ve bazofillerdeki reseptörlere bağlanır, hızlı degranülasyona ve histamin, lökotrienler ve prostaglandinlerin salınmasına yol açar.
Bu aracılar vazodilatasyon, bronkokonstriksiyon, ödem ve nötrofil aktivasyonuna neden olur ve inflamatuar bir yanıt oluşturur.
Bu reaksiyonlar damar sistemi, sindirim sistemi, cilt ve solunum sistemini ciddi şekilde etkileyebilir. Ayrıca gıda alerjisi, ürtikari, rinit ve astım gibi durumlar olarak da ortaya çıkabilirler.
Penisillin, asparaginaz, monoklonal antikorlar, kortikotropin, heparin, aşılar, lokal anestezikler ve klorheksidin gibi antiseptikler gibi çeşitli ilaçlar anafilaksisine neden olabilir.
Anafilaksi için tanı yöntemleri klinik olup semptomlara dayanır. Cilt testleri, örneğin derme içi penisilpolizin enjeksiyonu, daha sonra penisilin alerjisini tespit edebilir.
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Q1: What is anaphylaxis and how does it develop?
Anaphylaxis is a severe, immediate hypersensitivity reaction mediated by IgE antibodies. When IgE binds to allergens, it forms complexes that attach to mast cells and basophils, triggering rapid degranulation. This releases mediators like histamine, leukotrienes, and prostaglandins, causing vasodilation, bronchoconstriction, edema, and inflammation throughout the body.
Q2: Which drugs commonly trigger anaphylactic reactions?
Penicillin is responsible for approximately 75% of anaphylactic deaths due to widespread use. Other drugs causing anaphylaxis include asparaginase, monoclonal antibodies, corticotropin, heparin, vaccines, local anesthetics, and antiseptics like chlorhexidine. These reactions occur through IgE-mediated mechanisms similar to food and environmental allergens.
Q3: What body systems are affected during anaphylaxis?
Anaphylaxis primarily affects the cardiovascular, respiratory, gastrointestinal, and integumentary systems. Symptoms include urticarial rash, hives, angioedema, bronchoconstriction, wheezing, shortness of breath, and hypotension. Severe cases progress to anaphylactic shock, characterized by sudden blood pressure drops, respiratory distress, and potential cardiovascular collapse.
Q4: How is anaphylaxis diagnosed in clinical practice?
Anaphylaxis diagnosis is primarily clinical, based on symptom presentation. Skin tests, such as intradermal injection of penicilloylpolylysine, can later identify penicillin allergy. Detecting particular IgE in plasma confirms allergic reactions, though these tests are reserved for cases where the allergen cause remains unclear.
Q5: What are common allergens that cause anaphylaxis?
Common allergens include food items like peanuts and shellfish, environmental substances such as grass pollen and dust mites, insect stings, and pharmaceutical agents. Radiological contrast agents, vaccines, and latex also trigger anaphylaxis. These allergens bind to IgE antibodies, initiating the cascade of mast cell and basophil degranulation.
Q6: What mediators are released during anaphylaxis and what effects do they produce?
Mast cells and basophils release histamine, leukotrienes, and prostaglandins upon degranulation. These mediators cause vasodilation, bronchoconstriction, edema, and neutrophil activation, generating an inflammatory response. The resulting cascade produces symptoms ranging from mild urticaria to life-threatening cardiovascular collapse and respiratory distress.
Q7: How does anaphylaxis differ from other hypersensitivity reactions?
Anaphylaxis is an immediate, IgE-mediated hypersensitivity reaction occurring within minutes of allergen exposure. Unlike delayed hypersensitivity reactions, which develop over hours or days, anaphylaxis causes rapid degranulation of mast cells and basophils. This distinguishes it from other hypersensitivity types in onset speed and severity.