anafülaktoonkidena

Anafülaktoonkidena, or anaphylactoid reaction, is a non‑IgE‑mediated hypersensitivity that mimics anaphylaxis but does not rely on IgE antibodies. It presents with similar symptoms yet arises from alternative pathways rather than classic allergen sensitization.

Mechanism involves direct mast cell degranulation or activation of inflammatory pathways such as the complement system, leading to release of histamine and other mediators. Triggers include radiographic contrast media, certain opioids (notably morphine), vancomycin, some NSAIDs, and physical factors like cold exposure or exercise, with other drugs occasionally implicated.

Clinical features resemble those of anaphylaxis and may include sudden hypotension, bronchospasm, urticaria or angioedema, tachycardia, and abdominal symptoms. Distinguishing anafülaktoonikidenaktsioon from IgE‑mediated reactions can be difficult; a history of a non‑IgE trigger supports the diagnosis.

Diagnosis is primarily clinical, based on exposure history and presentation. Serum tryptase can be measured but may be normal in non‑IgE reactions; skin testing is not routinely helpful for non‑IgE triggers. Evaluation focuses on identifying the trigger and ruling out other causes.

Treatment requires immediate management similar to anaphylaxis: prompt administration of epinephrine, securing the airway, providing oxygen, and restoring circulation with intravenous fluids as needed. Adjunctive therapies include antihistamines and corticosteroids. The trigger should be removed, and patients should be monitored after stabilization. For future exposures, consider safer alternatives and, when appropriate, premedication or desensitization strategies based on clinical judgement.

Prognosis is generally favorable with rapid treatment, though severe reactions can be life‑threatening. Prevention emphasizes avoiding known triggers and using safer diagnostic or therapeutic options when possible.