Drug-Induced Anaphylaxis in Children

Abstract

Drug-induced anaphylaxis in children is less common than in adults and primarily involves beta-lactams and nonsteroidal anti-inflammatory drugs. Epidemiological studies show variable prevalence, influenced by age, gender, and atopic diseases. The pathophysiology includes IgE-mediated reactions and non-IgE mechanisms, like cytokine release reactions. We address drug-induced anaphylaxis in children, focusing on antibiotics, nonsteroidal anti-inflammatory drugs, neuromuscular blocking agents, and monoclonal antibodies. Diagnosis combines clinical criteria with in vitro, in vivo, and drug provocation tests. The immediate management of acute anaphylaxis primarily involves the use of adrenaline, coupled with long-term strategies, such as allergen avoidance and patient education. Desensitization protocols are crucial for children allergic to essential medications, particularly antibiotics and chemotherapy agents.

Keywords: anaphylaxis; children; drug; drug-induced anaphylaxis; hypersensitivity reaction.

Figure 1

Mechanisms of DIA (drug-induced anaphylaxis) indicating culprit drugs, cells involved, and biomarkers. C3aR, C3a receptor; C5aR, C5a receptor; COX-1, cyclooxygenase-1; FcεRI, high-affinity Fc receptor for immunoglobulin E; IgE, immunoglobulin E; IL-6, interleukin-6; IL-β1, interleukin- β1; LTC4, leukotriene C4; LTD4, leukotriene D4; LTE4, leukotriene E4; mABs, monoclonal antibodies; MRGPRX2, Mas-related G-protein-coupled receptor member X2; NMBAs, neuromuscular blocking agents; NSAIDs, nonsteroidal anti-inflammatory drugs (NSAIDs); PAF, platelet-activating factor; RCM, radio contrast media; TNF-α, tumor necrosis factor-α; 9α,11β-PGF2, 9α,11β-prostaglandin F2.