Management of drug allergy-clinical update

Abstract

The new classification of drug hypersensitivity reactions (DHRs) is based on phenotypes, endotypes, and biomarkers. Immediate and delayed reactions are the clinical phenotypic presentation while endotypes are based on cellular, biological mediators, and biomarkers. Complement activation, cyclooxygenase-1 inhibition, Mas-Related G Protein-Coupled Receptor-X2 (MRGPRX2), Cytokine release syndrome (CRS) is also included in DHRs due to mast cell activation e.g., radio contrast media, nonsteroidal anti-inflammatory drugs, monoclonal antibodies, oxaliplatin and taxanes, etc. Genetic predisposition of specific human leukocyte antigen alleles has been associated with the development of T cell-mediated symptoms of severe cutaneous adverse reactions (SCAR), which includes acute generalized exanthematous pustulosis, drug rash with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, and toxic epidermal necroplasia, due to antibiotics, retrovirus and anti-convulsant drugs, etc., drug desensitization (Ds), is a personalized treatment approach for immunoglobulin E (IgE), and Non-IgE mediated DHRs, for example, antibiotics, biologicals, chemotherapy, etc. This review will update on the mechanism of DHRs, the clinical approach of alternative drugs, and Ds in a high-risk patient.

Keywords

• acute generalized exanthematous pustulosis
• adverse drug reaction
• desensitization models
• desensitization
• drug allergy
• drug hypersensitivity reaction
• drug rash with eosinophilia and systemic symptoms
• high-affinity immunoglobulin e fcε receptor i
• immunoglobulin e
• scar
• stevens-johnson syndrome
• toxic epidermal necroplasia