Table of Contents
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are severe, life-threatening skin reactions often triggered by medications. Understanding their mechanisms helps in early diagnosis and management.
Overview of SJS and TEN
SJS and TEN are part of a spectrum of adverse drug reactions characterized by widespread skin and mucous membrane damage. SJS involves less than 10% of body surface area, while TEN affects more than 30%. Both conditions require prompt medical attention.
The Immune-Mediated Mechanism
The primary mechanism involves an immune response triggered by certain drugs. These drugs or their metabolites bind to skin proteins, forming a complex that the immune system recognizes as foreign. This leads to an immune attack on the skin cells.
Role of T Cells
Activated cytotoxic T lymphocytes (CD8+ T cells) play a central role. They release cytotoxic molecules such as perforin, granzyme B, and Fas ligand, which induce apoptosis (cell death) in keratinocytes, the predominant skin cells.
Genetic Predisposition
Genetic factors, particularly certain Human Leukocyte Antigen (HLA) alleles, increase susceptibility. For example, HLA-B*15:02 is associated with carbamazepine-induced SJS/TEN in Asian populations.
Pathogenesis of Skin Damage
The immune response causes widespread apoptosis of keratinocytes, leading to detachment of the epidermis. This results in skin sloughing, blister formation, and mucous membrane erosion.
Summary
In summary, SJS and TEN are severe immune-mediated reactions primarily driven by drug-specific cytotoxic T cells. Genetic predispositions and the formation of drug-protein complexes contribute to their development. Recognizing these mechanisms is crucial for prevention and treatment.