From the Guidelines
Contact dermatitis and Stevens-Johnson Syndrome (SJS) differ primarily in their cellular mechanisms, with SJS involving a more severe, widespread immune reaction causing extensive cell death and epidermal detachment, whereas contact dermatitis is a localized immune response limited to the area of contact. The key difference lies in the extent of immune activation and target cell destruction, with SJS characterized by the activation of cytotoxic T cells and natural killer cells that directly attack keratinocytes throughout the epidermis, leading to widespread apoptosis via the Fas-FasL pathway and granulysin release 1. In contrast, contact dermatitis is a localized reaction where T cells recognize specific allergens and release cytokines that cause inflammation limited to the area of contact, as described in the guidelines for the management of contact dermatitis 1.
The severity of SJS is further exacerbated by genetic predisposition, particularly HLA associations, and the involvement of drug-specific T cell reactions to medications like allopurinol, carbamazepine, or sulfonamides 1. The widespread epidermal detachment and mucosal involvement in SJS lead to life-threatening consequences, including multiorgan failure and significant long-term sequelae, such as ocular damage and psychological problems 1. In contrast, contact dermatitis is usually triggered by external allergens like metals or plants and is characterized by a more limited reaction.
The most recent guidelines for the management of SJS/TEN in adults and children emphasize the importance of early recognition, withdrawal of suspected medications, and supportive care to prevent long-term complications and reduce mortality 1. The use of IVIg, systemic corticosteroids, or ciclosporin in the context of SJS/TEN is still debated, and their effectiveness is not well established 1.
In summary, the difference in cellular mechanisms between contact dermatitis and SJS lies in the extent of immune activation and target cell destruction, with SJS being a more severe and widespread reaction that can have life-threatening consequences. The management of SJS/TEN should prioritize early recognition, withdrawal of suspected medications, and supportive care to prevent long-term complications and reduce mortality.
From the Research
Cellular Level Differences
- Contact dermatitis and Stevens-Johnson syndrome (SJS) are both type 4 hypersensitivity reactions, but they differ in their severity and extent of skin damage 2, 3.
- SJS is a more severe condition, characterized by widespread skin necrosis and detachment, whereas contact dermatitis is typically limited to a specific area of skin contact 4, 5.
- The extent of epidermal detachment is the primary difference between SJS and toxic epidermal necrolysis (TEN), with TEN being the more severe condition 6.
Immunological Mechanisms
- The pathogenesis of SJS and TEN involves genetic linkage with HLA- and non-HLA-genes, drug-specific T cell-mediated cytotoxicity, T cell receptor restriction, and cytotoxicity mechanisms 3.
- The immune response in SJS and TEN is characterized by the activation of cytotoxic T cells, which leads to the destruction of keratinocytes and the formation of skin lesions 2, 3.
- The use of immunosuppressive therapies, such as cyclosporine and TNF-α inhibitors, has been proposed as a treatment option for SJS and TEN, highlighting the importance of immunological mechanisms in these conditions 2, 6.
Treatment and Management
- The treatment of SJS and TEN typically involves the withdrawal of the suspected causative agent, supportive therapy, and the use of immunosuppressive agents, such as corticosteroids and intravenous immunoglobulin (IVIG) 2, 4, 5, 6.
- The use of corticosteroids in the treatment of SJS has been shown to be effective in reducing mortality and promoting recovery 4, 5.
- The management of SJS and TEN requires a multidisciplinary approach, involving dermatologists, immunologists, and other healthcare professionals 2, 3.