Abstract

OVERVIEW OF STEVENS-JOHNSONS SYNDROME- ITS ETIOLOGY AND TREATMENT

*N. Subrahmanyeswari P., Mohanavamsi Yemineni, P. Srinivasa Babu

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Abstract

Stevens–Johnson Syndrome (SJS) is a rare yet severe condition that primarily affects the skin and mucous membranes. It generally begins actually with flu-like symptoms and then progresses to certain painful skin rashes. The syndrome is usually triggered by adverse drug reactions or infections and is rooted in immune system dysfunction. A strong genetic correlation has been found with the HLA-B1502 allele, present in all affected patients in some populations, with Type IV hypersensitivity being the underlying immune mechanism. SJS and its more severe variant, Toxic Epidermal Necrolysis (TEN), result in extensive cell death that causes the outer layer of skin (epidermis) to separate from the underlying dermis. Sulfonamide antibiotics are a common cause. SJS is viewed generally as a milder form out of TEN. Risk factors include conditions like HIV/AIDS and systemic lupus erythematosus. It is commonly induced by medications such as corticosteroids, antibiotics, antihistamines, or intravenous immunoglobulin. Patients were observed to be typically required proper intensive medical care in the areas of burn or critical care units. Symptoms include inflammation, painful blisters in the mouth and eyes, and full-thickness damage to skin and mucosal tissues. Among drug-induced severe cutaneous adverse reactions (SCARs), SJS involves a distinct immune pathway, notably Type IVb hypersensitivity, which differs from other reactions like DRESS syndrome.

Keywords: Rare disease, immune dysfunction, HLA-B1502, Type IV hypersensitivity.