Erythema Multiforme Research Paper

Erythema multiforme a self limited acute inflammatory disorder affecting skin,muous membrane or both was first recognized by Bateman and Bulkley in 1817. In 1846, a first case was reported in America as “Herpes Iris.” Later, in 1866 Von Hebra, described the features under the term “erythema exsudativum multiforme” caused due to internal or systemic origin and not local in causation. According to him the patients with Erythema multiforme should have acrally distributed typical target lesions or raised edematous skin papules.In1968 Kenneth described an inflammatory oral disorder typial of EM but without any skin involvement. EM results from T-cell-mediated immune reaction to the precipitating agent, leading to cytotoxic immunological
Anaphylactic stomatitis shows urticarial skin reactions with other signs and symptoms of anaphylaxis which were absent in our cases. Erythema multiforme major is more aggressive form characterized by involvement of multiple mucosa accompanied by typical target skin lesions. Lesions of EM minor are single mucosal ulcerations and typical target lesions of skin. The oral mucosal ulcerations are usually irregular and large with necrotic tissue tags. Lip ulcerations are blood encrusted. The third category of EM, also described by many investigators as oral EM has the lesions confined to the oral mucosa and lips with no skin involvement. The most common drugs that trigger EM lesions are co‑trimoxazole, long acting sulfa drugs especially sulphonamides, phenytoin, carbamazepine and nonsteroidal anti-inflammatory drugs such as diclofenac, ibuprofen, and salicylates. Management of oral EM involves identification of triggering agent. Usually lesions can be treated palliatively with analgesics for oral pain, systemic and topical antibiotics to prevent secondary infection. Lesions of EM usually respond to topical steroids, for more severe cases systemic corticosteroids are