SJS, TEN, and SJS/TEN Stevens–Johnson syndrome, toxic epidermal necrolysis, and Stevens–Johnson syndrome/Toxic epidermal necrolysis overlap syndrome are a spectrum of Type IV, Subtype IVc, delayed hypersensitivity<unk> , i.e.<unk>  initiated by CD8+ T cells and natural killer T cells. They are characterized initially by fever and flu-like symptoms followed within days by skin as well as mucous membrane blisters and denudation. Differentiation of the three disorders is based on the extent of disease with SJS involving 30% of the total bodily skin area. This spectrum of disorders is complicated by inflammation in and damage to internal organs such as the liver and, less commonly, kidney and heart. More importantly, they are also complicated by sepsis due to the loss of skin and mucous membrane epithelial barriers. In one study, SJS, TEN, and SJS/TEN mortality rates were 4.8%, 19.4%, and 14.8%, respectively, with an important portion of the deaths due to bacterial sepsis, particularly in the acute, early stage of these disorders. The drugs most commonly triggering the SJS, TEN, and SJS/TEN spectrum of disorders are anti-infective sulfonamides, anticonvulsants (e.g. carbamazepine and lamotrigine), non-steroidal anti-inflammatory drugs, allopurinol, nevirapine, and chlormezanone. Allopurinol appears in some studies to be the most common instigator of these disorders. Any new biological or herbal remedy, it is suggested, should be considered a possible cause of these disorders under the proper clinical circumstances. DRESS syndrome The DRESS syndrome is a Type IV, Subtype IVb, hypersensitivity drug<unk>  i.e. a<unk> dependent on CD4(+) cells and the cell- and tissue-injuring action of eosinophils. Skin lesions inflict 73% to 100% of afflicted individuals; they are generally infiltrative macules and plaques. About 75% of cases exhibit facial edema. The syndrome is also associated with other maladies caused by high levels of blood eosinophils such as the various hypereosinophilia-related disorders: persistent asthma and allergic rhinitis and, more significantly, eosinophil-based and lymphocyte-based inflammation of the liver (>70% of cases), kidney (20% to 40% of cases), lung (~33% of cases), heart (4% to 27% of cases), and, uncommonly, the meninges, brain, gastrointestinal tract, and spleen. The disorder is lengthened and worsened in individuals that develop reactivation of latent viruses of the herpes viruses. The estimated mortality rate for the DRESS syndrome is about 10%. Allopurinol and sulfasalazine account for almost 66% of DRESS syndrome cases with minocycline being the third most common cause of the disorder; Strontium ranelate, leflunomide, dapsone, and nonsteroidal anti-inflammatory drugs (diclofenac, celecoxib, ibuprofen, and phenylbutazone) are less common causes of the disorder. AGEP AGEP is a rare Type IV, subtype IVd, hypersensitivity<unk> dependent on neutrophils and characterized by the rapid formation of skin pustules on an erythematous background. In one study of 28 patients, the disorder was complicated by involvement of the kidney (36% of cases), lung (27%), and liver (11%). It is the least<unk>  of the SCARs disorders, typically shows a mild course, and is rarely associated with<unk>  complications although superinfection of skin lesions may be life-threatening.
Severe cutaneous adverse reactions
Chronic toxicity
Acute toxicity
Progressive disease
Autoimmune/inflammatory syndrome induced by adjuvants
Serious Hazards of Transfusion
Allergies in children
Limited symptom attack