to a particular drug on the basis of their expression of specific cell receptor types. while the evidence supporting these ideas is limited, one study identified the preferential presence of the tcr-v-b and complementarity-determining region 3 in t-cell receptors found on the t cells in the blisters of patients with allopurinol-induced dress syndrome. this finding is compatible with the notion that specific types of t-cell receptors are involved in the development of specific drug-induced scars. adme variations in adme, i.e. an individual's efficiency in absorpting, distributing, metabolizing, and excreting a drug has been found to occur in cases of the dress syndrome. these variations influence the levels and duration of a drug or drug metabolite in tissues and thereby impact the drug's or drug metabolite's ability to evoke the dress syndrome. for example, the cyp2c9 gene codes for cyp2c9, a cytochrome p450 enzyme which metabolizes various substances including phenytoin. the cyp2cp*3 variant of cyp29c has reduced catalytic activity; individuals expressing this variant show an increased incidence of developing the dress syndrome when taking phenytoin apparently due to increases in the drug's blood and tissue levels. in a second example of a genetically based adme defect causing scars, japanese individuals bearing slow acetylating variants of the n-acetyltransferase 2 gene, (nat2), viz., nat2*6a and nat2*7b, acetylate sulfasalazine more slowly than individuals homozygous for the wild type gene. individuals expressing the nat2*6a and nat2*7 variants have an increased risk for developing dress syndrome-like reactions to this anti-inflammatory drug. none-genetic adme factors are also associated with increased risks of developing the dress syndrome. allopurinol is metabolized to oxipurinol, a product with a far slower renal excretion rate than its parent compound. renal impairment is associated with abnormally high blood levels of oxipurinol and an increased risk of developing the dress syndrome, particularly the more severe forms of this disorder. dysfunction of the kidney and liver are also suggested to promote this disorder in response to other drugs due to the accumulation of scars-inducing drugs or metabolites in blood and tissues. currently, it is suspected that the expression of particular hla proteins and t-cell receptors interact with adme factors to promote scars particularly in their more serious forms. viral reactivation during the progression of the dress syndrome certain viruses that previously infected an individual and then became latent are reactivated and proliferate. viruses known to do so include certain members of the herpesviridae family of herpes viruses viz., epstein–barr virus, human herpesvirus 6, human herpesvirus 7, and cytomegalovirus. individuals with dress syndrome may exhibit sequential reactivation of these four viruses, typically in the order just given. reactivation of these viruses is associated with a flare-up in symptoms, a prolonged course, and increased disease severity which includes significant organ involvement and the development of certain autoimmune diseases viz., systemic lupus erythematosus, autoimmune thyroiditis, and type 1 diabetes mellitus. while these viral reactivations, particularly of human herpes virus 6, have been suggested to be an important factor in the pathogenesis of the dress syndrome, studies to date have not clearly determined if they are a cause or merely a consequence of t cell-mediated tissue injury. preventative currently, screening individuals for the expression of certain hla alleles before initiating treatment of patients with dress-inducing drugs is recommended. these recommendations typically apply only to specific populations that have a significant chance of expressing the indicated allele since screening of populations with extremely low incidences of expressing an allele is considered cost-ineffective. individuals expressing the hla allele associated with sensitivity to an indicated drug should not be treated with the drug. these recommendations include: allopurinol: the american college of rheumatology guidelines for the management of gout recommend hla-b*58:01 screening before allopurinol treatment. this is provided in many medical centers in taiwan, hong kong, thailand, and mainland china. abacavir: the usa food and drug administration and recommends screening for hla-b*57:01 in the treatment of hiv with abacovir in caucasian populations. this screening is widely implemented. it has also been suggested that all individuals found to express this hla serotype avoid treatment with abacovir. current trials are underway to evaluate the ability of genetic screening to prevent the dress syndrome for dapsone and hla-b*13:01 in china and indonesia. similar trials are underway in taiwan to prevent phenytoin-induced dress syndrome in individuals expressing the cyp2c9*3 allele of cyp2c9 as well as a series of hla alleles. treatment immediate discontinuance of the offending drug or drug(s) is the first and critical step in treating any scars disorder. in the past, the mainstay treatment of severe cases of dress syndrome was the use, often at high-dosage, of systemic glucocorticoids, relying on the anti-inflammatory actions of these drugs to suppress the eosinophil- and t cell-induced tissue damage caused by the disorder. however, there have been no randomized control trials reporting on the systemic use of these drugs. rather, there are suggestions that treatment with systemic glucocorticoids is associated with a higher incidence of relapse compared to topical glucocorticoid treatment and may be associated with a higher rate of opportunistic infection. accordingly, less severe cases of this disorder may be better treated conservatively with general support and, where needed, topical glucocorticoids. severer cases, particularly those involving significant internal organ involvement, may require systemic corticosteroids and efforts to support heart, kidney, lung, or other organ dysfunctions. terminology dress syndrome is one of several terms that have been used to describe a severe idiosyncratic reaction to a drug that is characterized by a long latency of onset after exposure to the offending medication, a rash, involvement of internal organs, hematologic abnormalities, and systemic illness. other synonymous names and acronyms include drug-induced hypersensitivity syndrome (dihs or dhis), anticonvulsant hypersensitivity syndrome, drug-induced delayed multiorgan hypersensitivity syndrome, drug-induced pseudolymphoma, anticonvulsant hypersensitivity syndrome, allopurinol hypersensitivity syndrome, dapsone syndrome, and dapsone hypersensitivity syndrome.