Abstract:A broad spectrum of drugs is associated with AGEP, a T cell-mediated reaction. Genetic susceptibility and the possible role of other risk factors in AGEP should be further evaluated in larger studies of AGEP patients with a validated diagnosis.
“…In this process an intradermal infiltration of activated CD4 and CD8 T cells producing granulocyte-macrophage colony-stimulating factors (GM-CSF), with IFN-g and TNF-a with the release of perforin/granzyme B and FasL, which are responsible for keratinocyte death [23,24]. These T lymphocytes also produce IL8 (CXCL-8), which is responsible for neutrophil chemoattraction and activation [7,23,[25][26][27].…”
Section: Immunopathologymentioning
confidence: 97%
“…Urticaria is characterized by wheals, sometimes accompanied by angioedema. AGEP consists of edematous erythema followed by small nonfollicular sterile pustules that may be accompanied by a nonerosive mucous membrane [3,6,7]. Fixed drug eruptions (FDEs) consist of solitary or just a few pruritic, erythematous macules that evolve into edematous plaques; they recur at the same sites with reexposure and lead to hyperpigmentation [3,8,9].…”
Section: Pattern Of Responsesmentioning
confidence: 99%
“…CD4 þ and CD8 þ cells expressing high levels of the activation marker and IFN-g have been detected in the supernatant of carbamazepine-stimulated T-cell clones [10]. In AGEP, drug-specific T cells have been obtained from patch test sites and blood [25,26,53], producing large amounts of IL8/CXCL8 [7], with a predominant Th1 cytokine profile (GM-CSF and IFN-g) and TNF-a [47]. Some T-cell clones like CXCL8þ display a Th2 pattern (IL4 and IL5) [47].…”
Section: T Lymphocytes Recognition Of Drugmentioning
Current studies provide overwhelming evidence of the interaction between the organ involved, very often the skin, and immunocompetent cells. This is of relevance for diagnostic and therapeutic approaches.
“…In this process an intradermal infiltration of activated CD4 and CD8 T cells producing granulocyte-macrophage colony-stimulating factors (GM-CSF), with IFN-g and TNF-a with the release of perforin/granzyme B and FasL, which are responsible for keratinocyte death [23,24]. These T lymphocytes also produce IL8 (CXCL-8), which is responsible for neutrophil chemoattraction and activation [7,23,[25][26][27].…”
Section: Immunopathologymentioning
confidence: 97%
“…Urticaria is characterized by wheals, sometimes accompanied by angioedema. AGEP consists of edematous erythema followed by small nonfollicular sterile pustules that may be accompanied by a nonerosive mucous membrane [3,6,7]. Fixed drug eruptions (FDEs) consist of solitary or just a few pruritic, erythematous macules that evolve into edematous plaques; they recur at the same sites with reexposure and lead to hyperpigmentation [3,8,9].…”
Section: Pattern Of Responsesmentioning
confidence: 99%
“…CD4 þ and CD8 þ cells expressing high levels of the activation marker and IFN-g have been detected in the supernatant of carbamazepine-stimulated T-cell clones [10]. In AGEP, drug-specific T cells have been obtained from patch test sites and blood [25,26,53], producing large amounts of IL8/CXCL8 [7], with a predominant Th1 cytokine profile (GM-CSF and IFN-g) and TNF-a [47]. Some T-cell clones like CXCL8þ display a Th2 pattern (IL4 and IL5) [47].…”
Section: T Lymphocytes Recognition Of Drugmentioning
Current studies provide overwhelming evidence of the interaction between the organ involved, very often the skin, and immunocompetent cells. This is of relevance for diagnostic and therapeutic approaches.
“…Skin reaction may occur in less than 2-3 days [7]. Discontinuing the suspected drug and supportive therapy is the principal treatment [10]. Corticosteroids (oral, topical, systemic) may be given, but no significant difference has been reported between treatment regimens in the course and recovery period [11].…”
“…[1][2][3] Skin symptoms arise quickly within a few hours and resolve rapidly within a few days without treatment. The rash is commonly accentuated in the large folds.…”
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