RESUMO
Drug-induced hypersensitivity syndrome (DIHS), also referred to as drug reaction with eosinophilia and systemic symptoms (DRESS), is a severe hypersensitivity drug reaction affecting the skin and multiple internal organ systems. We report a 47-year-old man with DIHS/DRESS and comorbidities (fulminant type 1 diabetes mellitus, valsartan-induced photosensitivity, vitiligo and acute interstitial nephritis). Although acute interstitial nephritis usually appears in the early phase, his is a rare case of acute interstitial nephritis more than 2 years after the onset of DIHS/DRESS.
Assuntos
Síndrome de Hipersensibilidade a Medicamentos/complicações , Fadiga/tratamento farmacológico , Nefrite Intersticial/diagnóstico , Acetaminofen/efeitos adversos , Biópsia , Carbocisteína/efeitos adversos , Claritromicina/efeitos adversos , Creatinina/sangue , Síndrome de Hipersensibilidade a Medicamentos/tratamento farmacológico , Síndrome de Hipersensibilidade a Medicamentos/patologia , Quimioterapia Combinada/efeitos adversos , Medicamentos de Ervas Chinesas/efeitos adversos , Humanos , Rim/patologia , Masculino , Pessoa de Meia-Idade , Muramidase/efeitos adversos , Nefrite Intersticial/sangue , Nefrite Intersticial/etiologia , Nefrite Intersticial/patologia , Prednisolona/uso terapêutico , Pele/patologia , Fatores de TempoRESUMO
Bidens pilosa (BP) Linn. var. radiata is a plant used in traditional folk medicine. It is clinically effective in various diseases; the pathogenesis of most of these involves cyclooxygenase (COX)-2. To investigate the mechanism on which the clinical effectiveness of BP is based, we examined its effects on COX-2 expression and its major product, prostaglandin (PG)E(2), under conditions of inflammation. We induced inflammation in normal human dermal fibroblasts with interleukin (IL)-1beta and examined the effects of BP on COX-2 expression and PGE(2) production using Western blotting and competitive enzyme immunoassay, respectively. The functional involvements of mitogen activated protein kinases (MAPK) ERK1/2, p38, and JNK in COX-2 expression were also examined by Western blotting. IL-1beta-induced COX-2 expression was regulated by MAPK pathways, especially by p38. BP inhibited the phosphorylation of MAPKs, COX-2 expression, and subsequent PGE(2) production. The physiological activities and clinical effectiveness of BP observed under diverse conditions may be partly attributable to its ability to inhibit MAPK, mainly p38, activity, COX-2 expression, and subsequent PGE(2) production.