Bullous pemphigoid (BP) is an acquired autoimmune subepidermal bullous disease caused by autoantibodies against components of the basement membrane zone. Primarily, IgG autoantibodies bind to components of the hemidesmosome adhesion complex such as BP180 and/or BP230 antigens. 1 Topical corticosteroids are the cornerstone of mild BP treatment with or without systemic administration of tetracycline, diaminodiphenyl sulfone, or low-dose corticosteroids (0.2-0.3 mg/kg/day). Additional systemic treatments for moderate to severe BP include steroid pulse therapy or highdose corticosteroids (0.5-1.0 mg/kg/day), high-dose intravenous immunoglobulin (IVIG), immunosuppressive agents (azathioprine, mizoribine, cyclosporine, mycophenolate mofetil, and cyclophosphamide), plasma exchange therapy, and rituximab. 2 In this respect, corticosteroids are central to the treatment of BP and various other autoimmune and autoinflammatory diseases. Among the abovementioned agents, corticosteroids are metabolized by CYP3A4, a drug-metabolizing enzyme found in the liver. 3 As a result, combining corticosteroids with CYP3A4 inducers such as antiepileptic drugs increases the metabolism of corticosteroids, resulting in refractory to corticosteroids. 4 Because many agents can be CYP3A4 substrates and induce CYP3A4, we must be cautious of drug interactions when using CYP3A4 substrates such as corticosteroids.
| C A S E REP ORTA 63-year-old woman with epilepsy and intellectual disability presented with a 3-month history of pruritic and edematous erythema, which was followed by tense blister formations (Figure 1a). From her early childhood, she was given phenytoin, phenobarbital, sodium valproate, and zonisamide for treating epilepsy. Skin biopsy and direct immunofluorescence showed dermal eosinophilia (Figure 1b) and linear complement C3 deposition at the basement membrane (Figure 1c), respectively. Serum anti-BP180 antibody levels were also elevated (4730 U/mL). The diagnosis of BP was made collectively. Following that, the oral administration of 35 mg/ day (0.8 mg/kg) of prednisolone and 100 mg/day of minocycline as well as topical clobetasol propionate were initiated. However, her erythema was getting worse and thus she was admitted to our hospital. Her entire body was covered in edematous erythema with