The editorial by Dr. Stephan Kra ¨henbu ¨hl 1 concerning the study of Wang et al. 2 taught the readers of HEPATOLOGY a great deal about the mechanism of acetaminophen (AP)-induced hepatotoxicity. However, as the corresponding author for the paper of Wang et al., I feel obliged to respond to his comments concerning the dose of acarbose and ethanol used in our study.
Dr. Kra ¨henbu ¨hl stated that the daily dose of alcohol and acarbose ingested by our rats, approximately 14 mL of 10% alcohol and 16 mg acarbose per day, corresponded to approximately 200 g of alcohol and 3 g of acarbose by a 70 kg human subject, and concluded that the doses of both ethanol and acarbose that we chose were substantially higher than those normally ingested. 1 However, the extrapolation of the dose from rats to humans can also be made on the basis of body surface area, rather than on the conventional body weight basis. 3 In Wang et al., 2 21 to 22 mg/kg/d of acarbose evidently potentiated the hepatotoxicity of CC1 4 and/or AP, which was significantly increased when combined with 3.0 g/kg/d alcohol. This dose of acarbose is about four times higher than the recommended dose (5 mg/kg/d) for type 2 diabetics when calculated on the basis of body weight, which is a substantially high dose, as Dr. Kra ¨henbu ¨hl remarks. 1 However, the dose extrapolation based on body surface area produces a different result. Assuming that the body surface area is proportional to body weight (kg) to the power of 0.7, 4 i.e., (body weight) 0.7 , the doses of acarbose (21.5 mg/kg) and alcohol (3.0 g/kg) for a rat correspond to doses of only 421