Ishikawa S, Kato M, Tokuda T, Momoi H, Sekijima Y, Higuchi M, Yanagisawa N
Department of Medicine (Neurology), Shinshu University School of Medicine, Asahi Matsumoto, Japan.
Int J Eat Disord. 1999 Jul;26(1):111-4. doi: 10.1002/(sici)1098-108x(199907)26:1<111::aid-eat16>3.0.co;2-u.
A patient with a history of anorexia nervosa developed licorice-induced hypokalemic myopathy. With potassium replacement, high CPK blood level and myopathic signs returned to normal. However, the patient manifested persistent hypokalemia and impaired renal function to concentrate and acidify the urine. Renal biopsy demonstrated intense degeneration and vacuolation of tubules with a normal glomerus which was consistent with hypokalemic nephropathy. Prolonged hypokalemia in anorexia nervosa is sometimes attributed to surreptitious purging or taking diuretics, but it is necessary to check the urine pH, the urine-specific gravity, and the urine potassium level in order to find underlying renal damage even after hypokalemic myopathy is treated successfully.
一名有神经性厌食症病史的患者患上了甘草诱发的低钾性肌病。补充钾后，高肌酸磷酸激酶（CPK）血症水平和肌病体征恢复正常。然而，该患者仍表现出持续性低钾血症以及肾功能在尿液浓缩和酸化方面受损。肾活检显示肾小管有严重变性和空泡形成，肾小球正常，这与低钾性肾病相符。神经性厌食症患者的长期低钾血症有时归因于偷偷催吐或服用利尿剂，但即使低钾性肌病得到成功治疗，也有必要检查尿液pH值、尿比重和尿钾水平，以发现潜在的肾脏损害。
