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Licorice‐induced hypokalemic myopathy and hypokalemic renal tubular damage in anorexia nervosa
Author(s) -
Ishikawa Shozo,
Kato Masahiro,
Tokuda Takahiko,
Momoi Hiroki,
Sekijima Yoshiki,
Higuchi Makoto,
Yanagisawa Nobuo
Publication year - 1999
Publication title -
international journal of eating disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.785
H-Index - 138
eISSN - 1098-108X
pISSN - 0276-3478
DOI - 10.1002/(sici)1098-108x(199907)26:1<111::aid-eat16>3.0.co;2-u
Subject(s) - hypokalemia , anorexia nervosa , endocrinology , medicine , nephropathy , myopathy , urine , diabetes mellitus , psychiatry , eating disorders
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. © 1999 John Wiley & Sons, Inc. Int J Eat Disord 26: 111–114, 1999.