フロセミド長期服用による偽性バーター症候群 : その病態と絶食療法の有用性

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  • A Case of Long-term Furosemide-induced Pseudo-Bartter's Syndrome : Its disease course and usefulness of fasting therapy

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Metabolic mimicry of Bartter's syndrome induced by self-vomiting, laxatives abuse, and diuretics abuse has recently been reported. We here report a case of eating disorder with pseudo-Bartter's syndrome caused by long term ingestion of furosemide in which fasting therapy was useful in breaking the dependence on furosemide. A 22-year-old unmarried woman consulted our hospital complaining of overall physical rigidity and breathing difficulty. She had a 5-year history of ingestion of furosemide (400 mg/day) and many characteristic symptoms of Bartter's syndrome, including hypokalemia, metabolic alkalosis, elevated plasma renin activity and serum aldosterone level without hypertension, and insensitivity to the pressor effect of angiotensin-II infusion. Serum CPK and uric acid were elevated. Creatinine clearance was within the normal range. and Fishberg's concentration test disclosed a poor concentration ability. The needle biopsy specimen from the kidney showed a hypertrophy of the juxtaglomerular apparatus and a large number of secretory granules and mitochondria. The granules, some of which contained crystalloid structures, were of various shapes and sizes. Additionally, after she was hospitalized, she presented the characteristic behavior of eating disorders including anorexia, binge eating, and self-vomiting. The behavior was accelerated when we tried to prohibit the furosemide. Therefore, we diagnosed the case as eating disorder with pseudo-Bartter's syndrome due to furosemide abuse, and tried to decrease the intake of the drug. Three months later, when the daily dose of furosemide was decreased to 40mg, plasma renin activity and serum aldosteron levels returned to almost normal ranges. At this stage, she strongly resisted complete cessation of the furosemide, then we followed her condition as an outpatient. After one month, the dosage again increased to 120-160 mg/day and she revisited us complaining that she could not discontinue the drug by herself, and asked for help. We then introduced her into fasting therapy and she succeeded in discontinuing the furosemide. Her eating disorder returned to normal after the therapy and she became well enough to obtain a job as a nurses' aid. We feel that fasting therapy is useful in helping patients, with diuretics abuse induced pseudo-Bartter's syndrome, discontinue the drug. But in the case of eating disorders, a careful observation must be made. Among the possible reasons why the fasting therapy was successful are as follows. 1. Patients who have a desire to become thinner are willing to undergo fasting therapy. 2. Since fasting therapy has a strong externally imposed structure, it is effective in stopping the patients from seeking the drug. 3. During the period of fasting, there is an increase of sodium excretion and a negative sodium balance even when a sodium supplement is given, therefore fasting is effective in changing the cognitive distortion of the patients that they can not excrete enough urine without furosemide. 4. Since refeeding is started with a low salt and low calorie diet, sodium retention is rarely found. 5. A successful fasting therapy would elevate self-efficacy and in turn improve the behavioral patterns of the patients.

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  • 心身医学

    心身医学 34 (5), 415-421, 1994

    一般社団法人 日本心身医学会

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