OBJECTIVE: PseudoBartter's syndrome, a complex pattern of seemingly unrelated metabolic abnormalities, is frequently seen in patients with eating disorders, particularly those who indulge in purging behaviors. We present two cases that, despite divergent background histories and clinical presentations, possess the unifying pathophysiology that ultimately leads to this syndrome. METHOD: Case report and review of literature pertaining to Bartter's and PseudoBartter's syndromes. RESULTS: Purging behaviors commonly result in a state of profound dehydration and chloride depletion that leads to the metabolic abnormalities characteristic of inheritable sodium and chloride renal tubular transport disorders. In the eating disorder patient, these abnormalities lead to a propensity towards marked edema formation. DISCUSSION: The metabolic and clinical manifestations of PseudoBartter's syndrome are seen more commonly than previously thought. It is important to appreciate that a complex self-perpetuating pathophysiology leads to the hypokalemic metabolic alkalosis characteristic of PseudoBartter syndrome. The metabolic abnormalities characteristic of this phenomenon should therefore be viewed in this context and the resulting predilection towards marked edema formation should be borne in mind.
OBJECTIVE:PseudoBartter's syndrome, a complex pattern of seemingly unrelated metabolic abnormalities, is frequently seen in patients with eating disorders, particularly those who indulge in purging behaviors. We present two cases that, despite divergent background histories and clinical presentations, possess the unifying pathophysiology that ultimately leads to this syndrome. METHOD: Case report and review of literature pertaining to Bartter's and PseudoBartter's syndromes. RESULTS: Purging behaviors commonly result in a state of profound dehydration and chloride depletion that leads to the metabolic abnormalities characteristic of inheritable sodium and chloriderenal tubular transport disorders. In the eating disorderpatient, these abnormalities lead to a propensity towards marked edema formation. DISCUSSION: The metabolic and clinical manifestations of PseudoBartter's syndrome are seen more commonly than previously thought. It is important to appreciate that a complex self-perpetuating pathophysiology leads to the hypokalemic metabolic alkalosis characteristic of PseudoBartter syndrome. The metabolic abnormalities characteristic of this phenomenon should therefore be viewed in this context and the resulting predilection towards marked edema formation should be borne in mind.