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PseudoBartter syndrome in eating disorders

Authors

  • Amit Bahia MD, MPH,

    Corresponding author
    1. The A.C.U.T.E Center for Eating Disorders, Department of Medicine, Denver Health, Denver, Colorado
    2. Department of Medicine, University of Colorado Denver School of Medicine, Denver, Colorado
    • Department of Medicine, Denver Health, 660 Bannock Street, MC 4000, Denver, CO 80204
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  • Margherita Mascolo MD,

    1. The A.C.U.T.E Center for Eating Disorders, Department of Medicine, Denver Health, Denver, Colorado
    2. Department of Medicine, University of Colorado Denver School of Medicine, Denver, Colorado
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  • Jennifer L. Gaudiani MD,

    1. The A.C.U.T.E Center for Eating Disorders, Department of Medicine, Denver Health, Denver, Colorado
    2. Department of Medicine, University of Colorado Denver School of Medicine, Denver, Colorado
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  • Philip S. Mehler MD

    1. The A.C.U.T.E Center for Eating Disorders, Department of Medicine, Denver Health, Denver, Colorado
    2. Department of Medicine, University of Colorado Denver School of Medicine, Denver, Colorado
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Abstract

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. © 2011 by Wiley Periodicals, Inc. (Int J Eat Disord 2012)

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