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Cases Journal

, 2:46

First Online: 13 January 2009Received: 24 November 2008Accepted: 13 January 2009DOI: 10.1186-1757-1626-2-46

Cite this article as: Manzato, E., Mazzullo, M., Gualandi, M. et al. Cases Journal 2009 2: 46. doi:10.1186-1757-1626-2-46

Abstract

BackgroundIndividuals who suffer from Anorexia Nervosa refuse to maintain a minimally normal body weight, are intensely afraid of gaining weight and exhibit a significant disturbance in the perception of the shape and size of their body. Postmenarchal females with this disorder are amenorrohic. In the Binge-Eating-Purging subtype individuals regularly engage in binge eating and purging behaviour i.e self-induced vomiting or misuse of laxatives, diuretics, or enemas.

Hypokalaemia is often seen in chronic Anorexia Nervosa, especially that of the purging type ANp, and, as well as electrocardiographic anomalies, this can lead to tubulointerstitial nephritis hypokalaemic nephropathy with typical histological characteristics. The physiopathological mechanisms behind this damage are linked to altered stimulation of vasoactive mediators, and to the ammonium-mediated activation of the alternative complement pathway. However, it has not yet been ascertained whether a variant of the pathway specific for ANp 1, exists.

Case presentationWe describe herein a case of hypokalaemic nephropathy in a patient affected by chronic ANp who presented to our Centre for Eating Disorders.

ConclusionHypokalaemia can provoke cardiovascular alterations as well as muscular and renal complications, and thus potential renal damage needs to be investigated in patients suffering from long-term purgative anorexia.

AbbreviationsAnpAnorexia Nervosa, binge-purging type

BMIBody Mass Index

OGDSOesophagogastroduodenoscopy

ACEAngiotensin Converting Enzyme

ET-1Endothelin-1

EDRF-1Endothelium-Derived Relaxing Factor-1

PGE2Prostaglandin E2

APArterial Pressure

ESRDEnd Stage Renal Disease

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Autor: Emilia Manzato - Maria Mazzullo - Malvina Gualandi - Tatiana Zanetti - Giovanni Scanelli

Fuente: https://link.springer.com/







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