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Licensed Unlicensed Requires Authentication Published by De Gruyter June 18, 2014

Acute metformin intoxication: 2012 experience of Emergency Departement of Lodi, Italy

  • Giulia Acquistapace EMAIL logo , Marco Rossi , Mara Garbi , Pablo Cosci , Ciro Canetta , Anna Manelli and Giovanni Ricevuti

Abstract

Background: Metformin is a biguanide antihyperglycemic agent that decreases insulin resistance. It is removed through renal mechanisms and its clearance is reduced in renal failure. Metformin ingestion should always be considered in the differential diagnosis of any patient with metabolic acidosis and increased lactate level. Hemodialysis and continuous veno-venous hemofiltration (CVVH) are both efficient methods to treat metformin intoxication and correct metabolic abnormalities.

Methods: Patient 1: A 63-year-old man with type 2 diabetes mellitus presented to emergency department (ED) of Lodi (Italy) for dyspnea. He also reported having diarrhea for 10 days. Initial investigations revealed metabolic acidosis with hyperlactatemia and hypoglycemia (54 mg/dL), metformin concentration was 41 μg/mL (normal value <4 μg/mL). His hemodynamic condition became rapidly unstable and hypotension worsened despite CVVH being performed. Death occurred in 24 h. Patient 2: A 76-year-old man with type 2 diabetes mellitus presented to ED of Lodi for dyspnea. He referred a recent surgery amputation of the left foot’s fifth phalanx for osteomyelitis, in levofloxacin therapy. Initial investigations revealed metabolic acidosis with hyperlactatemia and severe hypoglycemia (20 mg/dL). Two hemodialysis sessions were performed with complete normalization of the serum concentration of metformin.

Results and conclusions: In our two cases the genesis of metformin intoxication was clear, powered by acute renal failure, but less obvious was the etiology of acute renal damage responsible for metformin accumulation. Damage due to renal hypoperfusion or the direct toxic effect of metformin should be considered. Additionally, for the second patient, we can also hypothesize that interstitial nephritis was exacerbated by levofloxacin.


Corresponding author: Giulia Acquistapace, MD, Università degli Studi di Pavia, Scuola di Specializzazione in Medicina d’Emergenza-Urgenza, via Emilia, 10/12, 2700 Pavia, Italy, Phone: +39 0371 372057, E-mail:

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Received: 2014-2-25
Accepted: 2014-5-16
Published Online: 2014-6-18
Published in Print: 2014-10-1

©2014 by De Gruyter

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