| Threshold for toxicity from hyperammonemia in critically ill children. | |
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MedLine Citation:
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PMID: 21703182 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND & AIMS: Hyperammonemia results from reduction of hepatocyte function or enzyme of urea cycle deficiency. Hyperammonemia contributes to cerebral edema that may lead to cerebral herniation. The threshold of toxicity of ammonemia is unknown. METHODS: We conducted a retrospective observational study in our pediatric intensive care unit. All children who developed hyperammonemia from January 2000 to April 2009 were included. Clinical and laboratory data at admission, specific treatments implemented, and ammonemias the first 7 days after inclusion were collected. The outcome assessed was 28 day mortality. Risk of mortality was estimated by a logistic regression model. RESULTS: Ninety patients with liver failure (63.3%) and primary or secondary urea cycle defect (23.3%) were included. Patients with urea cycle defects were more likely to receive ammonia scavengers than patients with liver failure (47.6% versus 3.5%). The 28 day mortality rate was 31.1%. Risk of mortality increased according to the ammonemia within 48 h: odds ratio 1.5, 1.9, 3.3, 2.4 for ammonemia above 100, 150, 200, and 300 μmol/L, respectively. Peak ammonemia ≥200 μmol/L within the first 48 h was an independent risk factor for mortality, with greater risk found in liver failure than in urea cycle defect. CONCLUSIONS: Our study identifies a threshold of exposure to ammonia (≥200 μmol/L) above which mortality increases significantly, especially in liver failure. Specific treatments of hyperammonemia are rarely used in liver failure when compared with urea cycle defect even though use of ammonia scavengers may help to decrease ammonemia. |
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Authors:
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Bruno Ozanne; John Nelson; Jocelyne Cousineau; Marie Lambert; Véronique Phan; Grant Mitchell; Fernando Alvarez; Thierry Ducruet; Philippe Jouvet |
Publication Detail:
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Type: Journal Article Date: 2011-05-18 |
Journal Detail:
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Title: Journal of hepatology Volume: 56 ISSN: 1600-0641 ISO Abbreviation: J. Hepatol. Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2011-12-16 Completed Date: 2012-05-21 Revised Date: 2012-08-24 |
Medline Journal Info:
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Nlm Unique ID: 8503886 Medline TA: J Hepatol Country: England |
Other Details:
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Languages: eng Pagination: 123-8 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved. |
Affiliation:
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CHU Sainte-Justine, Soins Intensifs, 3175 Chemin de la Côte Sainte-Catherine, Montréal (QC), Canada H3T 1C5. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Ammonia
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blood Brain Edema / etiology, physiopathology Child Child, Preschool Critical Illness Encephalocele / etiology, physiopathology Female Humans Hyperammonemia / complications, etiology, mortality, physiopathology* Infant Kaplan-Meier Estimate Liver Failure, Acute / complications, physiopathology Male Retrospective Studies Risk Factors Urea Cycle Disorders, Inborn / complications, physiopathology |
| Chemical | |
Reg. No./Substance:
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7664-41-7/Ammonia |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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