Acylcarnitines profile best predicts survival in horses with atypical myopathy.

François Boemer,Eric Richard,Gaby Van Galen,Johann Detilleux,Dominique-Marie Votion,Hélène Amory,Laurence Lefère,Christophe Cello,Gunther Van Loon,Christel Marcillaud-Pitel

doi:10.1371/journal.pone.0182761

François Boemer, Eric Richard + Show 8 more

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https://doi.org/10.1371/journal.pone.0182761

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Abstract

Equine atypical myopathy (AM) is caused by hypoglycin A intoxication and is characterized by a high fatality rate. Predictive estimation of survival in AM horses is necessary to prevent unnecessary suffering of animals that are unlikely to survive and to focus supportive therapy on horses with a possible favourable prognosis of survival. We hypothesized that outcome may be predicted early in the course of disease based on the assumption that the acylcarnitine profile reflects the derangement of muscle energetics. We developed a statistical model to prognosticate the risk of death of diseased animals and found that estimation of outcome may be drawn from three acylcarnitines (C2, C10:2 and C18 -carnitines) with a high sensitivity and specificity. The calculation of the prognosis of survival makes it possible to distinguish the horses that will survive from those that will die despite severe signs of acute rhabdomyolysis in both groups.

Highlights

Equine atypical myopathy (AM) is caused by hypoglycin A intoxication resulting from the ingestion of seeds or seedlings of certain Acer tree species, principally Acer pseudoplatanus in Europe [1,2,3]
These acyl-CoAs may be scavenged into acylcarnitines which subsequently leave the mitochondrion and reach the peripheral circulation leading to, in AM affected horses, a characteristic blood acylcarnitine profile consistent with a multiple acyl-CoA dehydrogenase
51 horses suspected of AM and for which blood samples were available were confirmed to be AM cases based on a MADD phenotype

Summary

Introduction

Equine atypical myopathy (AM) is caused by hypoglycin A intoxication resulting from the ingestion of seeds or seedlings of certain Acer tree species, principally Acer pseudoplatanus (sycamore maple) in Europe [1,2,3]. Acyl-CoA dehydrogenases catalyse the initial step in each cycle of fatty acid βoxidation and their reduced activity leads to accumulation of acyl-CoAs in the mitochondria. These acyl-CoAs may be scavenged into acylcarnitines which subsequently leave the mitochondrion and reach the peripheral circulation leading to, in AM affected horses, a characteristic blood acylcarnitine profile consistent with a multiple acyl-CoA dehydrogenase.

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