Creatine kinase, hypoglycin A, MCPA-carnitine and acylcarnitines in horses with atypical myopathy

Kód výsledku v IS VaVaI

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Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Creatine kinase, hypoglycin A, MCPA-carnitine and acylcarnitines in horses with atypical myopathy

Popis výsledku v původním jazyce

Atypical myopathy (AM) is a potentially fatal disease of grazing horses caused by the ingestion of sycamore seeds or seedlings containing hypoglycin A (HGA). HGA is transformed into toxic (methylenecyclopropyl)acetyl-CoA (MCPA-CoA), which inhibits acyl-CoA dehydrogenases that are necessary for fatty acid oxidation. The disease is expressed clinically as rhabdomyolysis accompanied by the elevation of creatine kinase (CK) activity and acylcarnitines (AC) concentrations in the blood of affected horses. The diagnosis of AM is based on the identification of elevated CK activity, accumulation of AC and the presence of MCPA-carnitine or HGA in the blood. However, the dynamics of change in these parameters during the disease are not known. Objectives: The aim of the retrospective study was to describe changes in CK activity, MCPA-carnitine, HGA and AC concentrations in the blood of horses with AM during the process of the disease. Methods: Jugular blood samples were collected from 18 horses affected by AM at various stages of the disease. Serum CK activity was measured in 72 serum samples, MCPA-carnitine, HGA and AC concentrations in 61 dry blood spots. These compounds were measured by flow injected analysis and liquid chromatography both coupled with tandem mass spectrometry. Results: Increased CK activity, MCPA?carnitine and HGA were detected in the blood in all horses. Ten of them survived (S group), five horses were euthanized, and three horses died (E + D group). The mean ? SD of peak CK activity in the S group was 243 288 ? 206 729 iu/l, in the E + D group 417 982 ? 317 594 iu/l. In all horses of the S group the elevation of CK activity persisted till the end of treatment (48 hours-17 days). The duration of MCPA-carnitine presence in the blood was variable in horses of the S group: it was present 7 days after the onset of clinical signs in one horse but was not detected 36 hours after the onset of clinical signs in another horse. AC concentrations (especially C2-C10) were elevated and decreased with ongoing recovery. HGA level was detected even 17 days after the onset of clinical signs. Conclusions: The elevation of CK activity and the presence of HGA in horses with AM persists after regression of clinical symptoms. Concentrations of MCPA-carnitine are variable, and in horses with ingestion of low doses of toxin can disappear within 48 hours. These dynamics can influence laboratory confirmation of AM.

Název v anglickém jazyce

Creatine kinase, hypoglycin A, MCPA-carnitine and acylcarnitines in horses with atypical myopathy

Popis výsledku anglicky

Atypical myopathy (AM) is a potentially fatal disease of grazing horses caused by the ingestion of sycamore seeds or seedlings containing hypoglycin A (HGA). HGA is transformed into toxic (methylenecyclopropyl)acetyl-CoA (MCPA-CoA), which inhibits acyl-CoA dehydrogenases that are necessary for fatty acid oxidation. The disease is expressed clinically as rhabdomyolysis accompanied by the elevation of creatine kinase (CK) activity and acylcarnitines (AC) concentrations in the blood of affected horses. The diagnosis of AM is based on the identification of elevated CK activity, accumulation of AC and the presence of MCPA-carnitine or HGA in the blood. However, the dynamics of change in these parameters during the disease are not known. Objectives: The aim of the retrospective study was to describe changes in CK activity, MCPA-carnitine, HGA and AC concentrations in the blood of horses with AM during the process of the disease. Methods: Jugular blood samples were collected from 18 horses affected by AM at various stages of the disease. Serum CK activity was measured in 72 serum samples, MCPA-carnitine, HGA and AC concentrations in 61 dry blood spots. These compounds were measured by flow injected analysis and liquid chromatography both coupled with tandem mass spectrometry. Results: Increased CK activity, MCPA?carnitine and HGA were detected in the blood in all horses. Ten of them survived (S group), five horses were euthanized, and three horses died (E + D group). The mean ? SD of peak CK activity in the S group was 243 288 ? 206 729 iu/l, in the E + D group 417 982 ? 317 594 iu/l. In all horses of the S group the elevation of CK activity persisted till the end of treatment (48 hours-17 days). The duration of MCPA-carnitine presence in the blood was variable in horses of the S group: it was present 7 days after the onset of clinical signs in one horse but was not detected 36 hours after the onset of clinical signs in another horse. AC concentrations (especially C2-C10) were elevated and decreased with ongoing recovery. HGA level was detected even 17 days after the onset of clinical signs. Conclusions: The elevation of CK activity and the presence of HGA in horses with AM persists after regression of clinical symptoms. Concentrations of MCPA-carnitine are variable, and in horses with ingestion of low doses of toxin can disappear within 48 hours. These dynamics can influence laboratory confirmation of AM.

Druh

O - Ostatní výsledky

CEP obor

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OECD FORD obor

40301 - Veterinary science

Projekt

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Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2020

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů