Myopathy in a Haflinger horse: An initiating search for a fatty acid oxidation deficiency

Abstract

SummarySo far, the area of fat metabolism disturbances has been poorly explored in the horse but, as in man, deficiencies in the β‐oxidation of fatty acids (FAOX) and in carnitine metabolism or carnitine transport potentially can be a cause of myopathy. A 9‐year‐old Haflinger patient with recurrent rhabdomyolysis and 5 healthy horses of various breeds with a mean age of 16 ± 5.9 years were used as a comparison. Blood biochemical analysis revealed elevated aspartate amino transferase, lactate dehydrogenase and creatine kinase activities. Plasma vitamin E concentration was low and selenium was within the reference range. Quantitative electromyography was indicative of myopathy based on the short duration and low amplitude motor unit action potentials. Staining of muscle biopsies was suggestive for a myopathy based on a disturbance in fat catabolism. Carnitine, acylcarnitines, very‐long‐chain fatty acids and organic acids screening in blood and urine established no differences between these parameters in the patient and control horses. Even though this patient was negative on FAOX or carnitine disturbances, the potency of the applied methods seems large and indicates a potential diagnostic value.