Sequential serum enzymes were followed in 12 ponies, eight of which received either continuous (N=4) or short term (N=4) to tansy ragwort (Senecio jacobaea). The disease process in the liver was concurrently monitored in four ponies utilizing percutaneous liver biopsies. The toxic principle, pyrrolizidine alkaloids, caused a progressive hepatopathy characterized by the sequential development of intranuclear inclusions in hepatocytes, biliary hyperplasia, micronecrotic foci, and fibrosis. Gamma glutamyl transferase was the first and most consistent enzyme to rise above control values. Alkaline phosphatase was also elevated in all of the ponies with a definite rise in value prior to death in six of the eight ponies. Glutamate dehydrogenase values elevated above control values in the majority of the ponies (six of eight), but, in general this change occurred early in the disease process. Two clinical patterns of disease progression were evident — a chronic disease process with death in six to 22 weeks (N=4) and a chronic-delayed disease process (N=4) where animals remained clinically normal until just prior to death at 38 to 58 weeks. In the latter cases, veterinarians need to be aware that clinicopathological indices may reflect normalcy in the mid-stage of disease while progressive hepatopathy is occur- ring. Practicalimplications of this study are the need for continued monitoring of animals at risk or recovering from tansy ragwort intoxication and encouragement of the use of percutaneous liver biopsies to evaluate definitive disease progression.
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