Effect of oral administration of excessive iron in adult ponies

Citation
Eg. Pearson et Cb. Andreasen, Effect of oral administration of excessive iron in adult ponies, J AM VET ME, 218(3), 2001, pp. 400-404
Citations number
27
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION
ISSN journal
00031488 → ACNP
Volume
218
Issue
3
Year of publication
2001
Pages
400 - 404
Database
ISI
SICI code
0003-1488(20010201)218:3<400:EOOAOE>2.0.ZU;2-5
Abstract
Objective-To evaluate the potential of excess dietary iron to cause hepatic lesions similar to those described in horses with suspected iron toxicosis or hemochromatosis. Design-Prospective study. Animals-6 adult male ponies. Procedure-4 ponies received 50 mg of iron/kg (22.7 mg/lb) of body weight ea ch day by oral administration of ferrous sulfate, which contained 20% eleme ntal iron; 2 ponies received only the carrier (applesauce). Complete blood counts, serum biochemical analyses, and hepatic tissue biopsies were perfor med, and serum iron concentrations were measured. Blood and tissue samples were obtained at days 0 and 2. and at the end of weeks 1, 3, 6, and 8 after administration of iron was initiated. Treatment was discontinued after 8 w eeks, and hepatic iron concentrations were measured at 28 weeks. Results-Hepatic iron concentrations, serum iron concentrations, percentage saturation of transferrin, and serum ferritin concentrations were increased , compared with baseline and control concentrations, by week 8. Adverse cli nical signs or histologic lesions in the liver were not detected in any pon ies. At 28 weeks, hepatic iron concentrations had decreased. Conclusions and Clinical Relevance-Histologic lesions were not seen in the hepatic biopsy specimens obtained from the ponies treated with ferrous sulf ate. It was concluded that it would be unlikely for iron toxicosis to devel op in adult ponies or horses during a period of < 8 weeks when food or wate r contained increased amounts of iron. It is suspected that previous report s of hepatopathies in animals with hemosiderin accumulation may represent a primary hepatopathy with secondary hemosiderin accumulation, especially if the only source of iron is via oral consumption.