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.