Equine Veterinary Data, Vol. 13, No. 12, 1992
Report by: Drs. Warwick M. Bayly and Gary P. Carlson
Speaking at the 10th Annual ACVIM Forum in San Diego, CA, Dr. Gary P. Carlson said iron is an essential structural component of vitally important biologic compounds such as hemoglobin, myoglobin, mitochondrial cytochrome and a variety of enzymes. Free iron is, however, an extremely reactive element that can catalyze free radical formation from molecular oxygen and hydrogen ions with disastrous consequences for biologic materials.
Animals have developed sophisticated mechanisms to conserve this essential element and at the same time to maintain iron in a safely bound or chelated form. Iron is one of the few elements for which internal balance is maintained by controlling intestinal absorption of dietary intake, rather than regulating excretion. The body does not have a regular means of excreting or eliminating excess iron when iron accumulates as a consequence of excessive iron administration or blood transfusion. Iron overload has been shown to cause acute massive hepatic necrosis in certain circumstances in calves, lambs and foals. Iron accumulation as the result of hemochromatosis in humans is reported to result in chronic liver damage. A critical balance must be maintained between the body's absolute requirement for iron and protection of the body from the potential adverse effects of iron overload.
Hematologic parameters, particularly the erythrocyte count, hemoglobin concentration and packed cell volume (PCV) have been used as indexes of readiness to race and performance potential. It has been recognized that when these parameters are abnormal, either too high or too low, horses often perform below expectation. Iron supplementation in the diet and or by parenteral injection is an almost universal practice for Thoroughbred horses in race training in North America.
The precise iron requirement of athletic horses has never been determined. There is some evidence from published studies that iron overload may be common in racehorses. However, these limited studies were not conducted on healthy horses in training, but were obtained from samples drawn from horses hospitalized in university veterinary hospitals for a variety of medical problems.
A variety of laboratory procedures have been used to assess iron status of humans and animals. While all these procedures have their indications, it is important to realize that they all have certain limitations. The classic hematologic description of iron deficiency anemia is a microcytic, hypochromic anemia. In adult horses these hematologic features are rarely recognized. These features occur only in the very late stages of profound iron depletion, which is usually the result of chronic blood loss. Additionally, other deficiencies or conditions which inhibit hemoglobin synthesis can result in similar hematologic findings.
Perhaps the earliest indication of iron depletion can be found in the evaluation of marrow iron with Prussian Blue staining. This subjective evaluation of iron stored does not provide a quantitative result but, in the hands of experienced individuals, can yield valuable information. However, bone marrow collection and evaluation does not lend itself to surveys of horses in race training. Serum ferritin has been suggested as a reliable guide to the status of iron stores in the liver, but has not yet been widely employed in veterinary medicine.
The most practical and useful procedures for the evaluation of iron status is the determination of serum iron and iron binding capacity. These parameters provide a measure of iron in the transport compartment. Transferrin, the iron transport protein in the serum, can be measured with special procedures. However, serum iron binding capacity is easier to determine and is generally used as an indirect, but very useful, estimate of transferrin. Ordinarily, about one-third of transferrin is saturated with iron. Normal serum iron is approximately 120 Fg/dl while iron binding capacity is 300-350 Fg/dl in most species. Fairly marked iron deficiency results in decreases in serum iron, while the iron binding capacity is often elevated. These changes may be noted in iron deficiency prior to the development of microcytosis or hypochromasia. Iron overload is characterized by increases in serum iron.
Carlson heads a research project where data was collected from a large group of horses in training. Most of the horses were relatively young, with maidens accounting for nearly one-third of the horses sampled. Over half of the horses had received intravenous iron during the 3 months prior to sampling. There was no significant relationship between the trainers perception of performance and serum iron. Interestingly, there were no significant differences in serum iron between horses which had never received injectable iron and horses that occasionally or regularly received parenterally administered iron.
Overall the serum iron and iron binding capacity of these horses in training were remarkably similar to values reported for clinically normal sedentary horses. Only a few horses were judged to be anemic, and none had low serum iron. Dietary iron supplementation was practiced by most trainers, and in many instances this supplementation seemed excessive. However, iron overload, as judged by serum iron concentration, did not appear to be a common problem in the group of horses sampled.