INVESTIGATING IRON STATUS
Serum iron concentrations can be inexpensively determined by using ferrozine-based methods. Samples must be collected carefully
to avoid ex vivo hemolysis, which may affect accuracy. However, low serum iron concentrations have poor specificity for IDA.
In many patients with chronic inflammatory, infectious, or neoplastic conditions, iron is sequestered in the bone marrow and
reticuloendothelial organs, and serum concentrations may fall below the reference range despite adequate iron stores.
This process appears to be triggered, at least in part, by increased hepcidin concentrations. This peptide hormone is produced
by the liver and plays a key role in iron homeostasis, uptake, and distribution.7 It is thought that inflammatory cytokines promote production of hepcidin.
Concurrent determination of total iron-binding capacity along with serum iron concentrations is necessary to confirm IDA.2 If iron is truly scarce, total iron-binding capacity usually increases and percent saturation falls to < 20%.
Serum ferritin concentrations are a more accurate way to assess iron status and are not affected by hemolysis. Ferritin is
an intracellular protein that stores iron in a nontoxic form and then releases it as needed. Under steady state conditions,
serum ferritin concentrations correlate reliably with total body iron stores.2 Species-specific ferritin assays are routinely offered by reference laboratories but are likely to cost more than the measurement
of serum iron concentrations.
In people, decreased reticulocyte volumes and subnormal reticulocyte hemoglobin concentrations have been shown to indicate
iron deficiency. These parameters have not been looked at extensively in veterinary patients, although one study in dogs suggests
that they may be a useful method to assess iron status in this species.8 Reference laboratories may be able to supply this information upon request.
Iron stores within the bone marrow can be readily assessed on examination of an aspirate or biopsy sample using special stains
such as Prussian blue. However, unless there is another reason to evaluate the bone marrow, noninvasive tests are preferable.
Iron supplementation and blood transfusion can rapidly affect the laboratory diagnosis of IDA. These therapies should be withheld
until appropriate samples have been collected.
CAUSES OF IDA
There are essentially only three causes of IDA: inadequate intake, compromised absorption, and chronic blood loss. Of these,
chronic blood loss is the most common cause of IDA in companion animals.
Because of growth and increased erythropoiesis, neonates have a higher need for dietary iron than adults do.1 Milk contains relatively little iron, so juveniles with even moderate parasitism may rapidly become iron-deficient. Adult
animals receiving unbalanced homemade diets, particularly vegetarian or vegan diets, are vulnerable to IDA. A life-stage-appropriate
diet approved by the Association of American Feed Control Officials should contain adequate amounts of iron to meet routine
Dietary iron is absorbed in the proximal small intestine through a protein called ferroportin. Uptake is adjusted to match need through hepcidin.7 When iron is abundant, hepcidin prevents enterocyte secretion of absorbed iron into the portal circulation. This surplus
iron is then simply lost from the body through normal enterocyte turnover. IDA has been reported in dogs with severe inflammatory
bowel disease, although it is unclear if iron deficiency in these patients was due to compromised iron absorption, occult
gastrointestinal (GI) blood loss, or a combination of both.9
Chronic blood loss can occur through the skin (e.g. severe flea infestation) or respiratory, urinary, or GI tracts. In general, patients with respiratory or urinary loss are
likely to have overt clinical signs, such as coughing, nasal discharge, dysuria, or gross hematuria, and are presented for
medical attention before IDA occurs. Animals with GI blood loss may experience vomiting, diarrhea, or hyporexia but are often
apparently well before signs related to anemia are noted.
Melena, characterized by a dark tarry stool, is a reliable indicator of blood loss through the GI tract but is only noted
when a substantial volume of blood enters the GI tract at one time. Studies have shown that about 500 mg/kg of hemoglobin
must enter the GI tract before melena is noted; that equates to about 100 ml of blood in a medium-sized dog.10 A patient with gradual-but-persistent loss from an ulcerative lesion may never have melenic stools.