Page 1585 - Clinical Small Animal Internal Medicine

172 Metabolic Bone Diseases 1523

calcium and increased phosphorus in the diet. The most Serum separator tubes should not be used as they lead
VetBooks.ir frequent cause of nutritional FOD is an all‐meat diet. to decreased PTH concentrations. In addition, visible
hemolysis of the sample interferes with the assay.
The ideal Ca:P ratio of a diet is 1:1. Meat and liver have
Second, there are several different assays available for
calcium to phosphorus ratios of 1:20 and 1:50 respec­
tively, and a diet based solely on these components can measuring PTH, including radioimmunoassays (RIA/
lead to clinical signs of FOD within four weeks. ERMA) and enzyme immunoassays (EIA/ELISA). In
Animals with nutritional hyperparathyroidism most addition, assays are available for whole PTH (W‐PTH),
commonly present with an ill‐defined lameness, disincli­ intact PTH, N‐terminal fragment of PTH, and C‐terminal
nation to move, and a failure to thrive. Some animals fragment of PTH. PTH undergoes proteolysis in the
may have angular limb deformities. In more severe cases, liver, blood, and other organs, forming N‐terminal and
pathologic fractures may occur with only mild trauma. C‐terminal fragments. The N‐terminal PTH fragment
Resorption of alveolar bone in the mandible and maxilla cannot bind to the PTH receptor and so does not elicit
may lead to loosening of teeth. A few animals may the classic response to PTH; it is in fact thought to inhibit
develop vertebral compression fractures, which in some PTH action. N‐terminal PTH fragments are increased in
cases may lead to neurologic signs. While another term chronic renal failure.
for fibrous osteodystrophy is rubber jaw, this is usually The W‐PTH assay is a third‐generation PTH assay
only seen in severe prolonged cases, and is more com­ that is specific for whole 1‐84 PTH, while the I‐PTH is a
mon in young animals with familial renal disease and second‐generation assay that, in addition to measuring
renal secondary hyperparathyroidism, rather than nutri­ 1‐84 PTH, also measures large N‐terminal PTH frag­
tional hyperparathyroidism. ments. Human two‐site RIA/IRMAs for I‐PTH have
been validated in both cats and dogs, as has a combined
W‐PTH/I‐PTH assay. Human EIAs may not cross‐react
Diagnosis
with canine or feline PTH. Canine‐specific I‐PTH ELISA
Biochemistry assays are also available. Reference ranges are assay spe­
Animals with nutritional fibrous osteodystrophy have cific and ideally should not be extrapolated from other
low to low‐normal plasma total and ionized calcium types/brands of assay.
concentrations. The calcium deficiency in the diet The third important point is that ionized calcium, total
stimulates PTH release, which subsequently leads to calcium, and phosphorus concentrations should be
osteoclastic resorption of calcium from bone, thereby measured on the same sample as PTH. These analytes
maintaining plasma calcium concentration to the detri­ are essential for the interpretation of the plasma PTH
ment of bone mineral content. If the dietary deficiency of concentration.
calcium is severe or the amount of calcium released from
the bones is inadequate then the dog or cat will have Radiography
hypocalcemia. The predominant change seen on radiography is gener­
The increased PTH concentration leads to increased alized osteopenia of all bones. It may be most obvious in
excretion of phosphorus from the kidney, and so results those bones with a greater proportion of cancellous bone
in an increase in the fractional excretion of phosphorus. which is more readily resorbed, such as the vertebrae.
Depending on the balance of dietary intake to renal The mandible may show a marked reduction in bone
excretion, plasma phosphorus concentrations may be density, particularly the alveolar bone around the teeth
low, normal or increased. (Figure 172.1). There may be evidence of pathologic frac­
Serum alkaline phosphatase concentrations are tures (see Figure 172.1), such as compression fractures in
increased due to increased bone remodeling but, along the vertebrae and infractions in the long bones. In more
with the phosphorus concentration, need to be inter­ severe cases, there may be complete fracture of the long
preted with caution as both may be increased in younger bones. The growth plates are normal in animals with
animals due to growth. fibrous osteodystrophy, but there may be increased radi­
Plasma intact PTH concentration will be increased but oopacity in the primary spongiosa directly beneath the
there are a number of cautions to be considered when growth plate (see Figure 172.1). The cortices appear
interpreting plasma PTH concentrations. The first is thinner and more porous. The limbs may show angular
collection of the sample. PTH is highly susceptible to deformities, and lordosis of the spine can be present.
proteolysis, so serum or plasma should be separated New technology such as dual‐energy X‐ray absorpti­
from red cells immediately (samples should be at room ometry (DEXA/DXA) and computed tomography (CT)
temperature for less than two hours) and tested directly, give a more accurate assessment of bone mineral density
refrigerated for no more than 24 hours or stored frozen than plain radiographs. Bone mineral density must be
at –20 °C. Samples should be shipped chilled/frozen. decreased by more than 30% before it is detected on