Page 933 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

908 CHAPTER 6

VetBooks.ir Table 6.3 Diets associated with increased risk of nutritional secondary hyperparathyroidism

• Grain with high phosphorous content and poor to average hay (i.e. oats [Ca 0.07%, P 0.37%] and grass hay [Ca 0.3%, P 0.3%])
• Increased grain to roughage ratio
• Supplementation with rice or wheat bran (i.e. rice bran [Ca 0.04%, P 1.8%] and wheat bran [Ca 0.12%, P 1.43%])
• Pasture or hay with oxalate:calcium ratios >0.5% (i.e. Setaria, Argentine or Dallas grass, and buffalo grass)

6.7 Horses that develop hypercalcaemia associated
with primary hyperparathyroidism have vague
clinical signs such as poor appetite and shifting
leg lameness. There are no clinical signs that are
specific for high blood calcium concentrations.

Differential diagnosis
Differential diagnoses for hypercalcaemia include
renal failure, primary hyperparathyroidism, nutri-
tional secondary hyperparathyroidism, vitamin D
toxicoses and malignancy (pseudohyperparathyroid-
ism). Intestinal parasitism should be considered in a
thin, young horse that is primarily unthrifty. Physitis
Fig. 6.7 Young horse with nutritional secondary should also be considered in a young horse with stiff-
hyperparathyroidism. Note the thin, unthrifty ness or pain in multiple limbs. However, if coarse
appearance and the enlarged head.
facial features are present, nutritional secondary
hyperparathyroidism should be strongly suspected.
phosphorous is unchanged (i.e. not increased),
because parathyroid hormone also promotes renal Diagnosis
tubular excretion of phosphate (although vitamin A PTH panel, which consists of measuring PTH,
D inhibits it). Chronic stimulation of the parathy- ionised calcium and PTH-related peptide, should
roid gland results in parathyroid gland hypertrophy be submitted when evaluating a horse with sus-
and hyperplasia. The net result is maintenance of a pected parathyroid disease. Comparisons between
normal serum calcium level at the expense of bone those constituents may assist clinicians in reaching
resorption. Primary hypoparathyroidism is an idio- a final diagnosis. A complete dietary history should
pathic condition in horses that results in profound be reviewed for evidence of a possible calcium/
life-threatening hypocalcaemia. phosphorous imbalance. Bone demineralisation can
be appreciated on radiographs once the bones are at
Clinical presentation least 30% demineralised; this occurs first in the skull
Affected horses usually look unthrifty (Fig. 6.7). (Fig. 6.8). Initially, there is decreased density of the
Clinical signs mainly involve the appendicular skel- laminae durae dentes, followed by decreased density
eton, the teeth and the skull. Bone demineralisation of the facial bones. In less advanced cases and in the
results in a stiff gait, lameness, painful joints, loose absence of concurrent renal disease, diagnosis can
teeth and painful mastication. Pathological fractures be made by measuring increased PTH or increased
can occur. Demineralisation and fibrous prolifera- fractional excretion of phosphorous in the urine
tion (hyperostotic fibrous osteodystrophy) in the (Table 6.4). Normal fractional excretion of phospho-
skull result in firm enlargements of the facial bones rous is 0.0–0.5%. Fractional excretion of phospho-
dorsocaudal to the facial crest, thickening of the rous of >0.5% is suggestive of nutritional secondary
mandibles and thickening of the nasal bones, even- hyperparathyroidism, and fractional excretion of
tually resulting in nasal obstruction. phosphorous of >4% is diagnostic. It is important