Page 180 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

170 ELECTROLYTE DISORDERS

dietary intake of phosphorus was mildly below the mini- to stand. In puppies that were radiographed, osteopenia
mal requirements in five of six cats. An unfavorable was noted, with pathologic fractures apparent in multiple
calcium to phosphorus ratio existed for all diets. long bones. In euthanized puppies, the long bones were
A case of type 2 vitamin D-dependent rickets was pliable, and cortices were thin. Parathyroid glands were
described in a 5-month-old Pomeranian dog with inter- prominent, and histologically, fibrous osteodystrophy
mittent lameness, and forelimb bowing and was present in bones. Nutritional secondary hyperpara-
thickening. 326 Vitamin D-dependent rickets type 2 is thyroidism was attributable to a diet low in calcium and
characterized by end-organ resistance to calcitriol. This an inappropriate calcium to phosphorus ratio. Diffuse
puppy was fed a commercial puppy food and had persis- osteopenia and myelopathy occurred in a puppy fed a
tent hypocalcemia with elevated PTH concentration. raw ground beef diet. 557 This 8-month old puppy had
Despite high-dose calcitriol therapy, hypocalcemia been fed a commercially available organic premix mixed
persisted. A case of type 2 vitamin D-dependent rickets with ground beef for the previous 4 months. Vitamin
was described in a 4-month-old cat examined because D-dependent rickets Type I developed following the
of vomiting, diarrhea, muscle tremors, and mydriasis of feeding of this nutritionally incomplete diet. While young
acute onset. 522 Serum tCa and tMg concentrations were animals may be more susceptible to nutritional secondary
decreased, and serum phosphorus, calcitriol, and PTH hyperparathyroidism, clinical signs can occur in adult
concentrations were increased, excluding hypoparathy- dogs fed incomplete diets. Osteopenia occurred in a
roidism as the cause of hypocalcemia. Calcitriol and cal- 6-year-old dog that had been fed a homemade diet for
cium salt supplementation resulted in the return to the previous year. 136 This homemade diet did not include
normocalcemia. Another case of vitamin D-dependent any vitamin or mineral supplements, and was deficient in
556
rickets type 2 was described in a 4-month-old kitten. both calcium and vitamin D. Plasma PTH concentration
In this kitten, serum iCa concentration was low, with was elevated, and circulating 25-hydroxyvitamin D con-
elevations of both PTH and calcitriol. Serum concentra- centration was low. Severe osteopenia of the skull bones
tion of 25-hydroxyvitamin D was within the reference was present, with facial enlargement.
range. The kitten was smaller than its littermates, had
bilateral forelimb swelling, and a hunched appearance. Secondary Hyperparathyroidism
Even with calcitriol therapy, the kitten failed to grow, Associated with Hyperadrenocorticism
had continual hypocalcemia, and died of unknown causes Hyperadrenocorticism has been associated with
7 months after diagnosis. elevations in serum PTH concentration. 461 In 68 dogs
Vitamin D-dependent rickets type 1 has been with hyperadrenocorticism, 92% had concentrations of
described in a 5-month-old kitten. 210 Vitamin D-depen- serum PTH above the reference range. Ionized calcium
dent rickets type 1 is characterized by a deficiency of was measured in 28 of these dogs, and was within or
1a-hydroxylase, which converts 25-hydroxyvitamin D to below the reference range in 20 dogs. However, the mean
calcitriol. The kitten was examined because of generalized iCa concentration in dogs with hyperadrenocorticism was
pain and reluctance to move. This kitten exhibited not significantly different from a group of 20 other hos-
hypocalcemia, elevated serum PTH concentration, with pital patients that did not have hyperadrenocorticism.
low serum calcitriol concentration. The serum concentra- Serum PTH concentration was significantly positively
tion of 25-hydroxyvitamin D was within the reference correlated to basal and post-ACTH cortisol
range. The kitten responded to calcitriol therapy. concentrations, and to serum alkaline phosphatase
Exotic animals may be at increased risk for the devel- concentration. The mechanism for the development of
opment of nutritional secondary hyperparathyroidism secondary hyperparathyroidism is unknown in these
because nutritional requirements are not always known. dogs, though glucocorticoids can decrease intestinal
Nutritional secondary hyperparathyroidism was absorption of calcium and increase urinary calcium
documented in a 3-month-old tiger cub that was fed only excretion. These effects may be sufficient to create a
beef with no calcium or vitamin supplementation. 622 This negative calcium balance, resulting in increased secretion
tiger cub was reluctant to walk, exhibited osteodystrophy of PTH.
of the lumbosacral vertebrae, and had an elevated serum The effect of trilostane treatment for hyperadreno-
PTH concentration. Clinical signs improved after admin- corticism on serum PTH and calcium concentrations was
istration of vitamin D and calcium. studied in 22 dogs. 559 With treatment, serum PTH
With the feeding of BARF (biologically appropriate concentrationsweresignificantlylower,andwerenotdiffer-
raw food, or bones and raw food) and other homemade ent from a control population that did not have hyperadre-
diets, the occurrence of nutritional secondary hyperpara- nocorticism. Serum calcium concentration increased
thyroidism is more likely. In a recent report, 6-week-old, significantly with trilostane therapy, even though there
large-breed puppies from two litters were fed a BARF diet was no significant difference in calcium concentration
on weaning. 138 Puppies were weak, exhibited pain, and between the pretreatment hyperadrenocorticism group
had abnormal-appearing joints, and some were unable and the control group. Serum phosphate concentrations