Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

VIII. Calcium and Phosphorus: Metabolic Bone Disease
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1994 ; Phalen et al. , 1990 ; Takeshita et al. , 1986 ). PU/PD can
be explained by the fact that in a hypercalcemic state, the
ability of the renal tubules to respond to antidiuretic hormone
decreases, thus inhibiting the reabsorption of water ( Meric,
1995 ). The calcifications found in the kidneys may also contribute
to the polyuria. Other clinical signs include muscle
weakness, painful joints, demineralization of the bone and
disorientation, the abnormalities eventually leading to death.
Calcium is regulated within narrow limits and slight elevations
above the reference range should be taken seriously.
At postmortem examination, metastatic calcifications
in the liver, kidney, gastrointestinal tract, heart, and blood
vessels can be found ( Dumonceaux and Harrison, 1994 ;
Lumeij, 1994b ; Macwhirter, 1994 ; Phalen et al. , 1990 ;
Takeshita et al. , 1986 ).
2 . Estrogen-Induced Hypercalcemia
Estrogen-induced (pseudo)hypercalcemia may be seen in
various avian species related to egg laying. About 4 days
before female pigeons are due to ovulate, tCa rises from
a normal value of about 2.2 mmol/L to a value of over
5.0 mmol/L at the time of ovulation. This rise in Ca is caused
by an increase in the protein-bound Ca resulting from the
estrogen-induced transport of yolk proteins to the ovary as
Ca complexes, whereby the concentration of iCa remains
constant ( Simkiss, 1967 ). Because tCa is the sum of biologically
active iCa, protein-bound Ca, and Ca chelated to
anions, tCa should always be interpreted in conjunction with
plasma proteins. When reference values for iCa are available
for the species under consideration, determination of iCa is
the method of choice (see Section VIII.A).
3 . Primary Hyperparathyroidism
Primary hyperparathyroidism may result from hyperplasia,
adenoma, or carcinoma of the parathyroid gland ( Lumeij,
1994c ). Although tumors of the parathyroid gland do occur
in avian species, primary hyperparathyroidism has not been
documented.
4 . Pseudohyperparathyroidism
Pseudohyperparathyroidism occurs when nonendocrine
tumors secrete hormone-like substances that cause hypercalcemia.
This phenomenon may be seen, for instance, in
malignant lymphoma. Hypercalcemia was reported in two
Amazon parrots ( Amazona spp.) associated with lymphocytic
leucosis ( de Wit et al ., 2003 ). Although a paraneoplastic
syndrome was suggested, this was not convincingly
demonstrated, and hyperproteinemia may have been the
reason for elevated tCa in these cases.
5 . Tertiary Hyperparathyroidism
Tertiary hyperparathyroidism might develop after prolonged
nutritionally secondary hyperparathyroidism, where
the chronically stimulated hyperplastic gland may develop
an adenoma ( Lumeij, 1994c ). In contrast to secondary
hyperparathyroidism, where the increased activity of the
parathyroid is a consequence of hypocalcemia, tertiary hyperparathyroidism
is associated with hypercalcemia.
6 . Calcium and Vitamin D 3 Toxicity
Oversupplementation of the diet with calcium and vitamin
D 3 is the most common cause of true hypercalcemia in birds.
Vitamin D 3 (1,25-dihydroxycholecalciferol) regulates
the absorption of calcium by the gut ( Lumeij, 1994c ). Birds
can synthesize vitamin D in their skin from 7-dehydrocholesterol
and therefore only need dietary vitamin D 3
when they lack ultraviolet light ( Lumeij, 1994c ; Nott and
Taylor, 1993 ). One can easily oversupplement a bird’s diet
because most commercial diets contain abundant vitamin
D 3 ( Dumonceaux and Harrison, 1994 ; Macwhirter, 1994) .
Vitamin D3 is considered to be in the toxic range at 4 to 10
times the recommended dose ( Brue, 1994 ). Avian species
that have been reported to be susceptible to hypervitaminosis
D 3 are the macaw, cockatoo, African grey parrot, toucan,
dove, and cardinal ( Phalen et al. , 1990 ; Takeshita et al. ,
1986 ; Dumonceaux and Harrison, 1994 ; Lumeij, 1994b ). In
literature on hypervitaminosis D in birds, there seldom is
discrimination between vitamin D 3 and D 2 . Because vitamin
D 2 (ergocalciferol) is 30 times less active than vitamin
D 3 ( Nott and Taylor, 1993 ), an excess of vitamin D 3 occurs
most easily. When amounts of vitamin D are expressed in
international chicken units (ICU), they refer to vitamin
D 3 . The baby macaws described by Takeshita et al. (1986)
showed symptoms when fed a diet containing 1000 to 4000
ICU vitamin D 3 /kg. Other workers reported that toxic effects
will appear when the birds are fed a diet containing more
than 2500 ICU vitamin D 3 /kg diet ( Brue, 1994 ; Harrison,
1991 ). The diet of the two birds reported by De Wit et al.
(2003) contained more than 25,000 ICU vitamin D 3 /kg.
Recommended calcium concentrations for maintenance
in avian diets are 5 to 10 g/kg. A level of 30 g calcium/kg
diet will result in toxicity ( Shane et al. , 1969 ). A high calcium
intake alone can cause calcifications in the kidneys
(Macwhirter, 1994) . Nutritional errors can be prevented by
the use of balanced commercial diets.
C . Physiological Marrow Ossification
Physiological marrow ossification is induced by the combined
effects of estrogens and androgens and can be
observed at about the same time as the estrogen-induced
hypercalcemia in female birds ( Simkiss, 1967 ). There is
a large increase in the quantities of Ca and P, which are
retained from the diet and laid down as medullary bone.
This medullary bone may completely fill the marrow spaces
of the long bones. It is most clearly seen in the limb bones
but occurs in most parts of the skeleton. This period of bone