Objective—To evaluate calcium balance and parathyroid
gland function in healthy horses and horses with
enterocolitis and compare results of an immunochemiluminometric
assay (ICMA) with those of an
immunoradiometric assay (IRMA) for determination of
serum intact parathyroid hormone (PTH) concentrations
Animals—64 horses with enterocolitis and 62 healthy
Procedures—Blood and urine samples were collected
for determination of serum total calcium, ionized calcium
(Ca2+) and magnesium (Mg2+), phosphorus, BUN,
total protein, creatinine, albumin, and PTH concentrations,
venous blood gases, and fractional urinary clearance
of calcium (FCa) and phosphorus (FP). Serum
concentrations of PTH were measured in 40 horses by
use of both the IRMA and ICMA.
Results—Most (48/64; 75%) horses with enterocolitis
had decreased serum total calcium, Ca2+, and Mg2+
concentrations and increased phosphorus concentrations,
compared with healthy horses. Serum PTH concentration
was increased in most (36/51; 70.6%) horses
with hypocalcemia. In addition, FCa was significantly
decreased and FP significantly increased in
horses with enterocolitis, compared with healthy horses.
Results of ICMA were in agreement with results of
Conclusions and Clinical Relevance—Enterocolitis
in horses is often associated with hypocalcemia;
79.7% of affected horses had ionized hypocalcemia.
Because FCa was low, it is unlikely that renal calcium
loss was the cause of hypocalcemia. Serum PTH concentrations
varied in horses with enterocolitis and concomitant
hypocalcemia. However, we believe low PTH
concentration in some hypocalcemic horses may be
the result of impaired parathyroid gland function. ( Am
J Vet Res 2001;62:938–947)
Objective—To clone and sequence the cDNA for
feline preproparathyroid hormone (preproPTH) and to
compare that sequence with other known parathyroid
hormone (PTH) sequences.
Sample Population—Parathyroid glands from 1
Procedure—A cDNA library was constructed in λ
phage from feline parathyroid gland mRNA and
screened with a radiolabeled canine PTH probe.
Positive clones were sequenced, and nucleic acid and
deduced amino acid sequences were analyzed and
compared with known preproPTH and PTH
Result—Screening of approximately 2 X 105 recombinant
plaques revealed 3 that hybridized with the
canine PTH probe; 2 clones comprised the complete
sequence for feline preproPTH. Feline preproPTH
cDNA consisted of a 63-base pair (bp) 5'-untranslated
region (UTR), a 348-bp coding region, and a 326-bp 3'-UTR. The coding region encoded a 115-amino acid
peptide. Mature feline PTH consisted of 84 amino
acids. Amino acid sequence analysis revealed that
feline PTH was > 83% identical to canine, bovine,
swine, equine, human, and macaque PTH and 69, 71,
and 44% identical to mouse, rat, and chicken PTH,
respectively. Within the region responsible for hormonal
activity (amino acids 1 to 34), feline PTH was >
79% identical to other mammalian PTH sequences
and 64% identical to the chicken sequence.
Conclusions and Clinical Relevance—The amino
acid sequence of PTH is conserved among mammalian
species. Knowledge of the cDNA sequence
for feline PTH may be useful to investigate disturbances
of calcium metabolism and alterations in PTH
expression in cats. (Am J Vet Res 2002;63:194–197)
Objective—To determine effects of experimentally induced hypercalcemia on serum concentrations and urinary excretion of electrolytes, especially ionized magnesium (iMg), in healthy horses.
Animals—21 clinically normal mares.
Procedures—Horses were assigned to 5 experimental protocols (1, hypercalcemia induced with calcium gluconate; 2, hypercalcemia induced with calcium chloride; 3, infusion with dextrose solution; 4, infusion with sodium gluconate; and 5, infusion with saline [0.9% NaCl] solution). Hypercalcemia was induced for 2 hours. Dextrose, sodium gluconate, and saline solution were infused for 2 hours. Blood samples were collected to measure serum concentrations of electrolytes, creatinine, parathyroid hormone, and insulin. Urine samples were collected to determine the fractional excretion of ionized calcium (iCa), iMg, sodium, phosphate, potassium, and chloride.
Results—Hypercalcemia induced by administration of calcium gluconate or calcium chloride decreased serum iMg, potassium, and parathyroid hormone concentrations; increased phosphate concentration; and had no effect on sodium, chloride, and insulin concentrations. Hypercalcemia increased urinary excretion of iCa, iMg, sodium, phosphate, potassium, and chloride; increased urine output; and decreased urine osmolality and specific gravity. Dextrose administration increased serum insulin; decreased iMg, potassium, and phosphate concentrations; and decreased urinary excretion of iMg. Sodium gluconate increased the excretion of iCa, sodium, and potassium.
Conclusions and Clinical Relevance—Hypercalcemia resulted in hypomagnesemia, hypokalemia, and hyperphosphatemia; increased urinary excretion of calcium, magnesium, potassium, sodium, phosphate, and chloride; and induced diuresis. This study has clinical implications because hypercalcemia and excessive administration of calcium have the potential to increase urinary excretion of electrolytes, especially iMg, and induce volume depletion.