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hypercalcemia by a similar mechanism as that of an excess of PTH. Osteolysis from primary bone tumors are a rare cause of hypercalcemia.
Other common disorders associated with hypercalcemia are hypoadrenocorticism chronic renal failure, and urolithiasis in cats. Although in these retrospective studies, a significant number of Addisonian animals were reported to be hypercalcemic, the pathogenesis of the hypercalcemia is unknown. Dogs and cats with chronic renal failure demonstrate hypercalcemia uncommonly, and it is thought that decreased renal calcium excretion and PTH-mediated osteoclastic activity from renal secondary hyperparathyroidism may be responsible. In the cat, idiopathic hypercalcemia of mild to moderate severity has been described. In some cases it has been associated with calcium oxalate urolithiasis and has resolved with discontinuation of an urinary acidification diet. The pathogenesis of hypercalcemia with this condition is unknown.
Endocrine etiologies of hypercalcemia in the dog
and cat include primary hyperparathyroidism and hypervitaminosis D. Primary hyperparathyroidism
may result from parathyroid hyperplasia, adenoma or adenocarcinoma, which are all rare in small animals. Hypervitaminosis D, most commonly results from
vitamin D-containing rodenticides or medications,
but may be seen with over supplementation with
vitamin D, especially in small dogs being given human vitamins. Infectious and inflammatory disorders such as blastomycosis, coccidioidomycosis, feline granulomatous disease, endometritis, and schistosomiasis rarely are reported to cause hypercalcemia in dogs and cats. A recent report also details hypercalcemia following renal transplantation in the cat.
Clinical signs
How does one recognize a hypercalcemic patient?
The clinical presentation of hypercalcemia can range from the animal with no clinical abnormalities in which hypercalcemia was found on a routine chemistry to a severly weak or even comatose one. Usually, the clinical signs of hypercalcemia are insidious and so mild that many owners fail to recognize that there is anything wrong with their pet. The most common clinical sign
of hypercalcemia is polyuria/polydipsia (PU/PD). This is
a direct effect of hypercalcemia on the concentrating ability of the kidney; however, hypercalcemia can also cause acute or chronic renal failure, also resulting in PU/ PD. Hypercalcemic animals may also present with signs of lower urinary tract disease since they are predisposed to urinary tract infections and the formation of calcium uroliths. Other less commonly recognized clinical signs include: muscle weakness/atrophy, depression, anorexia, vomiting, constipation, bone pain, pathological fractures, and cardiac arrhythmias. Signs related to specific tumors may also be present.
Evaluating the Hypercalcemic Patient
The clinical approach to the diagnosis of the hypercalcemic patient requires patience and thoroughness. A detailed history should be obtained
and questions regarding the possible exposure to rodenticides should be included. Owners should also be questioned about any nutritional supplementation they may be using that may contain vitamin D. The first thing that needs to be established is that the patient is truly hypercalcemic. Since approximately 1⁄2 of the plasma calcium is complexed or protein-bound, the total calcium level must be evaluated in light of the serum albumin concentration. The most ccurate way to determine serum calcium levels is to measure ionized calcium in the serum. It is this form that the body regulates through PTH and Vitamin D activity.
Once the presence of hypercalcemia has been established, ruling in or out the differential diagnoses listed above should be attempted. Physical examination should be thorough and include palpation of the neck area for parathyroid masses. Although this is a low-yield procedure since the majority of parathyroid masses
are too small to be palpated externally. Peripheral
lymph nodes should be carefully evaluated for size and firmness, changes in which may indicate the presence
of lymphoma. Abdominal palpation should be thorough including evaluation for masses and kidney size. Skeletal pain should be noted that may signal the presence of bone disease. Anal sacs should be thoroughly palpated to check for the presence of anal sac adenocarcinoma.
Biochemical work-up should be initiated by a CBC, chemistry profile, and urinalysis. The leukogram may reveal a leukocytosis that may signal an infectious or inflammatory process. The presence of lymphocytosis or of abnormal lymphocytes may suggest the presence of lymphoma. The hemogram may reveal a nonregenerative anemia that may indicate the presence of chronic disease, renal failure,or bone marrow invasion of neoplastic cells. A chemistry profile will allow evaluation of azotemia that may indicate renal failure. The phosphorous concentration must be carefully evaluated since hypophosphatemia along with hypercalcemia
may indicate hyperparathyroidism. Hyponatremia
or hyperkalemia may suggest the presence of hypoadrenocorticism, and hyperglobulinemia may signal multiple myeloma or chronic infection. A urinalysis should always be performed in order to fully evaluate the chemistry profile. Unconcentrated samples or isosthenuria may reflect the lack of renal concentrating ability caused by direct effect of hypercalcemia and not necessarily the presence of renal failure. A sediment examination should be performed to determine the presence of crystalluria or urinary tract infection. Urine culture should be performed if indicated.
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