Page 954 - Small Animal Internal Medicine, 6th Edition

926 PART VII Metabolic and Electrolyte Disorders

serum ionized calcium, PTH, and PTHrP concentrations; PTH concentrations are in the normal range or low; primary
and cervical ultrasound. hyperparathyroidism has not been confirmed in any of these
VetBooks.ir lymphoma-induced hypercalcemia and can be readily iden- cats. Increased serum PTHrP, 25-hydroxyvitamin D, or cal-
Sternal and hilar lymphadenopathy is common with
citriol concentrations have not been identified. Nephrocalci-
tified with thoracic radiographs. Radiographs of the thorax
increased urinary calcium excretion. Consistently effective
and abdomen can also be used to evaluate bones; discrete nosis and urolithiasis may develop, presumably secondary to
lytic lesions in the vertebrae or long bones suggest multiple treatment has not been identified primarily because the
myeloma. Hyperproteinemia, proteinuria, and plasma cell pathogenesis of this problem remains unknown. In addition,
infiltration in the bone marrow suggest multiple myeloma. the course of the disease is sometimes waxing and waning,
Cytologic evaluation of peripheral lymph node, bone marrow, which complicates confident correlation of improvement to
and splenic aspirates can be helpful in identifying lymphoma; treatments. Serum calcium concentrations have decreased in
involvement of the peripheral lymph nodes or spleen by some cats following a dietary change to a high-fiber diet, a
lymphoma can be present without causing their enlarge- diet designed for kidney disease, or a diet designed to manage
ment. Ideally, the largest lymph node should be evaluated. calcium oxalate urolithiasis, or after prednisolone treatment
Normal lymph node, bone marrow, and splenic aspirates do (initial dose, 5 mg q24h), but the response has been unpre-
not rule out lymphoma. dictable and often short-lived. Preliminary trials with oral
Measurement of serum ionized calcium, PTH, and PTHrP bisphosphonates (e.g., alendronate) have been promising in
levels from the same blood sample is helpful in differentiat- some cats with idiopathic hypercalcemia (see Treatment
ing primary hyperparathyroidism from HHM. Excessive section). Serum calcium, phosphorus, and renal parameters
secretion of biologically active PTHrP plays a central role in should be monitored periodically in affected cats and appro-
the pathogenesis of hypercalcemia in most forms of HHM. priate therapy initiated if hypercalcemia progressively
An increased serum ionized calcium concentration, a detect- worsens, deterioration in renal function occurs, or both (see
able serum PTHrP concentration, and a nondetectable Chapter 41).
serum PTH concentration are diagnostic for HHM. Lym-
phoma is the most common cause of detectable PTHrP con- Treatment
centrations, but other tumors, including apocrine gland Medical therapy should be directed at eradicating the under-
adenocarcinoma and various carcinomas (e.g., mammary lying cause of the hypercalcemia. Supportive therapy to
gland, squamous cell, bronchogenic), can also cause hyper- decrease the serum calcium concentration to less toxic levels
calcemia by this mechanism. In contrast, an increased serum is indicated if clinical signs are severe, if serum calcium
ionized calcium concentration, a normal to increased serum concentration is greater than 17 mg/dL (dog) or 16 mg/dL
PTH concentration, and a nondetectable PTHrP concentra- (cat), if serum ionized calcium is greater than 1.8 mmol/L
tion are diagnostic of primary hyperparathyroidism. Ultra- (dog) or 1.7 mmol/L (cat), if the calcium-phosphorus solu-
sonographic examination of the parathyroid complex may bility product ([Ca] × [Pi]) is greater than 60 to 70 (implying
reveal enlargement of one or more parathyroid glands (see metastatic mineralization of soft tissues), or if azotemia is
Fig. 47.2, and Video 47.1). Most parathyroid adenomas present. In dogs and cats, correction of fluid deficits, saline
measure 4 to 8 mm in greatest diameter, although parathy- diuresis, diuretic therapy with furosemide, and corticoster-
roid adenomas can exceed 2 cm. In contrast, the parathyroid oids are the most commonly used modes of therapy (Box
glands should be small (<2 mm in diameter) or undetectable 53.6). Prerenal azotemia is common in dogs with hypercal-
with hypercalcemia of malignancy. cemia secondary to water restriction imposed by owners
Trial therapy to determine the cause of hypercalcemia is concerned about the polyuria and polydipsia. Therefore
strongly discouraged. If the dog or cat is stable, eating, and diuretics should never be administered before volume
not significantly ill, it is recommended to wait a few days to replenishment is completed.
weeks and retest. Most of the causes of hypercalcemia are not The supportive therapy implemented should not interfere
occult, so the veterinarian is reminded to complete a thor- with attempts to establish a definitive diagnosis. As a general
ough history (including toxin and supplement exposure), rule, saline diuresis followed by diuretic therapy can be initi-
physical exam, cervical and abdominal ultrasonography, and ated without compromising the results of diagnostic tests.
assessment of PTH and PTHrP assays. Very rarely in dogs Because of the high incidence of lymphoma in animals with
the clinician is left with nebulous results and must con- hypercalcemia, glucocorticoids should not be administered
sider surgical exploration of the neck or trial therapy with unless the cause of the hypercalcemia has been identified.
L-asparaginase to see if hypercalcemia is alleviated. Calcitonin may be useful in the treatment of animals with
Idiopathic hypercalcemia is a common diagnosis in severe hypercalcemia and could be used in lieu of predni-
young and middle-aged cats established by ruling out other sone for treating hypercalcemia in animals without a defini-
causes of hypercalcemia. Hypercalcemia is usually mild tive diagnosis. Calcitonin inhibits osteoclast activity. It has
(<13 mg/dL), and cats are usually asymptomatic. Serum been used most commonly to treat hypercalcemia in dogs
phosphorus concentration and renal parameters are normal. with cholecalciferol rodenticide toxicosis. The decrease in
The cause is unknown. Results of a complete diagnostic serum total calcium concentration after calcitonin adminis-
evaluation, as described previously, are unremarkable. Serum tration is relatively small (≤3 mg/dL), and adverse reactions