Veterinary Medicine - March 2009 - (Page 128) A challenging case PEER-REVIEWED FOLLOW-UP Initially, the patient was evaluated every 30 days, and more recently, it has been evaluated every 60 to 90 days. The results of intermittent serum chemistry pro les, including electrolytes, have been normal. Treatment includes desoxycorticosterone pivalate every four weeks, and the oral prednisone has slowly been tapered to a physiological dose of 0.3 mg/kg daily. We instructed the owner to increase the prednisone dose in times of stress, such as boarding or illness. The patient is a clinically normal 2.5-year-old dog. dogs, but it also occurs in neonatal and pediatric dogs.3,7,8 Standard poodles, West Highland white terriers, great Danes, Leonbergers, Labrador retrievers, and Portuguese water dogs are overrepresented breeds.3,8 The link between hypoadrenocorticism and hypercalcemia Addison’s disease may cause electrolyte abnormalities including mild to moderate hypercalcemia.9,10 Hypercalcemia is noted at the time of diagnosis in 29% of patients with hypoadrenocorticism.3 The severity of hypercalcemia in Addison’s disease is typically proportional to the clinical severity of adrenal insuf ciency.7,9 Although the exact mechanism of hypercalcemia associated with hypoadrenocorticism remains DISCUSSION Hypoadrenocorticism, or Addison’s disease, is an endocrine disorder most commonly resulting from atrophy and destruction of the adrenal cortices. This deterioration leads to a de ciency of glu- dium reabsorption then occurs in the proximal tubule, which is associated with an increase in calcium reabsorption. 5. Since glucocorticoids antagonize vitamin D activity, glucocorticoid de ciency, as with hypoadrenocorticism, can result in increased intestinal absorption and increased bone resorption of calcium. Glucocorticoids may alter osteoblast differentiation in a manner that has not been identi ed. Thus, a lack of glucocorticoids may cause an increase in calcium resorption from bone. Many or all of these factors likely play a role in hypercalcemia associated with hypoadrenocorticism. The puppy in this report may have been at a higher risk to develop hypercalcemia because it had increased bone turnover due to growth. The serum calcium concentration on presentation in the patient in this case was 26.8 mg/dl (reference range = 8.8 to 11.4 mg/dl), almost double that of previously reported concentrations of hypercalcemia associated with hypoadrenocorticism. Reported ranges of calcium concentrations in dogs with hypoadrenocorticism are 6.8 to 15.9 mg/dl (reference range = 8.5 to 11.5 mg/dl),7 12 to 14.9 mg/dl (reference range = 8.5 to 11.6 mg/dl),9 and—the highest reported value—16.7 mg/dl (reference range = 8.5 to 11.5 mg/dl).11 Hypercalcemia has toxic effects on all cell types, with clinically important effects on the heart and the nervous, gastrointestinal, and renal systems. Dogs with hypercalcemia commonly experience polyuria, polydipsia, anorexia, lethargy, and weakness.13 The development of these clinical signs depends on the severity and rate of development of hypercalcemia.13 The mechanism of hypercalcemia associated with hypoadrenocorticism remains uncertain. cocorticoids alone or both glucocorticoids and mineralocorticoids.3,4 Many causes of this disease have been identi ed in people, including adrenal gland destruction (often autoimmune), tuberculosis, human immunode ciency virus, adrenoleukodystrophy, and congenital adrenal hypoplasia.5,6 In dogs, primary hypoadrenocorticism is usually due to autoimmune destruction of the adrenal glands.3 Less common causes include granulomatous disease, infarction, neoplastic metastasis, amyloidosis, trauma, and iatrogenic causes.3 Natural secondary hypoadrenocorticism is due to a lack of ACTH production by the pituitary glands, which rarely occurs in dogs.3 Hypoadrenocorticism is most common in young to middle-aged female uncertain, the following theories have been postulated8,11,12: 1. Dehydration leads to hemoconcentration and a relative increase in proteins that bind calcium. 2. Hyponatremia due to mineralocorticoid de ciency increases the af nity of plasma proteins for calcium. This increased protein binding of calcium leads to an elevated serum calcium concentration. 3. Decreased renal function and decreased glomerular ltration rate due to hypovolemia lead to increased tubular calcium reabsorption and decreased calcium excretion. 4. Increased serum calcium interferes with sodium and water retention in the distal renal tubules. A compensatory increase of so- Differential diagnoses for hypercalcemia Hypercalcemia in dogs has many differential diagnoses other than hypoadrenocorticism, including primary 128 March 2009 VETERINARY MEDICINE
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