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Basics ⬇

Basics

Definition

A pathologic, sustained, high, circulating concentration of PTH.

Pathophysiology

  • PTH-secreted by the parathyroid glands in response to changes in the concentration of ionized calcium in the serum; raises the serum calcium concentration through its effects on bone and renal tubular calcium resorption and vitamin D-dependent intestinal calcium absorption.
  • Can develop as a primary condition or be secondary to a disorder of calcium homeostasis; primary hyperparathyroidism is associated with benign (usually) adenoma of the parathyroid gland(s); secondary hyperparathyroidism can be caused by a deficiency of calcium and vitamin D associated with malnutrition or chronic renal disease.

Systems Affected

  • Cardiovascular
  • Gastrointestinal
  • Neuromuscular
  • Renal/Urologic

Genetics

  • None known for primary hyperparathyroidism, but its association with certain breeds suggests a possible hereditary basis in some cases.
  • Secondary hyperparathyroidism can develop in association with hereditary nephropathy, but is not inherited per se.

Incidence/Prevalence

  • Prevalence of primary form is unknown.
  • More commonly diagnosed in dogs than in cats.
  • Fairly common among causes of hypercalcemia, but much less common than hypercalcemia of malignancy in dogs.
  • Nutritional secondary hyperparathyroidism is decreasing in prevalence as the public becomes more educated in pet nutrition.
  • Chronic renal failure with secondary hyperparathyroidism is extremely common, more so in cats than in dogs.

Signalment

Species

Cat and dog

Breed Predilections

  • Keeshonden
  • Siamese cats

Mean Age and Range

  • Cats-mean age, 13 years; range 8–15 years
  • Dogs-mean age, 10 years; range 5–15 years

Predominant Sex

None

Signs

General Comments

  • Most dogs and cats with primary hyperparathyroidism do not appear ill.
  • Signs are usually mild and are due solely to the effects of hypercalcemia.
  • Signs become apparent when hypercalcemia is severe and chronic.

Historical Findings

  • Polyuria
  • Polydipsia
  • Anorexia
  • Lethargy
  • Vomiting
  • Weakness
  • Urolithiasis
  • Stupor and coma

Physical Examination Findings

  • Often unremarkable.
  • Parathyroid adenoma is not palpable in dogs but often is in cats.
  • Nutritional secondary disease is sometimes associated with pathologic bone fractures and general poor body condition.

Causes

  • Primary hyperparathyroidism-PTH-secreting adenoma of the parathyroid gland. In most cases only one gland is adenomatous. Malignant tumors of the parathyroid glands are uncommon and usually non-invasive.
  • Renal secondary hyperparathyroidism-renal calcium loss and reduced gut absorption of calcium due to deficiency in calcitriol production by the renal tubular cells.
  • Nutritional secondary hyperparathyroidism-a nutritional deficiency of calcium and vitamin D.

Risk Factors

  • Primary hyperparathyroidism-unknown.
  • Secondary hyperparathyroidism-coexisting renal tubular disease or calcium/vitamin D malnutrition.

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

  • The differential list includes causes of hypercalcemia.
  • Lymphoma-common in dogs, rare in cats.
  • Anal sac apocrine gland adenocarcinoma-dogs.
  • Other miscellaneous carcinomas-dogs and cats.
  • Myeloproliferative disease-cats.
  • Fibrosarcoma-cats.
  • Chronic renal failure.
  • Hypoadrenocorticism.
  • Vitamin D intoxication-rodenticides are not currently marketed in the United States, but exposure can come from plant sources and vitamin supplements.
  • Granulomatous diseases.
  • Idiopathic hypercalcemia in cats.

CBC/Biochemistry/Urinalysis

  • High serum calcium concentration.
  • Low or low-normal serum phosphorus concentration in primary hyperparathyroidism.
  • Hyperphosphatemia in secondary hyperparathyroidism or hypervitaminosis D.
  • BUN and creatinine concentrations are usually normal in patients with primary hyperparathyroidism, except those with hypercalcemia-induced renal failure.

Other Laboratory Tests

  • Serum ionized calcium determination is often normal in patients with chronic renal failure and high in patients with primary hyperparathyroidism or hypercalcemia associated with malignancy.
  • High serum PTH concentration is diagnostic for primary hyperparathyroidism in the absence of azotemia; assays that measure the intact PTH molecule are most useful. A normal serum PTH concentration in an animal with hypercalcemia may be considered abnormal and can signal parathyroid-dependent hypercalcemia.

Imaging

  • Radiography can be useful to assess urolithiasis, renal morphology, and bone density and to identify occult neoplasia.
  • Ultrasonography of the ventral cervical area sometimes reveals a parathyroid gland adenoma.
  • Ultrasound of the abdomen can reveal lymphadenomegaly, urolithiasis, or renal morphologic abnormalities.

Diagnostic Procedures

Surgical exploration of the ventral cervical area

Pathologic Findings

  • Parathyroid adenoma is usually a solitary, small (= 1 cm), round, light brown or reddish mass located in the proximity of the thyroid gland.
  • Occasionally multiple adenomas are found.
  • The histologic distinctions between adenomas, hyperplasia, and carcinomas of the parathyroid gland are often unclear.

Treatment ⬆ ⬇

Treatment

Appropriate Health Care

  • Primary hyperparathyroidism generally requires inpatient care and surgery.
  • Nutritional or renal secondary hyperparathyroidism in non-critical patients can be managed on an outpatient basis.

Activity

No alterations recommended

Diet

Calcium supplementation for secondary forms

Client Education

Explain signs referable to changes in calcium status, because hypocalcemia is a potential complication of parathyroidectomy.

Surgical Considerations

  • Surgery is the treatment of choice for primary hyperparathyroidism and is often important in establishing the diagnosis.
  • Percutaneous ultrasound-guided heat ablation has been used successfully for treatment of parathyroid adenoma, and may be recommended if available.
  • Percutaneous ultrasound-guided ethanol ablation has been reported to be less successful than surgery or heat ablation.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

  • Normal saline is the fluid of choice for treatment of hypercalcemia.
  • Diuretics (furosemide) and corticosteroids can be useful in treating hypercalcemia.
  • No medical treatment exists for primary hyperparathyroidism per se.
  • Renal secondary hyperparathyroidism is sometimes treated with calcitriol, but its use has not gained wide acceptance.
  • A new class of calcimimetic drugs is being used to treat renal secondary hyperparathyroidism in human patients, but studies of these drugs in dogs and cats have not been reported.

Contraindications

  • Do not use glucocorticoids until the diagnosis of lymphoma has been excluded; they can obfuscate the diagnosis.
  • Avoid calcium-containing fluids.

Precautions

Use furosemide only in patients with adequate hydration.

Alternative Drug(s)

Pamidronate has been used to treat hypercalcemia of various causes in dogs and cats.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • Postoperative hypocalcemia is relatively common after treatment of primary hyperparathyroidism. Recent studies have shown that preoperative ionized calcium and PTH concentrations are poor predictors of post-surgical hypocalcemia, so monitoring is essential in all cases.
  • Postoperative hypocalcemia requires treatment with vitamin D (calcitriol is recommended) and calcium supplements (see treatment of hypoparathyroidism), and ionized calcium should be monitored to guide dosage adjustments.
  • In patients with renal impairment, check serum concentrations of urea nitrogen and creatinine.

Prevention/Avoidance

  • No strategies exist for prevention of primary hyperparathyroidism.
  • Nutritional secondary hyperparathyroidism is prevented by proper nutrition.

Possible Complications

Irreversible renal failure secondary to hypercalcemia.

Expected Course and Prognosis

  • Untreated disease usually progresses to end-stage kidney or neurologic disease.
  • Prognosis for treatment of parathyroid adenoma is excellent.
  • Recurrence is seen in a small percentage of cases.
  • In animals that develop postoperative hypoparathyroidism, the return of normal parathyroid function is unpredictable and can take weeks to months.

Miscellaneous ⬆

Miscellaneous

Associatedconditions

Calcium-containing urolithiasis

Age-Relatedfactors

N/A

Pregnancy/Fertility/Breeding

N/A

Abbreviation

PTH = parathyroid hormone

Author Thomas K. Graves

Consulting Editor Deborah S. Greco

Client Education Handout Available Online

Suggested Reading

Arbaugh M, Smeak D, Monnet E. Evaluation of preoperative serum concentrations of ionized calcium and parathyroid hormone as predictors of hypocalcemia following parathyroidectomy in dogs with primary hyperparathyroidism: 17 cases (2001–2009). J Am Vet Med Assoc 2012, 241(2):233–236.

Feldman EC, Hoar B, Pollard R, Nelson RW. Pretreatment clinical and laboratory findings in dogs with primary hyperparathyroidism: 210 cases (1987–2004). J Am Vet Med Assoc 2005, 227(5):756–761.

Gear RN, Skelly BJ, Herrtage ME. Primary hyperparathyroidism in 29 dogs: Diagnosis, treatment, outcome and associated renal failure. J Small AnimPract 2005, 46(1):10–16.

Milovancev M, Schmiedt CW. Preoperative factors associated with postoperative hypocalcemia in dogs with primary hyperparathyroidism that underwent parathyroidectomy: 62 cases (2004–2009). J Am Vet Med Assoc 2013, 242(4):507–515.

Rasor L, Pollard R, Feldman EC. Retrospective evaluation of three treatment methods for primary hyperparathyroidism in dogs. J Am Anim Hosp Assoc 2007, 43(2):70–77.

Richter KP, Kallet AJ, Feldman EC, Brum DE. Primary hyperparathyroidism in cats: Seven cases (1984–1989). J Am Vet Med Assoc 1991, 199(12):1767–1771.

Schaefer C, Goldstein RE. Canine primary hyperparathyroidism. Compend Contin Educ Vet 2009, 31(8):382–389,