Hyperparathyroidism in dogs – symptoms and treatment

Overview

The parathyroids are small glands in the neck near the thyroid. There are usually 4, on both sides of the neck. They secrete parathyroid hormone, or PTH, which helps regulate blood calcium.

Primary hyperparathyroidism is rare in dogs. It usually progresses slowly, and the dog may appear relatively healthy for a long time. An increased blood calcium concentration is called hypercalcaemia.

The most common cause is a benign glandular tumour, or adenoma. Other possible changes are malignant carcinoma and glandular overgrowth, or hyperplasia. Secondary hyperparathyroidism associated with kidney disease or nutritional imbalance develops through a different mechanism.

Adenomas account for around 87% of primary hyperparathyroidism. Around 87% of primary cases involve only one parathyroid gland.

Causes

The gland keeps secreting hormone despite high calcium

Normally, high blood calcium reduces PTH secretion from the parathyroid glands. In primary hyperparathyroidism, this feedback fails and the abnormal gland secretes hormone independently. One or several glands may be overactive.

PTH increases blood calcium through effects on bone, kidneys and the intestine. In the kidneys, it increases phosphorus loss in urine and calcium retention. Prolonged hormone excess accelerates bone breakdown and release of minerals from the skeleton.

A tumour can also develop in parathyroid tissue in an unusual location, such as the mediastinum within the chest. No dietary or environmental cause is known for an ordinary sporadic parathyroid tumour.

The secondary form results from another disorder

In secondary hyperparathyroidism, PTH rises in response to an imbalance of calcium and other minerals. With chronic kidney disease, phosphorus accumulates and active vitamin D production decreases. Blood calcium may then be low or normal despite increased PTH.

The nutritional form can develop when a diet persistently contains too little calcium or too much phosphorus. The body corrects blood calcium by taking minerals from bone. This may weaken the skeleton even when blood calcium remains normal.

Risk factors

A dog developing primary hyperparathyroidism is usually over 7 years old. No difference in susceptibility between males and females has been identified. Keeshonds have a recognised dominantly inherited predisposition.

The mean age of dogs with primary hyperparathyroidism is around 11 years. Affected dogs have ranged from 6–17 years old. A positive genetic test in a Keeshond indicates predisposition, rather than current disease.

Hyperparathyroidism is also found more often than usual in Labrador Retrievers and German Shepherd Dogs, for example. Nutritional secondary disease particularly threatens growing large-breed puppies fed boneless raw meat. Chronic kidney disease predisposes to renal secondary hyperparathyroidism.

Typical symptoms

Signs may be so mild that they are interpreted as normal ageing. Around 32% of patients have no symptoms at diagnosis. A glandular nodule is not usually noticed by looking at or feeling the neck.

• Your dog drinks and urinates more than usual.

• Your dog tires or seems to have weak muscles.

• Appetite declines or your dog loses weight.

• Your dog has nausea or vomiting.

• Constipation makes passing faeces difficult.

• Your dog trembles or has difficulty getting moving.

Increased urination partly results from impaired kidney urine-concentrating ability during high calcium. Your dog drinks more to replace the fluid lost in urine. Urinary stones and urinary tract infections may be the first noticeable problem.

Complications and consequences

Kidneys and the urinary tract can be damaged

Urinary stones are found in around 31–33% of dogs with primary hyperparathyroidism. Urinary tract infections occur in around 29–30%. Stones are often calcium oxalate, associated with high blood and urine calcium.

A stone can sustain bacterial infection in the urinary tract. Persistently high calcium can cause calcium-phosphate deposits in the kidneys and other organs. Resulting internal organ damage may be permanent.

Prolonged hormone excess can weaken bone

In severe skeletal disease, immature connective tissue replaces bone. A fragile long bone can fracture after only minor trauma. A vertebral fracture can compress the spinal cord or nerves and impair movement.

Changes to facial bones may cause teeth to loosen or fall out. In renal secondary disease, advanced bone softening can impair normal jaw function. Severe skeletal deformities in the nutritional form do not always resolve completely even after diet correction.

High calcium may recur after successful treatment

Calcium rises again in around 10% of treated cases. In Keeshonds, recurrence is around 50%. It may involve a change in a previously untreated gland or incompletely removed tissue.

Diagnosis at the vet

Calcium and PTH are tested together

Suspicion often begins with repeatedly increased calcium on routine blood testing. Ionised calcium reflects biologically active calcium better than total calcium. An unexpected total calcium increase can be checked with another fasting blood sample.

PTH is interpreted alongside simultaneously measured ionised calcium. High calcium should normally suppress PTH to a very low level. PTH within the reference range can therefore be abnormal when calcium is increased at the same time.

Other causes of high calcium include tumours, kidney disease and Addison's disease. The PTH-like protein PTHrP may be measured when investigating hypercalcaemia caused by another tumour. General examination also assesses lymph nodes and anal sacs for possible other tumours.

Blood tests assess kidney function, phosphorus and other electrolytes. Urinalysis and, where needed, bacterial culture investigate concurrent urinary problems. Abdominal radiographs may reveal bladder or kidney stones.

Imaging locates the gland needing treatment

Neck ultrasound helps locate the abnormal gland before a procedure. An abnormal gland may measure only 4 millimetres. Examination therefore requires experience with these small neck structures.

Contrast-enhanced computed tomography may particularly help locate parathyroid tissue in an unusual position. Tissue removed surgically can be sent for microscopy to identify tumour type. If nutritional secondary disease is suspected, dietary calcium, phosphorus and vitamin D are assessed.

Treatment

The abnormal gland is removed or destroyed

The main curative treatment for primary disease is surgery or ablation, targeted destruction of the abnormal gland. Surgery succeeds in around 95–100% of patients. The overall cure rate for ablation treatments is around 90%.

Ethanol ablation has a success rate of 72–87%. Radiofrequency ablation succeeds in 72–98% of patients. Ethanol treatment is repeated in 2–16%. With radiofrequency treatment, 2–14% need another procedure.

Ablation can destroy glandular tissue using ethanol or radiofrequency heat. It too requires general anaesthesia and may need repeating. Ethanol treatment provides no tissue sample for microscopic tumour examination.

Surgery can often preserve the thyroid and other normal parathyroid glands. If high calcium has already impaired organ function, fluids and medication may be used before anaesthesia. High calcium can carry a risk of arrhythmias and blood pressure problems during anaesthesia.

If a procedure is not possible

Monitoring may be an option for an older dog with no or mild symptoms if other diseases make anaesthetic risk high. Calcium, kidney function and urinary stone formation are then monitored.

Calcium is monitored closely after the procedure

The other parathyroid glands may have been suppressed by prolonged high calcium. Recovery of their own hormone secretion usually takes days or longer. In a dog with severe skeletal disease, calcium can fall too low within 12–24 hours of surgery.

Post-procedure hypocalcaemia occurs in around 22–68% of patients. Symptomatic hypocalcaemia occurs in around 11%. It usually develops within 1–3 days but may appear as early as 12 hours. Low calcium only rarely lasts longer than 7 days.

Where necessary, the vet treats hypocalcaemia, excessively low blood calcium, with calcium and active vitamin D. It may require a prolonged hospital stay. Face rubbing, muscle twitching and seizures may indicate post-treatment hypocalcaemia.

If high calcium persists for at least 1 week after surgery, remaining abnormal tumour tissue must be investigated. The cause may be another abnormal gland or parathyroid tissue in an unusual location.

Secondary disease treatment targets the underlying cause

In the renal form, kidney disease and phosphorus balance are treated. The vet may use a phosphorus-restricted diet and phosphate binders. In the nutritional form, calcium, phosphorus and vitamin D are corrected to suit the dog's age and needs.

Prevention

There is no known dietary or environmental way to prevent a sporadic parathyroid tumour. Genetic testing can assess inherited predisposition in Keeshonds. Some breed-club guidance recommends breeding from Keeshonds with a negative PHPT genetic test or otherwise known to be genetically clear.

A Keeshond with a parathyroid tumour is not used for breeding. Balanced dietary calcium and phosphorus prevent the central cause of nutritional secondary disease. A diet based solely on boneless raw meat poses a particular risk to growing puppies.

Keeshond genetic testing can use a cheek-cell or blood sample.

Important for dog owners

A genetically positive but well Keeshond may have calcium and kidney values monitored through blood testing before symptoms develop. Blood calcium can remain high for a long time before outward illness becomes noticeable.

Record drinking, urination, appetite, weight changes and movement before treatment. Bring previous calcium and kidney results and details of all supplements and food. Before discharge, agree where calcium will next be measured and whom to contact if signs change. Keep discharge instructions and the medication list available in the evening too.

Post-treatment monitoring aims to detect low calcium before severe symptoms. The long-term outlook after surgery or ablation is generally excellent.

Ionised calcium is monitored twice daily for at least 5–7 days after the procedure. The dog rests for 3–5 days afterwards to reduce hypocalcaemia risk. After successful treatment, long-term calcium checks are recommended every 6–12 months.

Frequently asked questions

Is hyperparathyroidism always cancer?

No: the most common cause in dogs is a benign adenoma. Glandular overgrowth and a less common malignant tumour are also possible. Removed tissue can be examined microscopically to identify the change. Even a benign glandular tumour can cause excessive hormone secretion and high blood calcium.

Can PTH be normal even when a dog has hyperparathyroidism?

Yes, because PTH should be suppressed when blood calcium is high. In that situation, a hormone level within the reference range may indicate inadequate regulation. PTH and ionised calcium are therefore assessed from simultaneous results.

Does a positive PHPT genetic test mean a Keeshond is ill?

A positive genetic test does not show that the dog is already clinically affected. It indicates inherited predisposition. Monitoring calcium and kidney values helps detect disease changes even in a dog that seems well. Visible symptoms usually begin only at an older age.

Why can calcium fall too low after surgery?

Secretion by the other parathyroid glands may have been suppressed for a long time by high calcium. They need time to recover after the abnormal gland is removed. Blood tests are therefore monitored after surgery and low calcium treated if necessary.

Can changing diet cure primary hyperparathyroidism?

Curative treatment of a primary glandular lesion is usually surgery or ablation. Diet correction is different: it treats nutritional secondary disease. In the renal form, the underlying kidney disease and mineral balance are treated. Blood calcium may be normal or low in secondary hyperparathyroidism.