Feline hyperparathyroidism: pathophysiology, diagnosis and treatment of primary and secondary disease

Abstract

Practical relevance: Hyperparathyroidism exists in primary and secondary forms. Primary hyperparathyroidism has typically been considered a disease that uncommonly affects cats, but this condition is more prevalent than previous diagnoses would suggest. Secondary hyperparathyroidism may be caused by either nutritional influences (ie, nutritional secondary hyperparathyroidism) or chronic kidney disease (ie, renal secondary hyperparathyroidism). Tertiary hyperparathyroidism has yet to be documented in veterinary medicine, but it is possible that this condition occurs in some cats following longstanding renal secondary hyperparathyroidism.

Clinical challenges: Diagnosis of this group of calcium metabolic disorders presents a number of challenges for the clinician. For example, clinical signs can be non-specific and, especially in the case of primary hyperparathyroidism, there is often a low index of suspicion for the disease; careful sample handling is required for testing of parathyroid hormone (PTH) and ionized calcium levels; and there is currently no feline-specific assay for PTH, which has implications for test sensitivity and interpretation of results.

Aims: This article briefly outlines PTH and calcium physiology by way of introduction to a review of PTH measurement and interpretation. Various forms of feline hyperparathyroidism are then described, encompassing diagnosis and treatment options.

Figure 1

Regulation of extracellular fluid (ECF) calcium concentration by the effects of parathyroid hormone (PTH) and calcitriol (1,25[OH]₂D₃) on the gut, kidneys, bone and parathyroid gland

Figure 2

Graph detailing idealized set-point relationships between ionized calcium and the PTH secretory rate. Note that maximal parathyroid hormone (PTH) secretion is achieved as iCa declines as a normal homeostatic mechanism – this occurs as an attempt to prevent further decline in circulating iCa that could otherwise be lethal

Figure 3

Parathyroid mass on ultrasound examination in a 9-year-old domestic medium haired spayed female cat with hypercalcemia and mild depression. Note the hypoechogenic mass (solid arrows) below the thyroid (open arrow), which is the abnormal parathyroid gland (PTG; height 1.4 mm, length 2.8 mm). Even with the high frequency ultrasonographic technique available today, the normal feline PTG is too small to be seen. This mass was confirmed to be a PTG adenoma following surgical removal and histopathology. Courtesy of Dr John Mattoon, Washington State University College of Veterinary Medicine, USA

Figure 4

Surgical exploration of the cervical region in a cat with hypercalcemia. Note the enlarged parathyroid gland (black arrow) next to the thyroid gland (between white arrows). Courtesy of Dr Daniel Smeak, Colorado State University College of Veterinary Medicine, USA

Figure 5

Distal femoral fracture in a 2-month-old kitten eating an all-meat diet. Note that the bone has already healed as a functional malunion. The cortical thickness and bone mineral density are reduced, as is expected in cats with nutritional secondary hyperparathyroidism. Folding fractures of long bones are typical with this condition; pathological fractures can also occur in the pelvis and spine. This kitten additionally presented with humeral and pelvic fractures. After transitioning on to a complete and balanced diet, all fractures healed without surgical intervention and no new fractures were acquired. Courtesy of Dr Jonathan Dyce, The Ohio State University College of Veterinary Medicine, USA

Figure 6

Thyroid glands, parathyroid glands (PTGs) and kidneys at necropsy from a 7-year-old domestic shorthair cat with a 3 year history of chronic kidney disease (CKD). The cat’s CKD was acquired secondarily to potassium deficit nephropathy (kaliopenic nephropathy). Note that the renal cortices are irregular and pale. Also there is a large retention cyst near the renal pelvis. This cat’s PTH level was increased to 6 x the upper limit of the reference interval. Solid arrows denote the greatly enlarged PTGs that occur as part of renal secondary hyperparathyroidism. Open arrows denote the thyroid glands. The PTG enlargement is largely due to chief cell hyperplasia, although hypertrophy of chief cells also contributes. Courtesy of Dr Larry Nagode, The Ohio State University College of Veterinary Medicine, USA

Figure 7

Surgical exploration of the cervical region in a cat undergoing thyroidectomy for treatment of hyperthyroidism. Note the enlarged parathyroid gland (black arrow) to the left of the thyroid gland (white arrow). Courtesy of Dr Steven Birchard and Dr Mark Peterson, The Animal Medical Center, New York, USA