Parathyroid Disorders in Cats
The parathyroids are four small glands in the neck located near the thyroid gland. The parathyroid glands secrete the hormone PTH, which is essential to bone metabolism and blood calcium regulation. As the blood calcium level falls, the parathyroid glands compensate by releasing more PTH, which raises the calcium level in the blood by drawing calcium out of the bones. High serum phosphorus levels will also stimulate the body to secrete PTH. Accordingly, either a low serum calcium or a high serum phosphorus will cause an excess of PTH in the blood. When this situation goes unchecked, the bones become demineralized, thin, and often look cystic (small holes in the bone) on X-ray. Minor stress can cause a fracture.
There are several conditions related to abnormal parathyroid gland metabolism.
Low levels of parathyroid hormones are almost always associated with the inadvertent removal of the parathyroid glands during surgery for hyperthyroidism. In this case, cats have a low level of blood calcium and may have muscle tremors.
Treatment: Treatment involves oral or even intravenous calcium supplementation. Many cats adapt to this problem with time and medication, but it can be serious immediately after the surgery.
This rare condition is due to a parathyroid gland tumor that produces excess hormone. These are usually benign adenomas and are seen in older cats.
Treatment: Surgical removal of the affected gland is the only possible treatment.
Renal Secondary Hyperparathyroidism
This condition is the result of long-standing kidney disease that causes the cat to retain phosphorus. The high serum phosphorus stimulates the parathyroid glands to produce excessive amounts of PTH. Effects on the bones are the same as those of nutritional secondary hyperparathyroidism (page 366). However, signs of kidney failure are usually the main symptoms.
Treatment: Treatment is directed toward correcting the kidney disease.
Nutritional Secondary Hyperparathyroidism
The cause of this nutritional bone disease is a diet consisting primarily of organ meats, such as hearts, livers, and kidneys. Such a diet is too high in phosphorus and too low in calcium and vitamin D. (Vitamin D is necessary for calcium to be absorbed from the small intestine.)
Kittens are at particular risk because they require large amounts of calcium for growth and development. When a kitten's sole source of nourishment is meat, he's getting too much phosphorus and not enough calcium. This results in overactivity of the parathyroid glands.
Symptoms appear after the kitten has been on a high-meat diet for about four weeks. Affected kittens are reluctant to move, and they develop an uncoordinated gait and lameness in the back legs. The front legs are often bowed. Their thin bones are easily fractured. These fractures, often multiple, tend to heal rapidly and may even go unrecognized. Because the meat diet supplies adequate calories, kittens often appear well-nourished and have a healthy coat despite their metabolic bone disease.
Osteoporosis is the adult form of this disease. It occurs in older cats who receive large quantities of meat at the expense of other nutrients. Other feeding practices that can lead to osteoporosis include vegetarian diets, dog food diets, and diets that consist primarily of table scraps and leftovers.
Since adult calcium requirements are lower than those for kittens and adult cats have more calcium in their bones to draw out, bone demineralization takes longer (5 to 13 months). The first sign of demineralization is thinning of the jaw bones with exposure of the roots of the teeth. The loose teeth are then expelled.
Treatment: Dietary correction is required. Calcium and vitamin D supplements should not be given to kittens unless prescribed by a veterinarian for a specific deficiency. Oversupplementation can be just as dangerous as deficiencies.
Kittens with nutritional secondary hyperparathyroidism should be kept quiet and confined to prevent bone fractures while their diet is adjusted. Bone deformities tend to be permanent, so early recognition and treatment is important.
This article is excerpted from “Cat Owner’s Home Veterinary Handbook” with permission from Wiley Publishing, Inc.
Copyright © 2008 by Delbert Carlson, DVM, and James M. Giffin, MD. All rights reserved.
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