Secondary nutritional hyperparathyroidism in cats

Symptoms of alimentary hyperparathyroidism in cats Diagnosis Treatment Prognosis for alimentary hyperparathyroidism in cats Alimentary (secondary) hyperparathyroidism in cats is a metabolic disorder associated with excessive release of parathyroid hormone (PTH) in response to a lack of calcium, or an excess of phosphorus, or a lack of vitamin D in the body. This disease is more common in kittens and is associated with a diet unbalanced in calcium, phosphorus and vitamin D. Hence the name - “alimentary”, caused by poor nutrition. In this case, calcium from the bones migrates into the bloodstream, resulting in bone fragility and pathological fractures. Intestinal motility also decreases, which leads to constipation and bloating in kittens.

Symptoms of alimentary hyperparathyroidism in cats

The disease can occur without symptoms, mainly in adult animals. Kittens usually have:

lameness,
bone deformities,
spontaneous fractures,
pain syndrome,
convulsions,
constipation,
bloating.

If you suspect nutritional hyperparathyroidism in a kitten, you must limit its movement (put it in a cage or carrier) and take it to a veterinary clinic. The sooner the diagnosis is made and treatment is prescribed, the lower the risk of irreversible complications (the greatest danger is posed by pathological fractures of the spine, as a result of which the kitten may remain paralyzed).

Symptoms of the disease

In kittens and cats, the symptoms of this disease in the initial stages are quite mild. The first signs are that the animal becomes lethargic and apathetic, it experiences slight discomfort when moving, so the cat prefers to lie in one place. Gradually, painful sensations in the bones increase, which negatively affects behavior. The cat shows aggression when the owner tries to play with him; he can hiss at the owner and even bite him.

As the pathology begins to enter the active phase, the animal has difficulty moving and limps. If the cat is accustomed to an active lifestyle, then it may have multiple mini-fractures. Doctors have identified characteristic symptoms for a disease such as hyperparathyroidism:

intense pain in the muscles and bones of the cat;
the pelvic bone of the animal is subject to deforming changes;
tooth growth is disrupted and they may fall out;
the shape of the cat's sternum changes;
delays in the process of bowel movements and urination;
apathy alternating with aggression when the owner tries to play with the cat;
the pet sleeps a lot;
complete or partial paralysis of the paws;
The cat's abdomen is distended.

The owner must carefully monitor the first symptoms of a progressive disease and immediately take the cat for examination to a specialist. Otherwise, the animal faces serious danger in the form of disability and even death.

Diagnostics

To make a diagnosis, a survey of the owner is carried out, as a result of which an imbalance in the diet is discovered. Such kittens are usually fed natural products - cereals, meat, baby meat puree or industrial food, which does not contain information that the food is suitable for everyday feeding (a complete diet), which are not able to fully supply the kitten’s body with minerals, and are not balanced in phosphorus and calcium levels. To confirm nutritional hyperparathyroidism, an x-ray is taken, in which the animal has a noticeable decrease in bone density, pathological fractures, curvature of the spine, and tail creases are often visualized.

Causes

Causes of primary hyperparathyroidism include:

Malignant and benign tumors of the parathyroid gland.
Congenital disorders in which the parathyroid gland produces excessive amounts of parathyroid hormone.

Symptoms of the primary form of the disease are more common in older animals, with cats getting sick less often than dogs.

The secondary form of pathology develops due to:

Calcium deficiency, poor absorption of this substance by the body.
Kidney failure.
Gastrointestinal diseases.
Diseases of the thyroid gland.
Excess in the diet of foods rich in phosphorus.
Accelerated growth of kittens aged 1-7 months.

Treatment

Treatment of hyperparathyroidism in cats:

A cat with this disease is primarily recommended to limit its mobility to prevent spontaneous fractures. For example, this could be keeping in a small box or cage, usually for at least 1-2 months. Strict limitation of mobility is associated with the need to avoid further injuries and micro-traumas, and to heal existing bone damage as physiologically as possible, as well as to control pain. Restricting mobility for such a period is not scary and will not cause harm to health, unlike possible complications with free movement.
Premium commercial kitten foods are recommended that can fully supply the kitten's body with the necessary substances and contain optimal levels of calcium, phosphorus and vitamin D. For example, Hill's kitten, Royal Canine kitten, Eukanuba kitten, etc. Foods for adult cats are not recommended, since kittens' needs for calcium and phosphorus are much higher.
An animal with constipation is prescribed medications to soften the consistency of stool. For example, lactulose preparations or petroleum jelly.
For bloating and excessive gas formation, carminative medications may be prescribed. For example, containing simethicone.

In most cases, additional treatment for nutritional hyperparathyroidism is not required.

Alimentary (secondary) hyperparathyroidism (nutritional or juvenile osteodystrophy) - Vasiliev A.A.

NUTRITIONAL (SECONDARY) HYPERPARATHYROSIS (NUTRITIONAL OR JUVINYL OSTEODISTROPHY)

- an endocrine disorder characterized by excessive synthesis and secretion of the parathyroid hormone parathyroid hormone, which is involved in the regulation of extracellular calcium levels. Secondary hyperparathyroidism is a disease that occurs as a result of prolonged stimulation of the parathyroid glands by a reduced level of calcium in the blood, initially as a compensatory process, and then a chain of pathological processes occurs that develop in response to a chronic decrease in the level of calcium in the blood (hypocalcemia). The parathyroid gland controls the level of calcium in the blood, a hormonally caused disorder leads to impaired bone mineralization and improper skeletal development, which is a consequence of poor nutrition when kittens or puppies do not get enough calcium in their diet. A diet consisting mainly of meat and organ meats such as heart, liver and kidneys, etc. contains too high levels of phosphorus and very little calcium and vitamin D (vitamin D is necessary for the absorption of calcium in the small intestine), which leads to impaired growth and development of the skeleton, spontaneous fractures and lameness.

Exchange of calcium and phosphorus in the animal's body.

Calcium is one of the essential elements in the life of mammals. Calcium homeostasis is a very complex, balanced and multicomponent mechanism, the main links of which are calcium receptors on cell membranes that recognize minimal fluctuations in calcium levels and trigger cellular control mechanisms (for example, a decrease in calcium leads to an increase in the secretion of parathyroid hormone and a decrease in the secretion of calcitonin), and effector organs and tissues (bones, kidneys, intestines) that respond to calcium-tropic hormones by correspondingly changing Ca++ transport.

The main hormonal mediators of calcium homeostasis are parathyroid hormone, vitamin D and calcitonin.

Parathyroid hormone, produced by the secretory cells of the parathyroid glands, plays a central role in calcium homeostasis. Its coordinated actions on bones, kidneys and intestines lead to an increase in the transport of calcium into the extracellular fluid and an increase in the concentration of calcium in the blood.

Parathyroid hormone has both anabolic and catabolic effects on bone tissue, which can be distinguished as an early phase of action (mobilization of Ca++ from bones to quickly restore balance with extracellular fluid) and a late phase during which the synthesis of bone enzymes (such as lysosomal enzymes) that promote resorption and remodeling of bone tissue. The primary point of application of parathyroid hormone in bones is osteoblasts. Under the influence of parathyroid hormone, osteoblasts produce a variety of mediators that have a powerful stimulating effect on the differentiation and proliferation of osteoclasts. Thus, bone resorption by osteoclasts is stimulated indirectly through osteoblasts.

Vitamin D is the second strong humoral agent in the system of regulation of calcium homeostasis. Its powerful unidirectional effect causes an increase in calcium absorption in the intestines and an increase in the concentration of Ca++ in the blood.

ETIOLOGY, PATHOGENESIS OF HYPERPARATHYROIDSIS

The metabolism of calcium is closely related to the metabolism of phosphorus (mainly phosphate -P04), and their concentrations in the blood are inversely related. The ratio of calcium to phosphorus in the diet should be no less than 1:1 for dogs and 0.9:1 for cats and should not exceed 2:1 for both species. In the blood, the ratio of calcium and phosphorus for dogs and cats from 3-9 months. – 0.9-1.3, over 9 months. – 1.6-2.3.

The disease is observed in small kittens and puppies, which are fed primarily with meat or offal, because Meat food contains a lot of phosphorus and little calcium, which leads to a violation of the mineralization of the skeleton, its deformation, and in the case of a long course of the disease, fractures of the limbs. A calcium-poor diet stimulates the production of parathyroid hormone, as a result of which the deposition of calcium salts in the bones decreases, and the body begins, on the contrary, to take calcium from the bones (osteoresorption) in order to maintain a normal level of calcium in the blood.

In turn, insufficient calcium intake is often reported when feeding dogs and cats diets consisting of meat or meat by-products. Typically, meat diets contain approximately 0.02% Ca and 0.3% P, which provides a Ca to P ratio of 1:15–1:20, which causes secondary hyperparathyroidism.

The maximum osteoresorptive effect is observed in bones with a pronounced cortical structure (long tubular bones), while bones with a trabecular structure (vertebrae, iliac crest) can maintain their density. This effect has a certain differential diagnostic significance when, during an X-ray examination of patients with secondary hyperparathyroidism, a decrease in bone density is recorded in the area of the radius and tibia, less in the femur and often absent in the vertebrae.

Vivid clinical manifestations of bones are accompanied by cases of secondary hyperparathyroidism in young, actively growing animals. In them, the effect of excess parathyroid hormone manifests itself faster - deformations of the bones of the limbs, spine, fractures, etc. occur. A clear example is the clinical case of the cat Ushlepa, who was admitted to the clinic for observation by orthopedic doctors regarding X-shaped curvature of the lower extremities, thoracic lordosis, lumbar kyphosis and pelvic canal stenosis, the cause of which turned out to be severe primary hyperparathyroidism caused by a mono-diet (feeding meat birds).

Joints are also a weak link in the body of patients with primary hyperparathyroidism. The load on them increases due to erosive changes in the epiphyses and disruption of bone geometry. Another pathogenetic factor of arthropathy is the deposition of calcium salts in the synovial membranes, cartilage and periarticular, which leads to chronic trauma and severe pain throughout the life of the animal.

Neuromuscular changes in secondary hyperparathyroidism manifest themselves in weakness and fatigue. This is a reversible syndrome that quickly disappears after adequate help is prescribed.

CLINICAL SIGNS

The disease has a long-term hidden nature of development, the absence of pathognomonic symptoms up to the development of severe osteodystrophy with destruction of the skeleton. As a rule, the disease manifests itself between the ages of 3 and 7-8 months; purebred cats (Scottish, British, Sphynx, exotic) are often affected.

• Reduced activity and mobility, lack of interest in games, drowsiness;

• Lameness, even after jumping or falling from a small height;

• Incorrect positioning of the limbs (X-shaped);

• Constipation;

• Neatness of movement, lack of playfulness, curiosity and desire to “walk on the ceiling” characteristic of cats; the animal has difficulty overcoming obstacles and jumping on furniture.

Lameness is the most indicative symptom of the disease. The cause of lameness is calcium deficiency in the bones, as a result of which their fragility increases and stress tolerance decreases. In extremely severe conditions, subperiosteal greenstick fractures are possible.

LABORATORY DIAGNOSTICS OF SECONDARY HYPERPARATHYROIDIS

The key criteria for the laboratory diagnosis of hyperparathyroidism are three indicators: increased levels of parathyroid hormone and decreased or normal levels of calcium in the blood plasma, increased levels of phosphorus. The simultaneous detection of these three laboratory signs in a patient leaves virtually no doubt about the diagnosis of secondary hyperparathyroidism. Thus, with the classic bright variants of the course of the disease, its laboratory diagnosis cannot but amaze with its simplicity.

They learned to determine calcium in the blood a little over a hundred years ago - in 1907. In the blood, calcium is found in three main forms: the ionized fraction of the element - 50%, the fraction associated with proteins - 40-45%, the fraction consisting of complex phosphate and citrate connections - 5%. The main clinical laboratory parameters for studying this element in the body are the concentration of total calcium and the concentration of ionized (or free) blood calcium.

The range of normal values for total calcium in dogs is 2.25-2.85 and cats - 2.0-2.7 mmol/l; ionized calcium in dogs - 1.26-1.50 and cats -1.10-1.30 mmol/l.

In addition to its diagnostic value (to confirm the diagnosis of secondary hyperparathyroidism), the level of phosphorus in the blood serves as a differentiating criterion for distinguishing between primary (hyperfunction of the parathyroid gland, usually due to its degeneration) and secondary hyperparathyroidism caused by malnutrition during the period of intensive growth of the animal or chronic renal failure. In the second case, phosphorus levels tend to increase depending on the severity of renal dysfunction, which is associated with a loss of the ability to actively excrete phosphates. In addition to hyperphosphatemia, a distinctive feature of secondary hyperparathyroidism will always be a normal or reduced level of calcium in the blood.

The range of normal phosphorus values in dogs is 1.1-2.0 up to 6 months. – 0.9-2.1 and cats – 1.0-2.3 up to 6 months. 2.1-2.8 mmol/l;

Useful for diagnosing and establishing the severity of the disease are indicators of increased reorganization of bone matter and osteoresorption under the influence of prolonged excessive release of parathyroid hormone into the blood. Markers of osteoresorption include increased levels of alkaline phosphatase (its bone fraction). However, this indicator can increase in any form of hyperparathyroidism and other conditions associated with active restructuring of bone matter. Its values are more informative as indicators of the severity of damage to the skeletal system.

INSTRUMENTAL DIAGNOSTICS

X-ray research methods for secondary hyperparathyroidism include survey X-rays of the chest, abdominal cavity (allowing incidental detection of consolidated rib fractures, establishing spinal curvatures), as well as targeted X-ray examination of skeletal bones (diffuse thinning of the cortical bone, decreased bone density, hypertrophy of the periosteum, traces consolidated pathological fractures of the limbs, subperiosteal fractures, pronounced osteodystrophic changes in the skeleton).

The figures below illustrate these most common pathological changes in bones.

Secondary hyperparathyroidism can also occur in older cats as a result of chronic renal failure.

Increased activity of the parathyroid gland is a compensatory reaction of the body to hypocalcemia induced by meat foods or low calcium levels in the diet. The predominantly meat type of diet does not satisfy the cat’s body’s needs for microelements, primarily calcium, which is necessary for the normal growth of the animal.

This disorder occurs during periods of intense growth in young animals, as they require large amounts of calcium for growth and development.

TREATMENT

Treatment should be carried out by a specialist.

Treatment of patients with nutritional secondary hyperparathyroidism should be aimed at the main cause - normalization of the diet in terms of mineral composition.

Cage restriction to prevent bone fractures in animals with severe disease.

Laboratory studies and radiographs at intervals determined by your veterinarian are helpful in assessing improvement and response to therapy.

The purpose of monitoring is to track the dynamics of restoration of impaired functions (primarily the state of the skeleton), and to ensure that calcium metabolism indicators are normalized.

Animals without severe bone deformities have a good prognosis. Bone mineralization returns to normal within two to three months.

Prognosis for nutritional hyperparathyroidism in cats

The prognosis for proper treatment of nutritional hyperparathyroidism in cats is usually favorable if there are no fractures or curvatures of the spinal column that compress the spinal cord and internal organs. However, treatment of this pathology may require 3 or 5 months. Therefore, the owner must be prepared for a long-term restriction of mobility in his pet. Every 3 months it is recommended to conduct an X-ray examination to assess the dynamics. And do not neglect feeding recommendations; this is the most important element of therapy, without which recovery will not occur. It is optimal to use industrial feeds that are balanced in composition. Homemade diets for the correction of metabolic disorders should be prepared only by a professional nutritionist, and the mineral composition should be adjusted as the animal grows.

Feeding your beloved kitten “only fresh meat from the market” or baby meat food very often leads to the development of nutritional hyperparathyroidism in the pet!

Video about hyperparathyroidism in cats - interview with a veterinarian:

(c) Veterinary center for the treatment and rehabilitation of animals “Zoostatus”. Varshavskoe highway, 125 building 1. tel. 8 (499) 372-27-37

Clinical picture and symptoms of hyperaparathyroidism

The development of the initial stages of hyperparathyroidism is slow and asymptomatic. The early stages of hyperparathyroidism are characterized by muscle weakness, depression, and deterioration in performance in dogs.

As the disease progresses, thirst, increased urination, and decreased appetite are noted. The animal tries more and more to avoid contact with people, sometimes this behavior reaches the point of aggression towards humans.

In advanced cases, hyperparathyroidism in dogs and cats leads to lameness and even paralysis of the limbs. Fibrous bone degeneration is manifested by curvature of the limbs, swelling and pain in the joints. There is also frequent loosening and loss of teeth, and bone fractures.

How does the disease develop?

Calcium homeostasis is regulated by the combined actions of parathyroid hormone (PTH), vitamin D and calcitonin. Parathyroid hormone (PTH) is produced by the chief cells of the parathyroid glands in response to a decrease in the concentration of ionized calcium in the blood. As soon as a signal comes to the cells of the parathyroid glands about a decrease in calcium levels, PTH is released into the blood, which, in turn, stimulates osteoclastic resorption (the release of calcium from the mobile bone depot) of bone tissue and increases resorption (reabsorption). Thus, after prolonged release of parathyroid hormone, the skeleton is greatly weakened. Bone growth is weak, because their resorption exceeds the rate of formation of new bone tissue. To strengthen the bones, the body begins to replace bone tissue with fibrous tissue in limited areas of the bone, which leads to corresponding changes in the skeleton.

Hormones affecting calcium balance

The optimal amount of minerals in the blood, including calcium, is ensured by the action of hormones. One of these is parathyroid hormone, which is synthesized by the parathyroid organ. Under its influence, the calcium needed by the body is borrowed from the bones, and the kidneys begin to work to maximize the retention of these ions.

Mineral imbalance is followed by deterioration in well-being

The thyroid gland produces calcitonin, a specific hormone that has the opposite effect, thereby maintaining a healthy mineral balance. An incorrect balance can have detrimental consequences for your pet's health.

Etiology: why does hyperparathyroidism develop?

In a healthy pet, the ratio of calcium to phosphorus in the body should be the same. If the owner does not monitor the diet of the growing kitten, then he has an excess or deficiency of these substances, as a result of which hypercalcemia or hyperparathyroidism is diagnosed. The primary form of bone disease in kittens can occur due to hyperplasia of the parathyroid glands and is known as hyperparathyroidism. As a result of the disease, the amount of parathyroid hormone increases. Secondary nutritional hyperparathyroidism develops due to poor absorption of calcium. This phenomenon occurs due to impaired functioning of the gastrointestinal tract or thyroid gland.

Veterinarians note that calcium deficiency is associated with rapid growth of the kitten.