Secondary nutritional hyperparathyroidism in dogs. Hyperparathyroidism in cats - primary and secondary forms. Causes, treatment, prevention. Ca

Hyperparathyroidism affects both dogs and cats. In the body of sick animals, excessive production of parathyroid hormone is observed. The substance redistributes calcium ions from the bones, regulates the functioning of the kidneys. As a result of metabolic disorders, an increase in the concentration of calcium in the blood against the background of a decrease in the level of phosphorus occurs.

Types of pathology:

Primary hyperparathyroidism in dogs is primarily due to pathological changes in the thyroid gland, which produces parathyroid hormone. Older dogs are most commonly affected. Cats get sick less often. Oncological processes (adenoma, malignant tumors), parahyperplasia thyroid gland- the main reasons for the development of the primary form in animals.

Secondary metabolic disorder, due to increased production of parathyroid hormone, is associated with impaired renal function. Cats suffer from this form mainly due to the development of chronic renal failure. With kidney disease in the body of an animal, a violation occurs in the electrolytic balance: the concentration of calcium in the blood decreases, and the level of phosphorus increases.
As compensation, the parathyroid gland intensively produces parathyroid hormone, which has little effect on calcium levels. In the body, the content of calcitriol decreases, which is accompanied by a violation of mineralization in bone tissue.
Alimentary hyperparathyroidism caused in cats and dogs most often by errors in feeding. The disease develops against the background low level calcium and high doses of phosphorus in the diet. Young pets are the main risk group for nutritional hyperparathyroidism. Deficiency of calcium, magnesium, vitamin D and increased content in phosphorus products during the active growth of the skeleton of kittens and puppies leads to a gross violation of the metabolism of minerals.
The reason for this imbalance is often a mono-diet - feeding only meat, for example, chicken. Violation of the absorption of calcium and vitamin D from the intestine as a result of a long one can also lead to a alimentary form.

Juvenile hyperparathyroidism- a secondary form of pathology in furry patients. So it is often referred to by veterinarians.

The disease has uncharacteristic Clinical signs, and is often mistaken for rickets in young animals. Symptoms of hyperparathyroidism in dogs:

lagging behind breed standards;
the activity of the young pet is reduced, he does not want to take part in the games;
the owner often observes drowsiness, lethargy;
curvature of the bones of the limbs and spine;
permanent fractures;
deposition of calcium salts synovial membranes leads to severe pain syndrome;
after jumping, running, the dog has lameness;
chronic constipation.

Symptoms of hyperparathyroidism in cats:

loss of activity;
loss of appetite;
nausea, bloating;
loss of teeth;
soreness when stroking;
skeletal deformity;
neurological manifestations: paresis, convulsions;
against the background of metabolic disorders in the body, cats often develop urolithiasis, heart problems.

When contacting the owner about frequent fractures in the pet, curvature of the bones, lameness, the veterinarian may suspect secondary hyperparathyroidism in dogs. When collecting an anamnesis, important importance is given to the analysis of the diet of the animal. Predominantly this is how alimentary hyperparathyroidism is detected.

As a rule, subperiosteal fractures are observed in sick individuals. In this case, carry out radiographic examination. The picture clearly shows the zones of softening of the bone tissue, phenomena, creases of the tail, curvature of the vertebrae.

The differential diagnosis is carried out in relation to rickets in young pets and osteomalacia in adults. For this purpose, take blood for biochemical analysis. AT biological fluid carry out the determination of calcium and phosphorus. Informative method diagnosis is to measure the hormonal status of the parathyroid gland.

In some cases, to determine the cause of hyperparathyroidism, Thyroid ultrasound in order to exclude hyperplasia of the organ and identify neoplastic formations.

Treatment of hyperparathyroidism in dogs and cats:

With alimentary hyperparathyroidism in puppies, it is recommended to review the diet. Nutrition of a sick individual should be complete, with high content in calcium products. The level of phosphorus in the diet is minimized. When feeding with natural food, the animal is given meat of different varieties: chicken, beef, rabbit meat. At least once a day, the puppy should receive fermented milk products.
Along with calcium, the body must receive enough vitamin D. The pet should have regular sunbathing. On the recommendation of a doctor, vitamin supplements are introduced into the puppy's diet: meat and bone and fish meal, vitamin D concentrate, fish oil.

If primary hyperparathyroidism is found in an animal, then we can talk about the surgical removal of the neoplasm. Surgical intervention is reduced to resection of the damaged lobes of the parathyroid gland and is carried out in specialized institutions.
When hyperparathyroidism is detected in kittens first of all, they limit their activity: they are placed in a small box, cage or box. This is the prevention of spontaneous fractures. For the entire period of treatment, which can be 2-3 months or more, the animal is prescribed medical nutrition enriched with calcium. The best option would be to use specialized feeds with calcium.
Treatment metabolic disorder in advanced cases, it can not do without the use of medications. For example, borgluconate, calcium gluconate, calcium chloride are injected into the pet's body intravenously.
Therapy includes symptomatic treatment. Thus, sick animals often suffer chronic constipation with which vaseline oil will help.

Read more in our article on hyperparathyroidism.

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What is hyperparathyroidism?

Pets are prone to a number of metabolic diseases, among which owners often experience hyperparathyroidism. The disease affects both dogs and cats. In the body of sick animals, excessive production of parathyroid hormone is observed. The substance redistributes calcium ions from the bones, regulates the functioning of the kidneys. As a result of metabolic disorders in the body, an increase in the concentration of calcium in the blood occurs against the background of a decrease in the level of phosphorus.

Active excretion of calcium from the bone tissue, saturation of the blood with it leads to the destruction of bones, their thinning. Violation of the metabolism of minerals in the body is accompanied by the development of osteoporosis, urolithiasis. In advanced cases, the digestive system is involved in the pathological process.

Types of pathology

In veterinary practice, it is customary to distinguish between primary and secondary disease.

Primary and secondary (alimentary)

Primary hyperparathyroidism in dogs is primarily due to pathological changes in the thyroid gland, which produces parathyroid hormone. According to the observation of veterinary specialists, older dogs most often suffer from the primary form of the disease. Cats get sick less often.

Oncological processes (adenoma, malignant tumors), hyperplasia of the parathyroid gland are the main causes of the development of the primary form of impaired parathyroid hormone production in domestic animals.

A secondary metabolic disorder due to increased production of parathyroid hormone is associated with impaired renal function. Cats suffer from this form of the disease mainly due to the development of chronic renal failure. With kidney disease in the body of an animal, a violation occurs in the electrolytic balance: the concentration of calcium in the blood decreases, and the level of phosphorus increases.

As compensation, the parathyroid gland intensively produces parathyroid hormone, which has little effect on calcium levels. In addition, the content of calcitriol in the body decreases, which is accompanied by a violation of the mineralization of bone tissue.

Alimentary

Most often faced with alimentary hyperparathyroidism in dogs and cats, due to errors in feeding. The disease develops against the background of low levels of calcium and high doses of phosphorus in the animal's diet. Young pets with a high need for building material for bones - the main risk group for nutritional hyperparathyroidism.

The lack of calcium, magnesium, vitamin D and the increased content of phosphorus in the products during the active growth of the skeleton of kittens and puppies leads to a gross violation of the metabolism of minerals. The reason for this imbalance is often a mono-diet - feeding a young animal only with meat, for example, chicken.

Malabsorption of calcium and vitamin D from the intestines as a result of prolonged diarrhea can also lead to the alimentary form of the disease.

Juvenile

It is not uncommon for cat owners to hear from a veterinarian that a cat has juvenile hyperparathyroidism. Professionals call this term a secondary form of pathology in fluffy patients.

Symptoms in puppies and kittens, adults

The insidious disease has uncharacteristic clinical signs, and is often mistaken for rickets in young animals. The owner should carefully look at the state of health and know the symptoms of hyperparathyroidism in dogs:

Lagging behind breed standards.
The activity of the young pet is reduced. The puppy does not want to take part in the games. The owner often observes drowsiness, lethargy.
Curvature of the bones of the limbs and spine.
Permanent fractures.
The deposition of calcium salts in the synovial membranes leads to a pronounced pain syndrome.
After jumping, active movement, running, the dog has lameness.
Chronic constipation.

Weakness of the hind legs

With hyperparathyroidism in cats, the owner may observe the following symptoms:

Loss of activity.
Decreased appetite.
Nausea, bloating.
Loss of teeth.
Pain when stroking.
Skeletal deformity.
Numerous fractures.
Neurological manifestations: paresis, convulsions.

Against the background of a metabolic disorder in the body, cats often develop heart problems.

Animal diagnostics

When contacting the owner about frequent fractures in the pet, curvature of the bones, lameness, the veterinarian may suspect secondary hyperparathyroidism in dogs. When collecting an anamnesis, important importance is given to the analysis of the diet of the animal. A mono-diet, a monotonous diet of only cereals or only meat, the absence of vegetables and lactic acid products in the menu makes it possible to suspect alimentary hyperparathyroidism in a shaggy patient.

As a rule, subperiosteal fractures are observed in sick individuals. In this case, to confirm the diagnosis, the veterinarian conducts an x-ray examination. The picture clearly shows the zones of softening of the bone tissue, the phenomena of osteoporosis, tail creases, curvature of the vertebrae.

The differential diagnosis is carried out in relation to rickets in young pets and osteomalacia in adults. For this purpose, blood is taken from a sick animal for biochemical analysis. Calcium and phosphorus are determined in the biological fluid. An informative diagnostic method is the measurement of the hormonal status of the parathyroid gland.

In some cases, to determine the cause of hyperparathyroidism in pets in specialized clinics, ultrasound examination thyroid gland in order to exclude hyperplasia of the organ and identify neoplastic formations.

Treatment of Hyperparathyroidism in Dogs and Cats

In case of detection of alimentary hyperparathyroidism in puppies, the first thing a veterinarian recommends is to review the diet. The nutrition of a sick individual should be complete, with a high content of calcium in foods. The level of phosphorus in the diet is minimized. When feeding with natural food, the animal is given meat of different varieties: chicken, beef, rabbit meat.

In the event that the animal has primary hyperparathyroidism, then we can talk about the surgical removal of the neoplasm. Surgical intervention is reduced to resection of the damaged lobes of the parathyroid gland and is carried out in specialized institutions.

When hyperparathyroidism is detected in kittens, their activity is primarily limited. For this, a sick pet is placed in a small box, cage or box. This is done to prevent spontaneous fractures. For the entire period of treatment, which can be 2-3 months or more, the animal is prescribed a therapeutic diet enriched with calcium.

The best option would be to use specialized feeds that take into account the low need of the sick organism for phosphorus and the high need for calcium.

Treatment of metabolic disorders in advanced cases is not complete without the use of medications. For example, borgluconate, calcium gluconate, calcium chloride are injected into the body of a sick pet intravenously.

Therapy for hyperparathyroidism in pets, in addition to enriching the body with calcium, also includes symptomatic treatment. So, sick animals often suffer from chronic constipation. Vaseline oil can help solve the problem.

Such a serious metabolic disorder in four-legged family members as hyperparathyroidism often develops due to gross violation rules for feeding young animals. Deficiency in the diet of calcium and vitamin D, an excess of phosphorus is the main cause of the alimentary form of the disease. In cats, the disease often occurs against the background of chronic renal failure.

Treatment primarily includes diet food, the introduction of minerals and vitamins into the body of a sick pet. If neoplastic processes are detected, the veterinary specialist conducts prompt removal damaged lobes of the parathyroid gland.

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ETIOLOGY: idiopathic, sometimes congenital, but often caused by severe general hormonal disorders of the body:
More often than not, it is underproduction. parathyroid glands parathyroid hormone; as casuistry - accidental removal of the parathyroid glands during surgical intervention on the thyroid gland.
Other causes: The disease can also be caused by the following reasons:
- autoimmune disease;
- surgical destruction;
- neoplasms;
- atrophy associated with prolonged hypercalcemia;
- deficiency of magnesium;
- congenital agenesis;
- infarction of parathyroid adenomas;

PATHOGENESIS: the disease strongly disrupts the balance of Ca and P in the blood and causes severe hypocalcemia with all the ensuing consequences and clinical signs that are the result of the impossibility of adequate retention of serum calcium levels.
Parathyroid hormone is a polypeptide that is involved in the regulation of phosphorus and calcium metabolism in the body and facilitates their transfer through biological membranes.
A decrease in the concentration of parathyroid hormone in the blood leads to the development of hypocalcemia, hyperphosphatemia, a weakening of calcium and phosphate excretion, and alkalosis.
Hypoparathyroidism occurs in two forms: chronic and latent (excluding postoperative complications).

PECULIARITIES:
Clinic: diarrhea, epilepsy, obstruction, vomiting, appendages, grand mal and petit mal attacks, hypocalcemia;

General clinic:
1. Abnormal behavior, aggression, change in habits;
2. Abnormal proprioceptive positioning;
3. Abnormal pupillary light reflex;
4. Anorexia (lack of appetite, refusal to eat);
5. Ataxia;
6. Auscultation of the heart: Tachycardia, increased heart rate;
7. Bradycardia, heart rate slowdown;
8. Ventricular tachycardia, multifocal or monofocal;
9. Ventricular premature tone, multifocal or monofocal;
10. Excitation (delirium, mania);
11. Generalized weakness;
12. Generalized lameness, stiffness of movements;
13. Hyperesthesia, hypersensitivity;
14. Hypothermia;
15. Dehydration;
16. Dysuria, difficult, painful urination, stranguria;
17. Dysmetria;
18. Disorientation, memory loss;
19. Dyspnoe (difficulty breathing, with open mouth);
20. Dysphagia (difficulty swallowing);
21. Trembling;
22. Growth retardation;
23. Cataract (clouding of the lens);
24. Lymphadenopathy;
25. Fever, pathological hyperthermia;
26. Mydriasis, dilated pupil;
27. Fainting, syncope, convulsions, collapse;
28. Polydipsia, increased thirst;
29. Polyuria, increased volume of urination;
30. Precomeric salivation, ptyalism, salivation;
31. Prolapse of the third eyelid, protrusion of the nictitans membrane;
32. Vomiting, regurgitation, emesis;
33. Photophobia;
34. Spasms of the head, neck, face;
35. Spasms hind limbs;
36. Spasms of the forelimbs;
37. Spasms of the back;
38. Tachypnoe, Increased respiratory rate, polyp, hyperpnea;
39. Tenesmus. attempts;
40. Tetany,
41. Tetraparesis, paresis of all limbs;
42. Tremor;
43. Oppression (depression, lethargy);
44. Photophobia,

Symptoms. Puppies have a form of chronic intestinal osteodystrophy. The processes of calcium resorption in small intestine, and to restore its balance in the blood, calcium is mobilized from bone depots.
The depleted bone tissue is replaced by fibrous tissue. First of all, the bones of the jaws are affected, the expansion of the back of the nose becomes noticeable, the teeth are displaced, there are pains in the joints (especially in the maxillary).
Observed ectodermal disorders in the form of cataracts, loss of coat, fragility of claws, defects in tooth enamel and, in addition, cachexia.

Radiographically, a symptom of "bloating" of the bones of the upper and lower jaws is noted, their cortical layer is subject to osteolysis in places, alternating with areas of thickening. The general impoverishment of the bones of the skeleton with calcium is noted - osteoporosis.

Breeds.
In adult females, small and dwarf breeds hypoparathyroidism is like latent form tetany, activated only before estrus or during pregnancy and lactation (see "Tetany").

The diagnosis is made taking into account clinical and radiological signs and by determining the concentration of calcium in the blood.
- Clinical signs;
- rejection of other causes;
- measurement of serum levels of Ca and P;
- treatability;

TREATMENT: synthetic parathyroid hormone according to an individually selected dosage regimen - taking into account changes in the patient's state of health.
In acute cases, calcium gluconate is administered intravenously, diuretics, CO2 inhalation is used to cause a shift towards acidosis.
In chronically current hypoparathyroidism, dihydrotachysterol is prescribed to regulate the phosphorus-calcium balance: 1-15 drops of 0.1% oil solution daily.
The content of calcium and phosphates in the blood is determined again after 5-7 days from the start of treatment, then once a month.

DEVELOPMENT: prolonged.

FORECAST: doubtful to unfavorable.

Hyperparathyroidism in dogs and cats is a pathology endocrine nature, which occurs due to excessive production of parathyroid hormone. With this pathology, there is an increase in the level of calcium and a decrease in the content of phosphorus in the blood, damage to bone tissue in the form of increased fragility. Hyperparathyroidism can be primary or secondary. A secondary form of pathology in cats is called juvenile osteopathy.

Causes of the disease

Most often, primary hyperparathyroidism in dogs and cats appears as a result of adenoma, cancer, hyperplasia of the parathyroid glands.

The cause of secondary hyperparathyroidism in animals is considered to be an insufficient amount of calcium in the diet with an excess of phosphorus. This pathology can develop as a result of destructive lesions of the kidneys and chronic dystrophic changes small intestine.

Pathogenesis

A pathological increase in the production of parathyroid hormone leads to a violation of the exchange of phosphorus and calcium. With hyperparathyroidism, bone dystrophy develops. As a result of increased bone resorption, calcium from the bones moves into the bloodstream. This is accompanied by increased excretion of this element in the urine. There is a restructuring of the bone and acceleration of the processes of resorption of its parts. The bone apparatus of animals acquires softness and flexibility.

A manifestation of kidney damage is increased urination as a result of increased calcium excretion. A large number of calcium in the urine and bloodstream is the cause of the formation of urinary stones.

Clinical picture and symptoms of hyperparathyroidism

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

As the disease progresses, thirst, increased urination, and a decrease in appetite are noted. The animal is increasingly trying to avoid contact with people, sometimes this behavior comes to aggression towards humans.

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

Diagnosis of hyperparathyroidism

The main method for detecting hyperaparathyroidism in dogs and cats is the study of the content of calcium and phosphorus in the blood. To detect the pathology of the bone apparatus, it is necessary to conduct an x-ray examination. The X-ray sign of pathology is considered to be a thin cortical layer of the bone and the detection of bone cysts.

Hyperparathyroidism must be distinguished from diseases such as alimentary osteodystrophy, malignant hypercalcemia, etc.

Hyperparathyroidism in dogs and cats - treatment and prevention

On the early stages development of the disease can be successfully treated. Moreover, for this it is enough to switch to super-premium class food or make a balanced diet. Usually after a couple of months proper feeding the balance of calcium / phosphorus in the body is fully restored.

In advanced cases, surgery is necessary. Parathyroid adenoma is considered an indication for its surgical removal. After the operation, treatment is indicated that improves metabolic processes in the bone tissue. For this purpose, prescribe gluconate, calcium phosphate, vitamin supplements. Diet is also important. Conservative therapy is to reduce calcium in the blood and increase the content of phosphorus. First of all, it's about diet, rich in calcium. As drug treatment you can use phosphosan, etc. In case of kidney damage, intravenous sodium chloride is used. Large animals are injected with about a liter of such a liquid. Sodium citrate is used to reduce calcium levels in the blood. Calcitrin is used to preserve calcium in the bone apparatus. With pronounced inflammatory process in the joints use corticosteroids (prednisolone).

Secondary hyperparathyroidism, due to malnutrition, involves calculation of a balanced diet. If the disease is not advanced, then a properly selected super premium food or a balanced home diet is almost guaranteed to restore the calcium / phosphorus balance in the pet's body within a few months.

Common consequences of hyperparathyroidism

This disease rarely goes unnoticed. Usually this always results in growth retardation. Irreversible deformation is also possible pelvic bones which makes it difficult to defecate and urinate. In advanced cases of the disease, it is not recommended to give birth to ill animals.

Deformation chest often causes chronic diseases respiratory system. Neurological problems in animals also persist for life.

Secondary feeding hyperparathyroidism is a disease that has exclusively food etiology, is characterized by a violation of calcium-phosphorus metabolism with the development of osteodystrophy. It is based on a decrease in the intake of calcium from the intestines into the blood due to a lack of it in the feed (deficiency of intake) or prolonged chronic diarrhea(deficiency of assimilation).

IN AND. Kobyakov, E.V. Chernobay, Ph.D., "Don Veterinary Hospital", Rostov-on-Don

The main clinical signs of this pathology are impaired growth of puppies, curvature of the limbs, pain during movement, and fractures that are not associated with adequate physical impact. In such cases, veterinarians often diagnose rickets (a disease of growing animals characterized by impaired bone growth due to a lack of vitamin D in the diet). However, true rickets is rare in dogs and is difficult to model even experimentally. Whereas feed hyperparathyroidism is a fairly common pathology.

Rice. 1. Outbred puppy, 5 months old. Musculoskeletal dysfunction

Rice. 2. Doberman, 4 months old. Transfer of body weight when moving to the forelimbs, caused by pain in the pelvic limbs

The mechanism of regulation of calcium-phosphorus metabolism

It is known that about 40% of the total blood plasma calcium is associated with proteins, about 40% is present as cations and 20% in the form of compounds with organic matter. The ionized form of calcium is bound to the calmodulin protein and is biologically active. Phosphorus is present in plasma as sodium phosphate and compounds with organic substances. In the bones, a significant amount of calcium and phosphorus is deposited in the form of microcrystalline and amorphous hydroxyapatite.

Calcium metabolism in the body is regulated by parathyroid hormone (PTH), calcitonin, sex hormones and adrenal hormones.

PTH is a polypeptide hormone produced by the parathyroid glands, consists of 84 amino acid residues and is one of the main regulators of calcium metabolism in animals. The intensity of hormone secretion depends on changes in the level of calcium in the blood plasma. With a decrease in its concentration in plasma, parathyroid receptors that are sensitive to calcium activate the secretion of the hormone. In addition, PTH stimulates the release of calcium into the blood from bone tissue osteoclasts.

Rice. 3. Central Asian Shepherd Dog, 3.5 months old. Fracture of the upper third of the right thigh

The mechanism of action of PTH involves specific target cell membrane receptors - adenylate cyclase, cyclic adenosine monophosphate (cAMP) and protein kinase. When PTH acts on membrane receptors, adenylate cyclase is activated, which leads to the formation of cAMP inside the cell, which, in turn, increases the activity of protein kinase, which phosphorylates functionally important proteins. As a result, a number of biochemical reactions are triggered, which determine the physiological action of PTH.

In bone tissue, PTH increases the dissolution of hydroxyapatite, while phosphorus, calcium and bicarbonate are released into the extracellular fluid, but the content of phosphorus and bicarbonate in the blood does not increase due to increased loss of these substances in the urine, and the calcium content increases.

The action of PTH on the kidneys is to decrease phosphate reabsorption in the proximal and distal tubules and to increase calcium reabsorption in the distal tubules. PTH indirectly affects calcium absorption in the intestine, stimulating the production of D-1,25-dihydroxycholecalciferol in the kidneys, which can significantly increase calcium absorption from the intestine.

Diagnosis and treatment

Clinically, hyperparathyroidism is manifested by a violation of the musculoskeletal function, pain during movement, curvature of the long tubular bones, pathological fractures (Fig. 1-4). characteristic feature disease is a softening of the cortical layer of bone tissue. Sometimes it becomes so soft that it can be pierced with an ordinary injection needle (Fig. 5). At X-ray examination the architectonics of the cancellous bone is practically not visible, but diffuse osteoporosis is diagnosed - a uniform decrease in bone density, thinning of the cortical layer and expansion of the medullary canal (Fig. 6).

Rice. 4. Residual deformity of the bones of the forearms and metacarpus ( French Bulldog, male, 7 months)

Rice. 5. Puncture with an injection needle of the cortical layer of the tibia

Rice. 6. X-ray with secondary feeding hyperparathyroidism. Characteristic features: osteoporosis, cortical thinning femur, expansion of the medullary canal

Pathological fractures can occur even with minor physical impacts. As a rule, these are green stick fractures. When performing osteosynthesis, significant technical difficulties arise when trying to install a bone metal structure. In such cases, extrafocal osteosynthesis or celacast fixing bandages are preferable. Some types of pathological fractures in hyperparathyroidism do not require intervention at all, because. with an intact periosteum and limited mobility, such fractures grow together without fixation.

The main methods of treatment of secondary feeding hyperparathyroidism are diet therapy and the use of non-steroidal anti-inflammatory drugs (NSAIDs), in particular ketofen.

Diet therapy for hyperthyroidism

The effect of diet on the occurrence and course of hyperparathyroidism was studied by the authors in an experiment on 20 dogs of large and medium breeds with the corresponding diagnosis at the age of 3 to 6 months. At the beginning of the experiment and 2 months after it, a hematological study of all animals was carried out to determine the plasma levels of PTH, total calcium, inorganic phosphorus, total protein, and also carried out general analysis blood. Ten dogs (experimental group) were switched to the Purina JM Veterinary Diet (PVD JM). The remaining 10 dogs (control group) remained on the same diet ( natural products with the predominant use of meat) and received NSAIDs, tk. the owners of animals in this group did not agree with the concept of using ready-made rations.

In 1-2 weeks after the application of the PVD JM food, the dogs of the experimental group, in which certain clinical manifestations of hyperparathyroidism were observed in most cases before the experiment, began to move better, showed greater activity, and many of the manifestations of the pain syndrome ceased. After 2 months, the condition of the dogs almost returned to normal. The results of the study of animals of the experimental group are presented in table 1.

In the dogs of the control group, there was practically no improvement, two dogs were euthanized. All dogs of this group had curvature of the limbs, valgus deformity of the forearms, proximity of the hocks. Data from studies of animals in the control group are shown in Table 2.

conclusions

Secondary feeding hyperparathyroidism occurs, as a rule, in young dogs of predominantly large and medium breeds with a predominance of meat in the diet. It has been established that an imbalance of calcium and phosphorus in the blood plasma leads to decalcification of the bones, followed by a violation of the growth and development of the skeleton and the occurrence of pathological fractures. The study showed that the use prepared feed premium class, optimally balanced in composition nutrients, minerals and vitamins, prevents the development of secondary feeding hyperparathyroidism.

Table 1. Dynamics of the studied parameters in 10 dogs of the experimental group before the appointment of PVD JM and after 2 months of its use

Table 2. Dynamics of the studied parameters in 10 dogs of the control group before and after the experiment

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Hypercalcemia is a pathology detected, as a rule, in the biochemical analysis of blood serum. Disorders caused by hypercalcemia in dogs include lymphosarcoma, acute and chronic renal failure, vitamin D toxicosis, hypocorticism, anal sinus apocrine gland carcinoma, multiple myeloma, systemic mycosis, and primary hyperparathyroidism (PHP). Medical history, physical examination, complete blood count, urinalysis, biochemical analysis of blood serum, x-ray examination of the chest and abdominal cavity, cytological tests and biopsy usually give enough data to make a diagnosis. A preliminary diagnosis of RNR can be supported by measurement of serum parathyroid hormone (PTH) concentration, and histological confirmation of excised parathyroid tissue is required for a definitive diagnosis. RHP is a fairly uncommon cause of hypercalcemia, and the diagnosis may not be obvious. Multiple evaluation steps in a dog with hypercalcemia will not lead to a definitive diagnosis, as test results may be similar in dogs with lymphosarcoma and those with RNR. The following are the criteria for diagnosing dogs with hypercalcemia and RNR.

Differential diagnosis of hypercalcemia

Since hypercalcemia is almost always detected unexpectedly, it is not a mistake to do a second blood test to rule out laboratory error. In our experience, laboratory errors are extremely rare. When hypercalcemia is confirmed, the veterinarian should review the signs of the disease and the medical history with the owner of the dog to detect findings not noticed at first. Dogs over the age of 6 years, of any gender, are most predisposed to RHP disease. In dogs with RHP, unlike animals with many other diseases that cause hypercalcemia, the disease progresses unusually. Clinical signs are rather mild and usually include polyuria and polydipsia, muscle weakness, decreased activity, and increased appetite.

Based on the history of the disease, one can try to explain the hypercalcemia, which could result, for example, as a result of possible exposure to toxins containing vitamin D (these include some rodenticides - rodenticides); pain can be explained by lytic damage to the bones (multiple myeloma or breast tumor), difficulty eating - damage oral cavity caused by renal failure, and also characterized by an increase and decrease in the course of the disease, sometimes observed in hyperparathyroidism. The physical examination should also be repeated to determine the cause of hypercalcemia. It is necessary to palpate the spine and bones of the extremities to determine the presence of bone pain and examine the breast for the presence of neoplasia, the oral cavity for the presence of a rubber jaw or lesions characteristic of renal failure, the rectal region for the presence of apocrine gland carcinoma, heart rate and pulse characteristic of disorders associated with hypoadrenocorticism and peripheral lymph nodes- for the presence of their increases associated with lymphoma. In dogs with RHP, the physical examination is unremarkable, and the parathyroid glands are rarely palpable.

A thorough clinical and biochemical analysis of blood serum and urinalysis should be carried out. Urine specific gravity is usually less than 1.020 in dogs with hypercalcemia and kidney disease, hypoadrenocorticism, and hyperparathyroidism. These disorders often result in urinary tract infections. A general clinical blood test with RNR usually does not give any important information, in contrast to the normocytic normochromic non-regenerative anemia common in chronic renal failure, hypoadrenocorticism, and various neoplasias (eg, lymphoma). A biochemical analysis of blood serum is also carried out to assess the content of blood urea nitrogen, creatinine and serum phosphate concentration, an increase in which is characteristic of renal failure. Hyperkalemia and hyponatremia are characteristic of hypoadrenocorticism, hyperglobulinemia in myeloma; possible pathological activity of liver enzymes associated with various malignant neoplasms. Dogs with RNR usually do not have these pathologies, except in a small number of animals that show mild increases in serum alkaline phosphatase or blood urea nitrogen, creatinine, and phosphate. For this purpose, the only additional expense will be a repeated study of the level of calcium in the blood serum.

If the history, physical examination, and available database fail to determine the cause of the hypercalcemia, the next step in the diagnostic study is a chest x-ray. Its initial purpose is to evaluate the area of the cranial mediastinum to rule out the presence of lymphoma. If lymphadenopathy is detected, a biopsy is performed to confirm the diagnosis of lymphoma. X-ray examination also examines the lungs for neoplasia or systemic mycoses, the spine and ribs for lytic lesions caused by neoplasia, and the heart for microcardia caused by hypocorticism. X-rays dogs with RNR are usually unremarkable. Abdominal imaging is also evaluated, although it is preferable to ultrasound procedure. It makes sense to assess the size and consistency of the liver, spleen, mesenteric and sublumbar lymph nodes for the presence of pathologies that indicate malignant neoplasms(lymphomas). Diagnostic Imaging for Evaluation malignant tumor(lymphoma) is used for various tumors located in other organs, but tumors other than lymphoma are rare in hypercalcemia.

If possible, aspiration or biopsy of pathological areas should be performed to determine the presence or absence of neoplasia. An assessment of the size and consistency of the kidneys can be made, although renal failure should have been ruled out with primary analyzes blood. Dogs with RNR have intermittent renal mineralization and 30-40% have uroliths. The rest of the abdominal scans are unremarkable. If the conducted studies do not confirm a diagnosis other than RNR, the suspicion of this disease increases. However, until a specific cause of hypercalcemia is confirmed, the possibility of lymphoma should never be ruled out.

Confirmation of primary hyperparathyroidism

Additional tests are performed to confirm the diagnosis of RNR. Serum ionized calcium concentrations are markedly elevated in dogs with RNR, while in dogs with hypercalcemia-induced renal failure it is often normal or low. It is possible to measure the concentration of PTH in the blood serum. Normal or increased concentration confirms the diagnosis of RNR in dogs with hypercalcemia but without renal insufficiency. Dogs with renal insufficiency may also have elevated serum PTH levels. But based on data on renal parameters, serum phosphate and ionized calcium concentrations (usually normal to low in dogs with renal insufficiency), and other data, RNR can be differentiated from renal insufficiency. Serum PTH-associated protein (PTHrP) concentrations elevated in dogs with hypercalcemia are most commonly associated with lymphoma or carcinoma of the apocrine gland of the anal sinus. If the exact explanation for hypercalcemia remains unclear, we recommend response to treatment as a last resort. Lymph nodes, spleen, and liver, or a combination of these, should be aspirated or biopsied prior to prescribing drugs to rule out lymphoma. Here, special attention is paid to this disease, since some dogs this diagnosis difficult to confirm. In addition, if a dog with lymphoma is treated with glucocorticoids, it will be even more difficult to confirm the diagnosis.

Localization of parathyroid tissue causing hyperparathyroidism

Upon confirmation of the diagnosis of RNR, the most cost-effective and appropriate for the treatment of the patient will be an operational examination of the neck. Pathological change fabrics parathyroid glands with autonomous secretion is not always noticeable when online access, but experienced surgeons usually have no difficulty detecting the parathyroid tissue that causes hypercalcemia. Pathological adenoma, parathyroid carcinoma, or adenomatous hyperplastic tissue is usually larger and darker than healthy parathyroid tissue. It is useful for surgeons to know on which side of the neck, or a particular location within one side of the neck, a tumor or abnormal parathyroid tissue is likely to be found.

In humans, detection of abnormal parathyroid tissue is performed using Tc-99m-Sestamibi nuclear scintigraphy. There are reports of successful scintigraphy in two dogs with RNR. However, nuclear scintigraphy is not available everywhere, results for dogs with RNR are inconsistent, and the cost of such a procedure exceeds the cost of neck surgery.

Attracts attention ultrasound echography, because it is a widely available non-invasive method and is quite cost-effective. Ultrasound echography, like any diagnostic method, used in veterinary medicine, is carried out by the operator, and his skill to a large extent determines the value of the study. As the necessary equipment, various high-frequency transducers are obtained, and the experience of ultrasound echograph specialists increases, this diagnostic equipment will become even more effective. More than 90% of the dogs with RH that we examined by ultrasound showed a mass corresponding in size and location to the abnormal parathyroid tissue identified during surgery. In our clinic, ultrasound echography of the neck area has become a regular part of diagnostic examination dogs with hypercalcemia.

Attempts to determine the part of the neck with pathological parathyroid tissue using selective venous samples and measuring the concentration of PTH in the blood serum did not give satisfactory results. Venous drainage from the parathyroid glands occurs in jugular veins. Theoretically, the concentration of PTH in serum taken from the contralateral jugular vein and great circle blood circulation (head vein) should be similar, and the concentration of PTH in the blood serum from the pathological tissue of the parathyroid gland will be increased. Serum PTH concentrations were studied from both jugular veins and one cephalic vein in the group of dogs with RNR. There was no clear gradient distinguishing part of the pathological parathyroid tissue. It is possible that the results obtained were not consistent with the theory because the venous outflow did not occur as expected, because the received blood was not under the outflow from the parathyroid gland to the jugular veins, or for some other reason. Anyway this procedure has not been proven to be useful.

Initial treatment of hypercalcemia

Hypercalcemia impairs the tubular ability of the kidneys, reduces renal blood flow and lowers the level glomerular filtration. Progressive renal impairment leading to azotemia and renal tubular degeneration is most likely in animals with a sustained increase in ionized calcium levels. Therefore, it is necessary to produce targeted and appropriate clinical and laboratory assessment to minimize the delay between the initial establishment of hypercalcemia and the start of treatment.

In the meantime, treatment is indicated that lowers the level of calcium in the blood serum. Such treatment is particularly important in animals with azotemia or "increased" calcium-phosphorus product (eg, calcium x phosphorus > 70). But severe hypercalcemia alone is not an indication for surgery. Some dogs with RHP in our cohort had total serum calcium levels in excess of 19 mg/dL and ionized calcium concentrations in excess of 2 mmol/L. In these patients, phosphate concentrations were typically less than 3 mg/dl and products less than 60. These dogs showed no clinical signs of hypercalcemia other than clinically stable polyuria, polydipsia, and muscle weakness. And the electrocardiogram given state was uninformative.

If necessary, treatment is first infusion therapy to reduce serum calcium and maintain renal perfusion. After taking blood and urine for analysis, a catheter is inserted intravenously and the patient is re-hydrated within 6-12 hours. Subsequent increase in fluid volume by intravenous administration of 0.9% physiological saline promotes the release of calcium, and with the introduction of volumes from 120 to 180 ml / kg within 24 hours, diuresis of saline begins. This treatment is usually combined with the loop diuretic furosemide (2 mg/kg IV every 8 hours), which increases calciuresis. To prevent iatrogenic hypocalcemia, intravenous injections potassium chloride; at the initial stage, 16-20 mEq of potassium chloride per 1 liter of saline is usually sufficient. These general measures reduce the serum calcium level to the required range, although hypercalcemia may have a weak effect on some patients and completely inadequate on others.

If the above measures fail, other drugs may be needed to lower serum calcium levels. Effectively this effect is exerted by glucocorticosteroids. Prednisolone (2 mg/kg PO or IM every 12 hours) increases urinary calcium excretion, decreases intestinal absorption, and interferes with calcium absorption from bones. Glucocorticosteroids are of partial benefit in hypercalcemia caused by malignant lymphoma, however, such treatment does not allow to establish accurate diagnosis due to a reduction in neoplastic cell mass and should be discontinued if possible until the possibility of lymphoma has been ruled out. Refractive hypercalcemia can be treated with mithramycin or calcitonin (5 U/kg IM or SC every 8 hours). These are expensive and more complex treatments. Veterinarians Those who are not experienced in using these drugs should first consult with an oncologist or physician about the specifics of the treatment and the side effects it causes.

Treatment of primary hyperparathyroidism

Treatment of dogs with suspected RHD also serves to confirm the diagnosis. A total exploratory thyroid surgery is recommended, in which the surgeon examines both sides of the neck, as well as the ventral and dorsal surface lobe of the thyroid gland. In most dogs with RHP, the abnormal parathyroid tissue is discrete, darker in color, and larger than normal parathyroid tissue and is therefore easy to recognize and remove. Pathological parathyroid tissue is usually removed if possible, and thyroid gland usually removed along with the pathological internal mass. If it is not possible to observe a parathyroid mass and the diagnosis is certain, one thyroid/parathyroid complex should be removed and analyzed histologically. When observing two pathological parathyroid glands, both must be removed. Three or four abnormal parathyroid glands present a dilemma, and usually one of them is left in place. Two, three, or four abnormal parathyroid glands are rare, and their presence indicates hyperplasia rather than adenoma.

If before the operation the serum calcium concentration was above 11.5 mg/dl but less than 14.0 mg/dl, we simply measure it or the concentration of ionized calcium twice a day for 5-7 days after the operation. Treatment with vitamin D is prescribed only if the calcium concentration becomes less
8.0 mg/dl, ionized calcium less than 0.85 mmol/l, or clinical signs of tetany are observed (see previous article). If preoperative serum calcium is >15 mg/dL, postoperative hypocalcemia is more likely to occur and we start vitamin D treatment (dihydrotachysterol; 0.03 mg/kg daily in two divided doses, then taper off over 2 -6 months) the morning after the operation or immediately after it. Measurement of serum calcium is performed as described above, and parenteral calcium is prescribed only in case of tetany or in unavoidable cases.