What is primary, secondary and tertiary hyperparathyroidism. Secondary hyperparathyroidism: causes, symptoms and treatments

Hyperparathyroidism- a chronic endocrine disease caused by an increase in the production of the hormone of the parathyroid glands (parathyroid hormone, parathyreocrine, PTH) with tumors (adenomas) of the parathyroid glands, or their hyperplasia (non-tumor proliferation of organ tissue, accompanied by an increase in working function).

Anatomy of the parathyroid glands

The typical number of parathyroid glands is two pairs (observed in 80-85% of people). 15-20% of the world's population has from 3 to 12 glands. Congenital variations in the number of glands, as a rule, are not accompanied by pathological symptoms.

With a typical number of parathyroid glands, the weight of one gland normally ranges from 20 to 70 mg, and the dimensions, as a rule, do not exceed 6 * 3 * 1.5 mm. The glands are disc-shaped, and differ from the tissue of the thyroid gland in a yellow color.

The parathyroid glands are most often located on the posterior surface of the thyroid gland. At the same time, their upper pair is at the level of the upper and middle thirds of the thyroid gland, and the lower pair is at the level of its lower third.

However, the location of the parathyroid glands is highly variable. For example, the lower pair may be located in the mediastinum, maintaining a connection with the thymus gland (thymus), sometimes inside the gland itself.

As a rule, the parathyroid glands are located at the entrance to the thyroid gland of blood vessels or nerve branches. Often they are partially or completely immersed in the tissue of the thyroid gland, although they have their own capsule.

Additional parathyroid glands can be located in the anterior and posterior mediastinum, inside the tissue of the thyroid and thymus glands, on the posterior surface of the esophagus, in the pericardial cavity (in the heart sac), in the region of the bifurcation of the carotid artery.

The parathyroid glands are supplied with blood from the branches of the arteries of the thyroid gland, so they can be damaged during operations on the thyroid gland.

Functions of the parathyroid hormone

Despite their small size, the parathyroid glands play an important role in the life of the body, regulating the exchange of calcium and phosphorus.

Parathormone promotes the release of calcium from bone tissue and, thus, increases its concentration in blood plasma. In addition, parathyroid hormone increases intestinal absorption of calcium and reduces its excretion in the urine, which also leads to hypercalcemia.

An increase in the production of parathyroid hormone contributes to an increase in the excretion of phosphorus from the body in the urine (phosphaturia).

The regulation of the activity of the parathyroid glands occurs according to the feedback principle: with a decrease in the level of calcium in the blood, their activity increases, and with hypercalcemia, it decreases. Thus, with an excess of calcium in the blood, the size of the glands decreases, and prolonged hypocalcemia leads to working hyperplasia of the organs - an increase in their activity and size.

pathological physiology

Increased secretion of parathyroid hormone leads to leaching of calcium from the bones, and an increase in its concentration in the blood plasma (hypercalcemia).

The pathology of the skeletal system in hyperparathyroidism manifests itself in systemic skeletal fibrosis (replacement of bone tissue by fibrous tissue), accompanied by gross deformities of the skeletal system.

Due to the high level of calcium in the blood, calcification occurs in the internal organs (in medicine, this phenomenon is called "transfer of the skeleton to soft tissues"). In this case, the kidneys and the walls of blood vessels suffer the most. So in severe cases, patients die from kidney failure or gross circulatory disorders.

Another common complication is the formation of calcium phosphate stones in the upper urinary tract, which further aggravates the condition of the kidneys.

Calcium plays an important role in water and electrolyte metabolism, therefore, an increase in its concentration causes systemic effects, such as:

  • impaired conduction in the nervous tissue, which ultimately leads to muscle weakness, depression, memory and cognitive impairment;
  • arterial hypertension ;
  • increased gastric secretion, which can be complicated by the formation of gastric and duodenal ulcers.

Epidemiology

Among endocrine diseases, hyperparathyroidism ranks third in prevalence (after diabetes mellitus and hyperthyroidism).

Women get sick 2-3 times more often than men. With age, the likelihood of developing the disease increases (especially after menopause in women). As life expectancy increases in highly developed countries, the incidence of hyperparathyroidism is likely to rise.

The reasons

In accordance with the cause of the increased content of the hormone of the parathyroid glands in the blood, there are:
1. Primary hyperparathyroidism.
2. Secondary hyperparathyroidism.
3. Tertiary hyperparathyroidism.
4. Pseudohyperparathyroidism.

The clinical symptoms of all forms of hyperparathyroidism are largely similar, since in all the cases described above, calcium is washed out of the skeletal system, and persistent hypercalcemia develops, leading to many complications.

However, the underlying disease that caused the hyperparathyroidism syndrome will also affect the clinical picture. Therapeutic tactics in many cases will be different.

Primary hyperparathyroidism

Primary hyperparathyroidism is a syndrome of increased secretion of parathyroid hormone caused by the primary pathology of this endocrine organ.

In 85% of cases of primary hyperparathyroidism, a single benign tumor (adenoma) of one of the glands becomes the cause of the development of pathology. Less often (in 5% of cases) there are multiple adenomas affecting several glands. Even less common is parathyroid cancer.

Cases of primary diffuse hyperplasia of the parathyroid glands are extremely rare (often we are talking about hyperplasia of accessory glands located in the mediastinum, which greatly complicates topical diagnosis).

Typical adenomas develop predominantly in older people, most often in women during menopause. Rare cases of diffuse hyperplasia are characteristic of a young age and, as a rule, are combined with other diseases of the endocrine system. Parathyroid cancer often develops after irradiation of the head and neck.

Secondary hyperparathyroidism

Secondary hyperparathyroidism is a syndrome of increased concentration of parathyroid hormone in the blood, which develops in initially healthy parathyroid glands due to reduced calcium levels caused by other diseases.

Thus, in response to a lack of calcium in the blood, parathyroid hormones are released, causing hypercalcemia - this is a normal feedback regulation. However, in cases when it comes to severe chronic diseases leading to a sharp and prolonged decrease in the level of calcium in the blood, a serious pathology may develop over time - secondary hyperparathyroidism.

Most often, the causes of secondary hyperparathyroidism are severe kidney pathology and malabsorption syndrome (impaired absorption of nutrients in the gastrointestinal tract) - respectively, renal and intestinal (intestinal) forms of secondary hyperparathyroidism are isolated.

In patients on hemodialysis ("artificial kidney" apparatus), the syndrome of secondary hyperparathyroidism develops in 50-70% of cases. In patients who have undergone gastric resection, the level of parathyroid hormone increases in 30% of cases.

The development of secondary hyperparathyroidism in chronic renal failure is associated with impaired synthesis of active vitamin D in the kidney parenchyma, which leads to impaired calcium absorption and hypocalcemia.

Hypocalcemia in intestinal forms of secondary hyperparathyroidism is associated with impaired absorption of vitamin D and calcium in the gastrointestinal tract.

In addition, hypocalcemia develops in severe liver diseases (primary biliary cirrhosis) due to impaired vitamin D metabolism, as well as in rickets and rickets-like diseases in children.

Tertiary hyperparathyroidism

Tertiary hyperparathyroidism was first described in patients who successfully underwent kidney transplantation. It turned out that the complete restoration of all renal parameters did not eliminate the elevated level of parathyroid hormone in the blood and, accordingly, the symptoms of secondary hyperparathyroidism.

Thus, with prolonged stimulation of the parathyroid glands by a state of hypocalcemia, an irreversible working hyperplasia of their glandular tissue develops. This condition has been termed tertiary hyperparathyroidism.

The clinic of tertiary hyperparathyroidism is in many ways similar to the clinic of primary hyperplasia of the parathyroid glands.

Pseudohyperparathyroidism

Pseudohyperparathyroidism is a syndrome of hypercalcemia associated with the development of malignant tumors (some malignant neoplasms of the lungs, kidneys, breast, myeloma). Pseudohyperparathyroidism is often caused by the presence of parathyroid hormone-producing cells in the tumor. However, according to the latest scientific data, this is not the main and not the only cause of this pathology.

The fact is that an increase in the level of calcium in the blood is often not combined with a high level of parathyroid hormone. It is believed that some tumors produce substances similar in action to parathyroid hormone. Often, hypercalcemia is associated with local (cancer metastases) or diffuse (myeloma) effect of the tumor on bone tissue, accompanied by bone dissolution and calcium release into the blood.

Symptoms

Symptoms of Primary Hyperparathyroidism

Initial manifestations of the disease
Often, the initial stages of primary hyperparathyroidism are asymptomatic, which leads to late diagnosis of the pathology. In such cases, the level of parathyroid hormone and calcium in the blood is usually low, and are almost the only signs of the disease. Therefore, in most cases, pathology is determined by chance, during examination for other diseases.

Up to 80% of patients in the initial stage of the disease present non-specific complaints, such as:

  • weakness;
  • lethargy;
  • tendency to constipation;
  • Bad mood;
  • pain in bones and joints.
It should be noted that these symptoms are often not associated with primary hyperparathyroidism, and do not disappear after radical surgical treatment of the disease.

In more severe cases, the first manifestations of the disease are usually complaints from the muscular system. A high concentration of calcium in the blood disrupts neuromuscular transmission, and leads to a kind of myopathy.

First, weakness and pain appear in certain muscle groups, most often in the lower extremities. Patients complain of difficulty in normal walking (often stumble, fall), it is difficult for them to get up from a chair (support is needed), to enter a tram, bus, etc.

Looseness in the joints appears early, a duck gait and pain in the feet are very characteristic (flat feet develop due to a violation of the tone of the muscles of the foot). Thus, in severe primary hyperparathyroidism, patients are bedridden even before the appearance of pathological fractures.

Often the onset of the disease is the appearance of a kind of diabetes insipidus (polyuria and polydipsia with reduced urine density). This syndrome is associated with damage to the kidney tubules by massive release of calcium (calciuria) and loss of their sensitivity to antidiuretic hormone.

A characteristic early manifestation of damage to the skeletal system in primary hyperparathyroidism is the loosening and loss of healthy teeth.

In severe cases of the disease, severe weight loss develops associated with a sharp loss of appetite and polyuria, leading to dehydration. Sometimes patients lose up to 10-15 kg in the first 3-6 months of illness. Characterized by earthy color and dry skin. This appearance is associated both with general exhaustion and dehydration, and with the development of anemia, the genesis of which in primary hyperparathyroidism has not yet been fully elucidated.

Advanced clinical stage of the disease
Symptoms of the advanced clinical stage of primary hyperparathyroidism in severe and moderate course can be divided into the following groups:

  • bone;
  • articular;
  • renal;
  • gastrointestinal;
  • vascular;
  • ophthalmic;
  • neurological.
Based on the predominant lesion of any of the body systems, bone, renal, visceropathic (with a predominant lesion of internal organs) and mixed clinical forms of primary hyperparathyroidism are distinguished.

Skeletal lesion
Under the action of parathyroid hormone, calcium and phosphorus are intensively washed out of the bones, and osteoclasts are activated - bone tissue cells that contribute to bone dissolution. As a result, osteoporosis (partial resorption of bone tissue) occurs. Osteoporosis can be either diffuse (a general decrease in bone density) or limited (subperiosteal osteoporosis - a decrease in bone density directly under the periosteum). It can also manifest itself through the formation of cysts (cavities in the bones that can be filled with fluid).

Osteoporosis is a severe deformity of the bones. So, the pelvis takes the form of a "card heart", the femur - a "shepherd's stick", the chest becomes like a bell. As a rule, the spine suffers, especially the thoracic and lumbar vertebrae, which take the form of "fish". On the basis of pathological changes in the vertebrae, a general deformation of the spinal column occurs - kyphosis (posterior curvature with the formation of a hump), scoliosis (sideways curvature with a violation of the general symmetry of the body), kyphoscoliosis.

Due to a decrease in bone density, bone fractures occur even with a slight load, or spontaneously (pathological fractures). Unlike conventional ones, pathological fractures are less painful, which in some cases makes diagnosis difficult and leads to improper bone fusion, or to the formation of false joints (bone fragments do not grow together, but acquire pathological mobility), which leads to permanent disability. Fracture healing is slow. However, if the bones fuse together, a sufficiently dense callus is formed, so that repeated fractures in the same place do not happen.

Due to severe bone deformities, patients may lose 10-15 cm or more in height.

Joint damage is associated with both skeletal deformity and the deposition of calcium phosphate salts (false gout). In addition, elevated levels of parathyroid hormone can stimulate the deposition of uric acid crystals in the joints (true gout).

Damage to the nervous system, blood vessels and internal organs
The second target after bones in primary hyperparathyroidism is the kidneys. The severity of renal symptoms, as a rule, determines the prognosis of the disease, since renal failure, which develops as a result of prolonged hypercalcemia, is irreversible.

Direct damage to the renal parenchyma is exacerbated by the formation of calcium phosphate stones in the upper urinary tract. Characterized by coral stones that fill the entire pyelocaliceal system of the kidney.

Lesions of the gastrointestinal tract are manifested by symptoms such as:

  • nausea;
  • a sharp decrease in appetite;
  • constipation.
With a pronounced increase in the level of calcium, patients complain of sharp pains in the abdomen of various irradiations.

In the future, ulcerative lesions develop: duodenal ulcers are most characteristic, less often the stomach, esophagus and intestines are affected. In severe cases, erosive processes occur in many organs of the gastrointestinal tract with the formation of multiple ulcers. A tendency to bleeding, frequent exacerbations and relapses is characteristic.

Often there are calculous cholecystitis (formation of stones in the gallbladder), calcification of the pancreatic ducts with the development of pancreatitis. It is characteristic that with the development of pancreatitis, the level of calcium in the blood decreases due to the increased production of the hormone glucagon by the inflamed gland.

The pathology of the cardiovascular system in primary hyperparathyroidism is associated with arterial hypertension and calcium deposition in the walls of blood vessels. In severe cases, it is possible to develop lesions of many organs due to a violation of their blood supply.

Eye damage is caused by the deposition of calcium salts in the cornea (ribbon keratopathy).

The pathology of the nervous system manifests itself already in the early stages of the disease, and the severity of symptoms is highly dependent on the level of calcium in the blood. Characteristic:

  • depressive states of varying severity;
  • apathy;
  • decreased memory and cognitive abilities;
  • in severe cases - confusion, psychosis.

Symptoms of secondary and tertiary hyperparathyroidism

Secondary hyperparathyroidism occurs against the background of a disease that caused an increase in the production of parathyroid hormone (most often this is a pathology of the kidneys).

Since the cause of secondary hyperparathyroidism was a pathology that provoked prolonged hypocalcemia, and hyperproduction of parathyroid hormone was a kind of compensatory reaction, the level of calcium in the blood in such patients is usually within the normal range.

The most characteristic symptoms of secondary hyperparathyroidism are lesions of the skeletal system, since secondary hypothyroidism develops against the background of a lack of vitamin D, accompanied by calcium leaching from the bones, and parathyroid hormone enhances this process.

Among extraosseous manifestations, calcifications are most common in soft tissues and walls of large vessels. Very characteristic eye damage in the form of calcification of the conjunctiva and cornea, combined with chronically recurrent conjunctivitis.

Tertiary hyperparathyroidism develops with a long course of the secondary, so that even with the elimination of the disease that caused hypocalcemia and stable normalization of calcium levels in the blood, parathyroid hormone production remains elevated due to irreversible working hyperplasia of the parathyroid glands.

Symptoms of tertiary hyperparathyroidism are nonspecific, and in many respects are similar to secondary ones. Laboratory determined high levels of parathyroid hormone and calcium in the blood.

Hypercalcemic crisis

Hypercalcemic crisis is a rather rare complication of hyperparathyroidism caused by a sharp increase in the level of calcium in the blood, and is characterized by severe disorders of higher nervous activity, a deadly increase in blood clotting, up to the development of thrombosis and disseminated intravascular coagulation syndrome (DIC), as well as the development acute cardiovascular failure, capable of causing cardiac arrest.

In the case of complications of hyperparathyroidism hypercalcemic crisis, the mortality of patients can reach 50-60% or more.
Most often, the factors provoking the development of a dangerous complication are:

  • exacerbation of primary hyperparathyroidism in the absence of adequate treatment;
  • spontaneous pathological bone fractures (massive release of calcium into the blood);
  • dehydration;
  • immobilization (prolonged immobilization due to a serious illness, after surgery, etc.);
  • misdiagnosis with calcium and/or vitamin D supplementation;
  • erroneous prescription of antacids for duodenal ulcer caused by hyperparathyroidism;
  • treatment with thiazide diuretics without taking into account contraindications;
  • intake of foods rich in calcium and phosphorus (milk, nutritional supplements, as well as foods containing an increased amount of vitamin D).
Hypercalcemic crisis in hyperparathyroidism develops acutely. The patient's condition deteriorates sharply, symptoms characteristic of an acute abdomen appear: nausea, indomitable vomiting, peritonitis, constipation. Pain in a hypercalcemic crisis is sharp and often shingles. Therefore, such patients are often mistakenly diagnosed with acute pancreatitis.

The intense secretion of gastric juice characteristic of hyperparathyroidism against the background of extreme hypercalcemia can lead to the formation of multiple ulcers and the development of gastrointestinal bleeding.

A high fever develops rapidly with an increase in temperature to 39-40 degrees and above. There is muscle weakness, decreased tendon reflexes, bone pain. The skin becomes dry, itching appears, which often leads to scratching.

A variety of neuropsychiatric disorders are growing, from depression to pronounced psychomotor agitation (up to psychosis). With the progression of the pathology, consciousness becomes confused, and the patient falls into a coma.

In the future, due to the activation of blood coagulation factors, DIC may develop. With extremely high numbers of hypercalcemia, shock may develop. Death, as a rule, occurs due to paralysis of the respiratory center and/or cardiac arrest.

Hyperparathyroidism in children

Primary hyperparathyroidism in children, especially those under 10 years of age, is extremely rare. According to statistics, girls get sick more often than boys. As in adults, the most common cause of hyperparathyroidism in children is a solitary benign tumor (adenoma) of the parathyroid gland. Glandular hyperplasia is much less common.

In newborns, hereditary hyperparathyroidism occurs, due to a genetic defect in the receptors of parathyroid cells for calcium. The mechanism of development of this pathology is similar to secondary hyperparathyroidism - the parathyroid glands undergo working hyperplasia, since defective receptors register a reduced level of calcium.

There are two forms of this hereditary disease:
1. Severe homozygous - when pathological genes are obtained from both parents.
2. More benign - heterozygous, when the influence of the pathological gene is somewhat balanced by the normal gene.

The most common cause of secondary hyperparathyroidism in children, as well as in adults, is severe renal failure or malabsorption syndrome.

In young children, the secondary type of the disease often develops with rickets and rickets-like diseases.

Hyperparathyroidism, which developed at an early age, causes a lag in physical and mental development.

Treatment for children is the same as for adults.

Diagnostics

Primary hyperparathyroidism

P Since the initial stages of hyperparathyroidism are often asymptomatic, laboratory methods are of paramount importance in the diagnosis of the disease.

Primary hyperparathyroidism is characterized by such laboratory symptoms as:

  • increased levels of calcium in the blood;
  • reduced plasma phosphate levels;
  • increased excretion of calcium in the urine;
  • increased excretion of phosphates in the urine.
With a double determination of hypercalcemia, a preliminary diagnosis of primary hyperparathyroidism is made, and the level of parathyroid hormone in plasma is measured.

If an elevated level of parathyroid hormone confirms the diagnosis of hyperparathyroidism, a topical diagnosis is performed. To do this, use ultrasound (ultrasound), computed tomography (CT) and magnetic resonance imaging (MRI) of the head and neck.

Additionally, diagnostics of complications of hyperparathyroidism (osteoporosis, kidney damage) is carried out.

When making a diagnosis of primary hyperparathyroidism, it is necessary to conduct a differential diagnosis with diseases that occur with an increased level of calcium in the blood:

  • malignant tumors (bone metastases, multiple myeloma);
  • hypervitaminosis D;
  • secondary hyperparathyroidism;
  • rare causes (thyrotoxicosis, taking thiazide diuretics, hypervitaminosis A, Addison's disease, etc.).
It should be noted that with hypervitaminosis D, the level of parathyroid hormone in the blood is normal or reduced. Secondary hyperparathyroidism occurs against the background of the underlying disease, with normal levels of calcium in the blood.

Secondary hyperparathyroidism

Secondary hyperparathyroidism is characterized by an elevated level of parathyroid hormone with a normal concentration of calcium in the blood plasma.

Determining the level of parathyroid hormone is indicated for any pathology of the kidneys, accompanied by a decrease in the glomerular filtration rate to 60% or less.

Topical diagnosis and diagnosis of complications are carried out according to the same rules as in the primary form of the disease.

Differential diagnosis is primarily carried out between diseases that can cause secondary hyperparathyroidism. Therefore, the examination is always supplemented by the study of the pathology that led to prolonged hypocalcemia, which caused increased production of parathyroid hormone.

Tertiary hyperparathyroidism

This type of disease is characterized by an increase in the level of parathyroid hormone in the blood by 10-25 times with a normal calcium content. Such a diagnosis is made with the resistance of secondary hyperparathyroidism to ongoing conservative treatment, and the appearance of hypercalcemia.

Treatment

Hypercalcemic crisis

The relief of the hypercalcemic crisis is carried out in the endocrinology or intensive care unit.

All therapeutic measures are aimed at the speedy decrease in the level of calcium in the blood. First of all, under the control of the electrolyte composition of the blood, forced diuresis is carried out: within three hours, 3.0 liters of an isotonic sodium chloride solution are injected intravenously, in combination with the introduction of the diuretic furosemide 100 mg/hour.

In addition, the binding of free calcium in the blood is carried out using Complexone - a 5% solution of the sodium salt of ethylenediaminetetraacetic acid (Na 2 -EDTA). For 5-6 hours, a dose equal to 50 mg/kg of the patient's body weight is administered.

And finally, calcium is fixed in the bones with the help of Calcitrin (1-4 IU / kg of the patient's body weight).

To accelerate the excretion of calcium from the body, extracorporeal methods (blood cleansing outside the body) such as hemodialysis and peritoneal dialysis with calcium-free dialysate can be used.

Primary hyperparathyroidism

Practice has shown that the only effective treatment for primary hyperparathyroidism is surgery.

However, the initial stages of hyperparathyroidism most often occur without pronounced symptoms, and the preclinical period of the disease is 10 years or more. Given the solid age of most patients (most often, the pathology develops in older men and women during menopause), they pay attention to the indications for the operation, which are divided into absolute and relative.

Absolute indications for surgical treatment:

  • the level of calcium in the blood is more than 3 mmol / l;
  • episodes of hypercalcemia in the past;
  • severe renal dysfunction;
  • stones in the upper urinary tract (even if there are no symptoms of urolithiasis);
  • excretion of calcium in the urine more than 10 mmol per day;
  • severe osteoporosis.
Relative indications for surgical treatment:
  • severe comorbidities;
  • complexity of dynamic observation;
  • young age (up to 50 years);
  • the patient's desire.
Surgical treatment of primary hyperparathyroidism consists in removing the tumor producing parathyroid hormone.

In cases when it comes to diffuse hyperplasia of the parathyroid glands, a subtotal parathyroidectomy is performed - three glands and part of the fourth are removed, leaving an area that is sufficiently well supplied with blood. Relapses after such an operation occur in 5% of cases.

Patients for whom surgery is not indicated are prescribed constant monitoring:

  • continuous monitoring of blood pressure and calcium levels in the blood;
  • study of kidney function every 6-12 months;
  • bone densistometry and ultrasound of the kidneys once every two to three years.

Secondary hyperparathyroidism

Drug treatment of secondary hyperparathyroidism consists in the appointment of vitamin D preparations, and with a tendency to hypocalcemia - in combination with calcium preparations (up to 1 g / day).

The indication for subtotal parathyroidectomy is the failure of the ongoing conservative treatment. Surgical intervention is resorted to with an increase in the level of parathyroid hormone in the blood plasma by three or more times, as well as with hypercalcemia of 2.6 mmol / l or more.

Tertiary hyperparathyroidism

The term "tertiary hyperparathyroidism" generally refers to the state of increased production of parathyroid hormone in patients after kidney transplantation.

It should be noted that the reverse involution of hyperplastic parathyroid glands takes time - months, and sometimes even years. However, if the high level of parathyroid hormone and calcium in the blood does not decrease, despite Calcitriol therapy, and there is a real threat of complications, subtotal parathyroidectomy is indicated.

Hyperparathyroidism: description, diagnosis, treatment - video

Forecast

With timely diagnosis of primary hyperparathyroidism and successful removal of a tumor that produces parathyroid hormone, the prognosis is favorable. Restoration of the bone tissue structure occurs, as a rule, within the first two years after the operation. Pathological symptoms of hyperparathyroidism from the nervous system and internal organs disappear within a few weeks. parathyroid hormone. Increased production of the hormone is a consequence glandular hyperplasia , which in turn leads to a violation of phosphorus-calcium metabolism. So there is an increased excretion of phosphorus and calcium from the skeleton, an increase in osteoclastic processes and their excessive intake in large quantities into the blood.

Simultaneous increased release of phosphorus, as well as a decrease tubular reabsorption gives rise to hypophosphatemia and hyperphosphaturia , at the same time, signs and symptoms appear in the bone tissue osteomalacia . Most often, 2-3 times more than men, the disease affects women aged 25 to 50 years.

The cause of hyperparathyroidism is a tumor of the parathyroid glands.

Depending on the cause of the occurrence, hyperparathyroidism is divided into the following types:

  • Primary appears as a result of the formation of parathyroid adenoma in the vast majority of cases. And only in one out of ten cases of diseases the cause is the occurrence carcinomas or hyperplasia, the overgrowth and enlargement of normal gland cells.
  • Secondary hyperparathyroidism- there is an increase in function, pathological growth and enlargement of the glands, a prolonged low content of calcium with a simultaneous increase in the content of phosphates in the blood. There is an increase in production parathyroid hormone in chronic renal failure.
  • Tertiary- there is the development of benign tumors of the parathyroid glands, as well as increased production of parathyroid hormone due to prolonged secondary hyperparathyroidism.
  • Pseudohyperparathyroidism- there is a production of parathyroid hormone by tumors that did not arise from the cells of the parathyroid glands.

According to the severity of the disease is divided into

  • manifest shape.
  • asymptomatic (soft) form.
  • asymptomatic shape.

In addition, according to the degree of the disease, the disease is divided into bone , renal , visceral and mixed forms.

Symptoms of hyperparathyroidism

The danger of the disease is that it can proceed without symptoms and the detection or diagnosis of hyperparathyroidism occurs by chance during the examination. In the early stages of the disease, the patient develops rapid fatigue even with small loads, difficulty walking, and especially when climbing stairs, a characteristic waddling "duck" gait.

Patients experience emotional imbalance, resentment and anxiety, memory deteriorates, depression appears. The skin takes on an earthy gray color. In old age, various may appear.

In the future, signs of damage to various internal organs develop - cholelithiasis, osteoporosis, etc.

The late stage of bone hyperparathyroidism is characterized by softening and curvature of the bones, the appearance of scattered pain in the bones of the arms or legs, in the spine. Ordinary movements can lead to bone fractures, which are not painful, but slowly grow together, while sometimes false joints are formed.

because of deformable skeleton, the patient may even become shorter. With osteoporosis of the jaws, healthy teeth become loose or fall out. On the neck, a large in the region of the parathyroid glands. On the limbs appear visible periarticular calcifications .

At visceropathic hyperparathyroidism there is nausea, vomiting, a sharp weight loss. Patients complain of loss, stomach pain, flatulence. The examination reveals the appearance of peptic ulcers with, as well as various signs of damage to the pancreas and gallbladder, polyuria and symptoms of renal failure develop. The nutrition of organs and tissues is disturbed, a high concentration of calcium in the blood causes damage to the vessels of the heart, an increase in blood pressure,. With calcification of the ocular conjunctiva, the so-called "red eye" syndrome is observed.

In the renal form, the main symptoms of hyperparathyroidism: polyuria and alkaline urine. It is possible to develop bilateral nephrocapcinosis , which in turn can lead to uremia . The patient is concerned about high blood pressure, attacks of renal colic, dyspeptic disorders. An ulcer of the duodenum or stomach appears, perforation of the wall of the stomach and intestines is possible. Often possible chronic formation of stones in the gallbladder.

Diagnosis of hyperparathyroidism

Diagnosis of the disease is carried out on the basis of blood tests that determine calcium and phosphorus in the body and urine analysis.

If a high level of calcium is detected, other tests and studies are performed: ultrasound, X-ray, CT and MRI, which can detect osteoporosis, pathological ulcers of the gastrointestinal tract, cystic bone changes and other changes. Scintigraphy parathyroid glands reveals the localization of the location of the glands and their anomaly.

In secondary hyperparathyroidism, the defining disease is diagnosed.

The doctors

Treatment of hyperparathyroidism

Treatment of the disease is carried out in a complex combination of conservative therapy with medications and surgical surgery. Before surgery, conservative treatment is carried out, the purpose of which is to reduce Ca levels in the blood.

Operatively, malignant tumors of the parathyroid glands are removed, then radiation therapy is performed.

The prognosis of hyperparathyroidism is favorable with timely diagnosis of hyperparathyroidism and adequate surgical treatment. Full recovery of working capacity depends on the degree of damage to the bone tissue. If the treatment of hyperparathyroidism is started at an early stage, the patient recovers within a maximum of six months. In moderately severe cases, recovery lasts for 2 years. In advanced cases, disability is likely.

A less favorable prognosis for renal forms of hyperparathyroidism and depends entirely on the degree of kidneys before surgery. Without surgery - disability and death due to progressive cachexia and chronic renal failure.

At hypercalcemic crisis the prognosis depends on the timeliness of treatment, mortality is 32%.

List of sources

  • Endocrinology. Ed. N. Lavin. - Moscow: Practice, 1999;
  • Pathophysiology of the endocrine system / ed. ON THE. Smirnova. - M.: Binom, 2009;
  • Endocrinology / Dedov I.I. etc. M.: Medicine, 2007.

Hyperparathyroidism is a chronic pathology of the parathyroid glands, progressing due to the occurrence of tumors or increased growth of their tissues. Pathology is characterized by increased production of parathyroid hormone, which affects calcium metabolism. Its excess content in the blood causes calcium to be washed out of the bones, and this, in turn, leads to serious complications.

Among all endocrine diseases, hyperparathyroidism ranks 3rd - more often than this disease, only and occurs. Women suffer from pathology more often than men several times (especially women over the age of 45). Sometimes there is hyperparathyroidism in children - due to congenital pathology of the parathyroid glands.

The reasons

The disease occurs when a large amount of parathyroid hormone is produced by the parathyroid glands, which leads to an increase in the concentration of calcium in the blood and a decrease in the level of phosphorus. Everyone knows that calcium plays an important role in our body. It is necessary for the normal functioning of the bone skeleton, and is also an important component of teeth. In addition, with its help, signals are transmitted to the muscles that ensure their work.

Causes of increased calcium levels in the blood can be hereditary and physiological. Hereditary causes are congenital pathologies in the structure, number and functioning of the parathyroid glands. However, such causes are less common than physiological, that is, resulting from the vital activity of the organism.

The main causes of hyperparathyroidism are as follows:

  • lack of vitamin D;
  • tumors of various origins on the parathyroid glands;
  • intestinal diseases, in which absorption processes are disturbed in the organ;
  • hyperplasia of two or more parathyroid glands.

Depending on the cause, there are several varieties of this pathology. So, in medical practice, primary, secondary and tertiary hyperparathyroidism is distinguished. In addition, there is the so-called alimentary and pseudohyperparathyroidism.

Primary is caused by the direct pathology of this organ. Most often, this disease occurs when there is a benign adenoma on the organ, and less often (5% of cases), multiple tumors become the cause. Very rarely, primary hyperparathyroidism occurs as a result of a cancerous tumor on the parathyroid gland.

Also, this type of disease causes hyperplasia of the parathyroid glands.

Secondary hyperparathyroidism occurs as a result of a violation of calcium metabolism due to other pathological disorders in the human body. Due to the lack of this trace element in the blood, due to some internal disturbances, the parathyroid glands begin to actively produce calcitonin, which leads to development.

Most often, secondary hyperparathyroidism develops as a result of complex pathologies of internal organs, for example, kidney pathology and pathological disorders in the intestines. Accordingly, this type of disease can be of two forms:

  • renal;
  • interstinal.

Such a pathology as alimentary hyperparathyroidism refers to the secondary form and it occurs against the background of malnutrition. The disease occurs when the nutrition of children or adults is unbalanced and there is a lack of calcium in it. The treatment of hyperparathyroidism of this form is the simplest - it is necessary to normalize the amount of calcium entering the body with food.

Tertiary hyperparathyroidism is a rather rare form of the disease that causes a violation of the production of parathyroid hormone due to kidney transplantation.

The last type of pseudohyperparathyroidism. This is a condition that occurs with certain cancers, such as tumors of the mammary glands and lungs. Often this type of pathological disorder is observed due to the fact that cancer cells are able to produce substances that are similar in properties to parathyroid hormone.

Symptoms

Very often, at the beginning of its development, the disease is asymptomatic, so its diagnosis is difficult. There is only one sign that speaks of the disease - an increased content of calcium in the blood, which is detected by chance, during a patient's examination for other health problems or a physical examination.

Most people at the initial stage of the disorder have only general symptoms, such as:

  • Bad mood;
  • fatigue;
  • loss of appetite;
  • the appearance of constipation;
  • pain in the bones and joints.

Sometimes there may be unreasonable nausea, and even vomiting.

At the stage of progression of the disease, the symptoms become more pronounced and they are associated with impaired neuromuscular conduction. There is weakness in the muscles, pain in them, difficulty walking. To get up from a chair, a person with such a disorder needs support, and he also cannot climb stairs, get on a tram, etc. without assistance.

Other symptoms of this disorder are loose joints and the development of a "duck walk". Because of this disorder, people can be bedridden even before the bones become brittle and pathological fractures occur. It is the fragility of the bones and the occurrence of permanent fractures that are important symptoms of the progression of the pathology. And a person also loses teeth, and even those that were completely healthy.

In addition to those described above, other symptoms are observed with hyperparathyroidism, for example, a sharp decrease in body weight, development leading to dehydration, an earthy shade of the skin and their dryness, development. A person with this disorder looks haggard and tired.

In a severe course of the disease, violations of the internal organs are noted. In particular, the following symptoms may occur:

  • skeletal damage (, severe bone deformities, and, pathological fractures, false and true gout);
  • development, the nature of which is irreversible;
  • disruption of the digestive tract, resulting in the development of symptoms such as pain, nausea, vomiting, diarrhea, etc.;
  • development and.

If we talk about secondary and tertiary hyperparathyroidism, then their symptoms are usually associated with the musculoskeletal system. Eye damage is characteristic, manifested by permanent conjunctivitis.

One of the most severe, although rare complications of this pathology, is a hypercalcemic crisis, which is characterized by:

  • development of cardiovascular insufficiency;
  • increased blood clotting;
  • severe disorders of nervous activity.

Such a pathological condition can cause or lead to cardiac arrest, therefore, with the development of a hypercalcemic crisis, the mortality rate is about 60%.

Diagnostics

An important role in the treatment of pathology is the diagnosis of the disease at an early stage. The main importance in the diagnosis of the disease is given to laboratory methods of research, which allow to determine the increased content of calcium in the blood and the insufficient content of phosphorus.

Diagnosis also involves ultrasound of the parathyroid glands, CT and MRI.

When establishing a diagnosis of primary hyperparathyroidism, a differential diagnosis of this disease is necessary, with pathologies such as hypervitaminosis D or malignant tumors in the body.

Diagnosis of other forms of this disorder is carried out in a similar way. In addition, patients with any kind of this pathology need to be diagnosed with complications that could develop against its background.

Treatment

When a form of pathology is established, its treatment will depend on the data obtained during the diagnosis. To stop the hypercalcemic crisis, the patient is placed in the intensive care unit and forced diuresis is performed. Hemodialysis and other emergency measures are also indicated.

Treatment of hyperparathyroidism is mainly carried out surgically. Surgical treatment consists in removing a tumor on the gland, or removing excess (overgrown) tissue. The secondary form can be treated with medication - for this purpose, vitamin D preparations are prescribed. If conservative treatment does not work, subtotal parathyroidectomy is indicated.

Hyperparathyroidism is a pathological condition of the parathyroid glands associated with a violation of their work and the production of an excessive amount of parathyroid hormone. This leads to the release of calcium from bone tissue, an increase in its concentration in the blood and accumulation in other organs, usually in the kidneys. Hyperparathyroidism is more common in adults; in children, pathology is observed much less frequently. According to medical statistics, in families where there are patients with hyperparathyroidism, in 30% of cases the disease also manifests itself in children.

The parathyroid glands are located on the posterior surface of the thyroid gland. Their increased functioning leads to an excess of parathyroid hormone in the blood and its accumulation in the internal organs.

An increase in the function of the parathyroid glands, observed in childhood, can have a variety of reasons:

  • idiopathic hyperplasia (an increase in the size and function of the glands for an unknown reason);
  • rickets;
  • thyroid adenoma;
  • chronic disorder of the processes of digestion and absorption of nutrients in the small intestine;
  • sarcoidosis;
  • increased concentration of blood phosphates in chronic kidney disease (hyperphosphatemia);
  • tuberculosis;
  • hypervitaminosis D;
  • Williams syndrome;
  • necrosis of subcutaneous adipose tissue in newborns;
  • oncological diseases (leukemia, neuroblastoma, dysgerminoma, etc.);
  • genetic predisposition (familial benign hyperparathyroidism), etc.

To provoke the development of hyperparathyroidism in children can:

  • uncontrolled intake of hormonal drugs and antibiotics;
  • unfavorable ecology;
  • eating carcinogenic foods, etc.

Symptoms

The clinical picture of hyperparathyroidism in children is similar to that of adults. Signs of the disease:

  • irritability;
  • drowsiness;
  • weakness;
  • malaise;
  • problems with weight gain;
  • muscle weakness;
  • nausea and vomiting;
  • constipation;
  • fever;
  • mental disorders;
  • delayed physical development, etc.

Due to the fact that calcium is excreted into the blood in excess, it is deposited in the kidney parenchyma; this leads to the development of hematuria and renal colic. The leaching of calcium is accompanied by a pathological change in the structure of bone tissue.

There is loosening of the teeth or their late eruption. Children complain of pain in the back, abdomen and limbs. In patients with hyperparathyroidism, hallux valgus deformity of the knee joints, compression fractures of the vertebrae, gait disturbances, etc. can be observed. Prolonged hypercalcemia leads to seizures, mental retardation and blindness.

Diagnostics

Secondary hyperparathyroidism is most often discovered incidentally. Primary pathology is diagnosed using the following studies:

  • Analysis of urine;
  • blood chemistry;
  • biopsy and histological examination of bone tissue;
  • densitometry (determination of bone density);
  • MRI and CT of the head and neck;
  • Ultrasound of the thyroid gland together with parathyroid, etc.

How to treat


To correct the chemical parameters of the blood, the child is given forced diuresis.

Treatment of hyperparathyroidism in children is complex. Depending on the condition of the child and the stage of development of the disease, one or more methods of therapy are used:

  1. First of all, the patient is given forced diuresis to correct the chemical parameters of the blood. Within a few hours, up to 3.5 liters of isotonic sodium chloride solution is administered intravenously.
  2. Taking vitamin D supplements in a therapeutic dose.
  3. Chemotherapy is treatment with chemotherapy drugs.
  4. Surgical intervention (most often comes down to subtotal parathyroidectomy). Patients partially or completely remove the adenoma, if any, damaged parathyroid glands and adjacent tissues. Currently, such operations are performed using a minimally invasive, endoscopic method.
  5. Taking hormonal drugs - corticosteroids, bisphosphonates, calcitonin. Hormone therapy helps to inhibit the release of calcium from the skeletal system.
  6. Treatment with radioactive iodine, etc.

During the treatment of hyperparathyroidism in children, the intake of calcium-containing vitamins and medicines that increase its level in the body is canceled. In addition, additional treatment is prescribed with drugs that stop muscle and bone dystrophy.

With early diagnosis and timely surgical treatment, the prognosis is favorable. However, severe and extensive bone deformities can persist for life.

Diet for hyperparathyroidism

Proper nutrition in hyperparathyroidism is the key to stabilizing the patient's condition and speedy recovery. Children with this endocrine pathology must strictly follow a diet. Parents must:

  • exclude from the child's diet or limit to a minimum foods high in calcium (dairy and milk); babies with a congenital form of pathology are transferred from soy mixtures to food;
  • increase the amount of foods rich in phosphorus in the patient's menu,) and vitamin D (butter, cheese);
  • make sure that the child drinks (1-2 liters per day, depending on age);
  • use iodized or reduced sodium salt in cooking;
  • completely exclude "harmful" foods rich in carcinogens, preservatives, salt, fats, dyes.

Summary for parents


A child with hyperparathyroidism should drink enough water.

To prevent the development of hyperparathyroidism in children, it is necessary to ensure that foods containing

- endocrinopathy, which is based on excessive production of parathyroid hormone by the parathyroid glands. Hyperparathyroidism leads to an increase in the level of calcium in the blood and pathological changes occurring primarily in bone tissue and kidneys. The incidence of hyperparathyroidism among women is observed 2-3 times more often than among men. Hyperparathyroidism affects women aged 25 to 50 to a greater extent. Hyperparathyroidism can have a subclinical course, bone, visceropathic, mixed form, as well as an acute course in the form of a hypercalcemic crisis. Diagnosis includes the determination of Ca, P and parathyroid hormone in the blood, X-ray examination and densitometry.

General information

- endocrinopathy, which is based on excessive production of parathyroid hormone by the parathyroid glands. Hyperparathyroidism leads to an increase in the level of calcium in the blood and pathological changes occurring primarily in bone tissue and kidneys. The incidence of hyperparathyroidism among women is observed 2-3 times more often than among men. Hyperparathyroidism affects women aged 25 to 50 to a greater extent.

Classification and causes of hyperparathyroidism

Hyperparathyroidism can be primary, secondary or tertiary. The clinical forms of primary hyperparathyroidism can be varied.

Primary hyperparathyroidism

Primary hyperparathyroidism is divided into three types:

I. Subclinical primary hyperparathyroidism.

  • biochemical stage;
  • asymptomatic stage ("silent" form).

II. Clinical primary hyperparathyroidism. Depending on the nature of the most pronounced symptoms, there are:

  • bone form (parathyroid osteodystrophy, or Recklinghausen's disease). Manifested by deformation of the limbs, leading to subsequent disability. Fractures appear "on their own", without injury, heal for a long time and difficult, a decrease in bone density leads to the development of osteoporosis.
  • visceropathic form:
  • renal - with a predominance of severe urolithiasis, with frequent attacks of renal colic, the development of renal failure;
  • gastrointestinal form - with manifestations of stomach and duodenal ulcers, cholecystitis, pancreatitis;
  • mixed form.

III. Acute primary hyperparathyroidism(or hypercalcemic crisis).

Primary hyperparathyroidism develops when the parathyroid glands contain:

  • one or more adenomas (benign tumor-like formations);
  • diffuse hyperplasia (enlargement of the gland);
  • hormonally active cancer (rarely, in 1-1.5% of cases).

In 10% of patients, hyperparathyroidism is combined with various hormonal tumors (pituitary tumors, thyroid cancer, pheochromocytoma). Primary hyperparathyroidism also includes hereditary hyperparathyroidism, which is accompanied by other hereditary endocrinopathies.

Secondary hyperparathyroidism

Secondary hyperparathyroidism serves as a compensatory response to a long-term low level of Ca in the blood. In this case, increased synthesis of parathyroid hormone is associated with impaired calcium-phosphorus metabolism in chronic renal failure, vitamin D deficiency, malabsorption syndrome (impaired absorption of Ca in the small intestine). Tertiary hyperparathyroidism develops in the case of untreated long-term secondary hyperaparthyroidism and is associated with the development of an autonomously functioning parathyroid adenoma.

Pseudohyperparathyroidism (or ectopic hyperparathyroidism) occurs with malignant tumors of various localization (breast cancer, bronchogenic cancer), capable of producing a parathormone-like substance, with multiple endocrine adenomatosis types I and II.

Hyperparathyroidism is manifested by an excess of parathyroid hormone, which promotes the removal of calcium and phosphorus from bone tissue. Bones become fragile, soften, can bend, and the risk of fractures increases. Hypercalcemia (excessive level of Ca in the blood) leads to the development of muscle weakness, excretion of excess Ca in the urine. Urination intensifies, constant thirst appears, kidney stone disease (nephrolithiasis), deposition of calcium salts in the kidney parenchyma (nephrocalcinosis) develops. Arterial hypertension in hyperparathyroidism is due to the effect of excess Ca on the tone of blood vessels.

Symptoms of hyperparathyroidism

Hyperparathyroidism can be asymptomatic and diagnosed incidentally during examination. With hyperparathyroidism, the patient simultaneously develops symptoms of damage to various organs and systems - stomach ulcers, osteoporosis, urolithiasis, cholelithiasis, etc.

Early manifestations of hyperparathyroidism include fatigue during exercise, muscle weakness, headache, difficulty walking (especially when lifting, overcoming long distances), and a waddling gait is characteristic. Most patients note memory impairment, emotional imbalance, anxiety, and depression. Older people may present with severe psychiatric disorders. With prolonged hyperparathyroidism, the skin becomes earthy gray.

At the late stage of bone hyperparathyroidism, softening, curvature, pathological fractures (during normal movements, in bed) of the bones occur, diffuse pains occur in the bones of the arms and legs, and the spine. As a result of osteoporosis of the jaws, healthy teeth become loose and fall out. Due to the deformation of the skeleton, the patient may become shorter in stature. Pathological fractures are not painful, but heal very slowly, often with deformities of the limbs and the formation of false joints. Periarticular calcifications are found on the arms and legs. A large adenoma can be palpated on the neck in the area of ​​the parathyroid glands.

Visceropathic hyperparathyroidism is characterized by nonspecific symptoms and a gradual onset. With the development of hyperparathyroidism, nausea, stomach pains, vomiting, flatulence occur, appetite is disturbed, weight decreases sharply. Patients have peptic ulcers with bleeding of various localizations, prone to frequent exacerbations, relapses, as well as signs of damage to the gallbladder and pancreas. Polyuria develops, urine density decreases, unquenchable thirst appears. In the later stages, nephrocalcinosis is detected, symptoms of renal failure develop, progressing over time, uremia.

Hypercalciuria and hypercalcemia, the development of calcification and vascular sclerosis, leads to malnutrition of tissues and organs. A high concentration of Ca in the blood contributes to damage to the vessels of the heart and an increase in blood pressure, the occurrence of angina attacks. With calcification of the conjunctiva and cornea of ​​the eyes, red eye syndrome is observed.

Complications of hyperparathyroidism

Hypercalcemic crisis refers to severe complications of hyperparathyroidism that threaten the patient's life. Risk factors are prolonged bed rest, uncontrolled intake of Ca and vitamin D preparations, thiazide diuretics (reduce urinary Ca excretion). The crisis occurs suddenly with acute hypercalcemia (Ca in the blood is 3.5 - 5 mmol / l, at a rate of 2.15 - 2.50 mmol / l) and is manifested by a sharp exacerbation of all clinical symptoms. This condition is characterized by: high (up to 39 - 40 ° C) body temperature, acute pain in the epigastrium, vomiting, drowsiness, impaired consciousness, coma. Weakness sharply increases, dehydration of the body occurs, a particularly serious complication is the development of myopathy (muscle atrophy) of the intercostal muscles and diaphragm, and the proximal parts of the body. Pulmonary edema, thrombosis, bleeding, perforation of peptic ulcers may also occur.

Diagnosis of hyperparathyroidism

Primary hyperparathyroidism does not have specific manifestations, so it is quite difficult to make a diagnosis based on the clinical picture. It is necessary to consult an endocrinologist, examine the patient and interpret the results:

  • urinalysis

Urine acquires an alkaline reaction, calcium excretion in the urine (hypercalciuria) and an increase in the content of P in it (hyperphosphaturia) are determined. The relative density drops to 1000, there is often protein in the urine (proteinuria). Granular and hyaline cylinders are found in the sediment.

  • biochemical blood test (calcium, phosphorus, parathormone)

The concentration of total and ionized Ca in the blood plasma increases, the content of P is below normal, the activity of alkaline phosphatase is increased. More indicative in hyperparathyroidism is the determination of the concentration of parathyroid hormone in the blood (5-8 ng / ml and above at a rate of 0.15-1 ng / ml).

  • ultrasound

Ultrasound of the thyroid gland is informative only when parathyroid adenomas are located in typical places - in the region of the thyroid gland.

  • x-ray, CT and MRI

Radiography can detect osteoporosis, cystic bone changes, pathological fractures. Densitometry is performed to assess bone density. With the help of x-ray examination with a contrast agent, peptic ulcers in the gastrointestinal tract that occur during hyperparathyroidism are diagnosed. CT of the kidneys and urinary tract reveals stones. X-ray tomography of the retrosternal space with esophageal contrasting with barium suspension allows to identify parathyroid adenoma and its location. Magnetic resonance imaging is superior in information content to CT and ultrasound, visualizes any localization of the parathyroid glands.

  • scintigraphy of the parathyroid glands

Allows you to identify the localization of usually and abnormally located glands. In the case of secondary hyperparathyroidism, the defining disease is diagnosed.

Treatment of hyperparathyroidism

Complex treatment of hyperparathyroidism combines surgical surgery and conservative drug therapy. The main treatment for primary hyperparathyroidism is surgery, which consists in removing the parathyroid adenoma or hyperplastic parathyroid glands. To date, surgical endocrinology has minimally invasive methods of surgical interventions performed for hyperparathyroidism, including the use of endoscopic equipment.

If the patient has been diagnosed with a hypercalcemic crisis, an emergency operation is necessary. Prior to surgery, it is mandatory to prescribe conservative treatment aimed at lowering Ca in the blood: drinking plenty of fluids, intravenously - isotonic NaCl solution, in the absence of renal failure - furosemide with KCl and 5% glucose, livestock thyroid gland extract (under the control of Ca levels in the blood), bisphosphonates (pamidronic acid and sodium etidronate), glucocorticoids.

After surgery for malignant tumors of the parathyroid glands, radiation therapy is performed, and an antitumor antibiotic, plicamycin, is also used. After surgical treatment, the amount of Ca in the blood decreases in most patients, so they are prescribed vitamin D supplements (in more severe cases, Ca salts intravenously).

Forecast and prevention of hyperparathyroidism

The prognosis of hyperparathyroidism is favorable only in case of early diagnosis and timely surgical treatment. Restoration of the patient's normal working capacity after surgical treatment of bone hyperparathyroidism depends on the degree of damage to the bone tissue. With a mild course of the disease, performance is restored after surgical treatment within about 3-4 months, in severe cases - within the first 2 years. In advanced cases, limiting bone deformities may remain.

In the renal form of hyperparathyroidism, the prognosis for recovery is less favorable and depends on the severity of kidney damage at the preoperative stage. Without surgery, patients usually become disabled and die from progressive cachexia and chronic renal failure. With the development of a hypercalcemic crisis, the prognosis is determined by the timeliness and adequacy of the treatment, mortality in this complication of hyperparathyroidism is 32%.

With existing chronic renal failure, drug prevention of secondary hyperparathyroidism is important.

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