Primary hyperparathyroidism treatment. Primary hyperparathyroidism

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What is hyperparathyroidism?

Anatomy of the parathyroid glands

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 thyroid tissue by their yellow color.

The parathyroid glands are most often located on back surface thyroid gland. Moreover, their upper pair is located at the level of the upper and middle third 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.

Usually, parathyroid glands located at the entry points thyroid gland blood vessels or nerve branches. Often they are partially or completely immersed in the thyroid tissue, 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 area 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 parathyroid hormone

Parathyroid hormone promotes the release of calcium from bone tissue and thus increases its concentration in the blood plasma. In addition, parathyroid hormone increases calcium absorption in the intestine 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).

Regulation of the activity of the parathyroid glands occurs according to the feedback principle: when the level of calcium in the blood decreases, their activity increases, and with hypercalcemia it decreases. Thus, with excess 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

Pathology skeletal system in hyperparathyroidism, it manifests itself in systemic skeletal fibrosis (replacement of bone tissue with fibrous tissue), accompanied by gross deformations of the skeletal system.

Due to the high level of calcium in the blood, calcifications form in the internal organs (in medicine this phenomenon is called “transfer of the skeleton to soft tissues”). In this case, the kidneys and vessel walls suffer the most. So in severe cases patients die from renal failure or severe circulatory disorders.

Another common complication is the formation of calcium phosphate stones in upper sections urinary system, which further aggravates the kidney condition.

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

• disruption of conduction in nerve 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 stomach and duodenal ulcers.

Epidemiology

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 increase.

Causes

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

However, on clinical picture The underlying disease that caused hyperparathyroidism syndrome will also be affected. Treatment tactics will be different in many cases.

Primary hyperparathyroidism

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

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

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

Secondary hyperparathyroidism

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

The most common causes of secondary hyperparathyroidism are severe kidney pathology and malabsorption syndrome (impaired absorption of nutrients in the gastrointestinal tract) - renal and intestinal (intestinal) forms of secondary hyperparathyroidism are respectively distinguished.

In patients undergoing hemodialysis (artificial kidney machine), secondary hyperparathyroidism syndrome develops in 50-70% of cases. In patients who have undergone gastrectomy, parathyroid hormone levels increase in 30% of cases.

The development of secondary hyperparathyroidism in chronic renal failure is associated with impaired synthesis of active vitamin D in the renal 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 when serious illnesses liver (primary biliary cirrhosis) due to impaired vitamin D metabolism, as well as rickets and rickets-like diseases in children.

Tertiary hyperparathyroidism

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

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

Pseudohyperparathyroidism

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. Hypercalcemia is often associated with local (cancer metastases) or diffuse (myeloma) effects of the tumor on bone tissue, accompanied by bone dissolution and the release of calcium into the blood.

Symptoms

Symptoms of primary hyperparathyroidism

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

• weakness;
• lethargy;
• tendency to constipation;
• Bad mood;
• pain in bones and joints.

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

First there is weakness and pain in the separate groups muscles, most often in lower limbs. Patients complain of difficulties in normal walking(they often stumble and fall), it is difficult for them to get up from a chair (they need support), get on a tram, bus, etc.

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

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

Characteristic early manifestation 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 the disease. Characterized by sallow 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 is still not fully understood.

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;
• ophthalmological;
• neurological.

Skeletal lesion
Under the influence of parathyroid hormone, calcium and phosphorus are intensively washed out of the bones, and osteoclasts, bone tissue cells that promote bone dissolution, are also activated. As a result, osteoporosis occurs (partial resorption of bone tissue). Osteoporosis can be either diffuse ( general decline bone density) and limited (subperiosteal osteoporosis - decreased 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 causes severe bone deformation. Thus, the pelvis takes the shape of a “card heart”, the femur - a “shepherd’s stick”, rib cage becomes like a bell. As a rule, the spine suffers, especially the thoracic and lumbar vertebrae, which take on a “fish” shape. Due to pathological changes in the vertebrae, general deformation of the spinal column occurs - kyphosis (posterior curvature with the formation of a hump), scoliosis (sideways curvature with a violation of the overall 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 ordinary fractures, pathological fractures are less painful, which in some cases complicates diagnosis and leads to improper fusion of bones, or the formation of false joints (bone fragments do not heal, but become pathological mobility), which leads to permanent disability. Healing of fractures is slow. However, if the bones heal, a sufficiently dense callus is formed so that repeated fractures do not occur in the same place.

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

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

Defeat nervous system, blood vessels and internal organs
The second target after bone in primary hyperparathyroidism is the kidneys. Expressiveness kidney 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 aggravated by the formation of calcium phosphate stones in the upper urinary system. Coral stones are characteristic, filling the entire pyelocaliceal system of the kidney.

Defeats gastrointestinal tract manifested by symptoms such as:

• nausea;
• a sharp decrease in appetite;
• tendency to constipation.

Further development ulcerative lesions: duodenal ulcers are most common; the stomach, esophagus and intestines are less commonly affected. In severe cases, erosive processes occur in many organs of the gastrointestinal tract with the formation of multiple ulcers. Characterized by a tendency to bleeding, frequent exacerbations and relapses.

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

Pathology of cardio-vascular system in primary hyperparathyroidism is associated with arterial hypertension and calcium deposition in the walls of blood vessels. In severe cases, damage to many organs may develop due to disruption of their blood supply.

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

Pathology of the nervous system manifests itself already at early stages diseases, and the severity of symptoms depends greatly on the level of calcium in the blood. Characteristic:

• depressive states varying degrees expressiveness;
• apathy;
• decreased memory and cognitive abilities;
• in severe cases – confusion, psychosis.

Symptoms of secondary and tertiary hyperparathyroidism

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

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

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

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

Symptoms of tertiary hyperparathyroidism are nonspecific and are in many ways similar to secondary hyperparathyroidism. High levels of parathyroid hormone and calcium in the blood are determined in the laboratory.

Hypercalcemic crisis

If hyperparathyroidism is complicated by a hypercalcemic crisis, the mortality rate of patients can reach 50-60% or higher.
Most often, the factors provoking the development 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 (long-term immobilization due to serious illness, after surgery, etc.);
• erroneous diagnosis with the use of calcium and/or vitamin D supplements;
• erroneous prescription of antacid drugs for duodenal ulcers caused by hyperparathyroidism;
• treatment with thiazide diuretics without taking into account contraindications;
• eating foods rich in calcium and phosphorus (milk, nutritional supplements, as well as products containing increased amount vitamin D).

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

Developing quickly high fever with an increase in temperature to 39-40 degrees and higher. Muscle weakness, decreased tendon reflexes, and bone pain are observed. The skin becomes dry, itching appears, which often leads to scratching.

Various psychoneurological disorders are on the rise, from depression to severe psychomotor agitation (up to psychosis). As the pathology progresses, consciousness becomes confused and the patient falls into a coma.

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

Hyperparathyroidism in children

In newborns, hereditary hyperparathyroidism occurs, caused by 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 received from both parents.
2. More benign is 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 children younger age secondary type The disease often develops with rickets and rickets-like diseases.

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

Treatment for children is the same as for adults.

Diagnostics

Primary hyperparathyroidism

Primary hyperparathyroidism is characterized by: laboratory symptoms, How:

• increased levels of calcium in the blood;
• decreased level of phosphates in blood plasma;
• increased excretion of calcium in the urine;
• increased excretion of phosphates in the urine.

If an elevated level of parathyroid hormone confirms the diagnosis of hyperparathyroidism, topical diagnosis is performed. For this purpose, ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MRI) of the head and neck area are used.

Additionally, complications of hyperparathyroidism (osteoporosis, kidney damage) are diagnosed.

When diagnosing primary hyperparathyroidism, it is necessary to carry out a differential diagnosis with diseases that occur with elevated levels 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.).

Secondary hyperparathyroidism

Determination of parathyroid hormone levels is indicated for any kidney pathology, accompanied by a decrease in glomerular filtration rate to 60% or lower.

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

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

Treatment

Hypercalcemic crisis

All curative measures aimed at quickly reducing calcium levels in the blood. First of all, under the control of the electrolyte composition of the blood, forced diuresis is carried out: 3.0 liters of isotonic sodium chloride solution is injected intravenously over three hours, in combination with the administration of the diuretic furosemide 100 mg/hour.

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

Finally, calcium is fixed in the bones using Calcitrin (1-4 IU/kg of the patient’s body weight).

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

Primary hyperparathyroidism

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

Absolute indications for surgical treatment:

• blood calcium level 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.

• severe concomitant diseases;
• complexity of dynamic observation;
• young age (up to 50 years);
• patient's wishes.

In cases where we are talking about 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:

• constant monitoring of blood pressure and calcium levels in the blood;
• kidney function testing every 6-12 months;
• Carrying out bone densitometry and ultrasound of the kidneys once every two to three years.

Secondary hyperparathyroidism

The indication for subtotal parathyroidectomy is the failure of conservative treatment. TO surgical intervention resorted to when the level of parathyroid hormone in the blood plasma increases three times or more, as well as when hypercalcemia is 2.6 mmol/l or more.

Tertiary hyperparathyroidism

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

Hyperparathyroidism: description, diagnosis, treatment - video

Forecast

Hyperparathyroidism is a disease of the parathyroid glands, which is characterized by increased production of parathyroid hormone (PTH) by the organ. The disease code according to ICD 10 is E21. The result is dysregulation of calcium and phosphorus levels in the blood. An increase in calcium concentration causes hypercalcemia. The strength of bone tissue decreases, and the risk of injury and bone fractures increases.

Hyperparathyroidism develops more often in women (2-3 times more often than in men). With age, the number of cases increases; by the age of 50, 1% of women experience hyperparathyroidism. Until recently, the disease was considered rare. But thanks modern methods diagnostics it turned out that only cases of a significant excess of parathyroid hormones are rare.

Classification and reasons for development

There are forms of hyperparathyroidism:

• primary- occurs with primary damage to the parathyroid glands;
• secondary- manifests itself against the background of calcium deficiency and excess phosphorus in the blood;
• tertiary- formation of organ adenoma due to secondary hyperparathyroidism.

The mechanism of development of the disease is associated with an increase in the concentration of PTH, which is responsible for the exchange of phosphorus and calcium in the body, which entails:

• leaching of calcium from bones, its sedimentation in the kidneys and soft tissues;
• increased amount of phosphorus in urine;
• activation of the formation of active vitamin D3;
• promotion secretory activity pancreas and stomach.

Primary hyperparathyroidism occurs in 80% of cases in women. Its forms are distinguished:

• bone;
• renal;
• gastrointestinal;
• mixed.

Causes of development of primary hyperparathyroidism:

• parathyroid adenoma (80% of cases);
• diffuse organ hyperplasia (10%);
• hormone-producing cancer - carcinoma (2-3%).

10% of cases of hyperparathyroidism occur against the background of existing tumors.

Secondary hyperparathyroidism is a consequence of prolonged Ca deficiency. There is an increased production of parathyroid hormone due to a disturbance in calcium-phosphorus metabolism due to:

• vitamin D deficiency;
• renal failure;
• disturbances in calcium absorption in the small intestine.

Symptoms and manifestations of pathology

The clinical manifestations of hyperparathyroidism depend on its form. Symptoms of primary hyperparathyroidism may vary depending on its subtypes.

Common signs of the disease may be:

• increased blood pressure;
• weight loss;
• "duck" gait;
• fast fatiguability;
• muscle paresis, weakness;
• deterioration of brain activity;
• disturbance of emotional balance.

Bone form

This form of hyperparathyroidism is characterized by its own specific manifestations:

• frequent sudden bone fractures, their deformation at the fracture sites;
• formation of cysts in the bones (club-shaped swellings);
• aching pain in the joints, back, hands;
• decrease in height;
• pathological flexibility of bone tissue.

Renal type of pathology

Occurs in almost half of cases of primary hyperparathyroidism. The renal form is characterized by:

• renal colic;
• frequent urination;
• blood in urine.

The prolonged course of the disease leads to infection of the kidneys and the development of pyelonephritis. Pain appears in the lower back, the temperature rises. Hypercalcemia against the background of hyperparathyroidism in women contributes to the accumulation of calcium in the renal tissues (nephrocalcinosis).

Gastrointestinal form

With this type of disease, a stomach ulcer develops. In this regard, typical complaints arise:

• pain in the upper abdomen;
• heartburn or belching;
• weight loss;
• nausea and vomiting after eating;
• constipation;
• flatulence;
• icteric syndrome.

Women with blood calcium levels greater than 4 mmol/l may develop a hypercalcemic crisis. This is a condition characterized by:

• temperature increase to 39-40 o C;
• dehydration of the body;
• acute abdominal pain;
• severe weakness;
• vomit.

Patients experience loss of consciousness and coma. This condition is life-threatening and requires urgent resuscitation measures.

In secondary hyperparathyroidism, symptoms predominate in the vast majority of cases primary disease(usually of renal or gastrointestinal origin).

Diagnostics

Due to the variety of clinical manifestations of hyperparathyroidism, different specialists (nephrologist, gastroenterologist, endocrinologist) can diagnose it.

The diagnosis is made based on the results of studies:

• collecting anamnesis, interviewing the patient;
• X-ray of the spine, skull, bones of other parts of the body;
• general blood and urine analysis;
• blood test for calcium and phosphorus levels;
• FGDS (fibrogastroduodenoscopy);
• bone biopsy if necessary;
• Ultrasound, MRI, CT to identify the exact lesion.

Effective treatments

Treatment tactics are determined based on the causes of the disease, clinical manifestations, and severity. Therapy may consist of:

• taking medications;
• hemodialysis (for renal failure);
• surgical intervention;
• correction of nutrition and lifestyle.

On a note! In primary hyperparathyroidism with hypercalcemia below 3 mmol/l, the woman is usually under constant dynamic monitoring. Specific treatment not required.

Conservative therapy

When calcium levels are above 3 mmol/l, drug therapy is prescribed, the purpose of which is to eliminate hypercalcemia. If the case is not complicated renal disorders, a woman is advised to drink more water.

To slow down the leaching of calcium from bones, bisphosphonates are prescribed:

• Bondronat;
• Zometa.

While taking this group of medications there may be side effects in the form of muscle pain, fever, high creatinine in the blood.

Calcimimetics (Cinacalcet) can be prescribed to reduce PTH synthesis. But the effectiveness of such drugs for hyperparathyroidism has not yet been fully studied.

• fluoride-containing drugs (Coreberon);
• vitamin D metabolites (Calcitriol);
• regenerative agents (Osteochin).

Women during menopause are additionally prescribed female sex hormones to reduce the progression of osteoporosis.

Radical ways

Indications for surgery are:

• parathyroid tumors;
• critical degree of hypercalcemia;
• significant reduction in bone mass;
• kidney dysfunction.

For hyperparathyroidism, subtotal or total parathyroidectomy is performed. In the first case, about 50-70 g of organ tissue remains. In the second case, the glands are completely removed.

On the page read about characteristic symptoms and manifestations of pancreatic cancer.

Features and rules of nutrition

With hyperparathyroidism, women need to reconsider their diet. Nutrition should limit the consumption of foods with high content calcium, increase fluoride-containing foods.

The following should be excluded from the diet:

• milk and fermented milk products;
• salt;
• semi-finished products;
• coffee.

• fish;
• meat;
• grain crops;
• walnuts.

Traditional medicine

Proven recipes:

• Grind the walnut leaves. Place them in a jar. Pour vodka. Leave for 2 weeks in a dark place, seal tightly. Take 10 drops twice a day at first. Gradually increase the dosage to 1 teaspoon.
• Dry and grind the sunflower roots. Boil 1 spoon of roots in 0.5 liters of water for about 10 minutes. Drink 1 glass 3 times a day.
• Pour 0.5 liters of vodka into a glass of walnut partitions. Add 50 cloves. Leave for 2 weeks, shake occasionally. Drink 1 teaspoon on an empty stomach. Wash it down big amount clean water.
• Mix crushed walnuts, flax seeds, buckwheat honey(per glass). Take 1 time per week during the day. On this day, eat only the prepared remedy, drink tea or water. It should be remembered that this recipe is suitable only for women with the primary form of hyperparathyroidism.

Hyperthyroidism in women can be cured if it is detected in the early stages and treated promptly. At mild form pathologies, patients can quickly restore the functions of the parathyroid glands and normalize hormone levels. Progression of hyperparathyroidism may cause serious complications(especially dangerous renal form). If you suspect any problems with the endocrine system, you should contact a specialist and have your body examined.

The following video discusses the most common form hyperparathyroidism - primary: the main causes of development, stages of diagnosis and the essence of treatment:

With hyperparathyroidism, symptoms and treatment in women are closely related.

After all, there are several options for the course of the disease, according to which the necessary therapeutic regimen is selected.

Depending on what caused the disease, there are 3 main forms of the disease - primary, secondary and tertiary.

Primary hyperparathyroidism develops in connection with the occurrence of tumors of various etiologies on the parathyroid gland and tissue proliferation (hyperplasia).

Most often, this condition is a consequence of an adenoma. In this case, there is a rapid violation metabolic processes in the bones, which is associated with the active excretion of phosphates from the human body and accelerated absorption of calcium in the gastrointestinal tract.

At the same time, calcium is not absorbed in the bones, but is released into the blood, as a result of which it occurs much faster than its formation, which manifests itself in the form of thinning of the bones, the development of osteoporosis and osteodystrophy.

Primary hyperparathyroidism often leads to damage renal tubules and the formation of stones in the pelvis. The functioning of the urinary system is disrupted.

• blood calcium level more than 3 mmol/l;
• history of hypercalcemic crisis;
• impairment of kidney function, formation of stones in the pelvis, excretion of calcium in the urine;
• bone osteoporosis.

After surgical removal tumors definitely do histological examination sample in order to identify its good quality. If cancer is detected, the patient should undergo radiation therapy to prevent its relapse.

If there are contraindications to surgery, hyperparathyroidism is treated with drugs that reduce calcium levels in the blood.

For this purpose intravenous drip administration isotonic solution with further use of diuretics.

Drinking plenty of fluids is recommended. In some cases, the use of bisphosphonates and glucocorticoids is advisable.

Treatment of secondary disease

Treatment of secondary hyperparathyroidism involves first of all prescribing medications to normalize hormone levels endocrine gland in blood.

Conservative therapy of the disease is aimed at eliminating the cause that provoked the development of the disease, especially if it is a pathology of the gastrointestinal tract, in particular malabsorption syndrome.

After all, in this case there is a deterioration in the absorption of nutrients necessary for the formation of bone tissue.

Main directions in treatment:

1. Diet plays a key role in hyperparathyroidism. With the help of a properly selected menu, you can limit the intake of calcium from foods and increase the intake of phosphorus. Nutritional hyperparathyroidism is easier to correct if the patient drinks plenty of fluids. This will help remove from the body along with urine some microelements that provoke an increase in the level of the hormone in the blood.
2. Phosphate binders. Used to treat mineral and bone disorders in patients suffering from chronic kidney diseases. These include: Calcium Carbonate, Calcium Citrate, Calcium Acetate, etc.
3. Vitamin D. It has a beneficial effect on the work of osteoblasts - bone building cells. Helps increase calcium levels in bone tissue when it is deficient and prevents release into the blood.
4. Calcimimetics. Suppress the production of parathyroid hormone, normalizing calcium and phosphorus levels in the bones.
5. Vitamin D analogue. Used if there are contraindications to the use of the latter.

In the absence of positive dynamics from the ongoing conservative therapy the use of surgical intervention is indicated.

The main indication for surgery is progression of the disease, accompanied by deterioration in the functioning of other organs and systems.

Pathologies of the endocrine gland can develop at any age. In some cases, hyperparathyroidism is recorded in children.

The disease can provoke a severe deterioration in the child’s health. Therefore, if your baby is sick, there is no need to self-medicate.

You should contact a specialist as soon as possible for timely diagnosis diseases.

The sooner you start treatment, the greater the chances of recovering faster and preventing the development of complications.

For quotation: Dreval A.V., Tevosyan L.Kh. Primary hyperparathyroidism // Breast cancer. 2015. No. 8. P. 427

Normally, a decrease in the level of calcium in the blood stimulates the secretion of parathyroid hormone, and if this is observed constantly (for example, in the case of vitamin D deficiency), then this condition is called secondary hyperparathyroidism. It reflects a preserved mechanism for regulating parathyroid hormone secretion. In the case of autonomous production of parathyroid hormone caused by a parathyroid tumor (85% of cases), this pathological condition called primary hyperparathyroidism (PHPT).

At the same time, autonomously functioning primary hyperplastic parathyroid glands are also observed (15%), usually against the background of multiple endocrine neoplasia syndrome (MEN) - this is also PHPT, since no pathological process is detected that could lead to development of autonomously functioning hyperplastic parathyroid glands. On the other hand, prolonged hypocalcemia, usually due to chronic renal failure, vitamin D deficiency or malabsorption syndrome, can lead to the development of autonomous production of parathyroid hormone (PTH). In this case, when primary cause This hyperproduction is obvious, tertiary hyperparathyroidism is diagnosed (it is implied that it arose against the background of secondary hyperparathyroidism).

Taking into account the above, the diagnosis of diseases accompanied by hyperparathyroidism begins with verification of the hyperparathyroidism syndrome, and only after that its causes (primary, secondary or tertiary) are established. At the last stage, the localization of pathologically altered adenoma(s) is determined.

Definition

PHPT – primary, i.e. unprovoked reduced level calcium in the blood, hyperproduction of PTH, which leads to disruption of calcium homeostasis.

Epidemiology

The frequency is about 20 cases per 100 thousand population per year, and it is last years is growing due to improved diagnosis of hyperparathyroidism. The highest frequency is at the age of 50–55 years; in women it is detected 3 times more often than in men. The ratio of men to women in the age group over 60 years is 1:3.

PHPT ranks 3rd in terms of prevalence of endocrine diseases after diabetes mellitus and thyroid diseases.

Etiology

In approximately 85% of cases, PHPT is caused by a single parathyroid adenoma, and in only 15% it occurs with multiple parathyroid adenomas or multiple hyperplasia. Familial forms have been described as part of the manifestations of MEN1 or MEN2 syndrome or familial isolated hyperparathyroidism. Familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism also fall into this category.

Genetic disorders are represented by mutations in the genes of growth factors, proto-oncogenes, and tumor necrosis factors. Proliferation of parathyroid cells is associated with various gene mutations, for example, cyclin D1/PRAD1 (chromosome 11q), RET (chromosome 10q), MEN1, and inactivation of the tumor suppressor gene located at the 1p locus.

There is evidence of an association between head and neck irradiation and the development of of this disease.

Pathophysiology

In the case of PHPT caused by an adenoma, the normally functioning negative feedback between blood calcium levels and parathyroid hormone secretion is disrupted, as is the mechanism of suppression of parathyroid hormone secretion in response to hypercalcemia, since there is a defect in the calcium-sensing receptors that are located on the surface of the main cells of the parathyroid glands. Their calcium sensitivity threshold is reduced or completely absent. As a result, the production of parathyroid hormone increases, which causes a number of pathological changes in the body: the processes of bone resorption and bone formation are accelerated due to the activation of osteoblasts and cytokine-mediated induction of osteoclasts (with a long-term increase in the level of parathyroid hormone, resorption processes predominate); the renal threshold for phosphate reabsorption decreases (manifested by hypophosphatemia and hyperphosphaturia). Increased levels of parathyroid hormone and hypophosphatemia stimulate the synthesis of calcitriol (1,25(OH)2D3) in the renal tubules, which in turn significantly increases calcium absorption in the intestine.

A completely different mechanism for the development of PHPT in parathyroid hyperplasia is that an increase in the number of PTH-producing cells leads to unregulated hyperproduction of PTH. With PHPT, the following are often detected: hyperuricemia due to a decrease in the sensitivity of the renal tubules to antidiuretic hormone; a decrease in glomerular filtration rate (GFR), which, due to insufficient perfusion of the capillary network, causes a reduction in tubular secretion of urate, i.e., the excretion of uric acid is impaired. The level of uric acid decreases significantly after 1 week. after paraadenotomy.

Patients with PHPT often have a deficiency of vitamin D (25(OH)D), which aggravates the manifestations of hyperparathyroidism: more high performance parathyroid hormone before surgery, the weight of the adenoma and the severity of bone changes, as well as the degree of development of postoperative hypocalcemia (hungry bone syndrome) and an increase in cardiovascular mortality.

At an advanced stage of hyperparathyroidism, which is most often observed with PHPT from the bones, the following are observed: subperiosteal resorption of the distal phalanges, narrowing distal section clavicles, on a skull x-ray there are foci of resorption (described as “salt and pepper”), brown tumors of long bones.

Chronically increased urinary calcium excretion may be accompanied by the formation of kidney stones. Other symptoms of hyperparathyroidism are associated with hypercalcemia: muscle weakness, fatigue, nausea and vomiting, neuropsychiatric disorders such as depression, disturbances of consciousness, increased gastric secretion, which can lead to peptic ulcers, pancreatitis (rarely), in severe cases, coma and death.

Clinical manifestations

Symptoms of hyperparathyroidism, grouped by system, are presented in Table 1.

Since its introduction into the wider clinical practice blood calcium studies in the 1970s. expressed clinical manifestations PHPT began to be observed rarely, because the disease began to be diagnosed at the stage of an early biochemical sign - hypercalcemia. And in fact, in most cases it is subclinical (asymptomatic) PHPT.

PHPT can occur in mild and manifest forms. The mild form can be asymptomatic and low-symptomatic. In the manifest course, bone, visceral, mixed form and hypercalcemic crisis.

Diagnostics

Determination of calcium and parathyroid hormone levels in order to identify PHPT should be carried out in patients with recurrent urolithiasis, peptic ulcer stomach and duodenum, with insipidal syndrome, frequent low-energy fractures, cardiac arrhythmias, with neuroendocrine tumors, cancer of the gastrointestinal tract (GIT), as well as in relatives of patients with MEN syndrome and parathyroid cancer (to exclude familial forms).

Diagnostics is divided into 2 stages:

1. Verification of hyperparathyroidism, including PHPT.

2. Localization of the affected gland(s).

Cases in which both hypercalcemia and PTH overproduction are observed simultaneously are very rare, particularly in familial benign (hypocalciuric) hypercalcemia, lithium-induced hypercalcemia, and tertiary hyperparathyroidism. A relatively small percentage of patients with hyperparathyroidism (10–15%) have PTH levels at the upper limit of normal, but blood calcium levels are inappropriately high. In some patients, the level of serum calcium is normal against the background of elevated levels of parathyroid hormone (the so-called normocalcemic hyperparathyroidism). But in the latter case it is necessary to conduct a careful differential diagnosis with a number of conditions causing secondary hyperparathyroidism, such as low calcium intake, gastrointestinal disorders, vitamin D deficiency, renal failure, hypercalcemia of renal origin.

Secondary or tertiary hyperparathyroidism is diagnosed based on the clinical context. Hypercalcemia caused by cancer is usually associated with low level parathyroid hormone, although the level of PTH-like peptides may be increased.

If hyperparathyroidism is suspected in patients, the level of total or ionized calcium in the blood serum must be examined. In this case, hypercalcemia must be confirmed in more than one study before the patient is prescribed an in-depth examination. An increased level of total calcium may occur with hemoconcentration, for example, with hyperalbuminemia (while ionized calcium is normal).

In most patients, hypercalcemia is diagnosed late, since the determination of calcium levels is not included in the mandatory routine examination. This often leads to the detection of the disease at the stage severe complications.

An elevated level of intact PTH (second generation parathyroid hormone test kits) in combination with an elevated serum calcium level is diagnostic of PHPT. A study of 24-hour urinary calcium excretion is necessary to exclude familial hypocalciuric hypercalcemia.

Laboratory examination may reveal mild hyperchloremic acidosis, hypophosphatemia, and mild to moderately elevated urinary calcium excretion. With preserved renal function, a 24(OH)D level of >50 nmol/L is sufficient to suppress PTH secretion and prevent secondary hyperparathyroidism.

X-ray examination is used to determine the location of the affected parathyroid glands. Sometimes it is used in cases where there is insufficient data to diagnose PHPT. Since during surgery it is recommended to examine all parathyroid glands and remove those that look pathological, most surgeons believe that there is no point in performing an X-ray examination of the parathyroid glands when the patient is clinically indicated surgical treatment. However, if after surgical treatment the signs of hyperparathyroidism do not disappear or a relapse occurs, then an X-ray examination is very justified.

Ultrasound examination (US) of the neck area is safe and widely used to localize pathological parathyroid glands. But the accuracy of this study depends on the experience of the specialist, the size of the parathyroid glands and location, so the results obtained are very variable. Compared to x-ray examination Ultrasound accuracy reaches 75–80%.

Radioisotope scanning is carried out with a radioactive sestamibi tag. Sestamibi is commonly used for cardiac testing, but this radioisotope has been shown to accumulate in parathyroid adenomas (Figure 1).

Scanning sensitivity is 60–90%. The disadvantage of this method is manifested in the diagnosis of multiple adenomas - its sensitivity is reduced by 50%. In combination with single-photon emission computed tomography This method is very effective in localizing parathyroid adenomas, especially when they are ectopic or after ineffective surgical treatment.

Computed tomography and magnetic resonance imaging are also used to localize pathological parathyroid glands, especially when they are ectopic (eg, in the mediastinum).

Angiography and the study of parathyroid hormone in the jugular veins allow lateralization of pathological adenomas, but this technique is used only in certain research studies clinical centers and in specially selected patients.

Intraoperative ultrasound is also used to identify atypically located adenomas.

To identify visceral changes, the following studies are recommended: Kidney ultrasound (to detect nephrolithiasis or other pathology), GFR, gastroscopy, organ ultrasound abdominal cavity(to identify gastrointestinal pathology characteristic of PHPT), measurement of bone mineral density (BMD) ( radius, spine, proximal femur) to detect osteoporosis, x-ray of the hands and pelvis (to detect hyperparathyroid osteodystrophy), if indicated - tubular bones, electrocardiogram, echocardiography of the cardiovascular system.

A mild form of PHPT is diagnosed if the level of total calcium in the blood is higher than 0.25 mmol/l (1 mg/dl) of the upper limit of normal, there are no visceral manifestations, BMD is reduced by no more than 2.5 SD (T-score) in men under 50 years of age and women before menopause, no low-energy fractures.

The manifest form is diagnosed in the presence of visceral or osteovisceral complications and/or the level of total calcium in the blood is more than 0.25 mmol/l above the upper limit of normal.

Differential diagnosis

PHPT is differentiated from diseases and conditions accompanied by hypercalcemia, such as:

• destructive processes in bone tissue (metastases malignant tumors, myeloma, lymphoma, leukemia);
• Paget's disease;
• tertiary hyperparathyroidism;
• the use of thiazide diuretics, lithium preparations, overdose of vitamins A and D and theophylline intoxication;
• calcitriol-induced hypercalcemia in sarcoidosis;
• thyrotoxicosis, adrenal insufficiency;
• pseudohyperparathyroidism;
• long-term immobilization;
• familial hypocalciuric hypercalcemia;
• congenital lactase deficiency;
• Jansen's metaphyseal chondrodysplasia (a rare form of dwarfism).

In case of signs of diabetes (polydipsia, polyuria, nocturia), it is necessary to differentiate between diabetes mellitus and non-sugar diabetes (nephrogenic) diabetes.

Treatment

Indications for surgical treatment

It is now generally accepted that parathyroidectomy is preferred in all cases of symptomatic hyperparathyroidism or obvious end-organ damage. The operation is indicated if:

• undoubted symptoms of hypercalcemia. However, if the patient has only nonspecific symptoms hypercalcemia (abdominal pain, increased fatigue or moderate cognitive impairment), the effectiveness of surgical treatment is not always obvious;
• renal dysfunction;
• kidney stones;
• parathyroid bone lesions, especially osteitis fibrocystis;
• pancreatitis.

In the case of asymptomatic hyperparathyroidism, the indications for surgery (in accordance with the norms of the 2014 International Consensus) are the following:

• the level of total calcium in the blood is more than 0.25 mmol/l (1 mg/dl) above the upper limit of normal;
• the presence of visceral complications such as nephrolithiasis, nephrocalcinosis;
• urinary calcium excretion 10 mmol/day (optional indication in the USA);
• creatinine clearance<60 мл/мин (необязательное показание в Великобритании);
• BMD (T-score)<-2,5 СО (в США, малотравматичный перелом в анамнезе);
• age<50 лет.

Surgical removal of the parathyroid glands should only be performed by an experienced surgeon (at least 20 operations on the parathyroid glands per year).

For PHPT, various surgical techniques can be used, the choice of which depends on the nature of the lesion of the parathyroid glands, the experience of the operating surgeon and the equipment of the clinic: bilateral or unilateral revision of the parathyroid glands, minimally invasive parathyroidectomy with endoscopic control, minimally invasive radiofrequency ablation, removal of parathyroidoma using preoperative doses of technetril and radio probe (conductor) in the presence of a -chamber. There is also a technique for percutaneous administration of ethanol or calcitriol under ultrasound guidance (conservative destruction of the parathyroid glands), however, due to low efficiency and frequent side effects, this technique is not widely used.

To assess the effectiveness of surgical intervention, the method of intraoperative determination of the level of parathyroid hormone is used: before the start of the operation and 15 minutes after removal of the tumor or hyperplastic parathyroid glands. The method has high predictive and diagnostic value. If the level of parathyroid hormone decreases by 50%, surgery is considered successful; with a smaller decrease, it is necessary to continue to search for additional pathological parathyroid tissue.

In the case of hyperplasia, not all glands are removed, but if all, then it is recommended to implant the removed gland in a place that is easily accessible for possible removal.

Postoperative complications and outcomes:

• Paresis of the vocal cords due to damage to the recurrent nerve.
• Hypocalcemia:
  • transient due to suppression of PTH secretion by unremoved glands;
  • moderate and more or less constant, requiring treatment with oral medications containing calcium and vitamin D metabolites;
  • heavy;
  • due to depletion of calcium reserves in the bones (“starved bone”) (may develop in patients who had severe hypercalcemia before surgery);
  • in case of pre-existing bone disease accompanied by depletion of calcium reserves.
• Hypomagnesemia (very rare).

Treatment

Vitamin D supplements are prescribed before surgery, which reduces the risk of postoperative hypocalcemia. It is recommended to monitor calcium levels.

After surgery, calcitriol 1 mcg/day is prescribed (sometimes a larger dose is required) together with an oral calcium supplement 3 times/day. This treatment is prescribed for several weeks.

In less than 5% of cases, the calcium level is not normalized, for example, as a result of an inadequate volume of surgery, if lymph nodes and fatty tissue were mistaken for adenoma or hyperplasia, if more than one parathyroid gland is affected, in case of parathyroid cancer with metastases, as well as as a result of decreased kidney function. In this case, additional examination of the patient is required (arteriography and selective blood sampling for parathyroid hormone, performed by highly qualified specialists, multispectral computed tomography of the neck and mediastinum, exclusion of other causes of hypercalcemia) and repeated surgical treatment.

In the case of verified hyperplasia of the parathyroid glands (including MEN syndrome), patients should regularly determine the level of calcium in the blood for timely diagnosis of relapse of hyperparathyroidism.

If persistent hypoparathyroidism develops after surgery, the patient is prescribed continuous treatment with calcium supplements in combination with vitamin D. Such treatment is often accompanied by hypercalciuria, which increases the risk of developing urolithiasis. To reduce hypercalciuria, the target serum calcium value should be at the lower limit of normal.

If in the postoperative period an increased level of parathyroid hormone is observed in combination with a low calcium level, this indicates stimulation of the secretion of the remaining parathyroid glands due to hypocalcemia. A persistent increase in parathyroid hormone levels after surgery may be associated with vitamin D deficiency (25(OH)D).

Conservative tactics of patient management

• in case of moderate manifestations of hyperparathyroidism, without damage to target organs (with a mild form);
• in preparation for surgery (in order to prevent a hypercalcemic crisis; delayed surgical intervention);
• if there are contraindications to surgery or anesthesia;
• if the patient refuses surgery;
• with relapse of PHPT and absence of remission after parathyroidectomy.

In most patients, the disease does not progress for many years, but regular monitoring is required. In case of disease progression, surgical treatment is indicated.

Drug treatment

Drug therapy is carried out only in cases where surgical treatment is impossible for one reason or another.

Hormone replacement therapy:

• preserves bone mass;
• The long-term risk of breast cancer, venous thrombosis, heart disease or stroke should be considered.

Bisphosphonates:

• preserve bone mass;
• have a clinically insignificant effect on calcium levels in the blood and urine;
• The largest evidence base is available for alendronic acid, which has been studied in many clinical studies.

Calcium-sensitive receptor agonists, in particular cinacalcet (average effective dose - 30 mg 2 times / day):

• reduces the concentration of calcium in the blood, but not in the urine;
• increases the sensitivity of calcium-sensitive receptors, which leads to a decrease in PTH secretion;
• reduces the risk of visceral disorders.

The drug is also licensed for the treatment of: PHPT in patients for whom surgical intervention is contraindicated or clinically inappropriate, or the source of parathyroid hormone hyperproduction cannot be determined based on the results of the examination; severe secondary hyperparathyroidism in patients on dialysis; parathyroid carcinoma.

Monitoring of patients with hyperparathyroidism who are not treated surgically

The consensus of British and American experts regarding patients who cannot undergo surgical treatment is presented in Table 2.

Forecast

After successful surgery, most symptoms reverse. Within 1 year after surgery, BMD increases by 14–25%. High alkaline phosphatase activity and hypophosphatemia normalize within 6–8 months. .

Literature

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– endocrinopathy, which is based on excessive production of parathyroid hormone by the parathyroid glands. Hyperparathyroidism leads to increased calcium levels in the blood and pathological changes that occur primarily in bone tissue and kidneys. The incidence of hyperparathyroidism among women is 2–3 times more common than among men. Women between 25 and 50 years of age are more susceptible to hyperparathyroidism. 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 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 increased calcium levels in the blood and pathological changes that occur primarily in bone tissue and kidneys. The incidence of hyperparathyroidism among women is 2–3 times more common than among men. Women between 25 and 50 years of age are more susceptible to hyperparathyroidism.

Classification and causes of hyperparathyroidism

Hyperparathyroidism can be primary, secondary and 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, the following are distinguished:

• bone form (parathyroid osteodystrophy, or Recklinghausen's disease). It manifests itself as deformation of the limbs, leading to subsequent disability. Fractures appear “on their own”, without injury, heal long and difficult, and 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 (increase in the size 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 reaction to long-term low levels 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 hyperparathyroidism and is associated with the development of an autonomously functioning parathyroid adenoma.

Pseudohyperparathyroidism (or ectopic hyperparathyroidism) occurs with malignant tumors of various localizations (breast cancer, bronchogenic cancer), capable of producing parathyroid hormone-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 weak, soften, can bend, and the risk of fractures increases. Hypercalcemia (excessive levels of Ca in the blood) leads to the development of muscle weakness and the excretion of excess Ca in the urine. Urination increases, constant thirst appears, kidney stones develop (nephrolithiasis), and calcium salts are deposited in the kidney parenchyma (nephrocalcinosis). Arterial hypertension in hyperparathyroidism is caused by the effect of excess Ca on the tone of blood vessels.

Symptoms of hyperparathyroidism

Hyperparathyroidism can be asymptomatic and diagnosed accidentally 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 rapid fatigue during exercise, muscle weakness, headache, difficulty walking (especially when climbing or covering long distances), and a waddling gait is characteristic. Most patients report memory impairment, emotional imbalance, anxiety, and depression. Older people may experience severe mental disorders. With long-term hyperparathyroidism, the skin becomes an earthy gray color.

At the late stage of bone hyperparathyroidism, softening, curvature, pathological fractures (during normal movements, in bed) of the bones occur, and scattered pain occurs in the bones of the arms and legs, and the spine. As a result of osteoporosis, the jaws become loose and healthy teeth fall out. Due to skeletal deformation, the patient may become shorter. 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 pain, vomiting, flatulence occur, appetite is impaired, and weight decreases sharply. Patients are found to have peptic ulcers with bleeding of various locations, prone to frequent exacerbations, relapses, as well as signs of damage to the gallbladder and pancreas. Polyuria develops, urine density decreases, and unquenchable thirst appears. In the later stages, nephrocalcinosis is detected, symptoms of renal failure develop, progressing over time, and uremia.

Hypercalciuria and hypercalcemia, the development of calcification and vascular sclerosis, leads to impaired nutrition of tissues and organs. A high concentration of Ca in the blood contributes to damage to the heart vessels and increased blood pressure, causing angina attacks. When the conjunctiva and cornea of ​​the eyes become calcified, red eye syndrome occurs.

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 calcium and vitamin D supplements, thiazide diuretics (reduce calcium excretion in urine). The crisis occurs suddenly with acute hypercalcemia (Ca in the blood is 3.5 - 5 mmol/l, when the norm is 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 epigastric pain, vomiting, drowsiness, impaired consciousness, coma. Weakness sharply increases, dehydration occurs, and a particularly serious complication is the development of myopathy (muscle atrophy) of the intercostal muscles and diaphragm, proximal parts of the body. Pulmonary edema, thrombosis, bleeding, and 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 obtained:

• general urine test

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

• biochemical blood test (calcium, phosphorus, parathyroid hormone)

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

• ultrasound examination

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

• X-ray examination, CT and MRI

X-rays can detect osteoporosis, cystic bone changes, and pathological fractures. Densitometry is performed to assess bone density. Using an X-ray examination with a contrast agent, peptic ulcers in the gastrointestinal tract that occur with hyperparathyroidism are diagnosed. CT scan of the kidneys and urinary tract reveals stones. X-ray tomography of the retrosternal space with esophageal contrast with a barium suspension makes it possible to identify parathyroid adenoma and its location. Magnetic resonance imaging is more informative than CT and ultrasound and visualizes any location 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 underlying disease is diagnosed.

Treatment of hyperparathyroidism

Complex treatment of hyperparathyroidism combines operative surgery and conservative therapy with medications. The main treatment for primary hyperparathyroidism is surgery, which involves removing parathyroid adenoma or hyperplastic parathyroid glands. Today, 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, emergency surgery is necessary. Before surgery, it is mandatory to prescribe conservative treatment aimed at reducing Ca in the blood: drinking plenty of fluids, intravenous isotonic NaCl solution, in the absence of renal failure - furosemide with KCl and 5% glucose, extract of the thyroid glands of cattle (under the control of Ca level 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, most patients have a decrease in the amount of Ca in the blood, 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 bone tissue damage. In mild cases of the disease, performance is restored after surgical treatment within approximately 3-4 months, in severe cases - within the first 2 years. In advanced cases, work-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 surgical intervention, 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; the mortality rate for this complication of hyperparathyroidism is 32%.

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