Hyperparathyroidism - Information Overview

Hyperparathyroidism - fibrocystic osteodystrophy, Recklinghausen's disease - a disease associated with pathological hyperproduction of parathyroid hormone by hyperplastic or tumor-altered parathyroid glands.

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Epidemiology

According to most authors, hyperparathyroidism occurs with a frequency of 1:1000 people, women get sick 2-3 times more often than men. Hyperparathyroidism occurs mainly in people aged 20-50. Children, adolescents and the elderly rarely suffer from it. However, there are cases of congenital primary hyperparathyroidism.

In order to screen for hyperparathyroidism, serum calcium levels were measured in 50,000 people; several dozen serums with elevated calcium levels were found. It has recently become known that primary hyperparathyroidism can also occur with normocalcemia.

Causes hyperparathyroidism

There are primary, secondary and tertiary hyperparathyroidism.

In primary hyperparathyroidism (I HPT), hyperproduction of parathyroid hormone is usually associated with the development of an autonomously functioning adenoma of the parathyroid glands (parathyroid adenoma), less often - two or more adenomas, with diffuse hyperplasia or cancer of the parathyroid glands.

Secondary hyperparathyroidism (II HPT) is a reactive hyperproduction of parathyroid hormone by hyperfunctioning and/or hyperplastic OHTG in conditions of prolonged hyperphosphatemia and 1,25 (OH) ₂ D ₃ deficiency in chronic renal failure; chronic hypocalcemia in gastrointestinal diseases with impaired absorption ( malabsorption syndrome ).

Tertiary hyperparathyroidism (III HPT) is a condition associated with the development of adenoma of the OGD and its autonomous functioning under conditions of prolonged II HPT (according to the "hyperfunction-hyperplasia-tumor" principle). In I and III HPT, there is a violation of the feedback between the level of calcium in the blood serum and excessive secretion of PTH.

In 1891, pathologist F. Recklinghausen gave a classic description of widespread osteodystrophy, accompanied by the formation of cysts and brown tumors in the bones, and their histological characteristics. Although F. Recklinghausen mistakenly considered them to be the result of a chronic inflammatory process, it is undoubtedly these elements that make up the clinical and morphological picture of hyperparathyroid osteodystrophy.

The significance of hyperfunction of the parathyroid glands in the development of bone changes is substantiated by the classic studies of A. V. Rusakov (1924-1959), which showed that with hyperparathyroidism, the process of destruction of bone substance is sharply accelerated, which is combined with the replacement of fatty bone marrow with fibrous and giant cell tissue and the formation of new bone tissue (osteoblastic). At the same time, the rate of its restoration lags behind the rate of resorption, which explains the development of osteoporosis.

Giant cell growths (epulides) consist of cells that have the function of osteoblasts and osteoclasts, so they are called osteoclastomas (G. Lievre), or osteoblastoclastomas. The reasons for the formation of cystic elements in GPT are not completely clear. These are cavities containing a brownish liquid and mucoid substances. They can be single or multiple, like "soap foam". They are considered as a manifestation of hemorrhages or degenerative changes in bone tissue. It is known that there is a direct transition of bone blood vessels into the spongy spaces between the cells of bone tumor growths, where a channel is formed similar to the primary blood supply of embryonic mesenchyme. This nutritional feature causes the deposition of hemosiderin in them with the formation of a brown color of tumors.

In hyperparathyroidism, bone resorption occurs in a normal (osteoclastic) way. New formation (with the appearance of normal osteoblasts and the formation of osteoid) of young, still weakly mineralized bone occurs, in the structure of which there is a smaller amount of calcium than in the old mature bone. Hypercalcemia, so characteristic of hyperparathyroidism, from this point of view is a secondary, easily perceptible biochemical phenomenon. Under normal conditions, bone tissue reorganization occurs harmoniously, with the preservation of the natural bone structure. In hyperparathyroidism, this process is a manifestation of the sharpest acceleration of the normally existing and constantly acting change of bone regenerations. Reorganization is disorganized. Due to calcium depletion, bones become soft and flexible; under the influence of stress, curvatures and pathological fractures easily occur.

Renal changes in hyperparathyroidism include polyuria with hypoisosthenuria and thirst as one of the early manifestations. The pathogenesis of these symptoms undoubtedly involves the influence of increased calcium excretion with urine. Its excess damages the epithelium of the renal tubules, increasing the excretion of water. It should be remembered that idiopathic hypercalciuria (without hypercalcemia) also occurs with polyuria. It is also known that hyperparathyroidism increases the excretion of water by the kidneys. It has been proven that hyperparathyroidism reduces the sensitivity of the renal tubules to antidiuretic hormone (ADH). The mechanism of this effect is not clear enough.

The cause of persistent recurrent nephrolithiasis with frequent formation of bilateral multiple or coral stones in 10-15% of cases is hyperparathyroidism. Formation of kidney stones is associated with hypercalcemia and hypercalciuria, and the rate of development and severity of nephrolithiasis are not always parallel to the degree of bone destruction. In hyperparathyroidism, stones are usually oxalate, oxalate-phosphate and phosphate, less common are formations consisting of urates.

The most important manifestation of renal pathology in hyperparathyroidism is impregnation of the renal parenchyma with calcium salts - nephrocalcinosis. According to O. V. Nikolaev and V. N. Tarkaeva (1974), this is a manifestation of advanced damage to the distal sections of the renal tubules, when conglomerates of calcium salts block the lumen of the tubules and, increasing in size, become visible in the renal parenchyma radiographically. In this case, chronic renal failure occurs and progresses, accompanied by renal arterial hypertension, which is practically irreversible even if hyperparathyroidism is eliminated.

Hyperparathyroidism is characterized by the development of peptic ulcer disease with predominant damage to the duodenum, less often - the esophagus, stomach and small intestine. The genesis of peptic ulcer disease in hyperparathyroidism has not been established. Apparently, an important role in the development of parathyroid ulcers is played by hypercalcemia with arteriosclerosis and calcification of blood vessels in general and, in particular, the vessels of the stomach, as well as the duodenum, with impaired blood supply and trophism of the mucous membrane. The direct effect of parathyroid hormone on the mucous membrane of the gastrointestinal tract is not excluded (in an experiment, when parathyroid hormone was administered, hemorrhages, necrosis, increased secretion of gastric juice with an increase in the content of pepsin and hydrochloric acid were noted), although the assumption about the dominant role of hypersecretion of gastric juice with an increased content of hydrochloric acid in it is not confirmed by all authors.

Symptoms hyperparathyroidism

Hyperparathyroidism usually develops slowly and gradually. Symptoms of hyperparathyroidism are varied. Early symptoms (depending on the predominant nature of the lesion). There may be changes of a therapeutic (mainly gastrointestinal), urological, traumatic, rheumatological, dental, neuropsychiatric nature. The uncertainty of complaints in the initial period of hyperparathyroidism leads to incorrect or delayed diagnosis in the absolute majority of patients.

The first symptoms of the disease are usually general and muscle weakness, rapid fatigue. Weakness and pain in individual muscle groups, especially in the lower extremities, appear. It becomes difficult to walk (patients stumble, fall), get up from a chair (support is required on the hands), get on a tram, a bus, a duck gait and looseness in the joints develop, pain is felt in the feet (flat feet) due to muscle relaxation. All these symptoms are associated with hypercalcemia, which causes a decrease in neuromuscular excitability and muscle hypotonia. Patients are bedridden due to severe weakness, sometimes even before fractures appear. The skin is sallow, dry.

Some of the early signs of hyperparathyroidism are thirst and polyuria with a decrease in the relative density of urine. These phenomena are often regarded as diabetes insipidus. However, attempts at treatment with antidiuretic drugs (pituitrin, adiurecrin, adiuretin) are unsuccessful. This insipid syndrome is caused by impaired renal water reabsorption due to insensitivity of the renal tubules to antidiuretic hormone due to damage to the tubules by massive calciuria.

Weight loss often develops, associated with a sharp loss of appetite, nausea, vomiting, polyuria, dehydration; weight loss can reach 10-15 kg over 3-6 months of illness.

Very characteristic of the early stages of hyperparathyroidism are the loosening and loss of healthy teeth, which is explained by osteoporosis of the jaws and the destruction of the lamina dura of the alveoli, as well as the development of epuli of the jaws - cystic formations of parathyroid origin, usually containing giant cell or fibroreticular tissue or brown fluid.

One of the early signs of hyperparathyroidism is pain in the affected areas of the skeleton, especially in the feet, in the area of tubular bones, associated with walking, changing position, palpation of the changed areas. In later stages of hyperparathyroidism, skeletal deformation and frequent fractures that occur with minimal inadequate trauma (pathological fractures) dominate. The configuration of the chest, pelvis, spine, and limbs changes. Due to limb deformations and compression fractures of the vertebrae, patients decrease in height by 10-15 cm or more. Fractures in hyperparathyroidism are less painful than in healthy people. Healing occurs more slowly, with the formation of large strong calluses, so repeated fractures in the same place do not occur. Skeletal deformations are associated with improper healing of fractures, the formation of false joints, as well as curvatures due to insufficient mechanical strength of bones.

In the analysis of 77 case histories of individuals with bone and mixed forms of hyperparathyroidism, bone manifestations were observed with the following frequency: bone pain - in 72 patients, pathological fractures - in 62, bone deformities - in 41, pseudoarthrosis - in 76, osteoporosis - in 68, bone cysts - in 49 (including in the cranial vault - in 23), osteoporosis (and cysts) in the spine - in 43, subperiosteal resorption of the phalanges of bones - in 35, other bones - in 8, tooth loss - in 29, "Pagetoid" changes in the skull - in 8 patients.

V. V. Khvorov (1940) identifies 3 types of hyperparathyroid osteodystrophy: osteoporotic, “Pagetoid” types and fibrocystic (classical) form.

In hyperparathyroid osteodystrophy, osteoporosis is widespread, radiographically characterized by uniform granularity, a finely porous "miliary" pattern. As it progresses, the cortical layer of bones becomes thinner, the radiographic pattern of the bone structure is lost, bone cysts appear, which, increasing, deform the bone, causing local swellings and protrusions. There are also cysts with multiple bridges (like "soap bubbles"). They contain giant cell or fibroreticular tissue, sometimes impregnated with hemosiderin. These are "brown" tumors. The bones are deformed, curved, there are pathological fractures, often multiple. Most often, fractures occur in tubular bones, ribs, vertebrae. The pelvic bones are sharply deformed, acquiring the shape of a "card heart", the femur - a "shepherd's stick", the rib cage resembles a bell, the vertebrae (usually thoracic and lumbar) - "fish", deformations of the spine ( kyphosis, scoliosis, kyphoscoliosis) develop. Changes in the joints occur in the form of deforming arthrosis.

Very characteristic are the phenomena of subperiosteal resorption - subperiosteal resorption of bone substance, most often - in the terminal phalanges of bones, less often - in the area of the acromial end of the clavicle, the upper edges of the ribs. The cortical layer of the dental alveoli disappears. Epulides of the upper and lower jaws are pathognomonic. In the area of the cranial vault, against the background of osteoporosis, there are sometimes areas of reorganization with spotted sclerosis ("Pagetoid" type). Hyperparathyroidism causes various changes in internal organs. In this regard, in addition to the bone form, visceropathic and mixed forms of the disease are also distinguished. However, such a division is arbitrary and reflects only the most striking manifestations of the disease that prevail during the examination in specific patients.

Among the renal manifestations of hyperparathyroidism, in addition to polyuria with hypoisosthenuria, an alkaline reaction of urine is often noted, which is associated with the relative inability of the kidneys to excrete hydrogen ions caused by parathyroid hormone. Later, nephrocalcinosis, progressive chronic renal failure and uremia predominate, which are a consequence of further stages of nephron damage and, as a rule, are irreversible. Changes in the kidneys also cause arterial hypertension, which often accompanies hyperparathyroidism. Stone formation in the urinary tract is a common phenomenon of hyperparathyroidism and occurs in almost % of patients. It can also be a consequence of hypercalciuria. Stones are bilateral, multiple, often massive, with a tendency to recurrence.

Stones in hyperparathyroid nephrocalculosis are almost always radiopaque and are detected in general images of the urinary system. They can be of various shapes, typical are "coral" stones that fill the entire renal pelvis and calyces. The deposition of calcium salts in the tubular system (nephrocalcinosis) also has a characteristic radiographic picture - a basket-like shadow of the kidneys.

Disseminated nephrocalcinosis is a manifestation of severe kidney damage, accompanied by progressive renal failure, often with an unfavorable prognosis.

It should be noted that renal failure and nephrolithiasis may progress after removal of parathyroid adenoma, i.e. after elimination of hyperparathyroidism.

Gastrointestinal symptoms of the disease include nausea, sometimes vomiting, loss of appetite, flatulence, and constipation. Acute hypercalcemia causes abdominal pain with varying irradiation. Organic lesions of the gastrointestinal tract are also characteristic: peptic ulcers localized in the duodenum, less often in other parts of the intestine, in the stomach, esophagus, occurring with a high level of gastric secretion, with bleeding, frequent exacerbations and relapses. Multiple ulcers of various localizations, deep callous ulcers, erosive gastritis and enterocolitis are encountered.

Pancreatic diseases ( pancreatitis, pancreatic calculus, pancreatic calcinosis), calculous cholecystitis are not uncommon. The course of these diseases in hyperparathyroidism is no different from the usual one. It is interesting that in pancreatitis the level of calcium in the blood serum decreases, possibly due to the action of glucagon, which is secreted in excess during pancreatitis.

Hyperparathyroidism is characterized by ECG changes - shortening of the ST interval. Neurological symptoms consist of symptoms of decreased neuromuscular excitability, decreased tendon reflexes and secondary radicular syndromes against the background of compression changes in the spine. Mental disorders in hyperparathyroidism are varied: rapid mental exhaustion, irritability, tearfulness, daytime sleepiness. Some patients experience depression, others - mental agitation, especially pronounced in hyperparathyroid crisis.

Changes in calcium and phosphorus metabolism are pathognomonic for hyperparathyroidism: hypercalcemia with hypercalciuria, hypophosphatemia with an inconstant level of phosphorus excretion in the urine, high activity of alkaline phosphatase. The latter reflects the activity of the osteoblastic process in the bones of the skeleton. A direct indicator of the activity of the parathyroid glands is a study of parathyroid hormone in the blood.

Hypercalcemic crisis

A severe complication of hyperparathyroidism is hyperparathyroid hypercalcemic crisis - a condition of a sharp and rapid increase in calcium in the blood due to hyperproduction of parathyroid hormone. A life-threatening condition for the patient occurs when its level reaches 3.5-5 mmol / l (14-20 mg%). Factors that provoke the development of hyperparathyroid crisis are spontaneous pathological bone fractures, infections, intoxication, immobilization, pregnancy, dehydration, a calcium-rich diet, taking antacid and alkalizing drugs. Hyperparathyroid crisis develops suddenly. Nausea, uncontrollable vomiting, thirst, muscle and joint pain, acute abdominal pain of unclear localization ("acute abdomen"), an increase in body temperature to 40 ° C, and impaired consciousness appear. Calcium metastases may occur in soft tissues, lungs, brain and kidneys. Due to sharp spasms in the abdominal organs, bleeding, ulcer perforation, pancreatitis, etc. may occur, which requires surgical observation.

During a crisis, renal failure may increase, developing into uremic coma (oliguria, increased levels of urea, creatinine, residual nitrogen, and a sharp retention of phosphate). Mental disorders progress, which can occur in two ways: with drowsiness, lethargy, development of stupor, or, conversely, with sharp agitation, hallucinations, delirium, and seizures. Hypercalcemic crisis may cause cardiovascular failure, collapse, pulmonary edema, pulmonary and renal infarction, and thrombosis of the main vessels. The ECG shows a shortening of the ST interval, flattening or inversion of the T wave in leads II and III. The blood contains a sharply increased calcium content, and a decrease in the content of phosphorus, magnesium, and potassium. With the development of acute renal failure, the phosphorus content may increase.

The prognosis depends on the timeliness of diagnosis and treatment, but the mortality rate is high and amounts to 50-60%.

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Diagnostics hyperparathyroidism

Diagnosis of hyperparathyroidism, especially in the early stages of the disease, is difficult. It is based on anamnesis, clinical, radiological, biochemical and hormonal parameters. Pathognomonic clinical signs are changes in the organs of vision - calcifications in the eyelid area, keratopathy, from the ECG - shortening of the ST interval.

Important information for the diagnosis of hyperparathyroidism is provided by the X-ray examination method. Repeated X-ray examination of bones with standard density X-ray contrast agents, skeletal scanning with ¹³¹ 1-diphosphonates, and γ-photon absorptiometry are used to characterize the state of the skeleton in dynamics.

Hyperparathyroidism is based on disturbances in phosphorus-calcium metabolism. Study of biochemical parameters reveals an increase in calcium content in the blood serum; this is the most important sign of hyperparathyroidism. The normal calcium level is 2.25-2.75 mmol/l (9-11.5 mg%). In hyperparathyroidism, it is increased to 3-4 mmol/l, and in conditions of hyperparathyroid crisis - up to 5 mmol/l and more. Sometimes there are patients with normocalcemic hyperparathyroidism. However, in most of them, a decrease in serum calcium content occurs in the late stages of the disease and is explained by impaired renal function, progressive serum phosphate levels (due to a decrease in its clearance), which is a poor prognostic sign. The active fraction of serum calcium is ionized calcium. Its level is 1.12-1.37 mmol/l. This fraction is of the greatest biological significance; approximately the same amount of calcium is in a bound state (mainly with albumin, to a lesser extent with globulins).

When assessing the total serum calcium content, an adjustment should be made depending on the albumin level: if the serum albumin content is less than 40 g/L, 0.1 mmol/L is added to the total calcium level being determined (in mmol/L) for every missing 6 g/L of the substance. Conversely, if its content is more than 40 g/L, 0.1 mmol/L of calcium is subtracted for every excess 6 g/L of albumin.

For example, total serum calcium is 2.37 mmol/l, albumin is 34 g/l, correction is (2.37±0.1) = 2.47 mmol/l; serum calcium is 2.64 mmol/l, albumin is 55 g/l, correction is (2.64+0.25) = 2.39 mmol/l; serum calcium is 2.48 mmol/l, albumin is 40 g/l, correction is not required. This is especially important in conditions of dysproteinemia. The activity of calcium binding to serum proteins depends on pH and decreases in conditions of acidosis. In primary hyperparathyroidism, an increase in the concentration of chlorides and acidosis are observed in 85-95 and 67% of patients, respectively.

Hyperparathyroidism is characterized by increased calciuria (normal = 200-400 mg/day). The serum phosphorus content is reduced in hyperparathyroidism and increases only with the development of chronic renal failure. The excretion of phosphorus in the urine is an inconstant value (both in healthy people and in hyperparathyroidism) and has no clear diagnostic value.

An important biochemical indicator in hyperparathyroidism is the study of the activity of alkaline phosphatase. The main activity of this enzyme characterizes the intensity of metabolic processes in bone tissue (bone fraction of the enzyme). The highest activity rates (up to 16-20 Bodansky units with a norm of 2-4 units) are determined in fibrocystic osteitis (in comparison with osteoporotic and especially visceropathic forms). Indicators of the activity of the destructive process in the organic matrix of the bone are the content of sialic acids and oxyproline in the blood, as well as the intensity of excretion of the latter in the urine. Oxyproline is a product of collagen degradation, the level of sialic acids reflects the intensity of destruction of mucopolysaccharides of the bone matrix.

A direct and more informative diagnostic method is to determine the level of parathyroid hormone in the blood, which is always elevated in hyperparathyroidism. According to research, primary hyperparathyroidism occurs with an increase in parathyroid hormone levels by 8-12 times compared to the upper limit of the norm and reaches 5-8 ng/ml or more.

Functional tests are used to diagnose hyperparathyroidism, allowing one to assess the degree of autonomy of the parathyroid glands. Most of them in healthy people and in the absence of autonomous adenomas of the parathyroid glands cause an increase in the level of parathyroid hormone in the blood, and in the presence of an adenoma do not significantly change the already initially increased activity of parathyroid hormone secretion:

• with insulin hypoglycemia; insulin at a dose of 0.05 U/kg (administered intravenously) causes an increase in parathyroid hormone levels to 130% within 15 minutes compared to its basal content;
• with adrenaline; in doses of 2.5-10 mcg/min it increases parathyroid hormone levels. Data on the effect of norepinephrine on parathyroid hormone secretion are contradictory;
• with secretin; in healthy individuals, the level of parathyroid hormone increases sharply without changing the calcium content in the blood, probably due to the short-term action;
• with calcitonin; increases the level of parathyroid hormone and decreases the calcium content in healthy people; increases the level of the first and decreases (but not to the norm) the content of the second in primary hyperparathyroidism (the level of parathyroid hormone does not change only with a very sharp initial increase and the presence of adenoma of the parathyroid glands with complete autonomy). In hypercalcemia of other etiologies, calcitonin does not affect the content of parathyroid hormone in the blood, which allows differentiating hyperparathyroidism from other forms of hypercalcemia;
• determination of osteocalcin - a bone protein containing y-carboxy-glutamic acid (bone Gluprotein) in serum and y-carboxyglutamic acid (y-Glu) in urine, reflecting increased bone resorption and being biochemical markers of primary hyperparathyroidism.

The following types of research are used for the purpose of topical diagnostics.

Non-invasive methods:

• radiography (tomography) of the retrosternal space with contrasting of the esophagus with a barium suspension (Reinberg-Zemtsov test), which allows detecting adenomas of the parathyroid glands adjacent to the esophagus, with a diameter of at least 1-2 cm;
• radioisotope scanning of the parathyroid glands with ⁷⁵ 5e-selenium-methionine, which has the ability to actively accumulate in the parathyroid glands. To block also a sufficiently high incorporation of ⁷⁵ 5e-selenium-methionine into the thyroid gland, which interferes with the detection of parathyroid adenomas; the study is carried out against the background of suppression of thyroid function with triiodothyronine. To increase the activity of the parathyroid glands, a diet with a reduced calcium content is prescribed before the test;
• ultrasound examination (echotomography) is a highly sensitive and specific method;
• computed tomography (tomodensitometry);
• thermography.

Invasive methods:

• selective arteriography with contrast agents and dyes. The most commonly used is a 1% solution of toluidine blue in a 5% glucose solution;
• Venous catheterization with selective blood sampling to determine parathyroid hormone.

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Differential diagnosis

Hyperparathyroidism is a disease with polymorphic symptoms, involving various organs and systems of the body. It can occur under the "masks" of systemic bone diseases of genetic and metabolic nature, imitate chronic renal failure, urolithiasis, gastric ulcer and duodenal ulcer, pancreatitis, diabetes insipidus, etc. The most difficult differential diagnosis of hyperparathyroidism with bone diseases.

Fibrous dysplasia is a congenital disease that manifests itself in childhood, while hyperparathyroidism most often affects middle-aged people. It occurs with changes in one (monostotic form) or several bones (polyostotic form), there are cases with damage to the bones of one half of the body. The foci of this disease radiologically resemble parathyroid cysts, but they are located against the background of an unchanged skeleton. Violations of the general condition of the patient, gross changes in calcium-phosphorus metabolism are usually not observed.

The combination of fibrous dysplasia with early sexual and physical development and "coffee" colored spots on the skin (mainly in girls) constitutes the picture of F. Albright syndrome. In 1978, S. Fankoni, S. Prader found insensitivity to parathyroid hormone in patients with this syndrome, as in pseudohypoparathyroidism type I.

Paget's disease (deforming, "disfiguring" osteitis or osteodystrophy) presents difficulties in differential diagnostics, especially with the "Pagetoid" form of hyperparathyroidism. This is a disease of unclear origin, typical for elderly and senile people, leading to active destruction and intensive predominant renewal of bone tissue. It begins asymptomatically and with mild bone pain against the background of a good general condition. The calcium and phosphorus content in the blood is unchanged, the alkaline phosphatase level is elevated, there is no general osteoporosis. On the contrary, the rebuilt bone has multiple areas of compaction with a characteristic "cotton wool" pattern. The predominant localization of the lesion is also different in these diseases. In Paget's disease, the skull and iliac bones are most often changed, renal function is not impaired. There is no tendency to nephrocalculosis.

Osteogenesis imperfecta is a genetic disease that is detected in childhood. Due to the characteristic color of the sclera, it is called "blue sclera syndrome". In most cases, it occurs with pathological fragility of bones, the development of lush bone calluses in their place, and short stature. There are bone malformations, increased joint mobility, and hearing loss. The general condition of patients does not change significantly. Biochemical shifts are observed only occasionally, but functional tests can give the same indicators as with hyperparathyroidism.

In malignant tumors of various organs with bone metastases, the metastatic process in the bones leads to the development of pathological fractures and compression fractures of the vertebrae. Radiographically, clearly defined foci of enlightenment are detected against the background of unchanged bone structure. The level of calcium and phosphorus in the serum is usually normal, but the calcium content may be elevated. It is necessary to take into account the ability of some types of tumors to ectopically produce parathyroid hormone or peptides with PTH-like activity (pseudohyperparathyroidism) and prostaglandins, which cause hypercalcemia. Some cytostatic drugs also have a hypercalcemic effect. Diseases of the blood system can also occur with hypercalcemia (for example, chronic leukemia).

Important is differential diagnosis with multiple myeloma ( plasmacytoma, Kahler-Rustitsky disease), which has many similar signs with hyperparathyroidism: decreased bone mass, cyst-like enlightenment in the bones, hypercalcemia. The difference is the acuteness of the process in multiple myeloma, increased ESR, the presence of Bence-Jones protein (in secreting myeloma of light chains) in the urine, paraproteinemia, the presence of M-gradient in serum protein electrophoresis, plasmacytoid infiltration of the bone marrow, rapid development of amyloidosis, the absence of subperiosteal resorption of the skeletal bones.

A differential diagnosis is required between hyperparathyroidism and reticuloendotheliosis (eosinophilic granuloma, xanthomatosis), neurofibromatosis, sarcoidosis; idiopathic osteoporosis (post-menopausal, senile, juvenile), osteomalacia (puerperal, senile), as well as hypercalcemia due to intoxication with vitamin D; Barnett's syndrome, which occurs with a predominant diet of alkalizing dairy foods, and benign familial hypocalciuric hypercalcemia - a hereditary autosomal dominant disease.

Treatment hyperparathyroidism

The main type of treatment for primary and tertiary hyperparathyroidism is surgery - removal of a parathyroid adenoma or several adenomas. Surgery is especially necessary (for emergency indications) in the case of hyperparathyroid crisis. In secondary hyperparathyroidism, surgery is indicated in the case of a combination of persistent increase in parathyroid hormone and calcium in the blood, disturbance of the calcium and phosphorus ratio, metabolic disorders in bone tissue, and the appearance of soft tissue calcification. In surgical treatment of primary hyperparathyroidism caused by parathyroid cancer (4.5-5% of cases), it is necessary to remove the tumor together with the adjacent lobe of the thyroid gland. In hyperparathyroidism associated with hyperplasia of the parathyroid glands, subtotal or complete removal is indicated (in the latter case, their intramuscular implantation is desirable). A typical postoperative complication is persistent hypoparathyroidism (2-3% of cases) and transient hypoparathyroidism.

Conservative treatment before surgery is aimed at reducing the calcium level in the blood. Patients with hyperparathyroidism should be prescribed a diet with an increased amount of phosphates and a reduced calcium content. In acute hyperparathyroidism, an isotonic sodium chloride solution is administered intravenously (up to 3-4 l/day) to increase glomerular calcium excretion. In the absence of renal failure and dehydration, furosemide (lasix) is administered intravenously, intravenously, by drip, 80-100 mg every 2-3 hours in combination with sodium and potassium chloride and 5% glucose solution to force calcium excretion. It should be remembered that thiazide diuretics cannot be used for these purposes, since they reduce calcium excretion and increase hypercalcemia. Treatment with diuretics is carried out under control of the level of potassium in the blood (risk of hypokalemia), other electrolytes, a calcium antagonist is used - magnesium sulfate, 10 ml of a 25% solution intramuscularly. To bind calcium in the absence of renal failure, a 2.5% solution of sodium citrate (up to 250 ml by drip) or sodium-potassium phosphate buffer is administered intravenously:

Na ₂ HP0 ₄ - 81 mmol (11.583 g); KH ₂ P0 ₄ - 19 mmol (2.622 g).

5% glucose solution - up to 1000 ml (instead of glucose solution, you can add 1 liter of distilled water), pH 7.4.

1 liter of this composition contains 100 mmol (3.18 g) of atomic phosphorus, it is administered intravenously over 8-12 hours. If necessary, the composition can be re-administered after 24 hours. The following is given orally:

Na ₂ HP0 ₄ - 3.6 g;

Na ₂ P0 ₄. 2H ₂ 0 - 1 g;

6 ml fruit syrup / 60 ml water.

This prescription contains 6.5 mmol of phosphorus (0.203 g). Na ₂ HP0 ₄ can be taken orally, in capsules of 1.5 g (up to 12-14 g per day).

To increase calcium fixation in bones during a crisis, calcitrin is used at 10-15 units intravenously, by drip or 5 units intramuscularly every 8 hours - under control of the calcium level in the blood. Glucocorticoids are administered (hydrocortisone - up to 100-150 mg / day) to reduce the body's response to metabolic stress and suppress calcium absorption in the intestine; diphosphonates. Mithramycin at a dose of 25 mcg / kg of body weight intravenously can be used as a parathyroid hormone antagonist in the absence of an effect from other drugs in patients without renal and hepatic insufficiency. Peritoneal dialysis or hemodialysis with calcium-free dialysate is carried out according to indications. In acute HPT crisis, symptomatic cardiac therapy is prescribed, dehydration is combated. After removal of a parathyroid adenoma or several adenomas, tetany often develops, the treatment of which is carried out according to general principles.

For the fastest possible restoration of bone structure after surgery, a calcium-rich diet, calcium supplements (gluconate, lactate), vitamin D3, anabolic steroids, physiotherapy exercises, massage, and electrophoresis with calcium phosphate on areas of the skeleton with the greatest decalcification are recommended.

If surgical treatment is impossible due to the presence of concomitant diseases or if patients refuse surgery, long-term conservative treatment is carried out.

Forecast

The prognosis is favorable with timely diagnosis of primary hyperparathyroidism and removal of the adenoma. Restoration of the bone structure occurs within 1-2 years, internal organs and their functions - within a few weeks. In advanced cases, bone deformations remain at the fracture sites, limiting work capacity.

With the development of nephrocalcinosis and renal failure, the prognosis worsens sharply. The prognosis of secondary and tertiary hyperparathyroidism, especially that developed in connection with chronic renal failure, is usually unfavorable. The life expectancy of patients depends on the effectiveness of the treatment of the underlying disease. In the intestinal form of secondary hyperparathyroidism, it improves with therapy with calcium preparations and active forms of vitamin D3 - 250HD3 and 1,25(OH) _2D3, which enhance the absorption of calcium in the intestine.

The patients' ability to work is restored with timely radical treatment. The time it takes for patients to return to normal life depends on the degree of damage and the nature and intensity of postoperative therapy. Without radical treatment, patients become disabled.