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Parathyroid adenoma

Parathyroid adenoma is a benign tumor of the parathyroid gland that produces parathyroid hormone. The parathyroid glands are two pairs of small glands that are located on the sides of the thyroid gland in the neck. The disease is manifested by increased production of parathyroid hormone and various clinical manifestations, which most often include increased calcium in the blood, osteoporosis, urolithiasis and stomach ulcers. This is called hyperparathyroidism.


  • Primary hyperparathyroidism.


Primary hyperparathyroidism is caused by excessive secretion of parathyroid hormone and is accompanied by severe hypercalcemia.

Primary hyperparathyroidism is often asymptomatic and manifests itself as a generalized violation of calcium, phosphorus and bone metabolism.  The cause is parathyroid adenoma.  A small number of patients have primary parathyroid cancer.

Increased absorption of calcium from food and the release of calcium from the bones leads to an increase in its concentration in the blood. At the same time, the bone tissue begins to lose its strength, and osteoporosis develops, the outcome of which is fractures. Fractures occur with minimal load (jumps, a light blow to the limb, an unsuccessful change in the position of the body). The growth may decrease, due to the development of compression fractures of the vertebrae, the posture changes, the limbs are deformed. Typically, the appearance of muscle weakness, rapid fatigue. Primary hyperparathyroidism leads to the deposition of calcium from the blood in the walls of blood vessels and heart valves. A decrease in the elasticity of blood vessels due to the deposition of calcium in their wall leads to a deterioration in the contractility and conductivity of blood vessels, while the "upper" blood pressure increases, and the difference between the "upper" and "lower" pressure increases. The result of increased blood pressure and decreased vascular elasticity is an increased risk of heart attacks and strokes.

High levels of calcium in parathyroid adenoma impair attention, reduces the intellectual abilities of patients. With a high concentration of calcium, consciousness may deteriorate until the onset of a coma.

Severe forms of primary hyperparathyroidism lead to the death of the patient due to vascular disorders, coma, fractures.


  • Secondary and tertiary hyperparathyroidism


A feature of secondary and tertiary hyperparathyroidism is an increase in all four parathyroid glands at once. Usually one of the parathyroid glands is larger and "outstrips" the others in size, but still the pathological process develops immediately in all the glands – this is the main difference between secondary and tertiary from primary hyperparathyroidism.

Secondary hyperparathyroidism is a syndrome of increased concentration of parathyroid hormone in the blood, which develops in the primary healthy parathyroid glands due to reduced calcium levels caused by other diseases. Most often, secondary hyperparathyroidism develops in patients with chronic renal failure ("chronic kidney disease") and requiring hemodialysis.

Tertiary hyperparathyroidism is a form of the disease that is accompanied by the development of adenomas in the parathyroid tissue. Tertiary hyperparathyroidism is currently only established in patients after a successful kidney transplant if they do not have a normalization of the level of calcium and parathyroid hormone in the blood.


  • Symptoms of hyperparathyroidism. 


Up to 80% of patients in the initial stage of the disease present such non-specific complaints as: weakness; lethargy; pain in the bones and joints; decreased appetite; nausea; tendency to constipation. These symptoms are often not associated with primary hyperparathyroidism, and do not disappear after radical surgical treatment of the disease.


  • Diagnosis of parathyroid adenoma


Specific laboratory changes make it possible to diagnose the vast majority of cases of parathyroid adenomas.

Typical laboratory changes are:


  • increased levels of ionized calcium and parathyroid hormone in the blood;
  • decreased blood phosphorus levels (not found in all cases of primary hyperparathyroidism);
  • an increase in the level of calcium in the daily urine.


When identifying characteristic laboratory signs, it is already possible to say with confidence that the patient has a parathyroid adenoma. Due to the fact that the treatment of adenoma is always surgical, the next stage of diagnosis is to establish the location of the adenoma.  To identify the location of the adenoma, two methods are usually used: ultrasound of the parathyroid glands and scintigraphy. If both of these methods provide similar information about the location of the adenoma, you need to consult an endocrine surgeon to decide whether to perform the operation. Additional methods of investigation are computed tomography of the neck with intravenous administration of a contrast agent, which allows in a large number of cases to determine the location of the adenoma even with its atypical location.


  • Treatment of parathyroid adenoma.


Treatment of adenoma is only surgical. Removal of parathyroid adenoma is the most effective way to eliminate hyperparathyroidism and related complications. No drug provides the same effectiveness as surgery.  Currently, the least traumatic way to treat parathyroid adenoma is selective parathyroidectomy-removing only the adenoma without examining the rest of the parathyroid glands. This operation can be performed even through a skin incision 1.5-2 cm long, including using video equipment.

In non-missed cases, especially only with changes in the bones, the operation gives a good therapeutic effect. Kidney changes are more difficult to treat and are often irreversible by the time of surgery. In addition to surgery, symptomatic therapy, treatment of osteoporosis and other manifestations of calcium metabolism disorders are indicated.

Diagnosis and treatment of parathyroid diseases should take place with the participation of an endocrinologist, an endocrine surgeon and an oncologist in a specialized department.

GBUZ Moscow Clinical Scientific Center named after Loginov MHD