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Diseases of the parathyroid glands

The parathyroid glands develop from the 3rd and 4th gill arches in close connection with the thymus gland; 4 small glands are located on the upper and lower poles of the thyroid gland. When surgery on the thyroid gland should be remembered that relatively often there is angenesis of one or two glands or their atypical location. The parathyroid glands consist of main cells, the cytoplasm of which, when stained with hematoxylin and eosin, has a color from pale to dark pink, depending on the glycogen content. The main cells of polygonal shape with a diameter of 12-20 microns, have rounded, centrally located nuclei. In addition, they contain lipofuscin and secretory granules. The main cell is the main source of parathyroid hormone. Oxyphilic cells are found in a small amount. They are larger than the main cells, have acidophilic cytoplasm and densely packed mitochondria. Glycogen granules are found in these cells, but there are few or no secretory granules in them. In early childhood, isolated fat cells appear in the parathyroid glands; By the age of 25, fatty tissue amounts to 30% of the volume of the glands.

The metabolic function of the parathyroid hormone is to maintain serum calcium levels. Parathyroid hormone acts on calcium metabolism: 1) mobilizes calcium from the bones; 2) reduces the excretion of calcium in the urine; 3) activates vitamin D in the renal tissue [promotes the formation of l, 25- (OH) 2D3] and thereby increases the absorption of calcium in the gastrointestinal tract; 4) increases the excretion of phosphate in the urine. Thus, parathyroid hormone contributes to an increase in serum calcium levels while reducing the amount of phosphates.

All diseases of the parathyroid glands are divided into two large groups depending on their influence on the function of the glands - hyperparathyroidism and hypoparathyroidism.

Hyperparathyroidism is divided into primary, which develops as a result of the lesion of the gland itself and is accompanied by autonomous hypersecretion of the parathyroid hormone, leading to hypercalcemia and hypophosphatemia, and secondary, associated with enhanced production of the parathyroid hormone, but only in response to some diseases that cause hypocalciasis, but only in response to certain diseases that cause hypocalcosia,

Primary hyperparathyroidism. It is characterized by damage to the parathyroid glands, accompanied by an increase in the secretion of the parathyroid hormone and, as a consequence, the development of hypercalcemia and hypophosphatemia. The most common cause of primary hyperparathyroidism is adenomas, their proportion reaching 80%. The second most common cause (10–15%) is primary hyperplasia of the parathyroid glands. Carcinoma accounts for less than 5%.

Adenomas. They are well encapsulated, soft, brown or red. Solitary adenomas usually have a mass of 0.5-5.0 g, but can be much larger. They consist mainly of main cells, but often contain foci of oxyphilic or transitional cells, usually concentrated in the form of islets in the mass of main cells. Although the main cells look completely normal, they may be slightly larger than usual. Often there are two-nuclear cells. Cells are located in the form of layers, trabeculae or follicles. Although it is believed that oxyphilic cells do not function, sometimes hyperfunctioning adenomas consisting of oxyphilic cells occur.

In large adenomas marked areas of necrosis or hemorrhage. For unknown reasons, most adenomas are localized in the lower glands. Ectopic adenomas are also observed, for example, in the thymus or thyroid gland, near the pericardium or behind the esophagus, therefore during surgical intervention there are difficulties with their detection and removal. In those cases when two or more adenomas are simultaneously detected in the same or different glands, they must be differentiated from nodular hyperplasia. In adenomas, in contrast to nodular hyperplasia, there is a capsule, around which is located normal tissue of the parathyroid gland, the latter can be compressed due to the expansive growth of the tumor. Typical is a small amount or absence of stromal fat adenoma, while in the hyperplastic gland there are separate fat cells. Finally, with a functioning adenoma, the intact glands do not enlarge. In adenomas, monoclonality can be detected, whereas hyperplasia is polyclonal.

Primary hyperplasia. It can develop sporadically or with syndromes of multiple endocrine neoplasia. In all these cases, the anatomical changes are identical. Although in classical cases all 4 glands are involved in the process, asymmetry is often observed, sometimes very pronounced, with a marked predominance of an enlarged one or two glands.

Macroscopically, the glands look normal, but signs of hyperplasia may be noticeable. The total mass of all glands rarely exceeds 1.0 g, more often it is less than 0.5 g. Hyperplasia can be diffuse or nodular and most often affects the main cells, the cytoplasm of which becomes pale and vacuolated. Sometimes cells with optically empty cytoplasm or oxyphils predominate. Nodules can be surrounded by underdeveloped delicate fibrous bundles. When hyperplasia cells lie in the form of solid layers or form nests, trabeculae or follicular structures. There is usually a slight variability in the size of cells and nuclei, however, binuclear cells are also found.

One of the features of primary hyperplasia is the presence of fat cells in the hyperplastic regions, although the total amount of fatty tissue in the glands decreases. Uneven involvement in the pathological process of the glands sometimes creates difficulties in diagnosis, one or two mostly enlarged glands can be mistakenly removed as adenomas. In such cases, hyperparathyroidism re-develops soon after the operation. Indeed, only in 7% of cases an increase in all glands is observed, and in almost 50% of cases only two glands increase. This asymmetry is more characteristic for nodular than for diffuse hyperplasia.

Carcinoma. Less than 5% of cases of primary hyperparathyroidism are caused by carcinomas. These tumors are a gray-white formation of irregular shape, which sometimes have a mass of 10 g and usually grow in one parathyroid gland. Small carcinomas are often confused with adenomas. The tumor consists of solid layers of enlarged main cells, less often other types of cells separated by fibrous septa.
The diagnosis of carcinoma is very complex, it is reliable only when signs of invasive growth and metastasis are found. The prognosis is relatively favorable, death occurs mainly due to complications associated with hyperparathyroidism.

Secondary hyperparathyroidism. Most often it occurs in patients with renal insufficiency (uremic hyperparathyroidism), as well as in severe deficiency of vitamin D and osteomalacia. A rare disease is pseudohypoparathyroidism, characterized by impaired response of target organ receptors to the parathyroid hormone. In this disease, secondary hyperparathyroidism can also develop. The development of hyperparathyroidism in renal failure is associated with phosphate retention and hypocalcemia, leading to compensatory hyperfunction of the parathyroid glands. In addition, kidney disease can contribute to hypocalcemia by reducing the synthesis of l, 25- (OH) 2D3 С simultaneous impairment of calcium absorption in the small intestine, as well as with the state of skeletal resistance to the calciumcemic action of vitamin D and the parathyroid gland of unknown nature. It is noted, however, that uremic hyperparathyroidism can develop without hypocalcemia. Similarly, vitamin D deficiency can directly stimulate parathyroid hormone secretion. So, in patients with renal failure and less often with some other diseases, secondary hyperfunction of the parathyroid glands occurs, with hyperplasia of mainly main cells and skeletal changes - fibrocystic osteitis and osteomalacia (renal osteodystrophy).

Anatomical changes in secondary hyperparathyroidism are the same as in primary hyperplasia. All glands are usually affected, less often one, two or even three. As with the primary disease, hyperplasia can be diffuse or nodular and affect mainly the main cells interspersed with areas of transparent watery and oxyphilic cells. The amount of fat is usually reduced or the fatty tissue is replaced by hyperplastic cells. As with primary hyperparathyroidism, metastatic calcification can develop.

In many cases, the glands return to normal if the main clinical parameters are under control (for example, after a kidney transplant). With long-term secondary hyperplasia, however, normalization of gland function may not occur, since secondary hyperplasia may turn into an autonomous adenoma.

Manifestations of hyperparathyroidism are diverse, the most characteristic are the following:

• kidney damage due to stone formation and calcification of the renal parenchyma due to an excess of calcium in the urine, the resulting renal failure is the most serious complication of hyperparathyroidism;

• resorption of calcium from the bones leads to the development of osteoporosis and fibrocystic osteitis, which threatens with the appearance of pathological fractures;

• hypercalcemia leads to the deposition of calcium in the internal organs (metastatic calcification), this complication is more pronounced in secondary hyperparathyroidism;

• changes in the gastrointestinal tract include anorexia, nausea, peptic ulcers;

• characterized by neurological and neuromuscular manifestations (lethargy, weakness, convulsions, memory loss);

• Eye damage is characterized by the development of cataracts and corneal calcifications.

Hypercalcemia. One of the main effects of primary and secondary hyperparathyroidism is hypercalcemia. However, it should be remembered that an increase in serum calcium levels may be caused by other causes. Important causes of hypercalcemia include the effects of certain tumors. There are two main mechanisms of hypercalcemia for tumors. In the first mechanism, the primary tumor or bone metastases stimulate the function of osteoblasts and thus contribute to the leaching of calcium from the bones. This is characteristic of myeloma and some other hemoblastosis, metastasis of breast cancer. The second mechanism is the synthesis of tumor substances by the action of parathyroid hormone. Such a mechanism of hypercalcemia is characteristic of squamous cell lung cancer, kidney cancer, bladder cancer, and ovarian cancer.

Hypoparathyroidism. There are a large number of probable causes of parathyroid hormone secretion deficiency leading to hypocalcemia. The main ones are the following:

• erroneous removal of all glands during thyroidectomy, removal of parathyroid glands by mistake instead of lymph nodes during radical surgery on the neck in some forms of malignant tumors, removal of too much of the parathyroid gland in the treatment of primary hyperparathyroidism (for example, removal of 3 glands in a patient who has no additional 4th gland);

• congenital absence of all glands in Di Georgy syndrome;

• autoimmune disease - polyglandulo-autoimmune syndrome with simultaneous insufficiency of the adrenal glands and ovaries, mucous-cutaneous candidiasis, pernicious anemia;

• rare hereditary syndromes;

• syndromes accompanied by hypomagnesiemia (magnesia enhances the effect of parathyroid hormone).

Acutely developed hypoparathyroidism is accompanied by a sharp drop in serum calcium levels and an increase in neuromuscular excitability, leading to tetanic convulsions; death can occur due to laryngism. With long-term hypoparathyroidism, in addition to tetany, hypercalcification of bones, cataracts, and hypoplasia of the teeth due to the defective formation of enamel matrix and nail anomalies develop.

Pseudohypoparathyroidism. This rare disease is inherited in an autosomal recessive manner, characterized by signs of hypoparathyroidism in combination with parathyroid hyperplasia and parathyroid hormone hypersecretion. It is caused by the resistance of receptors of target cells to the action of parathyroid hormone, especially in the kidneys and the skeleton. In this little-studied disease, hypocalcemia is combined with skeletal abnormalities and calcifications in the internal organs. Relatives of such patients often have similar skeletal abnormalities without signs of damage to the parathyroid glands. This condition was called pseudo-pseudo-hypoparathyroidism; its genesis has not been studied.

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