The causes and pathogenesis of hypoparathyroidism
Last reviewed: 19.10.2021
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It is possible to single out the following basic etiological forms of hypoparathyroidism (in decreasing order of frequency): postoperative; associated with radiation, vascular, infectious lesions of the parathyroid glands; idiopathic (with congenital underdevelopment, absence of parathyroid glands or autoimmune genesis).
The most common cause of hypoparathyroidism is the removal or damage of the parathyroid glands (one or several) during imperfect operations on the thyroid gland, which is associated with their anatomical proximity, and in some cases - with an unusual arrangement of glands. It is important their trauma during surgery, violation of innervation and blood supply of the parathyroid glands. The incidence of the disease after surgery on the thyroid gland varies, according to different authors, from 0.2 to 5.8%. Postoperative hypoparathyroidism is more common in patients who underwent extirpation of the thyroid gland for malignant tumors. Characteristic of the development of the disease after operations on the parathyroid gland for hyperparathyroidism. In these cases, hypoparathyroidism is associated with the removal of the most active tissue with insufficient (suppressed) activity of the remaining parathyroid glands, with a sharp drop in hormonal activity and calcium level in the blood serum and with a decrease in total calcium resources in the body due to bone pathology.
Hypoparathyroidism can be caused by radiation damage of the parathyroid glands during remote irradiation of the head and neck organs, as well as endogenous irradiation in the treatment of diffuse toxic goiter or thyroid cancer with radioactive iodine ( 131 1).
The parathyroid glands can be damaged by infectious factors, inflammatory diseases of the thyroid gland and surrounding organs and tissues ( thyroiditis, abscesses, phlegmon of the neck and mouth cavity), amyloidosis, candidamycosis, hormone-inactive tumors of the parathyroid gland, hemorrhages in the tumor of the parathyroid glands.
Latent hypoparathyroidism is revealed on the background of provoking factors such as intercurrent infections, pregnancy, lactation, calcium and vitamin D deficiency in the diet, shift of the acid-base state towards alkalosis (with vomiting, diarrhea, hyperventilation), poisonings (chloroform, morphine, ergot, carbon monoxide).
There is a hypoparathyroidism of an unclear genesis, which is called idiopathic. This group includes patients with impaired development of the 3rd and 4th gill arches (Di George syndrome), congenital dysplasia of the parathyroid glands, as well as with autoimmune disorders that cause isolated gland failure or multiple hormonal insufficiency that includes this disease. In the genesis of idiopathic hypoparathyroidism undoubtedly the importance of genetic family factors, as well as some congenital metabolic disorders. The relative deficiency of parathyroid hormone can be associated with the secretion of parathyroid hormone with reduced biological activity or insensitivity of target tissues to its action. Hypoparathyroidism can be observed in children whose mothers suffer from hypomagnesia and hypoparathyroidism.
In the pathogenesis of the disease, the main role is played by absolute or relative deficiency of parathyroid hormone with hyperphosphataemia and hypocalcemia, the development of which is associated with impaired calcium absorption in the intestine, a decrease in its mobilization from the bones, and a relative decrease in tubular reabsorption in the kidneys. Lack of parathyroid hormone leads to a decrease in the level of calcium in the blood both independently and indirectly, due to a decrease in the synthesis in the kidneys of the active form of vitamin D 3 - 1, 25 (OH 2 ) D 3 (cholecalciferol).
Negative calcium and positive phosphorus balance disrupt electrolyte balance, calcium / phosphorus and sodium / potassium ratios change. This leads to a universal violation of the permeability of cell membranes, in particular in nerve cells, to a change in the processes of polarization in the region of synapses. The resulting increase in neuromuscular excitability and general vegetative reactivity leads to increased convulsive readiness and tetanic crises. In the genesis of tetany, a significant sol belongs to the disruption of the metabolism of magnesium and the development of hypomagnesemia. This facilitates the penetration of sodium ions into the cell and the release of potassium ions from the cell, which also contributes to increased neuromuscular excitability. The same action has also the resulting shift of the acid-base state towards alkalosis.
Pathanatomy
The anatomical substrate of hypoparathyroidism is the absence of parathyroid glands (congenital or in connection with surgical removal), underdevelopment and atrophic processes due to autoimmune damage, impaired blood supply or innervation, radiation or toxic effects. In the internal organs and walls of large vessels with hypoparathyroidism, the deposition of calcium salts is possible.