Causes of rickets
The main etiologic factor of rickets is vitamin D deficiency. At the same time, rickets is considered as a multifactorial disease, in which there is a discrepancy between the high demand of a growing child in phosphorus-calcium salts and the inadequate development of regulatory systems ensuring the supply of these salts to the tissues.
There are two ways to provide the body with vitamin D: the intake of food and the formation of the skin under the influence of ultraviolet rays. The first way is associated with the intake of cholecalciferol (vitamin D3) with products of animal origin (cod liver, fish caviar, egg yolk, to a lesser extent - female and cow's milk, butter). In vegetable oils, ergocalciferol (vitamin D2) can occur. The second way is associated with the formation of vitamin D in the skin of 7-dehydrocholesterol under the influence of ultraviolet rays with a wavelength of 280-310 microns. It used to be believed that these two ways of providing vitamin D are equivalent. However, recently it became known that more than 90% of vitamin D is synthesized by ultraviolet irradiation, and 10% comes from food. Under favorable conditions, the necessary amount of vitamin D is formed in the baby's skin. In case of insufficient insolation due to climatic conditions (smoke, atmospheric air, clouds, fogs), the intensity of vitamin D synthesis decreases.
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Formation of active metabolites of vitamin D
Entering the body, vitamin D is converted into more active metabolites through complex transformations in the liver and kidneys.
The first stage of activation is due to the fact that the vitamin D that enters the digestive tract or formed in the skin is transported to the liver, where it is converted into 25-hydroxycholecalciferol, or calcidiol, under the influence of the enzyme 25-hydroxylase, the main form of vitamin D circulating in the blood. In healthy children, the content of 25-hydroxycholecalciferol in the serum is about 20-40 ng / ml.
The second stage of vitamin D metabolism is repeated hydroxylation in the kidneys, where 25-hydroxycholecalciferol is transferred with the help of vitamin D-binding protein (transcalciferin). At the level of mitochondria of the kidneys, the most active metabolite is formed - 1,25-dihydroxycholecalciferol, or calcitriol, as well as 24,25-dihydroxycholecalciferol. The formation of the main metabolite - calcitriol - occurs with the participation of the renal enzyme 1-a-hydroxylase. The concentration of calcitriol in blood plasma is about 20-40 pg / ml.
The content of metabolites of vitamin D in the blood serves as an objective criterion for the provision of the child with vitamin D.
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The basic physiological function of vitamin D
The main physiological function of vitamin D is the control of the transport of calcium ions in the body (hence the name "calciferol" - "carrier calcium") - by regulating the absorption of calcium ions in the intestine and enhancing reabsorption in the renal tubules, as well as stimulating the mineralization of bone tissue. When the level of calcium and inorganic phosphates in the blood decreases or when the secretion of parathyroid hormone increases, the activity of renal 1-a-hydroxylase and the synthesis of 1,25-dihydroxycholecalciferol are sharply increased.
At normal and elevated levels of calcium and phosphorus, another enzyme of the kidneys, 24-hydroxylase, is activated in the plasma, with the participation of which 24,25-dihydroxycholecalciferol is synthesized, which contributes to the deposition of calcium and phosphates in the bone tissue and suppresses the secretion of parathyroid hormone.
In recent years, the concept of the role of vitamin D has been significantly supplemented by data on the conversion of this vitamin in the body, which led to a change in views on vitamin D as a typical vitamin. According to modern ideas, vitamin D should be considered a potent hormone-active compound, as, like hormones, it affects specific receptors. It is known that the metabolite of vitamin D (1,25-dihydroxycholecalciferol) transmits a signal to the gene device (DNA) of cells and activates genes that control the synthesis of functional transport proteins for calcium ions. Target organs for this metabolite are the intestines, kidneys, bones. In the intestine, vitamin D stimulates absorption of calcium and equivalent amounts of inorganic phosphates. In kidneys with his participation, active reabsorption of calcium and inorganic phosphates takes place. Vitamin D regulates the mineralization of cartilage tissue, bone apatites. It is believed that the metabolite plays an important role in the embryogenesis of bone tissue.
Vitamin D is involved in the regulation of the activity of the enzymes of the main bioenergetic cycle of Krebs, enhances the synthesis of citric acid. It is known that citrates are part of the bone tissue.
Vitamin D and its active metabolites affect the cells of the immune system, therefore, with vitamin D deficiency, infants develop secondary immune deficiency (phagocytosis activity, interleukin 1 and 2 production, interferon production).
Neuroendocrine regulation of phosphorus-calcium metabolism is carried out by the secretion of parathyroid hormone. The decrease in the level of ionized calcium, associated with vitamin D deficiency, serves as a signal for increasing the level of parathyroid hormone. Under the influence of parathyroid hormone, calcium of bone apatites passes into a soluble form, due to which the level of ionized calcium can be restored. The antagonist of parathyroid hormone is calcitonin. Under its influence, the content of ionized calcium in the blood serum decreases, the processes of bone mineralization increase.
What causes rickets?