- Rickets symptoms
- Rickets reasons
- Treatment of Rickets
the polietiologichny exchange disease caused by discrepancy between the high need of the growing organism for salts of phosphorus and calcium and insufficiency of the systems providing their transport and inclusion in metabolism. Rickets is characterized by the bone disturbances caused by an insufficient mineralization of osteoid (the forming intercellular matrix of a bone). At children 1 years are more senior and a similar state call adults by osteomalacy and osteoporosis.
Rickets - a frequent disease of children of the first year of life. Though its true prevalence is unknown, at many children reveal these or those residual phenomena of this disease (anomaly of a bite and growth of teeth, deformation of a skull, a thorax, lower extremities, etc.). The children having rickets enter further into group of often ill children.
The first symptoms of a disease arise usually on the 2-3rd month of life. The behavior of the child changes: there are a concern, fearfulness, hypererethism, starts at external irritants (loud noise, sudden flash of light). The dream becomes superficial and alarming. Sweating, especially on skin of a pilar part of the head and the person amplifies, note a resistant red dermographism. Sweat has an acid smell and irritates skin, causing an itch. The child rubs the head about a pillow, sites of baldness on a nape appear. The physiological hyper tone of muscles characteristic of this age is replaced by a hypomyotonia. There is a pliability of seams of a skull and edges of a big fontanel, thickenings on edges are outlined in places of costochondral joints ("rachitic beads").
On the roentgenogram of bones of a wrist reveal an insignificant osteoporosis. At a biochemical blood analysis find normal or even the increased concentration of calcium and decrease in concentration of phosphates; increase in activity of an alkaline phosphatase is possible. In the analysis of urine reveal a fosfaturiya, increase in amount of ammonia and amino acids.
The period of a heat is necessary most often for the end of the first half of the year of life and is characterized by even more considerable frustration from a nervous system and a musculoskeletal system. Processes of osteomalacy, especially pronounced at the acute course of rickets, lead to a softening of flat bones of a skull (craniotabes) with the subsequent, often unilateral flattening of a nape. There are a pliability and deformation of a thorax with impression in the lower third of a breast ("the shoemaker's breast) or its protrusion ("chicken", or "keeled", a breast). The curvature of long tubular bones is characteristic Au-shaped (more rare H-shaped). The narrowed ploskorakhitichesky basin forms. The expressed softening of edges is resulted by deepening in the area of a diaphragm attachment (a harrisonov a furrow). The hyperplasia of ossiform fabric prevailing at the subacute course of rickets is shown by formation of hypertrophied frontal and parietal hillocks, a thickening in wrists, costochondral joints and interphalangeal joints of fingers of hands with education so-called "brasletok", "rachitic beads", "pearls threads".
On roentgenograms of long tubular bones scyphoid expansions of metaphyses, blurring and an illegibility of zones of preliminary calcification are visible.
Clearly the hypophosphatemia, a moderate hypocalcemia, hyperactivity of an alkaline phosphatase are expressed.
Improvement of health and condition of the child are characteristic of this period. Static functions improve or normalized. On roentgenograms find changes in a type of uneven consolidation of regions of growth. Content of phosphorus in blood reaches norm or exceeds it a little. The small hypocalcemia can remain, and even sometimes amplify.
Period of the residual phenomena.
Normalization of biochemical indicators and disappearance of symptoms of active rickets demonstrate transition of a disease from an active phase in inactive - the period of the residual phenomena. Symptoms of the postponed rickets (residual deformations of a skeleton and a hypomyotonia) can is long to remain.
Severity and course of rickets.
Rapid development of all symptoms, the expressed neurologic frustration, considerable hypophosphatemia, dominance of processes of osteomalacy are characteristic of the acute course of rickets. Moderately expressed or almost imperceptible neurologic disturbances, minor changes of biochemical composition of blood, a prevalence of processes of an ossiform hyperplasia are inherent to a subacute current. Existence of a recurrent course of rickets is called into question now.
The main reasons for deficit of phosphates and salts of calcium at children of early age the following.
* Prematurity (the most intensive intake of calcium and phosphorus to a fruit happens pregnancies in recent months).
* Insufficient intake of calcium and phosphorus with food owing to the wrong feeding.
* The increased need for minerals in the conditions of intensive growth (rickets - a disease of the growing organism).
* Disturbance of transport of phosphorus and calcium in a GIT, kidneys, bones because of immaturity of fermental systems or pathology of these bodies.
* Adverse ecological situation (accumulation in an organism of lead salts, chrome, strontium, deficit of magnesium, iron).
* Genetic predisposition (for example, are more inclined to development of rickets and boys, children with swarty skin and a blood group of A(II) whereas children with 0(I) blood group have rickets less often transfer it heavier).
* Endocrine disturbances (disturbance of functions parathyroid and thyroid glands).
* Ekzo-or endogenous deficit of vitamin D.
Exchange of vitamin D in an organism is very difficult. Initial forms - ergocalciferol (D2 vitamin) and the cholecalciferol (D3 vitamin) arriving with food (the last is also formed in skin under the influence of Ural federal district), - biologically maloaktivna. The first hydroxylation of initial forms of vitamin D happens to their transformation into the intermediate (transport) metabolite called by 25 hydrocholecalciferol in a liver. 25 hydrocholecalciferol are 1,5-2 times more active than an initial form. Then there is transport 25 hydrocholecalciferols in kidneys where it is exposed to a hydroxylation again and 1,25 dihydrocholecalciferol and 24,25 dihydrocholecalciferol turn into active gormonopodobny metabolites. These metabolites together with hormones parathyroid and thyroid glands provide phosphorus-calcium exchange.
True exogenous deficit of vitamin D, how many the inborn and acquired disturbances of functions of intestines (malabsorption of various genesis), a liver, kidneys, hereditary defects of metabolism of vitamin D matter not so much. Determination of content of metabolites of vitamin D in blood in the 80th of the 20th century allowed to establish true security of an organism with this vitamin. It turned out that the vast majority of pregnant women, with clinical and biochemical signs of rickets of a hypovitaminosis of D has no women in childbirth, and also children of early age that allowed to draw a conclusion that rickets and hypovitaminosis of D - ambiguous concepts. A hypovitaminosis is registered with an identical frequency as at receiving vitamin D in the preventive purposes, and at not getting it. Besides, not always a hypovitaminosis of D is followed by disturbance of phosphorus-calcium exchange. Classical hypovitaminosis of D proceeds with the normal content of phosphorus in blood, and typical rickets is first of all a hypophosphatemia. Among children with rickets only at 15-20% decrease in concentration of metabolites of vitamin D in blood is revealed. There is an opinion that rickets - not a disease, but a borderline, scarce case, a peculiar diathesis. At the same time "physiological" bases of rickets (except feeding habits) consider intensive remodeling of 75-80% of a bone tissue on the first year of life and the forced hypokinesia breaking electrostatic regulation of creation of a bone.
It is necessary to consider that concentration of phosphorus and calcium in blood is also regulated by some hormones. Parathormone which content at rickets increases reduces a reabsorption of phosphates in renal tubules, at the same time stimulating a vitamin D hydroxylation in kidneys, absorption of calcium in intestines and a calcium resorption from a bone, thus liquidating a hypocalcemia. Observe as well change of activity of a thyroid gland as the calcitonin stimulates inclusion of calcium in a bone and transition of low-active metabolites of vitamin D to highly active.
Treatment of Rickets:
Treatment of rickets has to be complex, long and directed to elimination of the reasons which caused it. The great value is attached to the nonspecific treatment including rational feeding, the organization of the mode corresponding to age of the child, long stay in the fresh air with sufficient insolation, remedial gymnastics and massage, a hardening, treatment of associated diseases.
Specific treatment of rickets includes purpose of vitamin D, drugs of calcium and phosphorus.
After the termination of a course of treatment appoint vitamin D in preventive doses (100-200 ME/days, no more than 400 ME/days). It is necessary to remember that increase in a preventive dose can lead to a hypervitaminosis of D. Recently there were messages on need of individual approach at purpose of vitamin D (after determination of content in blood of its active metabolites). Many pediatricians suggest to appoint to children not vitamin D, and a complex of vitamins (for example, Podivit of Baby, Biovital gel for children, etc.) as rickets often is followed by a polyhypovitaminosis. Except vitamin D these complexes surely include the vitamin A reducing risk of development of a hypervitaminosis of D. If at treatment of rickets use vitamin D, recommend to appoint it in moderate doses. Usually use drugs of D3 vitamin (kolekaltsiferol) - Videcholum, Vigantolum. Many authors give preference to water-soluble D3 vitamin as it is better acquired in a GIT and renders more long effect in comparison with Solutio oleosa.