Good to know 

Reasons for overgrowth. Constitutional height. If the child is significantly ahead of peers in growth Family tallness

Tall statureimplies a high rate of linear growth of the child, exceeding the average for a given chronological age and gender. Tall stature- not a disease, but more often a sign of excessive physical development, however, it is one of the leading symptoms of such endocrine pathology as gigantism and acromegaly. Gigantism- a disease associated with excessive production of growth hormone by the adenohypophysis. The reason for the development of gigantism is the pathology of the hypothalamic-pituitary region, which develops as a result of tumors, neuroinfection, intoxication, and traumatic brain injury.

Gigantismmore often observed in boys of pre- and pubertal age. Characterized by high rates of dew, fatigue, weakness, decreased performance and school performance, headaches, dizziness, and possibly visual impairment. Body proportions are preserved. They note a quick hand and stop, a delay in sexual development. In the presence of a growing pituitary adenoma, along with cerebral symptoms, visual acuity and narrowing of the visual fields gradually decrease.

Acromegalyis extremely rare in children. With acromegaly, there is a different sensitivity of peripheral tissues to growth hormone. All cerebral symptoms are more pronounced than with gigantism. Children often complain of bone pain, muscle weakness, loss of smell. The disproportionate growth of the skeleton and soft tissues is characteristic: an increase in the superciliary and zygomatic arches, the lower jaw and spaces between the teeth, a significant thickening of all bones, an increase in the phalanges of the fingers and calcaneus, the appearance of bone outgrowths - spikes. The growth of soft tissues leads to a characteristic disfigurement of the face due to thickening of the nose, ruining the auricles. An increase in the size of the tongue causes dysarthria, a thickening of the vocal cords - coarsening of the voice. There are symptoms of hypogonadism.

TO rare genetic forms of tall stature include: Marfan syndromes are characterized by: tall stature, "spider" fingers, dolichocephaly, chest deformity, scoliosis, underweight, heart defects, ophthalmic disorders; Sotos' symptoms are characterized by: acromegaly, lack of coordination, mental retardation; Pyle's symptoms are characterized by: disproportionate long lower limbs, valgus deviation of the knee joints, limited extension of the elbow joints; homocystinuria is characterized by: osteoporosis, a tendency to fracture, optic nerve atrophy, arterial thrombosis, mental retardation, a phenotype as in Marfan's syndrome.

Hermaphroditismaccompanied by an abnormal (bisexual) structure of the external genitalia. anomalies in the structure of the external genitalia in persons with a female genetic sex (karyotype 46 XX) are commonly referred to as "false female hermaphroditism", anomalies in persons with a male genetic sex (karyotype 46 XY) - "false male hermaphroditism", with the exception of a rare form - true hermaphroditism , in which the presence of a 46 XY, 46 XX or 46 XY\46 XX karyotype is possible. The external genitalia are bisexual with varying degrees of virilization. The internal genitalia, as a rule, have female features: there is a uterus (often one-horned), a vagina, tubes. At puberty, patients, as a rule, are dominated by female features.

Diagnosis of hermaphrodism

It is necessary to begin the examination of children, first of all, with the determination of sex chromatin and karyotype. The detection of positive sex chromatin and the 46XX karyotype is more likely to indicate false female hermaphroditism. An accurate diagnosis can only be made with laparotomy, macroscopic and histological examination of the gonads. In the case of negative sex chromatin, a differential diagnosis should be made between various forms of false male hermaphroditism.

The presence of the uterus, tubes and vagina with a karyotype of 46 XY and a mosaic of 46 XY \ 45 X0 suggests the presence of testicular dysgenesis syndrome. Much less often, gonadal bisexuality (true hermaphroditism) can be detected. With a karyotype of 46 XY and the absence of the uterus and the upper third of the vagina, one should think about the syndrome of incomplete masculinization.

A significant difficulty is the differential diagnosis between the incomplete form of masculinization and the incomplete form of testicular feminization. The difference is revealed only in the pubertal period, when in children with an incomplete form of testicular feminization, the mammary glands spontaneously begin to develop, the figure develops according to the female type, and with the syndrome of incomplete masculinization, all signs of the male puberty are noted.

Treatment of hermaphrodism

For all forms of false female hermaphroditism the choice of the female sex is not in doubt. With congenital dysfunction of the adrenal cortex, adequate and timely initiated therapy with cortisol preparations makes it possible to avoid further vilirezation and creates the prerequisites for further physiological formation of the ovaries. With false male hermaphroditism with a satisfactory development of the cavernous bodies of the penis, the male sex is chosen and masculinizing plastic surgery of the genitals is performed. With true hermaphroditism the choice of female gender is desirable. Produce feminizing plastic of the genitals.

Complaints about high growth less common than short, as many parents take pride in their children being tall. However, some teenagers (mostly girls) show concern and consider themselves too tall during the pubertal growth spurt. The reasons for the height are listed below.

Causes of Prematurity or High Growth:
I. Obesity:
- Puberty occurs earlier, so the final growth centile is smaller than in childhood

II. Secondary:
- Hyperthyroidism
- Excess sex hormones - premature puberty for whatever reason
- Excess adrenal hormones and androgens - congenital adrenal hyperplasia
- True (excessive GH secretion)

III. Syndromes:
- Tall and too long legs:
Marfan syndrome
homocystinuria
Klinefelter's syndrome (47 XXY and XXY karyotype)

Proportional high growth at birth:
maternal diabetes
primary hyperinsulinism
Beckwith's syndrome

Sotos syndrome is accompanied by head enlargement, facial features and learning difficulties

Centile intervals of height and weight of children

In most cases high growth inherited from tall parents. Overeating in childhood, which causes obesity, stimulates early development and leads to tall stature. However, since in this case puberty usually occurs somewhat earlier than average, the final height may not be too high.

Secondary endocrine diseases are rare. Both congenital adrenal hyperplasia and early puberty lead to early fusion of the epiphyses, so that after early rapid growth, its rate decreases and the final growth is not much higher than normal.

Marfan syndromes(loose fibrous connective tissue disease) and Klinefelter (XXY) cause tall stature with disproportionately long legs, and the XXY condition is also accompanied by infertility and learning difficulties.

tall kids may experience discomfort as a result of being treated like adults because they look older than their chronological age. Prepubertal or early pubertal overgrowth in adolescent girls can be managed with estrogen therapy to induce early closure of the epiphyses.

However, since this treatment leads with varied results and dangerous side effects, it is rarely used. In cases of particularly pronounced tall stature, the possibility of surgical destruction of the epiphyses on the legs may be considered.

A child's advance in growth can be called a state when the child's growth rate is significantly ahead of the average, i.e. is outside the 95th centile in the table of growth indicators for children of this age (outside the norm).

If the child is much ahead in growth, first of all, it is necessary to draw the attention of the pediatrician observing the child to this condition and examine the child with specialists (endocrinologist, cardiologist, genetics, etc.).

Tall stature in healthy children.

The increase in cases of so-called constitutional high growth, which has no pathological basis and is characteristic of quite healthy children, has become a relatively new pediatric problem. Excessively high growth of girls often makes parents seek medical help. According to certain indications, such children can be treated with hormonal drugs that inhibit growth and enhance the maturation of the skeleton. Most often, diethylstilbestrol, estrogen conjugates, estradiol are used for these purposes. In relation to the predicted final growth, such a “treatment” for 1.5–2 years can result in a growth retardation of 4–8 cm.

The tallness of healthy boys very rarely causes concern for parents and the children themselves. Only in cases of Marfan's disease, where in parallel with the intensive growth of the skeleton and in proportion to it, aortic aneurysmatization increases, there may be indications for inhibition of growth by adrenal androgens or testosterone.

However, regardless of the reasons for tall stature, it is necessary to monitor the child's health, since the active growth of the skeleton entails the active growth of internal tissues and organs, which can adversely affect their functioning. This is especially true for the heart. Parents need to be especially careful during periods of active skeletal growth (5-7 years and 12-16 years). If active growth is accompanied by internal pains or disturbances in the activity of internal organs, you should consult a doctor.

Possible reasons for the advance of the child in growth are tall stature.

Tall stature of a pathological nature is much less common than short stature. It is necessary to distinguish between transient forms of tall stature and tall stature that persists until the end of the elongation period.

Transient forms include a large length and body weight in the fetal fetus of a woman suffering from diabetes mellitus. Sometimes, already in postnatal development, an accelerated growth of children with hyperfunction of the thyroid gland or increased production of adrenal androgens is temporarily observed.

Persistent forms of tall stature may be of a chromosomal nature, in particular, they are characteristic of carriers of an additional Y chromosome - sets 47 XYY or 48 XXYY. Congenital syndromes, a component of which is tall stature, or gigantism, are extremely rare. These include Wiedemann-Beckwitht syndrome, Berardinelli's lipodystrophy, Marfan's disease, and one of the forms of amino acid metabolism disorders - homocystinuria.

The congenital form of cerebral gigantism is characterized not only by tall stature, but also by its combination with profound mental retardation and anomalies of the craniofacial region.

Gigantism in children, which occurs in the process of postnatal development, may also have a pituitary nature, i.e. determined by hyperproduction of somatotropic hormone of the pituitary gland. In the vast majority of cases, the cause of such overproduction is a tumor of the adenohypophysis.

Diagnosis of the causes of tall stature

To clarify the diagnosis, parents should be interviewed and determine if there is a hereditary-constitutional form that does not require any treatment. In some cases, if the presence of a genetic-chromosomal pathology is suspected, a consultation with a geneticist and genetic analysis may be required. In addition, an analysis should be carried out to determine the level of growth hormones - STH and IGF-1, amino acids, glucose in the blood, as well as examinations for the content of thyroid hormones. In some cases, MRI, tissue biopsy (if the adrenal glands are affected), radiography, ultrasound, and so on may be required.

When taking an anamnesis, attention should be paid to indicators of height and weight at birth. So, with Marfan, Beckwith-Wiedemann, Simpson-Golabi-Bemel, Banayan-Riley-Ruvalkab syndromes and constitutional tallness, high values ​​of body length at birth are noted.

tall stature treatment

In the event that comorbidities are the cause of tall stature, they should be treated. So, for example, with tumors of the adrenal glands, they are removed, followed by replacement therapy. Otherwise, if indicated, hormonal therapy may be given to slow growth to a socially acceptable level.

Tall stature is understood as the excess of a child's height by more than 2.0 SDS (standard deviation coefficient) - 2.3 percentiles - for a given age, sex and population.

In children, primary, secondary and idiopathic tall stature is distinguished.

Primary include:

  • syndromes with violation of sex chromosomes - Klinefelter (47 XXY), 47 XYY, fragile X-chromosome, 47 XXX;
  • dysmorphic syndromes due to metabolic or connective tissue disorders - Marfan's syndrome, homocystinuria, total congenital lipodystrophy (Berardinelli's syndrome);
  • dysmorphic syndromes with symmetrical tall stature (Banayana - Riley - Ruvalkaba, Eleyalde, Marshall - Smith, Nevo, Simpson - Golabi - Bemel, Sotos, Vever);
  • dysmorphic syndromes with partial (asymmetric) tall stature (Beckwith - Wiedemann, Klippel - Trepone - Weber, Proteus).

Secondary tallness includes:

  • hyperproduction of growth hormone against the background of volumetric formation of the pituitary gland;
  • hyperinsulinism;
  • exogenous constitutional obesity;
  • familial glucocorticoid deficiency;
  • conditions that cause tall stature in children and normal growth or short stature in adults - premature sexual development (PPR), exogenous influence of estrogens or androgens, thyrotoxicosis, congenital adrenal hyperplasia;
  • conditions that predetermine normal growth in children and tall stature in adults - deficiency of gonadotropic hormones, aromatase, dysfunction of estrogen receptors.

Idiopathic (normal) tall stature includes genetic (familial or constitutional) and non-familial idiopathic forms.

Examination steps

It provides for the collection of anamnesis, clinical examination using instrumental and laboratory methods.

Anamnestic data:

  • clarification of the height of the parents with the calculation of the genetic (target) growth and determination of the growth corridor of the child; genetic (target) height for a boy = (mother's height in cm + father's height in cm)/2 plus 6.5 cm; for a girl = (mother's height in cm + father's height in cm) / 2 minus 6.5 cm; growth corridor in boys: on the somatogram (growth curve) the father's height is marked - one border, the mother's height plus 13 cm - the second border; in girls: mother's height - one border, father's height minus 13 cm - the second border;
  • growth of sibs, grandparents;
  • gestational age, pregnancy and childbirth;
  • height and weight of the child at birth;
  • the growth rate of the child from the first months of life until the moment of going to the doctor;
  • the timing of the onset of puberty in parents;
  • patient's disease throughout life.

Clinical examination:

  • measuring the height and weight of the patient;
  • measuring the ratio of the length of the upper body to the length of the lower, measuring the ratio of the span of the arms to the length of the body (body proportions);
  • assessment of the presence of dysmorphogenesis stigmas (congenital developmental features);
  • assessment of sexual development (Tanner stage);
  • assessment of intelligence, sense of smell.

Laboratory and instrumental examination:

  • general and biochemical (creatinine, urea, potassium, sodium, calcium, phosphorus, alkaline phosphatase, glucose, liver enzymes) blood test;
  • X-ray of the left hand and wrist with assessment of bone age and calculation of predicted growth using index tables;
  • predicted (final) height of the child in cm = height of the child in cm/% of bone maturity x 100%;
  • hormonal examination (the spectrum depends on the suspected pathology) - growth hormone (GH), insulin-like growth factor-1 (IGF-1), insulin-like growth factor-binding protein-3 (IFRB-3), luteinizing hormone (LH), follicle-stimulating hormone ( FSH), testosterone, estradiol, dehydroepiandrosterone, 17-hydroxyprogesterone, insulin / C-peptide, thyroid stimulating hormone (TSH), free thyroxine (T4 s), antibodies to thyroid peroxidase (TRO) and TSH receptors;
  • oral glucose tolerance test (OGTT) with the determination of GH levels every 30 minutes for 2 hours. Normally, in response to hyperglycemia, there is a decrease in GH levels up to the minimum detectable (suppression). With gigantism, there is no decrease in growth hormone below 1 ng / ml, in 30% of cases there is a paradoxical release of growth hormone in response to a glucose load;
  • examination by an ophthalmologist (fundus, visual fields), consultation with a neurologist;
  • cytogenetic analysis;
  • the content and spectrum of amino acids (methionine and homocysteine ​​in urine and blood serum);
  • CT (MRI) of the brain and pituitary gland with obligatory contrast enhancement;
  • molecular diagnostics.

Differential diagnosis of tall stature in children

On fig. Figure 1 presents an algorithm for the differential diagnosis of diseases accompanied by tall stature in children, starting from the neonatal period.

According to the time of occurrence, tall stature is distinguished:

  • fetal macrosomia or prenatal tallness syndrome;
  • postnatal advance of physical development, leading to tall stature in childhood;
  • postnatal advance of physical development, leading to tall stature in adults.

Fetal macrosomia associated with hyperinsulinemia and hypoglycemia

Fetal macrosomia. It is divided into diseases associated with the presence or absence of hyperinsulinemia and hypoglycemia (Fig. 2).


Newborns from mothers with diabetes

Long-term uncompensated disorders of carbohydrate metabolism in pregnant women are the most common cause of the birth of a child with macrosomia. Prolonged hyperglycemia in a pregnant woman with undiagnosed (gestational), sub- or decompensated diabetes mellitus leads to hyperplasia of β-cells of the fetal pancreas, causing an increase in the secretion of fetal insulin. Chronic hyperinsulinemia stimulates an increase in the expression of IGF-1, which is manifested by increases in the concentration of IGF-1 at birth. On the other hand, insulin, having an anabolic effect, has a growth-stimulating effect on the fetus.

In the presence of severe placental dysfunction, vascular disorders in a newborn from a mother with diabetes, intrauterine growth retardation, congenital malformations (heart, urinary system, eye, caudal dysgenesis, microcephaly) can be observed. A common problem is transient early postnatal hypoglycemia. Mothers with uncompensated diabetes mellitus have an increased risk of giving birth to premature babies, children with hyaline membrane disease, hypocalcemia, prolonged hyperbilirubinemia, thrombosis (renal veins), and transient cardiomyopathy.

Persistent neonatal hyperinsulinemic hypoglycemia (PHG)

This is a group of congenital diseases that are based on a defect in the development or functioning of pancreatic β-cells, causing uncontrolled secretion of insulin. The latter leads to increased utilization of glucose and the development of severe hypoglycemia. The incidence of PHH is 1 case per 50,000 newborns in the European population.

There are two forms of PHH in newborns: focal (isolated) and diffuse hyperplasia of pancreatic β-cells. Most familial and sporadic cases of the disease have an autosomal recessive pattern of inheritance. In some familial forms of PHH, mutations are found in the KCNJ11 and ABCC8 genes (SUR1 and Kir6.2 subunits of the pancreatic KATP channel).

The classic clinical manifestation of PHH is macrosomia for a given gestational age and persistent symptomatic hypoglycemia in the first days of life.

Correction requires a high rate of glucose supply - more than 10 mg / kg / minute. Laboratory criteria for hyperinsulinemic hypoglycemia include low levels of ketone bodies and free fatty acids, high levels of insulin and C-peptide.

Beckwith-Wiedemann Syndrome (WWS)

A group of syndromes is described, which are accompanied by macrosomia of the newborn with an increase in internal organs. They are based on excessive secretion of insulin-like growth factor - 2 (IGF-2). The most common disease is the Beckwith-Wiedemann syndrome (synonym: visceromegaly, omphacele and macroglossia syndrome). The incidence of WBS is 1 in 13,700 newborns.

The reason for the GLS is a change in the number of growth-regulatory genes located at the end of the short arm of the 11th chromosome (11p15.5). Molecular abnormalities in this disease are complex and explain the variability of the phenotype. 10% of patients with GBS have chromosomal abnormalities. In the other 90% of cases, molecular defects of known genes involved in the pathogenesis of the syndrome and candidate genes detected in sporadic cases are determined.

Minimal diagnostic features of PBS include macroglossia, hernia of the umbilical cord, macrosomia, notches on the earlobes, and hypoglycemia.

Frequent anomalies are macroglossia and omphacele (less often, the divergence of the rectus abdominis muscles). Macrosomia is noted from birth (the length of the newborn is more than 52 cm and the weight is more than 4 kg) or develops postnatally. Microcephaly or hydrocephalus may be seen; protruding neck; bite anomalies associated with hypoplasia of the upper jaw and relative hyperplasia of the lower; exophthalmos; relative hypoplasia of the orbits. Hemihypertrophy and pigmented nevi often occur.

There are visceromegaly (hepatomegaly, splenomegaly, nephromegaly, pancreatomegaly, less often - cardiomegaly), hyperplasia of the uterus, bladder, clitoris, thymus.

In 30–50% of patients, hyperinsulinemic hypoglycemia is observed due to hyperplasia of pancreatic β-cells. In most cases, it is transient in nature and is stopped by the introduction of glucose and diazoxide. In some patients, partial pancreatectomy is required to normalize glycemia. Moderate mental retardation is usually associated with hypoglycemia.

Patients with RBS have an increased risk of developing embryonic tumors (Wilms tumor, hepatoblastoma, adrenocortical carcinoma, gonadoblastoma).

Simpson-Golabi-Bemel syndrome (GBS)

The disease belongs to the X-linked syndromes with prenatal and postnatal tall stature. Minimal diagnostic signs are macrosomia (birth weight 4,000–5,000 g), anomalies of the facial part of the skull, polydactyly, nail hypoplasia.

Other phenotypic manifestations are similar to those of WBS. Macroglossia, visceromegaly, hyperinsulinemic hypoglycemia, and a tendency to embryonic tumors are noted. The height of men reaches 192–210 cm.

GBS syndrome is based on functional disorders of the gene that plays a role in the control of the growth of embryonic mesodermal tissue, glypican 3 (GPC3). A potential relationship between the receptor of this gene and IGF-2 is discussed, which may explain the similar clinical features of GBS and RBS syndromes.

Perlman syndrome

This rare genetic disorder is characterized by prenatal macrosomia, renal hamartoma, susceptibility to fetal tumors (Wilms' tumor), hypoglycemia associated with pancreatic islet cell hyperplasia, and facial dysmorphia. Most patients die in the neonatal period. The cause of the disease is currently unknown.

Fetal macrosomia with normal insulin levels

Sotos syndrome

The population frequency of Sotos syndrome (cerebral gigantism syndrome) is unknown. Most cases are sporadic. Family forms of the syndrome have an autosomal dominant type of inheritance. Minimal diagnostic features include acromegaly, overgrowth, mental retardation, and incoordination. At birth, an increase in body weight and height over the 90th percentile is characteristic. There is an acceleration of growth in the first years of life, the growth of patients exceeds the 97th percentile. Growth acceleration continues up to 4-5 years. Sexual development occurs at normal times, early puberty may occur.

The results of the levels (basal and during OGTT) of GH, IGF-1, IFRSB-3 have normal values. There are no specific laboratory and instrumental signs of the syndrome.

Macrocephaly with protruding frontal tubercles, prognathia, hypertelorism, antimongoloid incision of the eyes, protruding lower jaw, macroglossia, high palate, and strabismus are observed. Scoliosis, enlarged feet and hands, syndactyly of the toes are described. Increased risk of neoplasia, in particular hepatic carcinoma, Wilms tumor, ovaries, parathyroid glands. The degree of mental retardation is moderate. Convulsions, lack of coordination are noted.

Marshall-Smith Syndrome

This disease belongs to rare genetic syndromes and is characterized by prenatal tallness, progression of bone age, mental retardation, facial stigmas, large hands and feet, thickening of the proximal and middle phalanges of the fingers. The main cause of death of patients in early childhood is pulmonary insufficiency. The molecular cause of the syndrome is currently unknown.

Around us there are low, up to 150 cm, and high, up to 2 meters, women and men. These figures are in no way connected with mental abilities; for us, these are variants of the norm. They say that success and self-esteem of a person depend on growth. It is believed that tall women are more ambitious than their short girlfriends, and “short” men compensate for the missing centimeters with a successful career and financial situation.

There are those among us who stand out sharply from the crowd. Moreover, for parents of short stature, a son can grow up to two meters, and for tall parents, the daughter will not reach one and a half. In adulthood, growth is very difficult to influence. It is important for parents to regularly measure the growth of the child. As a rule, dwarfs do not grow more than 130 cm, and giants exceed 2 meters.

Children need to be closely monitored

Health problems can affect growth: chronic diseases of the respiratory system, heart and blood vessels, gastrointestinal tract, hormonal disorders. Regular use of drugs containing hormones, for example, to relieve asthma attacks, also slows down growth.

It happens that babies who were born with a weight and height below the norm grow poorly.

How children grow

1 year of life: + 25 cm.

2 year of life: + 8-12 cm.

Annual growth: + 4–6 cm.

If in the third year of life the child has grown less than 4 cm, it is necessary to show it to the endocrinologist. Sometimes parents do not pay attention to the fact that their baby is lagging behind their peers in growth, and they realize only in adolescence, when it is already difficult to fix anything. If they turned to specialists in time, the child would be helped to grow up.

Despite the care of parents and proper nutrition, 10% of these children, even after 4 years, lag behind their peers. A similar delay can also occur in those children who have one of the parents below 160 cm. But there is no reason to panic - in most children, doctors find only the so-called constitutional growth retardation. There is no pathology, but the child remains the smallest in the class for a long time. As a rule, in such children, puberty begins later - at the age of 14-16: thus, nature prolongs their growth time. Their parents grew up in much the same way: for a long time they went to the closing lessons in physical education, and then suddenly they waved and found themselves in the top five. These are boys and girls with late puberty. They do not need any treatment, they will catch up, and even surpass their peers by the age of 16-18.

But in some cases, a special examination - carried out only in a hospital - reveals a deficiency of growth hormone (GH) in the body. GH is produced by the pituitary gland under the control of the structures of the hypothalamus. Its deficiency may be genetically determined or associated with disorders in the endocrine system. Previously, the fate of such children was a foregone conclusion, they were doomed to dwarf growth: the boy did not grow above 140 cm, and the girl - 130 cm. Today they can be helped.

FOR LOVERS OF CALCULATIONS

There are formulas that allow you to calculate the genetically based growth of your child. Their error is quite large: plus or minus 5–10 cm.

Girls \u003d (father's height in centimeters + mother's height in centimeters) / 2 - 6.5 cm.

Boys = (father's height in centimeters + mother's height in centimeters) / 2 + 6.5 cm

What is responsible for growth?

Somatotropic hormone (GH), or the so-called "growth hormone", is responsible for growth in the human body. Sex hormones and the thyroid gland, insulin are also important, however, in relation to growth, they are active only in the presence of a normal level of growth hormone. It turns out that a deficiency of one or more of the listed hormones or an excess of adrenal hormones entails growth retardation and without appropriate treatment, the matter will not move forward.

Fortunately, endocrine growth retardation is found in less than 1% of children. A real lack of growth hormone leads to dwarfism (nanism): then boys grow no more than 140 cm, girls - up to 130 cm. The sooner parents turn to an endocrinologist and receive treatment, the more likely that a small patient will grow to an average height or even higher. Moreover, if the first child was found to be deficient in growth hormone, and the parents are planning a second one, in most cases the second child does not repeat this hormonal problem.

YOU SHOULD KNOW IT

Bone (or biological) age indicates whether the growth and overall development of the bones corresponds to how many years and months the child is. This is a more accurate indicator than height or body weight. In the bones of children there are so-called growth zones, due to which the skeleton can increase. These growth zones gradually close by the end of puberty, the skeleton ossifies and growth stops. Bone age allows doctors to understand how long the child will grow, whether it is necessary to look for hormonal pathology or there is no reason for this. True, even in healthy children, the deviation of bone age from the real one can be up to 3 years.

For the child to grow well

Dairy products, as calcium is a building material for a growing organism.

Vegetables and fruits. Especially useful carrots containing beta-carotene. In order for this microelement to be better absorbed, raw carrots must be rubbed and seasoned with sour cream or butter.

Protein products - meat, fish, caviar (in the absence of food allergies).

Those children who spend a lot of time outdoors, play outdoor games, and go in for sports grow better. By the way, if you want your child to be taller, when you choose a sports section, give preference not to power sports, but to basketball, volleyball, tennis.

Sleep plays a special role: 70% of the growth hormone - somatotropin - is produced at night. If you put your baby to bed late, he sleeps restlessly, wakes up often, the production of growth hormone is disrupted.

Vegetarianism and observance of religious fasts for children is unacceptable, as well as fast food, semi-finished products (sausages and sausage - there is almost no complete protein in them).

Vitamins and minerals. First of all - vitamin D, with a lack of which rickets develops. Now the recommendations of doctors are to give it to all children in a prophylactic dose, about 10 micrograms per day.

calcium and iodine. At 6–10 years of age, children should receive 800–1200 mg of calcium and 150 micrograms of iodine per day. And teenagers - 1200-1500 mg of calcium and 200 micrograms of iodine. The best source of calcium is cottage cheese, but you can’t eat that much, so about half of the calcium should be taken in tablets. Another option is foods fortified with calcium. As for iodine, only those who live by the sea get enough of it: drinking water and seafood are rich in iodine there. Iodized salt is not enough, so iodine supplements are another essential for growth.

________________________________________________________

If the child is a giant

“Grows well, tall, which means good health,” says the proud father, patting his son on the shoulder, who for three months waved a head higher than him. This is partly true: if the body develops rapidly, it means that it is healthy. However, it is precisely this - the rapid growth rate - that makes adolescence a time of increased health risk.

Gigantism (or macrosomia, tall stature) develops in children with incomplete processes of ossification of the skeleton. It is more common in adolescent boys, and is determined already at the age of 9-13 years, progresses throughout the entire period of physiological growth. With gigantism, the child's growth rate and its performance by the end of puberty reach more than 1.9 m in women and 2 m in men, while maintaining a relatively proportional physique.

The growth of adults from 175 cm to 200 cm is considered as subgiant. People over 200 cm are considered giants.

"Not everything is good, what is a lot"

The child is growing fast. Too fast - compared to peers. As a result:

The vessels do not keep up with the development of tissues, which worsens their nutrition;

Different parts of the same organs develop unevenly, creating structural defects and interruptions in normal functioning;

Bones that are soft during this period are amenable to curvature due to alternating weakness and tension of different muscle groups pressing on them.

All this leads to the emergence of adolescent diseases. Their specificity is that a “banal” problem overlooked during rapid maturation can seriously “knock down” a young organism in just six months.

If the child grows and recovers proportionally, there should be no problems. Worse, if the child is rapidly gaining centimeters, he is also rapidly losing kilograms. These are the children - thin and tall - at risk. They most often develop so-called growing pains. In second place in the risk group are fast-growing and sedentary children who spend a lot of time at a computer or TV: their muscles are very weak, and it is difficult for them to “keep” extra centimeters on themselves.

Cause of tall stature

1. Constitutionally-hereditary;
2. Endocrine

3. Chromosomal-genetic;
4. Premature sexual development in young children.

What threatens high growth

- Mitral valve prolapse.It occurs in about every 10th schoolchild between the ages of 12 and 15. It is caused by the fact that the mitral valve grows faster than the tissue of the heart (myocardium). The result is a condition similar to heart disease.

- Rachiocampsis.Growing bones, including the spine, easily take the form that the muscles and loads on the upper shoulder girdle force them to take. If they are significant, then the child has a chance to earn scoliosis - a lateral curvature of the spine. In most cases, six months of physical therapy and massage will be enough to correct posture. In advanced cases, you will need a special corset.

- Visual impairment.The vicious chain "growth - poor posture" has one more link - visual impairment. This is a direct consequence of the wrong position at the table while reading, as well as the lack of illumination of the workplace. The disease can progress until the end of puberty, gaining diopter by diopter. Glasses and vitamins stop the deterioration of vision, but do not return it, because the key point in vision is the weakening of the muscles of the eye, which they do not affect. The eye muscles are strengthened by hardware vision correction on a video simulator, computer or lens, as well as special massage and treatment.

- Stretch marks.Many children, whose growth is accompanied by weight gain, develop large red, and then whitish stretch marks on the body. This happens due to the fact that the skin of adolescents is thinned, easily stretched and injured, and the subcutaneous fat layer grows faster than the skin. As a result, the skin is stretched and replaced at the growth sites with connective tissue. However, sometimes the cause of stretch marks is hormonal imbalances, which may or may not be related to growth.

REFERENCE

Children-"giants" complain of fatigue and weakness, dizziness, headaches, blurred vision, pain in the joints and bones. Decreased memory and performance leads to poor school performance. Gigantism is characterized by hormonal disorders, a disorder of mental and sexual function.

Can growth disorders be identified and treated?

It is good when signs of dwarfism or gigantism are seen in childhood. If the child is 2 years behind or ahead of his peers in growth, you need to consult a doctor.

Of course, this takes into account the constitution and height of the parents. Doctors should conduct a comprehensive examination of the child. The level of somatotropic hormone in the blood is determined, and an X-ray examination of the skull is also performed. Treatment is carried out by an endocrinologist. In case of lack of growth hormone, replacement therapy is prescribed. This means that until a certain age, the child will drink pills that contain somatotropic hormone. Often with dwarfism, there is a lack of thyroid hormones and sex hormones. They can also be replaced with drugs. This treatment works well if started before 5–7 years of age. In parallel with hormones, drugs are prescribed that improve metabolism and promote muscle growth. And parents should also take care of good nutrition for their child, since bones need a lot of “building material” to grow bones.

Treatment of gigantism is carried out depending on the cause of its occurrence. It is necessary to start therapy in childhood - only then children with short stature will “catch up” with their peers, and very tall ones will stop growing at an “accelerated” pace.

Thank you for your help in preparing the material of the endocrinologist of the NMC Anna Petrova and pediatrician Svetlana Sofronova.