Reasons for high growth. If the child is significantly ahead of his peers in growth Constitutional tallness in girls

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

GigantismIt is more often observed in boys of pre- and pubertal age. Characterized by high rates of dew, fatigue, weakness, decreased performance and performance at school, headaches, dizziness, and possible visual impairment. Body proportions are preserved. Rapid development of the hands and feet and delayed sexual development are noted. In the presence of a growing pituitary adenoma, along with general cerebral symptoms, visual acuity gradually decreases and visual fields narrow.

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

TO rare genetic forms of tall stature include: Marfan syndrome is characterized by: tall stature, “spider” fingers, dolichocephaly, chest deformation, scoliosis, underweight, heart defects, ophthalmological 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 fractures, optic nerve atrophy, arterial thrombosis, mental retardation, a phenotype similar to Marfan 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 usually designated by the term “false female hermaphroditism”, anomalies in persons with a male genetic sex (karyotype 46 XY) are called “false male hermaphroditism”, with the exception of a rare form - true hermaphroditism , in which the presence of karyotype 46 XY, 46 XX or 46 XY\46 XX is possible. The external genitalia have a bisexual structure with varying degrees of virilization. Internal genitalia, as a rule, have female features: there is a uterus (often one-horned), a vagina, and tubes. At puberty, patients tend to have predominantly female characteristics.

Diagnosis of hermaphrodism

It is necessary to begin examining children, first of all, by determining sex chromatin and karyotype. Detection of positive sex chromatin and karyotype 46 XX most likely indicate false female hermaphroditism. An accurate diagnosis can only be made by 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 karyotype 46 XY and mosaic 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 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 during puberty, 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 the signs of the male puberty are noted.

Treatment of hermaphrodism

In front of everyone forms of false female hermaphroditism the choice of the female gender is beyond doubt. In case of congenital dysfunction of the adrenal cortex, adequate and timely therapy with cortisol drugs avoids further villization and creates the preconditions for further physiological formation of the ovaries. With false male hermaphroditism with satisfactory development of the corpora cavernosa of the penis, the male gender is selected and masculinizing genital plastic surgery is performed. With true hermaphroditism The choice of female gender is desirable. Feminizing genital plastic surgery is performed.

430 Chapter 13 Neuroendocrine diseases

growth hormone and IGF-1, growth hormone level against the background of OGTT

more than 2 ng/ml, MRI or CT signs of pituitary adenoma.

Newborns with Sotos syndrome (cerebral gigantism) are characterized by an increase in body weight and length, a convex forehead, dolichocephaly, macrocephaly, high Gothic palate, hypertelorism with anti-Mongoloid arrangement of the palpebral fissures, and prognathia. Such children experience mental retardation and impaired motor coordination. Skin and

soft tissues are somewhat thickened. With age, body growth increases

occurs, but puberty usually occurs earlier, as a result of which the epiphyses of the tubular bones close. This is why most patients with Co-syndrome

Tosa in adulthood have normal growth.

The clinical picture of Beckwith-Wiedemann syndrome is well reflected by another accepted name for the syndrome - EMG syndrome (omphalocele, macroglossia, gigantism - from the English. Exomphalos, Macroglossia, Gigantism). Indeed, a newborn with Beckwith-Wiedemann syndrome has large sizes, omphalocele, macroglossia, hyperplasia of the medullary layer of the kidneys, hyperplastic

gap of pancreatic islet cells, which often becomes the cause

development of hypoglycemia.

The typical appearance of patients with Marfan syndrome or Marfan-like syndromes (homocystinuria, MEN 2b syndrome,

congenital contractural arachnodactyly), primarily

due to a decrease in the upper segment of the body (sitting height) in relation to the lower, exceeding the arm span of the body length and arachnodactyly.

For the clinical picture of MEN 2b syndrome, see the section “Syn-

"drome of multiple endocrine neoplasia type 2."

For the clinical picture of Klinefelter's syndrome, see

"Delayed puberty syndrome."

In addition, high growth is associated with an increased risk of developing

development of certain diseases and disorders: idiopathic scoliosis and other postural disorders, varicocele, spontaneous pneumothorax, depression, osteoporosis, etc.

Etiology

Constitutional tallness.

Endocrine diseases.

GDM or decompensated diabetes in the mother during pregnancy.

Somatotropinoma of the pituitary gland (pituitary gigantism) and other causes of hypersecretion of growth hormone.

PPS syndrome.

Thyrotoxicosis syndrome.

Exogenous-constitutional obesity.

Hypogonadism syndrome.

Hereditary syndromes including somatotropinoma

pituitary gland

MEN 1 syndrome (Wermer syndrome).

McCune-Albright syndrome.

Carney syndrome.

Familial acromegaly.

Hereditary syndromes characterized by tall stature.

Sotos syndrome (cerebral gigantism).

Weaver-Smith syndrome.

Beckwith-Wiedemann syndrome.

Simpson–Golabi–Bemel syndrome.

Marfan syndrome.

MEN syndrome 2b.

Homocystinuria.

Congenital contractural arachnodactyly (Beals syndrome).

Fragile X syndrome (Martin–Bell syndrome).

ACTH resistance syndromes.

Familial glucocorticoid deficiency 1st type.

Syndrome "3A" (Allgrove syndrome).

Syndromes of androgen/estrogen resistance and aromatase deficiency (testicular feminization syndrome, etc.).

Congenital generalized lipodystrophy (lipoatro-

physical diabetes, Seip–Lawrence syndrome, Berardinelli–Seip syndrome).

Neurofibromatosis type I (Recklinghausen's disease).

Klinefelter's syndrome.

XYY syndrome (prison basketball team syndrome)

Diagnostics

If a newborn has excess body length, the first step should be

The first step is to look for diabetes in the mother. If the mother does not have diabetes

it is necessary to exclude congenital diseases, first of all

including Sotos and Beckwith-Wiedemann syndromes.

Diagnostic algorithm

In childhood, tall stature is diagnosed according to the algorithm presented in Fig. 13-1.

Be sure to find out: the height of parents and siblings; height and weight at birth; rate of growth throughout life.

Physical examination

During the physical examination, the following is carried out:

measurement of height, growth rate, body weight;

assessment of the presence of stigmata of disembryogenesis (congenital features maxillofacial area, ears, etc.);

intellectual development;

432 Chapter 13 Neuroendocrine diseases

Rice. 13-1. Diagnostic algorithm.

sexual development;

the ratio of the length of the upper body to that of the lower;

ratio of arm span to body length.

Laboratory and instrumental studies

Include:

determination of karyotype;

hormonal blood test(IGF-1, TSH);

bone age assessment;

calculation of estimated final growth;

urine test for homocysteine;

molecular genetic research.

In table 13-6 indicates the main principles of diagnosis

main diseases causing tall stature.

Table 13-6. Principles for diagnosing the main diseases causing tall stature

Diagnosis of other diseases that cause tall stature is based on the characteristic clinical picture and the results of molecular genetic studies.

Treatment of constitutional tall stature

Therapy is considered appropriate if the expected window

final growth of more than three standard deviations (for individuals

Caucasian race is more than 195 cm for boys and 180 cm for girls). The indications for prescribing pharmacotherapy are:

idiopathic scoliosis and psychosocial problems associated with high growth.

To treat tall stature, pre-pubertal growth can be slowed down.

growth so that timely puberty begins at a lower height, or reduce pre-pubertal growth, accelerating the onset

puberty.

Sex hormone therapy is aimed at accelerating the onset of puberty. If treatment is started early, the likelihood of reduced final height increases. The most appropriate time to prescribe therapy is prepuberty

434 Chapter 13 Neuroendocrine diseases

period (bone age for girls - 10, for boys - 12.5 years).

Therapy after the onset of puberty is no longer as effective.

tivna. The administration of sex hormones at bone ages greater than 14 years can lead to an increase in final height.

Treatment of constitutional tall stature with somatostatin analogues and growth hormone receptor antagonists is not yet used in widespread clinical practice.

Treatment of girls

Girls with constitutional tallness are prescribed

ethinyl estradiol orally 0.15–0.3 mg 1 time per day. If necessary, the dose of ethinyl estradiol can be increased to 0.5 mg/day if the patient tolerates the drug well. Application of con-

jugated estrogens (7.5–10 mg/day) are also quite effective

effective. If uterine bleeding occurs, cyclic use of sex hormones is indicated; dydrogesterone orally 10 mg 2 times a day is added to estrogens from the 16th to 25th day of the menstrual cycle or norethisterone orally 5 mg once a day from the 16th to 25th day. th day of the menstrual cycle. Treatment must be continued until the epiphyses are closed, otherwise

growth may continue after estrogen withdrawal.

If ethinyl estradiol is poorly tolerated, estradiol valerate can be replaced (the dose is increased gradually from 2 to 6 mg/day).

Treatment of boys

In practice, the need to treat boys with testosterone drugs is extremely rare.

Testosterone (mixture of esters) intramuscularly 250 mg once a day

week or 500 mg once every 2 weeks for 6–12 months.

Treatment of tall stature in other diseases

Sex hormones are used to limit growth in syn-

drome of Marfan.

For Beckwith–Wiedemann and Sotos syndromes, symptomatic

matic treatment.

Treatment of pituitary somatotropinoma - see “Acromegaly and pituitary gigantism”.

Treatment of MEN 2b syndrome - see “Multiple endocrine neoplasia syndrome type 2”.

Treatment of Klinefelter syndrome - see “Delayed puberty syndrome”, “Klinefelter syndrome” (hypergonadal

tropic hypogonadism).

SHORT STALLING SYNDROME

Classification

Idiopathic growth hormone deficiency.

Idiopathic growth hormone deficiency (classical

Neurosecretory dysfunction (NSD).

Growth hormone deficiency of organic origin: congenital

given and acquired form.

Other causes of short stature

Idiopathic short stature: familial, non-familial.

Clinically defined syndromes with chromosomal aberration: Turner, Down, gonadal dysgenesis.

Clinically defined syndromes without chromosomal aberration: Silver-Russell, Noonan, Recklinghausen, de Lange,

Williams, Bloom, Prader-Willi, Rubinstein.

Intrauterine growth retardation with postnatal short stature, without stigmata.

Intrauterine growth restriction with postnatal short stature

loss, with stigmas: due to perinatal infections,

mother taking drugs, smoking or alcohol abuse, etc.

Skeletal dysplasia: achondroplasia, hypochondroplasia, osteogenesis imperfecta, etc.

Diseases of bone metabolism: mucopolysaccharidosis, mucolipidosis, etc.

Metabolic diseases: glycogen storage disease,

lipid storage disease, phenylketonuria, etc.

Iatrogenic short stature.

Diagnostics

See “Growth Measurement and Evaluation.”

Growth deficiency is determined using percentile tables of variation.

ants of normal height. Analyze the child's growth curve with

taking into account the boundaries of his final height, calculated on the basis of the average height of his parents:

predicted final height for a boy = [(father's height + mother's height + 13 cm)/2] ± 10 cm predicted final height for a girl =

[(father’s height + mother’s height – 13 cm)/2] ± 10 cm.

If the extrapolated final height of a child based on birth data

hundred at the time of examination, taking into account bone age, is lower

limits of the calculated final growth interval, then it follows

talk about pathologically low growth.

Assessing the proportionality of the skeleton is important first of all

to exclude various forms of skeletal dysplasia as causes of short stature. In particular, it is advisable to calculate the “upper/lower segment” coefficient and arm span.

The degree of ossification of the epiphyseal growth zones is an important criterion in the diagnosis of dwarfism and the prognosis of final growth.

With primary growth deficiency, the delay in bone maturation is either absent or mild (skeletal dysplasia, syndromic forms of dwarfism, intrauterine growth retardation,

436 Chapter 13 Neuroendocrine diseases

genetic short stature). For secondary growth deficiency,

especially for pituitary dwarfism, significant

lag in bone age from chronological age (>2 years).

X-ray examination of the skull carried out in order to visualize the shape and size of the sella turcica and the condition of the skull bones. With pituitary dwarfism, the sella turcica is often small in size. Characteristic changes in the sella turcica are observed in craniopharyngioma: thinning and porosity of the ster-

nok, widening of the entrance, supra or intrasellar foci usually

messages. With increased intracranial pressure, increased digital impressions and divergence of cranial sutures are visible.

At CT and MRI of the brain in patients with idiopathic

hypopituitarism is revealed by morphological and structural

Toural changes: hypoplasia of the pituitary gland, rupture or thinning of the pituitary stalk, ectopia of the neurohypophysis, empty sella syndrome. CT and MRI of the brain are indicated for any suspicion of intracranial pathology (space-occupying process).

Constitutional growth retardation and puberty (CGRP) and familial short stature (or normal variant short stature)

growth) fit into the concept of normal growth options.

Children from parents with short stature, as a rule, are short in stature to the same extent as their parents, due to genetically programmed growth potentials. Children from parents with a history of

severe growth retardation and puberty, with a high degree of probability

will inherit this developmental pattern.

Children with CGRP have normal height and body weight at birth, grow normally until 1–2 years of age, then the growth rate decreases.

and the growth curve is slightly below the 3rd percentile

and parallel to it. Bone age usually corresponds to

age of growth, growth rate - at least 5 cm per year. In samples for

stimulation reveals a significant release of GH (>10 ng/ml),

but the integrated daily secretion of GH in the blood is reduced. Pu-

bertat is normal, but delayed due to bone age lag and occurs when bone maturation is reached in boys at 11.5–12 years, in girls at 10.5–11 years. The timing of achieving final growth is shifted in time; final growth is usually

normal and without hormonal therapy.

There is evidence of effective treatment with recombinant hormones

human growth monopoly of children with CGRP, intrauterine growth retardation, familial short stature, Turner, Russell-Silver, Prader-Willi syndromes, Fanconi anemia, Itsenko-Cushing disease, glycogenosis, with a condition after irradiation for leukemia and brain tumors, after kidney transplantation, with chronic renal failure,

skeletal dysplasias. At the same time, there is no reliable data on the higher final growth of children with CGRP receiving

treated with growth hormone than those who did not receive it, despite

that over a certain period of time (2–3 years) treatment with GH

significantly accelerates the growth rate.

In boys with CCRP over 12 years of age with a delay in bone age of at least 2 years from the chronological age, short-term treatment with short courses of small doses of anabolic steroids (nerobolil♠, retabolil♠) is possible. Wherein

Strict monitoring of the child’s growth is necessary (at least once every

6 months). If bone maturation progresses rapidly, treatment is discontinued.

Pituitary dwarfism (somatotropic insufficiency)

A single measurement of GH in the blood for the diagnosis of somatotropic insufficiency has no diagnostic value due to the pulsed nature of GH secretion and the possibility of obtaining extremely low (zero) basal values

GH even in healthy children. In this regard, spontaneous

secretion of growth hormone in the blood, determine the peak of GH release against the background of stimulation, examine IGFs and their binding proteins in the blood.

Provocative tests are based on the ability to differentiate

ny pharmacological drugs stimulate the secretion and release of GH by somatotrophs. In clinical practice, the most widely used tests are insulin, clonidine, GH-releasing hormone, arginine, levodopa, pyridostigmine bromide (Table 13-7).

Total somatotropic insufficiency is diagnosed when the peak release of GH against the background of stimulation is less than 7 ng/ml, partially

significant deficiency - at the peak of GH release from 7 to 10 ng/ml.

A necessary condition for carrying out GH-stimulating

samples - euthyroid state of the thyroid gland. In case of hypothyroidism, it is necessary

We are taking a preliminary course of treatment with thyroid drugs for 3–4 weeks. In addition, obese children have a reduced GH response to stimulation.

For simultaneous assessment of several pituitary functions

tions, it is convenient to conduct combined tests with various gi-

pothalamic releasing hormones [insulin + thyrotropin-releasing hormone

(TRH) + luliberin (LHRH test), GH releasing hormone + TRH +

LHRH test, GH releasing hormone + corticoliberin (CRH) +

LHRH + TRH test]. For example, when testing with GH-releasing hormone + thyroliberin + luliberin, GH-releasing hormone (1 μg/kg), thyroliberin (7 μg/kg, maximum 400 μg), luliberin (100 μg) are sequentially injected into the intravenous cannula. The presence of basal low levels of TSH and free T4 in combination with the absence or prolonged response of TSH to TRH indicates concomitant secondary hypothyroidism. Absence of gonadotropin release response to LHRH (increase more than 2 times the basal level) in combination with low

basal levels of sex hormones indicates secondary

hypogonadism.

The most diagnostically significant constants in identifying

GH deficiency in children - IGF, in particular IGF-1 (somatomedin C) and IGF-2.

To treat pituitary dwarfism, genetically engineered human growth hormone preparations are used as HRT. Currently, the following somatotropin preparations are approved for use in Russia:

genotropin ♠ (Genotropin♠);

norditropin Simplex♠ (Norditropin Simplex♠);

Saizen ♠ (Saizen♠);

humatrope ♠ (Humatrope♠);

Rastan ♠ .

skin daily at 20:00–22:00.

Treatment must be continued until the growth zones are closed or until

achieving socially acceptable growth.

When pituitary dwarfism is combined with multiple deficiency of adenohypophysial hormones, appropriate

HRT with thyroid drugs (L-thyroxine), glucocorticoids

dami (hydrocortisone), sex steroids.

Shereshevsky–Turner syndrome (gonadal dysgenesis)

Short stature is the most common clinical manifestation

phenomenon of Shereshevsky-Turner syndrome. This syndrome should be suspected primarily in girls with unexplained growth retardation. Considering the mosaic forms of syndro-

Shereshevsky–Turner ma (45 ХО/46 ХХ, 45 ХО/46 Х i(Хq), 46

Xi(Xq), 45 XO/46 X, rX, etc.) with a minimal set of typical clinical symptoms or even their absence, all girls with growth retardation (height SDS ≤2 SDS) are required to have a karyotype study at the first stage of the diagnostic search.

The growth pattern in girls with Shereshevsky–Turner syndrome is represented by moderate intrauterine growth retardation

(average length and body weight of newborns is approximately 1 SD

below normal values ​​and averages 48.3 cm and 2800 g, respectively), at a relatively normal rate

growth from birth to 3 years of life, progressive decline

The average height for Shereshevsky–Turner syndrome is

on average 142.0–146.8 cm.

In addition to growth retardation, clinical symptoms include

lymphatic edema of the hands and feet during the neonatal period,

a short neck with wing-shaped folds of varying expression

ness, low hair growth on the back of the neck, ptosis of the eyelids (usually

bilateral), micrognathia, epicanthus, Gothic palate, deformed

mation of the ears, barrel-shaped chest with widely spaced nipples, scoliosis, valgus deviation of the elbow-

joints, Madelung deformity, shortening and thickening of the fingers, typical dermatoglyphics, nail dysplasia, multiple pigmented nevi.

Provocative tests for growth hormone stimulation are performed only in patients with Shereshevsky–Turner syndrome, whose

the growth curve deviates from that for this syndrome.

Most patients have a normal growth hormone response to stimulation during childhood. Reduced levels of growth hormone in

period of puberty are probably associated with low levels of sexual

Changes in the production of hormones by the adrenal glands result in a variety of health effects. With their excessive activity, puberty occurs faster. If disturbances affect the medulla of the glands, the person develops arterial hypertension. Decreased adrenal function can lead to the development of Addison's disease, or, as it is also called, bronze disease. It is characterized by: skin pigmentation, exhaustion, decreased blood pressure, low sugar levels. With bronze disease, the body's resistance decreases. Dysfunction of the endocrine system can also manifest itself in changes in the activity of the gonads. Hormone production increases, mainly due to the development of malignant tumors. When the functions of the gonads decrease, a disease such as eunuchoidism is diagnosed. This disease manifests itself in excessive growth of the limbs with their abnormal lengthening, the appearance of a tendency towards obesity, underdevelopment of the genital organs and the absence of some secondary sexual characteristics.

Complaints about high growth less common than short, since many parents are proud that their children are tall. However, some teenagers (mostly girls) become concerned and consider themselves too tall during the puberty growth spurt. The reasons for tall stature are given below.

Causes of premature development or high growth:
I. Obesity:
- Puberty occurs earlier, so the final height centile is lower than in childhood

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

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

Proportional tall height at birth:
maternal diabetes
primary hyperinsulinism
Beckwith syndrome

Sotos syndrome is accompanied by an enlarged head, characteristic facial features and learning difficulties

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

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

Tall kids may feel uncomfortable with being treated like adults because they look older than their chronological age. Prepubertal or early pubertal overgrowth in adolescent girls can be managed using estrogen therapy to induce early epiphyseal fusion.

However, since this is a treatment leads to varied results and has 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.

Tallness is an excess of normal growth rates by more than two points. Growth is programmed genetically and depends on many factors.

This condition may be accompanied by increased fatigue, poor posture, problems in sexual development, and so on.

Causes of tall stature

The cause of tall stature may be a hereditary predisposition. In addition, endocrine diseases can also cause increased growth. In some cases, genetic-chromosomal pathologies are noted. Sometimes tallness is explained by early sexual development.

Constitutional-hereditary tall stature is most often diagnosed in boys. This condition is assessed as normal. At the same time, neither mental nor physical development suffers. When examining the blood, no significant changes are observed. This is the most common cause of tall stature.

In addition, increased growth of the child's skeleton can be observed as a result of the presence of a growth hormone-secreting tumor, cerebral gigantism, Beckwith-Wiedemann syndrome, hymicystonuria, untreated congenital adrenal hyperplasia, obesity, as well as increased production of estrogens and androgens.

Symptoms of tallness

The main sign of pathology is high growth, that is, its non-compliance with norms. There are ways to determine a child's future growth. So, for boys it is calculated by the formula: father’s height plus mother’s height, divided by two and plus 6.5 centimeters. For girls, the last digit is minus. Exceeding the normal indicators by two or more indicators is tall.

With increased growth, changes are observed in the vascular and muscular systems. In addition, such people are prone to high blood pressure in the future. In addition, they have a longer recovery period after illnesses.

It should also be noted that high growth causes the child to have complexes. Girls are often embarrassed by their height and try in every possible way to hide it. They begin to stoop, which leads to the formation of spinal diseases. As a result of the fact that the muscular skeleton does not have time to form at the same speed as the bone skeleton, there is a lack of weight compared to height. In addition, given that the heart is also a muscular organ, tall children often experience problems in the functioning of this organ. This manifests itself in the form of weakness, dizziness, heart pain, and so on.

Diagnosis of tall stature

To clarify the diagnosis, parents should be interviewed and determine whether there is a hereditary-constitutional form that does not require any treatment. In addition, an analysis should be carried out to determine the level of growth hormone, amino acids, serum in the urine, glucose in the blood, as well as examinations for hormone levels.

In some cases, tomography, tissue biopsy (if the adrenal glands are affected), radiography, ultrasound, and so on may be required.

Treatment of tall stature

There is currently no specific treatment for tall stature. The use of hormonal drugs can lead to serious side effects, which makes it necessary to abandon this technique.

If the cause of tall stature is concomitant diseases, they should be treated. For example, in case of adrenal tumors, they are removed followed by replacement therapy.

Prevention of tall stature

There is no specific prevention for this pathology. If a disease is suspected, the child should be examined to rule out diseases of vital organs.