Manifestations of growth hormone deficiency. GH hormone: functions, normal levels in the blood, causes of disorders

Insufficiency of GH in adults is manifested by a complex of disorders of the physical and mental state. Frequency GH deficiency among adults has not been established, however, since its most common causes are pituitary or peripituitary tumors (both before and after treatment), it can be assumed that it is approximately 10:1 000 000 per year and, apparently, does not depend on floor.
Etiology and pathogenesis. Most congenital forms of GH deficiency (pituitary dwarfism - see section 2.5) are genetic diseases. The most common form is panhypopituitary dwarfism, which is inherited in a recessive manner and is transmitted autosomally or via the X chromosome. TO congenital forms also include idiopathic GH-RH deficiency associated with a defect in the development of the hypothalamic-pituitary system (anencephaly, holoprosencephaly, segtooptic dysplasia; congenital pituitary aplasia, congenital hypoplasia pituitary gland, pituitary ectopia).
Acquired forms of GH deficiency, which can develop at any age, are caused primarily by tumors of the chiasmatic-sellar region: craniopharyngiomas, hamartomas, neurofibromas, germinomas, pituitary adenomas, meningiomas, cholesteatomas, tumors of other parts of the brain - glioma of the optic chiasm, undifferentiated tumors. GH deficiency may manifest or be aggravated due to surgical or radiation damage to the pituitary gland or pituitary stalk during the treatment of tumors of the chiasmal-sellar region. A schematic representation of the sequence of decrease in the secretion of tropic hormones of the pituitary gland depending on the size of the tumor is given in Fig. 2.9. Insufficiency of GH may accompany the “empty” sella syndrome, the formation of suprasellar arachnoid cysts, hydrocephalus, be a consequence of viral or bacterial encephalitis and meningitis, nonspecific (autoimmune?) hypophysitis or vascular pathology (pituitary aneurysm; pituitary infarction), general toxic damage the body during chemotherapy or radiation therapy (especially head and neck tumors).
As already noted, children may experience constitutional delays in growth and puberty, and psychosocial (deprivation) dwarfism. Growth disorders may also be based on peripheral resistance to the action of growth hormone (Laron syndrome, pygmy dwarfism) or IGF-I, as well as biologically inactive growth hormone.
GH is one of the key regulators of metabolism, acting in various organs, tissues, systems throughout life. This hormone is produced impulsively, and the amplitude of the impulses and their frequency are maximum during puberty and gradually decrease with age. The secretion of GH is inversely proportional to body weight and the amount of fat in the body and directly proportional to osteogenic activity and T concentration. The activity of somatotrophs of the adenohypophysis is controlled by two hypothalamic neurohormones of the hypothalamus: GH-releasing hormone and somatostatin (see section 2.1). In addition, other exo- and endogenous factors influence the secretion of GH (Table 2.4).

Physiological effects of growth hormone. At the molecular level, the biological effect of GH (GH-receptor complex) is carried out through binding to a receptor on the cell surface (additional receptor molecules) with the subsequent formation of a receptor complex. The effect of GH can be direct and indirect - through the synthesis and release of IGF. The production of these factors, controlled by GH, occurs not only in the liver, but also in other tissues. Their growth and stimulating effects affect many tissues, especially cartilage and bone.
There are two main insulin-like growth factors - IGF-1 and IGF-2. IGF-1 is a single-chain peptide consisting of 70 amino acids and has more than 40% homology with proinsulin. IRF-2 is also homologous to proinsulin and is structurally very similar to IRF-1. Although both IRFs have growth-stimulating activity and are present in human serum, being associated with IRF-binding proteins, they differ significantly in receptor specificity and, in all likelihood, perform different functions. biological functions. IGF not only stimulates the growth of many tissues of the body, but also, together with GH itself, acts on the hypothalamus and pituitary gland according to the mechanism feedback, controlling the secretion of GH-releasing hormone and somatostatin, as well as the secretion of GH by pituitary somatotrophs.
IRFs can act locally as a paracrine or autocrine factor. There are at least 6 known IGF-binding blood proteins that play a regulatory role by controlling the bioavailability and action of IGF.
HGH improves absorption nutrients and synthesis of muscle fibers, delays protein catabolism and stimulates anabolic processes. This hormone directly stimulates the differentiation of preadipocytes into adipocytes, increasing the number of fat cells, but at the same time exhibits lipolytic activity. As a result of its action, the amount of abdominal fat decreases and the total body fat mass decreases.
GH receptors are present in various departments brain, including the pituitary gland and hypothalamus. It is possible that these receptors in the choroid plexus contribute to the transfer of GH across the blood-brain barrier. In the brain, GH affects the level of endorphins.
GH stimulates the proliferation of chondrocytes in the growth zones of long bones. These zones (epiphyseal plates) are the sites of bone formation and in the prepubertal period determine the growth of bones in length. GH affects chondrocytes, increasing local production of IGF-1. However, even after the closure of the epiphyseal growth zones, it maintains bone mineral density and, together with sex steroids and calcium-regulating hormones, influences the processes of restructuring bone tissue. Under its influence, the production of osteocalcin (a marker of bone formation activity) increases. Through IGF-1, growth hormone increases the production of vitamin D, which enhances the absorption of calcium in the gastrointestinal tract, as well as the reabsorption of phosphorus in the kidneys. The regulating effect of this hormone on the reabsorption of salts in renal tubules defines it important role in maintaining the body's water balance. STH appears to increase plasma renin activity (PRA), resulting in increased synthesis of angiotensin and aldosterone.
Clinical picture of GH deficiency. GH deficiency in adults has only recently been identified as an independent nosological group. The basis for this was observations of patients with interpituitary insufficiency. Despite replacement therapy of such patients with corticosteroids, thyroid and sex hormones, they had a decrease in the basal metabolic rate of the kidneys and cardiovascular system, and in the volume of circulating blood. These changes could be associated with loss of GH secretion after surgical or radiation damage to the pituitary gland. Subsequently, other characteristic
symptoms of GH deficiency. With this condition, the structure of the body changes: patients look more overweight due to an increase in the mass of adipose tissue; they have a decrease in the amount of fluid in the body (especially extracellular), and such a decrease can reach 15%. Body weight in men increases by 2.4-7.5 kg, in women - by 3.3-3.6 kg. Excessive adipose tissue usually located on the abdomen and visceral cavities, resulting in a significantly increased waist/hip ratio. When studying the ratio of muscle and adipose tissue in the soft tissue of the thigh, it was revealed that patients with GH deficiency have 65% muscle tissue and 35% adipose tissue, while in healthy people 85% muscle tissue and 15% fat are noted (according to X-ray CT). With GH deficiency, the mineral density of spongy and trabecular bones also decreases. Degree of reduction bone density varies from osteopenia to AP. Not only does bone mass per unit volume decrease, but the microarchitecture of the bone is also disrupted, which significantly increases the risk of fractures (3-5 times compared to the population of the corresponding age and gender). Cases of loss of bone density in the spine by 10-20% and in the forearm by 20-30% have been described. In such patients, oxygen consumption is reduced (by 25-30%) and heart rate (by an average of 10%).
It has long been noted that in patients who have undergone hypophysectomy, there is a decrease glomerular filtration and renal blood flow, despite ongoing hormone replacement therapy with glucocorticoids, thyroid and sex hormones. These changes can be considered to be associated with a decrease in extracellular fluid and cardiac output. Insufficiency of growth hormone is accompanied by an increase in the blood levels of total cholesterol, LDL, SONP and triglycerides and a decrease in the concentration of HDL. Among patients with hypopituitarism, hyperlipidemia (72-77%) and hypercholesterolemia (18%) are more often observed than in the general population. They were found to have thickening of the intima of the vessels, an increase in atheromatous plaques on their walls and a decrease in the elasticity of the aorta. The concentration of fibrinogen and plasminogen inhibitor activator-I in the serum increases significantly, which helps to reduce fibrinolytic activity. Retrospective studies have led to the conclusion that it is GH deficiency that may be the main factor in increasing mortality from cardiovascular pathology in patients with hypopituitarism (Fig. 2.10).
In patients with GH deficiency, the risk of death from cardiovascular diseases 1.95 times higher than in the control group of the corresponding age and gender.
Long-term observations of patients with GH deficiency reveal increased emotional lability and fatigue, memory impairment, decreased ability to concentrate. All this causes depression and social isolation. Problems also arise in the area of ​​sexual relations.

As already noted, GH deficiency can be isolated or combined with panhypopituitarism. In the latter case, the clinical picture includes symptoms of secondary hypogonadism, secondary hypothyroidism, secondary adrenal insufficiency; symptoms of diabetes insipidus.
Diagnosis of somatotropic insufficiency. When diagnosing somatotropic deficiency in adults, it is necessary to take into account medical history, in which one can find indications of the presence of growth hormone deficiency since childhood, tumors of the chiasmatic-sellar region, tumors of the pituitary gland, postoperative damage to the pituitary gland, post-radiation damage (proton therapy, gamma therapy organic diseases pituitary gland and brain), total radiation exposure (liquidators of the Chernobyl accident), symptom of the “empty” sella turcica, hypophysitis.
This category of patients complains of fatigue, excess body weight, violation of psychological comfort, decreased quality of life associated with poor general health, impaired self-control, lack of positive emotions, depression, increased anxiety, decreased “vitality” and vitality, inadequate emotional reactions, social isolation.
For patients, in order to clarify the cause of the development of GH deficiency, especially in the absence of a burdened anamnesis, it is advisable to conduct a brain examination using X-ray CT or MRI methods. In addition, it is necessary to conduct anthropometry, which will immediately allow one to assess disturbances in the ratio of muscle and fat tissue; It is advisable to evaluate the thickness of the fat folds on the abdomen, shoulder blade, waist/hip ratio, body mass index (BMI).
The study of the cardiovascular system includes an echocardiographic study of the heart (assessment of myocardial thickness, contractile function of the heart). Assessment of cardiovascular risk factors: determination of total cholesterol levels and study of the lipid spectrum of the intima of the aorta, carotid and femoral arteries.
Determination of bone density can be carried out on the basis of x-ray examination ( thoracic spine), densitometry (ultrasound or x-ray).
Hormonal diagnostics. The main criterion for verifying GH deficiency is hormonal testing. However, it is known that normally there are significant fluctuations in the level of GH (1 - 10 ng/ml, or 46-465 pmol/l with radioimmune determination of the hormone), therefore it is not possible to diagnose GH deficiency in adults based on the basal level of GH in the blood. In this regard, the diagnosis of GH deficiency should be based on data from the peak response secretion of GH during provocative tests: with insulin, arginine, clonidine, GH-RG.
It has now been proven that the most informative test for diagnosing GH deficiency in adults is the insulin tolerance test (ITT, insulin-induced hypoglycemia test). Insufficient response secretion of GH in response to ITT has absolute diagnostic accuracy in differentiating patients with organic GH deficiency. According to the latest literature data, it is believed that the levels of IGF-1 and IGF-2 binding protein-3 (IGFBP-3) are uninformative indicators for diagnosing GH deficiency in adults.
ITT is carried out on an empty stomach, at 8 a.m. by intravenous administration of an insulin solution of 0.05-0.1 units/kg body weight. Take venous blood performed before insulin administration and then at intervals of 15-30 minutes for 2 hours. At the same intervals, blood sugar levels are monitored. The test results can be considered reliable if during the test the blood sugar level is 2 mmol/L or less. If the peak release of GH on the ITT is less than 5 ng/ml, complete GH deficiency is diagnosed.
Speaking about the diagnosis of GH deficiency, it should be noted that in the majority of patients in whom the cause is surgery for a tumor of the chiasmatic-sellar region and/or radiation therapy, GH deficiency is severe (often combined with a deficiency of other tropic hormones), and these patients do not need dynamic determination of growth hormone. At the same time, in 25% of patients with isolated idiopathic GH deficiency who received in childhood replacement treatment with GH drugs, in adults it is found normal level STG.
Treatment of GH deficiency should be aimed at compensating for hormonal deficiency, and, in cases where this is possible, at eliminating the cause of the disease.
Scheme replacement therapy in adults with GH deficiency, as in children, depends on the degree of general interstitial-pituitary insufficiency. In the presence of panhypopituitarism, hormone replacement therapy is usually started with adrenal cortex preparations. In severe cases, these drugs are administered parenterally (hydrocortisone 50-200 mg/day), and when the symptoms of hypocortisolism decrease, they switch to oral prednisolone (5-10 mg daily) or cortisone (25-50 mg/day). Mineralcorticoid deficiency is eliminated by administering a 0.5% solution of DOXA 0.5-1 ml intramuscularly daily; and then Cortinef is prescribed at 0.05-0.1 mg/day.
Compensation for thyroid insufficiency should begin after the elimination of hypocortisolism, since thyroid hormones enhance metabolic processes and can aggravate hypocortisolism. Synthetic L-thyroxine (50-150 mcg daily) or combination preparations containing thyroxine and triiodothyronine (thyrocomb, tireotom) are used. Treatment with thyroid drugs must be carried out under the control of heart rate and ECG, since in patients with hypothyroidism the sensitivity of the myocardium to these drugs is increased.
Insufficiency of the gonads in women is compensated with combined estrogen-progestogen drugs, which restore menstrual cycle(divina, cycloprogenova, etc.) according to a certain scheme. To restore fertility, gonadotropins are used (clostilbegit, etc., 50-100 mcg for 5-9-11 days of the cycle). In men, long-acting androgen preparations are used (omnodren, sustanon-250, 1 ml once every 3 or 4 weeks) or oral testosterone preparations (andriol, etc.).
Recently, data have been obtained on the positive effect of GH drugs (genotropin, humatrope, norditropin), used for 4-6 months, on body structure, heart function, kidney function, physical activity and overall quality of life.
During treatment with these drugs, there was an increase in “useful” body weight by 6% and an increase muscle mass by 5%, the volume and strength of the quadriceps femoris muscle increased.
GH medications in individuals with deficiency of this hormone significantly contributed to an increase in cardiac output and maximum pressure on exhalation, which had a positive effect on respiratory function. In the immediate and long-term periods of treatment, an increase in HDL levels and acceleration of LDL clearance were observed. Improvement in bone tissue metabolism during therapy with GH drugs is confirmed by an increase in the concentration of osteocalcin and procolagen-3, which indicates an increase in the processes of bone formation. There is an increase in mineralization of the lumbar spine and femoral neck. Many authors emphasize a significant improvement in the general condition of patients. There is an increase in the levels of not only growth hormone, but also IGF-1, IGF-SB-3 in the blood, as well as opioid peptides in cerebrospinal fluid(already 1 month from the start of treatment).
Currently, for replacement therapy, recombinant human GH preparations are used at a dose of 0.25 U/kg body weight once a week (starting from 0.125 U/kg).
Patients need comprehensive restorative therapy. For osteopenia and AP, it is necessary to use osteotropic agents (active metabolites of vitamin D3, bisphosphonates, calcium supplements). This category of patients also requires psychotherapeutic assistance as part of a social rehabilitation program.
Contraindications to GH therapy: malignant neoplasms, progressive growth of intracranial tumors. Relative contraindication is accompanying diabetes.
The prognosis depends on the nature and course of the underlying disease that causes the development of GH deficiency, as well as on the careful selection of doses and regimens of hormone replacement therapy. The patients' ability to work is reduced.

Somatotropic insufficiency (growth hormone deficiency) occurs in a large number of diseases and syndromes. In most cases, this disease manifests itself as dwarfism syndrome (from the Greek nanos - “dwarf”). Dwarfism is a condition characterized by a sharp lag of a child in growth and physical development from his peers, which is associated with an absolute or relative deficiency of growth hormone in the body. Since growth hormone is produced endocrine gland brain, which is called the pituitary gland, then nanism is pituitary.

People with dwarf stature include men with a height below 130 cm, and women with a height below 120 cm. The smallest height of a dwarf described in the literature was 38 cm. Pituitary dwarfism occurs with a frequency of 1 case per 5000 newborn children. There are no differences in the incidence of men and women. Most frequent form growth hormone deficiency is idiopathic (65-75%). It should be noted that with the introduction of MRI studies into practice and the improvement of genetic research methods, the proportion of patients with idiopathic growth hormone deficiency is gradually decreasing, since it is increasingly possible to identify specific causes of somatotropic deficiency. In addition to disruption of the formation of growth hormone in the pituitary gland, some other causes can lead to pituitary dwarfism. These include: the formation of a hormone with an incorrect chemical structure and a congenital defect in the receptors sensitive to this hormone, as a result of which they do not respond in any way to the production of somatotropin by the pituitary gland.

For the most part, somatotropic insufficiency is caused by genetic defect. However, other reasons for the development of this disease may be: underdevelopment of the pituitary gland, its incorrect location in the brain, the formation of cysts, compression by a tumor, trauma to the central nervous system. In addition, infectious and toxic damage central nervous system in early childhood: intrauterine viral infections, tuberculosis, syphilis, malaria, toxoplasmosis, neonatal sepsis, inflammation of the brain and its membranes. Changes in internal organs with dwarfism include thinning of the bones, delayed growth and ossification of the skeleton. Internal organs, muscles and subcutaneous fat are poorly developed.

For a long time, growth hormone deficiency was regarded only as a problem in childhood endocrinology. The main goal of treatment was the achievement of normal growth by the child. Only relatively recently it was discovered that the presence of somatotropic insufficiency in adults is the cause of a whole complex of serious metabolic disorders. This condition requires constant monitoring specialists and providing the necessary medical treatment. Growth hormone deficiency, first occurring in adulthood, occurs in 1 case per 10,000 population.

The main signs of dwarfism are a sharp lag in the growth and physical development of the child. Children with classic somatotropic insufficiency are born with normal body weight and length. They begin to lag behind in development starting from 2-4 years of age. This development of the disease is explained by the fact that the hormone prolactin, which enters the child’s body with mother’s milk, in the first years of early childhood can give children an effect similar to growth hormone. In the case of hereditary growth hormone pathology in children with delayed growth and sexual development, in most cases, upon questioning, it is possible to identify similar cases of short stature in the family of one of the parents. In adults who did not receive the necessary treatment in childhood, child-like body proportions are noted.

The facial features are small (“doll face”), the bridge of the nose is sunken. The skin is pale with a yellowish tint, dry, sometimes there is a bluish coloration and marbling of the skin. In untreated patients, an senile appearance appears early, the skin becomes thinner and wrinkled. The distribution of subcutaneous adipose tissue ranges from wasting to obesity, in which excess adipose tissue is deposited predominantly in upper half torso. Hair can be either normal or dry, thin, brittle. Secondary hair growth, which should appear during puberty, is absent in most cases. Muscular system poorly developed. In boys, as a rule, the penis is extremely small, and sexual development is delayed. Most children with growth hormone deficiency have a concomitant deficiency of hormones that promote the development of reproductive organs (gonadotropins).

Laron syndrome is an endocrine disease, which is based on the loss of sensitivity of body cells to growth hormone as a result genetic mutation. The manifestations of this deviation are approximately the same as in the case of pituitary dwarfism. Features in this case are: a high degree of growth retardation from birth, bone age lags behind the passport level, but is faster than the child’s growth; sexual development begins at a relatively normal time in 50% of children; growth spurts may occur. In addition, with Laron syndrome there is high risk the appearance of various congenital malformations, the most common of which are: shortening of the phalanges of the fingers, cataracts, involuntary movements eyeballs(nystagmus), narrowing of the aortic lumen, cleft lip, congenital dislocation hip joint, blue sclera.

The main methods by which pituitary dwarfism can be identified and confirmed are: anthropometry (measurement of height) and comparison of its results with the proper values ​​for the age of the child being studied; dynamic monitoring of the child's growth. In children with growth hormone deficiency, the growth rate does not exceed 4 cm per year. To exclude various congenital diseases skeletal dysplasia, it is necessary to evaluate body proportions. When conducting an X-ray examination of the bones of the hands and wrist joints, the so-called bone (x-ray) age is determined. In the case of pituitary dwarfism, a significant delay in ossification is detected. X-rays of the skull reveal the size and shape of the sella turcica (the bony receptacle of the pituitary gland), characteristic of childhood. Regardless of the fact that all of the above examination methods are highly informative, the most accurate method for correct setting The diagnosis of pituitary dwarfism is to determine the level of somatotropic hormone in the blood serum. A single determination of the level of growth hormone in the blood for diagnosing somatotropic deficiency is not important due to the fact that the hormone is released episodically during the day, which can lead to the determination of a low level even in healthy children.

Growth hormone deficiency in adults is accompanied by disorders of all types of metabolism and very diverse manifestations. As a result of impaired fat metabolism, obesity develops. Impaired protein synthesis leads to a decrease in the mass and strength of skeletal muscles, and depletion of the heart muscle is noted. Quite often one can note the appearance of hypoglycemic conditions (occur when there is a deficiency of glucose in the blood), which are accompanied by excessive sweating during night sleep and the appearance of headaches in the morning.

In case of growth hormone deficiency, the most striking manifestation is changes in the human psyche. There is a tendency to frequent depression, anxiety states, a person gets tired quickly, suffers general health, emotional reactions are disrupted. Over time, a tendency towards social isolation of people suffering from this disease begins to be clearly visible.

Among people with growth hormone deficiency who receive treatment without growth hormone, there was a twofold increase in the mortality rate from cardiovascular disease. The reason for this is a change in the composition of their blood, an increase in the amount of fat in it, which begins to settle on inner surface walls blood vessels, leading to the development of atherosclerosis.

With a lack of somatotropin, a decrease in bone mass occurs as a result of disruption of all types of metabolism, including mineral metabolism. This increases bone fragility, which leads to an increase in the incidence of fractures.

Treatment. The basis of treatment for pituitary dwarfism is replacement therapy with growth hormone preparations. The drug of choice in this case is human growth hormone, obtained by genetic engineering. Somatotropin in the treatment of classical growth hormone deficiency is administered daily in the form subcutaneous injections V evening time(20.00-22.00). The use of growth hormone for Laron syndrome does not bring any effect.

Hyposomatotropism (somatotropic insufficiency) is an absolute or relative deficiency of somatotropic hormone, which is accompanied in childhood by growth retardation (pituitary dwarfism) and severe metabolic disorders in adults.

Etiology and pathogenesis

Growth hormone deficiency can be congenital or acquired; absolute and relative; organic and idiomatic; isolated and combined with insufficiency of other tropic hormones of the adenohypophysis.

Congenital deficiency of somatotropic hormone ( STG) May be:

1. hereditary, i.e. caused by various genetic disorders;
2. idiopathic disorder of somatoliberin secretion;
3. anatomical defects in the formation of the hypothalamic-pituitary zone (aplasia or hypoplasia of the pituitary gland, cystic degeneration of the pituitary gland).

The development of acquired GH deficiency is possible due to:

1. tumors of the hypothalamic-pituitary zone (craniopharyngeoma, hamartroma, pituitary adenoma, germinoma, etc.) and other parts of the brain or suprasellar cysts;
2. traumatic brain injury, including surgical trauma during neurosurgical interventions;
3. neuroinfections (meningitis, encephalitis, etc.);
4. infiltrative diseases (histiocytosis, sarcoidosis, syphilis);
5. vascular pathology (aneurysm of the pituitary vessels, pituitary apoplexy);
6. radiation exposure (irradiation of the head, less often the neck);
7. toxic effects (chemotherapy).

Congenital and acquired growth hormone deficiency, which develops due to the reasons listed above, is absolute. Relative growth hormone deficiency is a consequence of peripheral resistance to growth hormone. It develops for a reason genetic disorders(pathology of the growth hormone receptor gene - Laron syndrome); development of biologically inactive growth hormone or resistance to somatomedin (IGF-1).

The pathogenesis of GH deficiency is associated with a deficiency in the action of the hormone at the level of peripheral tissues and the effect of somatomedins (IGF-1 and IGF-2), which determine linear growth, growth of organs and tissues and other metabolic effects. Until the last decade, growth hormone deficiency was regarded as a prerogative of childhood due to the main and most obvious symptom of the disease - lag in linear growth and physical development children, however, it has now been proven that in adults, a lack of GH has clinical manifestations that have a significant impact on the quality of life.

Symptoms

GH deficiency in adults is characterized by a decrease in muscle mass due to muscle wasting and atrophy, an increase in body weight due to the formation of visceral. A decrease in muscle mass leads to a decrease in muscle strength and endurance, patients complain of weakness and constant fatigue. At the same time, bone tissue mineralization decreases due to increased osteoclast activity and a slowdown in bone remodeling processes with the development of osteopenia and osteoporosis and an increased risk of fractures.

In patients with GH deficiency, cardiac output decreases due to myocardial dystrophy, which aggravates poor exercise tolerance, suppressed emotional reactions are noted, an anxious or depressive state appears, and memory is impaired. Men experience sexual weakness; women may experience impaired fertility. These factors lead to a significant decrease in the quality of life and may be accompanied by social isolation of the patient.

Metabolic disorders characteristic of GH deficiency in adults are characterized by insulin resistance, hyperlipidemia and the development of atherosclerosis, inhibition of fibrinolysis.

Diagnostics

The diagnosis of GH deficiency is established by clinical signs based on medical history and results laboratory research. Additional diagnostic tests are performed to verify the cause of the disease.

Laboratory confirmation of the diagnosis is:

• decrease in the basal level of growth hormone, fluctuations in the level of growth hormone during the day. To obtain an evidentiary basis, functional tests with various stimulants (insulin, arginine, clonidine, glucagon, L-dopa, pyridostigmine).
• a decrease in the level of IGF-1 and its recall protein IGF-SB-3 is the most accurate method for diagnosing GH deficiency, while the optimal determination of IGF-SB-3.

Treatment

Treatment is carried out with synthetic growth hormone (somatotropin) at a dose of 0.3 mg/day in men and 0.4 mg/day in women intramuscularly. Side effects of treatment - arthralgia, peripheral edema, myalgia, parasthesia - in most cases do not lead to the abolition of replacement therapy, which is accompanied by a significant improvement in the quality of life.

Direct participation in proper development child's body takes growth hormone (GH). extremely important for a growing organism. The correct and proportional formation of the body depends on HGH. And an excess or deficiency of such a substance leads to gigantism or, conversely, growth retardation. In the body of an adult, somatotropic hormone is contained in smaller quantities than in a child or teenager, but still has important. If the GH hormone is elevated in adults, this can lead to the development of acromegaly.

General information

Somatotropin, or growth hormone, is a growth hormone that regulates the development processes of the entire organism. This substance is produced in the anterior lobe of the pituitary gland. The synthesis of growth hormone is controlled by two main regulators: somatotropin-releasing factor (STGF) and somatostatin, which are produced by the hypothalamus. Somatostatin and STHF activate the formation of somatotropin and determine the time and amount of its elimination. HGH - the intensity of lipid, protein, carbohydrate and mineral metabolism depends on it. Somatotropin activates glycogen, DNA, accelerates the mobilization of fats from the depot and the breakdown of fatty acids. STH is a hormone that has lactogenic activity. The biological effect of somatotropic hormone is impossible without the low molecular weight peptide somatomedin C. When GH is administered, “secondary” growth-stimulating factors—somatomedins—increase in the blood. The following somatomedins are distinguished: A 1, A 2, B and C. The latter has an insulin-like effect on fat, muscle and cartilage tissue.

The main functions of somatotropin in the human body

Somatotropic hormone (GH) is synthesized throughout life and has a powerful effect on all systems of our body. Let's look at the most important functions such a substance:

• The cardiovascular system. STH is a hormone that is involved in the regulation of cholesterol levels. A deficiency of this substance can provoke vascular atherosclerosis, heart attack, stroke and other diseases.
• Leather. Growth hormone is an essential component in the production of collagen, which is responsible for the condition. skin. If the hormone (GH) is reduced, collagen is synthesized in insufficient quantities and, as a result, the aging process of the skin accelerates.
• Weight. At night (during sleep), somatotropin is directly involved in the process of lipid breakdown. Violation of this mechanism causes gradual obesity.
• Bone. Somatotropic hormone in children and adolescents ensures the elongation of bones, and in an adult - their strength. This is due to the fact that somatotropin is involved in the synthesis of vitamin D 3 in the body, which is responsible for the stability and strength of bones. This factor helps to cope with various diseases and severe bruises.
• Muscle. STH (hormone) is responsible for the strength and elasticity of muscle fibers.
• Body tone. Somatotropic hormone has positive influence for the whole body. Helps maintain energy good mood, deep sleep.

Growth hormone is very important for maintaining a slim and beautiful body shape. One of the functions of somatotropic hormone is the transformation of adipose tissue into muscle tissue, this is what athletes and everyone who watches their figure achieve. STH is a hormone that improves joint mobility and flexibility, making muscles more elastic.

In older age, normal levels of somatotropin in the blood prolong longevity. Initially, somatotropic hormone was used to treat various senile ailments. In the world of sports, this substance was used for some time by athletes to build muscle mass, but growth hormone was soon banned for official application, although today it is actively used by bodybuilders.

STH (hormone): norm and deviations

What are the normal values ​​of growth hormone for humans? IN at different ages the indicators of such a substance as growth hormone (hormone) are different. The norm for women also differs significantly from normal values for men:

• Newborns up to one day - 5-53 mcg/l.
• Newborns up to one week - 5-27 mcg/l.
• Children aged from one month to one year - 2-10 mcg/l.
• Middle-aged men - 0-4 mcg/l.
• Middle-aged women - 0-18 mcg/l.
• Men over 60 years of age - 1-9 mcg/l.
• Women over 60 years of age - 1-16 mcg/l.

Somatotropic hormone deficiency in the body

Particular attention is paid to somatotropin in childhood. GH deficiency in children is a serious disorder that can cause not only stunting, but also delayed puberty and general physical development, and in certain cases, dwarfism. This violation can be caused by various factors: pathological pregnancy, heredity, hormonal disorders.

An insufficient level of somatotropin in the body of an adult affects general condition metabolism. Low growth hormone levels are associated with various endocrine diseases, also, a deficiency of somatotropic hormone can provoke treatment with certain medications, including the use of chemotherapy.

And now a few words about what happens if there is an excess of somatotropic hormone in the body.

STH is increased

An excess of somatotropic hormone in the body can cause more serious consequences. Height increases significantly not only in adolescents, but also in adults. The height of an adult can exceed two meters.

In this case, there is a significant increase in the limbs - hands, feet, undergoes major changes and the shape of the face - the nose and become larger, the features become coarser. Such changes can be corrected, but in this case it will be necessary long-term treatment under the supervision of a specialist.

How to determine the level of growth hormone in the body?

Scientists have found that the synthesis of somatotropin in the body occurs in waves, or in cycles. Therefore, it is very important to know when to take STH (hormone), i.e. at what time to do an analysis for its content. This kind of research is not carried out in regular clinics. The content of somatotropin in the blood can be determined in a specialized laboratory.

What rules should be followed before conducting an analysis?

A week before the analysis for growth hormone (growth hormone), it is necessary to refuse an X-ray examination, as this may affect the reliability of the data. During the day before blood sampling, you should adhere to the strictest diet excluding any fatty foods. Twelve hours before the test, avoid eating any foods. It is also recommended to stop smoking, and within three hours it should be completely eliminated. A day before the test, any physical or emotional stress is unacceptable. Blood sampling is carried out in the morning, at this time the concentration of somatotropic hormone in the blood is maximum.

How to stimulate the synthesis of somatotropin in the body?

Today on pharmaceutical market There are a large number of different drugs with growth hormone. The course of treatment with such drugs can last several years. But such medications should only be prescribed by a specialist after careful medical examination and in the presence of objective reasons. Self-medication may not only not improve the situation, but can also cause many health problems. In addition, you can activate the production of somatotropic hormone in the body naturally.

1. The most intense production of growth hormone occurs during deep sleep, which is why you need to sleep at least seven to eight hours.
2. Rational diet. The last meal should be at least three hours before bedtime. If the stomach is full, the pituitary gland will not be able to actively synthesize growth hormone. It is recommended to have dinner with easily digestible foods. For example, you can choose low-fat cottage cheese, lean meat, egg whites, and so on.
3. Healthy menu. The basis of nutrition should be fruits, vegetables, dairy and protein products.
4. Blood. It is very important to monitor the level of glucose in the blood; its increase can cause a decrease in the production of somatotropic hormone.
5. Physical activity. For children excellent option There will be sections for volleyball, football, tennis, and sprinting. However, you should know: the duration of any strength training should not exceed 45-50 minutes.
6. Fasting, emotional stress, stress, smoking. Such factors also reduce the production of growth hormone in the body.

In addition, conditions such as diabetes mellitus, pituitary gland injuries, and increased blood cholesterol levels significantly reduce the synthesis of growth hormone in the body.

Conclusion

In this article, we examined in detail such an important element as growth hormone. The functioning of all systems and organs and the general well-being of a person depend on how its production occurs in the body.

We hope you find the information useful. Be healthy!