Traditional medicine

Hypercorticism symptoms in women. Iatrogenic hypercortisolism and hypocortisolism

Excessive production of glucocorticoids (produced by the adrenal cortex), which can be caused either by pathology of the adrenal glands themselves (tumor, nodular hyperplasia), or by overproduction of ACTH (pituitary adenoma). In the first case, this condition is usually referred to as Itsenko-Cushing syndrome, in the second - Itsenko-Cushing disease.

Pathogenesis of hypercortisolism

The basis Itsenko-Cushing's disease constitutes a feedback violation in functional system hypothalamus-pituitary gland - adrenal cortex, characterized constantly high activity pituitary gland and corticotropic hyperplasia or, much more often, the development of ACTH-producing pituitary adenomas and hyperplasia of the cortex of both adrenal glands. As a result, the rate of production and the total daily excretion of almost all fractions of corticosteroids increases with the development of symptoms of hypercortisolism. At the core Itsenko-Cushing syndrome lies the formation of an autonomous benign or malignant tumor adrenal gland or adrenal dysplasia.

Symptoms of hypercortisolism

For typical symptoms of hypercortisolism characterized by generalized damage to almost all organs and systems, decreased growth rate, increased body weight, uneven distribution of fat, hirsutism, stretch marks, hyperpigmentation, primary or secondary amenorrhea, osteoporosis, muscle weakness. In terms of symptoms and manifestations, Itsenko-Cushing syndrome is not much different from Itsenko-Cushing disease.

Features of Itsenko-Cushing's disease in children are the uniform distribution of fat in 70% of patients, and only 30% have a classic distribution. Typical for Itsenko-Cushing's disease in children is growth retardation (nanism). One of characteristic features defeats bone skeleton with Itsenko-Cushing's disease in children, there is a violation of the order and timing of ossification of the skeleton bones, and sometimes the appearance of other signs of pathological ossification.

Neurological signs found in children with Cushing's disease vary in severity, but are unstable and transient. This is apparently due to the fact that in most cases they are based on functional changes caused by cerebral edema, or dynamic changes intracranial pressure due to high hypertension.

With Itsenko-Cushing's disease in children, regardless of gender, there is a delay in sexual development with premature appearance sexual hair growth, which can be explained by excess production of the adrenal glands along with glucocorticoids and androgens. Children with Itsenko-Cushing's disease have a tendency to mild bleeding, hemorrhagic rashes are often observed, which is associated with changes in the blood coagulation system (a significant increase in heparin in the blood, a decrease in the prothrombin index), as well as with thinning and atrophy of the skin due to a decrease in the content of tissue proteins and increasing capillary permeability.

Depending on the degree of myopathic syndrome, trophic disorders, osteoporosis, steroid diabetes, hypertension, mental disorders, immunodeficiency and sexual dysfunction, various degrees severity of the disease.

At mild form there is a combination of 3-4 signs characteristic of hypercortisolism - most often dysplastic obesity, trophic disorders skin, moderate hypertension and sexual dysfunction, mild osteoporosis.

At moderate severity Itsenko-Cushing's disease develops almost all the symptoms of hypercortisolism.

The severe form is characterized by the presence of complications in the form of cardiac decompensation vascular system, severe osteoporosis with fractures, etc. Depending on the rate of increase clinical symptoms A distinction is made between a rapidly progressing (over 3-6 months) course and a torpid course of the disease.

Diagnosis of hypercortisolism

The main diagnostic criteria are data on increased activity of the pituitary-adrenal system and the results of topical diagnostics. Itsenko-Cushing's disease is characterized by a simultaneous increase in the blood levels of cortisol and ACTH, as well as increased daily urinary excretion free cortisol and 17-OX.

When erased clinical picture and a slight increase in adrenal cortex function, to prove the presence of pathological and exclude functional hypercorticism, use the results of a small dexamethasone test, based on the ability of dexamethasone to suppress ACTH secretion.

A large dexamethasone test allows you to differentiate Itsenko-Cushing's disease and Itsenko-Cushing syndrome (A large test with dexamethasone is carried out for 3 days - 2 mg of dexamethasone is given 4 times a day or 8 mg per day. The test is considered positive. If on the second and third days the release of 17-OX is reduced by more than 50%).

For Itsenko-Cushing's disease the test is positive, but with corticosteroma it is negative. The purpose of topical diagnosis for Itsenko-Cushing's disease is to identify macro- or microadenoma of the pituitary gland and bilateral adrenal hyperplasia.

For Itsenko-Cushing syndrome- a tumor of one adrenal gland is detected with reduced or normal sizes another. To solve this problem use x-ray method research - pathology sella turcica, ultrasound of the adrenal glands, computed tomography, nuclear magnetic resonance imaging, angiography of the adrenal glands.

Differential diagnosis of hypercortisolism

With severe hypercortisolism differential diagnosis carried out between Itsenko-Cushing's disease and corticosteroma, syndrome of ectopic ACTH production. In the erased form - with pubertal juvenile dyspituitarism or hypothalamic pubertal syndrome (PUDS).

PUD is characterized by dysfunction of the hypothalamic-pituitary system. Clinical manifestations of this condition are uniform obesity, multiple fine striae, transient hypertension, tall stature (in early puberty), accelerated or normal bone differentiation, folliculitis. Pathognomonic for PUB are stretch marks on the skin ranging from whitish to purplish-red. The development of secondary sexual characteristics begins on time, but proceeds quickly and ends prematurely.

The outcome of PJP can be spontaneous recovery or, less commonly, transition to hypothalamic syndrome, Itsenko-Cushing's disease.

Treatment of hypercortisolism

In the treatment of these patients, importance is attached to diet therapy, dehydration therapy, and nootropic drugs. Treatment of Itsenko-Cushing's disease surgical, radiation and medication. Both their combination and monotherapy are used.

Itsenko-Cushing syndrome, or hypercortisolism, is a disease based on an excess amount of glucocorticoids in the body.

Glucocorticoids are hormones synthesized by the adrenal cortex. Their action is aimed at regulating all types of metabolism. Main functions:

increased blood sugar levels;
stimulation of protein breakdown;
suppression of inflammation, participation in the regulation of immunity;
reduction in synthesis rate bone tissue;
stimulation of red blood cell formation;
increased action of adrenaline and norepinephrine;
inhibition of the synthesis of sex hormones.

The most active glucocorticoid is Cortisol.

What is Itsenko-Cushing syndrome?

This is a complex name for various diseases and conditions accompanied by the development of hypercortisolism.

There are several varieties of this disease depending on the reason:

Itsenko-Cushing's disease (the disease is based on excessive synthesis of ACTH, leading to excessive stimulation of the adrenal cortex);
ACTH- or corticoliberin-ectopic syndrome (excessive synthesis of hormones is associated with the presence of a hormone-producing tumor consisting of cells of the adrenal gland or pituitary gland, located outside these organs);
iatrogenic syndrome (occurs when taking large doses of drugs containing glucocorticosteroids);
hypercortisolism syndrome as a result of tumor processes in the adrenal gland itself (adenoma, adenocarcinoma).

Important! The most common (up to 80%) cause endogenous hypercortisolism is a microadenoma (less than 2 cm) of the pituitary gland. Hyperplastic processes of adrenal tissue are less common (about 15%). The prevalence of iatrogenic hypercortisolism is about 2%. The rarest are ectopic hormone-producing tumors (up to 1%).

In other etiological variants of the disease, metabolic changes are similar to Itsenko-Cushing's disease, but there is no increased level ACTH.

Important! There is a so-called “functional hypercortisolism”. This disease is not associated with pathology endocrine system, and an excess of glucocorticoids is provoked by factors such as overweight, diabetes, alcoholism, pregnancy. Clinically, the symptoms repeat the classic Itsenko-Cushing syndrome.

There is also a disease characterized by the opposite phenomenon: a decrease in cortisol synthesis. This condition occurs with congenital dysfunction of the adrenal cortex.

Symptoms of hypercortisolism

The symptoms of Itsenko-Cushing syndrome are quite typical, with them the habitus changes ( appearance) patient, called "Cushingoid". It includes:

Obesity. More than 85% of people with this disease are overweight.

The patient’s appearance is that of a “colossus with feet of clay.” There is excess fat deposition in the abdomen, back, chest, and face. Relatively thin limbs are characteristic.

This habit is associated with the ability of glucocorticoids to increase the absorption of glucose from food consumed. The second aspect is the stimulation by these hormones of fat synthesis (lipogenesis) in the abdomen and face. The effect on the subcutaneous fatty tissue of the extremities is the opposite: it causes its breakdown (lipolysis).

Changes in the skin.

Important! Due to the occurrence secondary immunodeficiency patients are prone to developing severe infectious and inflammatory diseases, including sepsis.

Destructive processes in muscles. Against the background of excess cortisol, active breakdown of proteins occurs, including muscle tissue. The result is weakness and muscle atony.

Osteoporosis. One of the most severe symptoms. It appears due to the ability of glucocorticoids to inhibit bone tissue synthesis. As a result, the patient has high risk fractures even with minor trauma.
Cardiomyopathy: as a result of the breakdown of proteins in the muscle tissue of the heart, its contractile function is reduced.
Diabetes mellitus, developing as a result of hyperglycemia due to increased absorption of carbohydrates under the influence of glucocorticoids against the background normal level insulin.
Violation of the synthesis of sex hormones. These hormones are also produced in the adrenal cortex. Hypercortisolism leads to their excess.

Also, in addition to hirsutism, women may develop amenorrhea and infertility.

Feminization of men is observed less frequently; the main symptoms are testicular atrophy, decreased libido, and infertility.

Important! Women with Cushing's syndrome planning pregnancy should undergo careful preparation, because Excess cortisol often causes miscarriages or complicated births.

Diagnosis of hypercortisolism

To make a diagnosis of Itsenko-Cushing syndrome, physical, laboratory and instrumental methods are used.

Physical methods include examining the patient, weighing, calculating BMI, measuring abdominal circumference, and determining muscle tone and strength.

Laboratory methods:

determination of the level of cortisol in urine. In the presence of this endocrine pathology, a 4-fold or more increase in the indicator is observed.
conducting pharmacological tests (dexamethasone test).

Purpose of the event small sample- difference between endogenous and exogenous hypercortisolism. The analysis is carried out within 3 days. On the first day, the level of cortisol in the blood is measured in the morning. Next, the patient takes 1 tablet (0.5 mg) of dexamethasone 4 times a day for 2 days. On the morning of day 3, cortisol levels are measured again. If the amount of the hormone decreases by 2 or more times, then this is an exogenous (functional) pathology; decreases by less than 2 times - endogenous.

When a diagnosis of an endogenous disease is made, large sample. The regimen is the same, but the dose of the drug is increased to 2 mg per dose. If the cortisol level has decreased by half, then this is Cushing's disease; if there is no decrease, then the source of excess glucocorticoids is the pathology of the adrenal glands themselves.

Instrumental methods are used to determine tumor processes in the area of the adrenal glands and pituitary gland. Mainly used are CT, MRI and ultrasound.

Important! A patient diagnosed with hypercortisolism needs to undergo comprehensive survey: ECG, blood sugar measurement, glucose tolerance test, cardiac ultrasound, skeletal radiography.

Treatment of Itsenko-Cushing syndrome

The main goal of treating hypercortisolism is to normalize the level of cortisol in the blood. Depending on the cause of the pathology, the following methods are used:

In case of iatrogenic etiology of the disease, glucocorticosteroid preparations are replaced with analogues.
The presence of a tumor process is an indication for surgical treatment.
If surgical treatment is not possible or if functional hypercortisolism antisecretory therapy is used.

In addition, symptomatic treatment is actively carried out, aimed at normalizing weight, blood sugar levels, and eliminating osteoporosis.

Itsenko-Cushing syndrome is a serious endocrine disease leading to the death of the patient without timely treatment. Therefore, if you have any symptoms of the disease, you should consult a doctor.

...glucocorticoid drugs have a versatile effect on the body, many of which are not fully understood. The high biological activity of glucocorticoids allows their use in the most severe clinical situations. They are often included in the complex emergency measures help with emergency conditions. However, many aspects of the use of glucocorticoids remain controversial.

HYPERCORTICISM
(hyperglucocorticoidism)

IN recent years glucocorticoids are widely used to treat many patients with severe chronic diseases (bronchial asthma, diffuse diseases connective tissue, glomerulonephritis, etc.). In this regard, there is high probability the appearance of drug-induced hypercortisolism, which corresponds to the clinical picture of Itsenko-Cushing's disease and syndrome (Stern N. et al., 1996).

Corticosetroid drugs for chronic diseases have to be prescribed in large doses (60 – 90 mg of prednisolone or more per day) for a long time (sometimes for years), which contributes to the rather rapid development of iatrogenic “Cushingoid”. Even long-term use of small doses of glucocorticoids (30 - 40 mg of prednisolone, cortisone per day) causes the development of Cushingoid syndrome.

The occurrence of Cushing's syndrome with the use of natural or synthetic corticosteroids is not considered a toxic effect or complication. It's an inevitable companion this treatment. Some Cushingoid symptoms can also be observed during long-term treatment of tuberculosis patients with drugs of the isoniazid group (tubazid, GINK, isoniazid). This is due to hypothalamic disorders during treatment with these drugs, which lead to hypersecretion of ACTH. Cushing's syndrome develops when long-term treatment ACTH, depot synacthenomes, which cause hypersecretion and hyperplasia of the adrenal cortex.

Exogenous Cushing's syndrome, caused long-term use glucocorticoids, - the most common reason secondary osteoporosis. The severity of the disease is directly proportional to the total dose of glucocorticoids and the duration of treatment. In addition, the development of osteoporosis is promoted by insufficient physical activity patients (Hunt T., 1999).

At the same time, glycogenesis increases, and fat is redistributed in the body (dysplastic type of obesity). In addition, immunogenesis is inhibited, hypertrichosis develops, associated with the moderate androgenic effect of steroid metabolites, mental disorders appear, including psychosis, sometimes euphoria occurs, in women the menstrual cycle is disrupted with the appearance of oligo-opsomenorrhea up to amenorrhea and infertility.

There is an appearance drug-induced damage to retinal vessels. joins drug-induced hypertension. But more often when using products with high content mineralocorticoids (fludrocortisone, cortinef). In this regard, sodium and chlorine retention and potassium loss occur. The excretion of potassium in the urine increases, hypokalemia appears, which leads to salt-losing (hypokalemic) kidney syndrome with polyuria and then polydipsia, and the specific gravity (density) of urine decreases. In such cases, one thinks about the syndrome diabetes insipidus. The adrenal cortex atrophies, but clinical manifestations There is no adrenal insufficiency while the patient is taking the drug. Diabetes mellitus with iatrogenic hypercortisolism develops in approximately 1% of patients. “Steroid” diabetes is not prone to acidosis and occurs in a milder form, but in in rare cases it gets harder. Its course is no different from normal.

Treatment of iatrogenic hypercortisolism practically absent, it is mostly symptomatic. Correction of protein metabolism is carried out by including protein-rich foods in the diet, as well as by using anabolic steroids. Treatment of diabetes mellitus consists of prescribing insulin or glucose-lowering drugs. Hypokalemia requires appropriate nutrition and administration potassium preparations. Weakening the iatrogenic effect of glucocorticoids is achieved by taking the full daily and two-day doses in the morning.

HYPOCORTICISM

Inhibition of the function of the adrenal cortex occurs under the influence medicines, acting cytotoxically or selectively inhibiting the synthesis of corticosteroids. A special group consists of patients treated with glucocorticoids for non-endocrine diseases. As a result, the function of the hypothalamic-pituitary-adrenal system decreases. The production of ACTH decreases, and atrophy of the adrenal cortex develops.

It should be remembered that hypocortisolism, created by oversaturation of the body with glucocorticoid drugs, manifests itself only after cessation of treatment with these drugs. Usually this is a picture secondary hypocortisolism, which in stressful situations may suddenly develop into an acute Addisonian crisis. A withdrawal syndrome may develop, occurring as acute adrenal insufficiency. It usually occurs in patients with rapid withdrawal of hormones, with prolonged use, with autoimmune diseases. Clinical symptoms may be absent, and only reduced cortisol secretion in tests with ACTH indicates insufficiency of the hypothalamic-pituitary-adrenal system (Lavin N., 1999).

Iatrogenic adrenal insufficiency should be suspected in the following cases::
1 - in any patient receiving prednisolone at a dose of 15 - 30 mg/day for 3 - 4 weeks; in such patients, after discontinuation of glucocorticoid therapy, inhibition of the hypothalamic-pituitary-adrenal system may persist for 8 to 12 months;
2 - in any patient receiving prednisolone at a dose of 12.5 mg/day for 4 weeks; suppression of the hypothalamic-pituitary-adrenal system can persist for 1 to 4 months.

Have a cytotoxic effect on the adrenal glands DDT preparations and its derivatives (in lately they are discontinued). Ketoconazole and its derivative, metopyrone, as well as triparanol, naphthal, and pyramidin derivatives inhibit the synthesis of corticosteroids. Clinical manifestations of hypocortisolism are complaints of fatigue, muscle weakness, weight loss, apathy, loss of appetite, hypotension.

Itsenko-Cushing syndrome and disease (hypercortisolism) is a symptom complex that develops when the adrenal glands produce excessive corticosteroid hormones. If the disease occurs as a result of disorders in the hypothalamic-pituitary system, which lead to an increase in the production of ACTH (adrenocorticotropic hormone) and, as a consequence, cortisol, then they actually speak of Itsenko-Cushing’s disease. If the appearance of symptoms of the disease is not associated with the functioning of the hypothalamic-pituitary system, then we're talking about about Itsenko-Cushing syndrome.

Causes of hypercortisolism

In some cases, the cause of hypercortisolism is a pituitary adenoma.

Exogenous or drug-induced hypercortisolism can be caused by long-term use of drugs containing glucocorticoid hormones (prednisolone, dexamethasone, etc.) in the treatment of any diseases, for example bronchial asthma, systemic lupus erythematosus, etc. In such cases, it is necessary to reduce the dose of drugs to a maintenance dose (minimum acceptable) to control this disease.
Ectopic ACTH production is a condition in which tumors of various origins outside the pituitary gland they produce adrenocorticotropic hormone, for example, thymus, or.
Tumors of the adrenal glands, and most often excess production of cortisol occurs with benign tumors of these glands (adenoma).
Familial form of Itsenko–Cushing syndrome. In most cases, this disease is not inherited, but there is hereditary syndrome multiple endocrine neoplasia, in which a person has an increased likelihood of developing tumors, including those of the adrenal glands.
– benign tumor pituitary gland, leading to hyperproduction of ACTH and, as a consequence, excessive production of cortisol by the adrenal cortex. Hypercorticism, resulting from damage to the pituitary gland, is actually called Itsenko-Cushing's disease. According to statistics, this disease is five times more common in women, and tumors of other endocrine glands are often detected simultaneously.

Symptoms of hypercortisolism

Itsenko–Cushing syndrome has quite pronounced external signs, by which the doctor may suspect this disease.

The overwhelming majority of patients exhibit obesity, characteristic of hypercortisolism. The distribution of fat occurs according to the dysplastic (Cushingoid) type: an excess amount of fatty tissue is determined on the back, abdomen, chest, and face (moon face).

Muscle atrophy, volume reduction muscle mass, decreased muscle tone and strength, especially noticeable violation of the tone of the gluteal muscles. “Sloping buttocks” is one of the typical signs of the disease. Atrophy of the anterior muscles abdominal wall may eventually lead to hernias of the white line of the abdomen.

Skin changes. In patients, the skin becomes thinner, has a marbled tint, is prone to dryness, flakes, and there are areas increased sweating. A vascular pattern is visible under the thinned skin. Striae appear - purple-purple stretch marks, most often appearing on the skin of the abdomen, thighs, mammary glands, and shoulders. Their width can reach several centimeters. In addition, many different rashes such as acne and spider veins. In some cases, with Itsenko-Cushing's disease, hyperpigmentation is observed - dark and light spots that stand out in color appear on the skin.

One of the severe complications of Itsenko-Cushing syndrome is associated with thinning of bone tissue, resulting in fractures and bone deformations; over time, patients develop scoliosis.

Heart dysfunction is expressed in the form of cardiomyopathy. Heart rhythm disturbances occur arterial hypertension, over time, patients develop heart failure.

In 10–20% of patients, steroid diabetes mellitus is detected, although there may be no damage to the pancreas and significant changes blood insulin concentrations.

Excessive production of adrenal androgens leads to hirsutism in women - male pattern hair. In addition, sick women experience disorders menstrual cycle up to amenorrhea.

Diagnosis and treatment of Itsenko–Cushing syndrome

In the urine with this pathology, an increased level of the hormone cortisol is detected.

The examination begins with screening tests: a urine test to determine the level of daily excretion of free cortisol, tests with dexamethasone (a glucocorticosteroid drug), which help identify hypercortisolism, as well as conduct preliminary differential diagnosis syndrome and Itsenko-Cushing's disease. Further studies are needed to identify pituitary adenomas, adrenal tumors or other organs and complications of the disease ( ultrasound diagnostics, radiography, computer and magnetic resonance imaging, etc.).

Treatment of the disease depends on the results of the examination, i.e. on the specific area in which it is detected pathological process, leading to the occurrence of hypercortisolism.

Today the only truly effective method Treatment of Itsenko-Cushing's disease resulting from pituitary adenoma is surgical (selective transsphenoidal adenomectomy). This neuro surgery indicated when identifying a pituitary adenoma with a clear localization established during examination. Usually this operation gives positive results in the vast majority of patients, restoration of the normal functioning of the hypothalamic-pituitary system occurs quite quickly, and in 70–80% of cases there is stable remission diseases. However, relapse may occur in 10–20% of patients.

Surgical treatment of Itsenko–Cushing's disease is usually combined with radiation therapy, as well as by the method of destruction of hyperplastic adrenal glands (since the mass of the glands increases as a result of prolonged hormonal imbalance).

If there are contraindications to surgical treatment pituitary adenomas ( serious condition patient, presence of severe concomitant diseases etc.) is carried out drug treatment. Drugs are used that suppress the secretion of adrenocorticotropic hormone (ACTH), an increase in the level of which leads to hypercortisolism. Against the background of such treatment, if necessary, it is necessary to carry out symptomatic therapy antihypertensive, hypoglycemic drugs, antidepressants, treatment and prevention of osteoporosis, etc.

If the cause of hypercortisolism is tumors of the adrenal glands or other organs, then their removal is necessary. When removing the affected adrenal gland in order to prevent hypocorticism in the future, patients will need long-term replacement hormone therapy under constant monitoring doctor

Adrenalectomy (removal of one or two adrenal glands) is rarely used in recent years, only when it is impossible to treat hypercortisolism in other ways. This manipulation leads to chronic adrenal insufficiency, requiring lifelong hormone replacement therapy.

All patients who have been or are undergoing treatment for this disease require constant monitoring by an endocrinologist, and, if necessary, other specialists.

Which doctor should I contact?

If these symptoms appear, you should contact an endocrinologist. If, after examination, a pituitary adenoma is detected, the patient is treated by a neurologist or neurosurgeon. If complications of hypercortisolism develop, treatment is indicated by a traumatologist (for fractures), a cardiologist (for increased blood pressure and rhythm disturbances), and a gynecologist (for disorders of the reproductive system).

It is known that the hormones produced by the adrenal cortex perform very important functions in the body. With insufficient or excessive secretion of hormones, the cortex develops various diseases. Itsenko-Cushing syndrome is a complex of symptoms resulting from excessive synthesis of cortical hormones in the adrenal glands. There are several types of this disease, and they all have similar symptoms. Reasons this state multitude. This could be a tumor, hormonal imbalance or other problems in the body. Subclinical hypercortisolism can be completely asymptomatic.

Itsenko-Cushing syndrome, or hypercortisolism syndrome, occurs due to the fact that the hypothalamus secretes a lot of corticoliberins - substances that stimulate the pituitary gland to increased production of adrenocorticotropic hormone (ACTH), and this, in turn, causes excessive synthesis of hormones of the adrenal cortex.

What types of adrenal hyperfunction are there?

The photo shows the examination process during kidney disease

There are primary and secondary hypercortisolism:

The causes of primary hyperfunction are mainly adrenal tumors - corticosteromas. They are mainly hormonally active, that is, they produce hormones. A lot of glucocorticoids and some androgens and mineralocorticoids are released into the blood. Also, the cause of this type of disorder may be tumors located in other organs that synthesize ACTH-like compounds.
Secondary hypercortisolism occurs due to disturbances in the functioning of the hypothalamic-pituitary-adrenal system. Brief description The mechanism for the development of this condition is found above. Another cause of secondary hypercortisolism may be a pituitary adenoma, which stimulates increased production of ACTH, which in turn leads to a large release of cortical hormones into the blood.

According to the forms of its course, adrenal hyperfunction syndrome is divided into 3 types:

The subclinical form occurs in the presence of so-called inactive adrenal tumors. In 10 patients out of 100, corticosteroma is detected, which secretes cortisol in small quantities, which does not cause clinical manifestations. But based on some signs, we can conclude that there is hypercortisolism syndrome. The patient may experience increased blood pressure, disturbances in reproductive system, diabetes mellitus.
Iatrogenic hypercortisolism is also called drug-induced or exogenous. It occurs in patients who long time were treated with synthetic corticosteroids. What is it and in what cases is it used? Long-term corticosteroids are indicated for inflammatory diseases such as rheumatism, various pathologies kidneys, blood diseases and chronic diseases connective tissue. Also this group drugs are prescribed to people who have undergone organ transplantation. Exogenous hypercortisolism occurs in 70% of cases.
Functional hypercortisolism occurs in obese people diabetes mellitus, liver diseases, hypothalamic syndrome, depression. This condition is also diagnosed in pubertal-adolescent dyspituitarism, pregnancy and alcoholism.

Clinical manifestations of the disease

The main symptoms of hypercortisolism:

Constant fatigue
Sleep disturbance up to insomnia
Progressive weakness
Decreased appetite
Painful sensations in the abdomen
Change in body weight
Nausea and vomiting
Constipation followed by diarrhea
Increasing muscle weakness
Decreased muscle tone of the skeleton and internal organs
Hyperpigmentation of the skin and mucous membranes - melanosis.
Depression
Dry skin and increased flaking
Increased amount of hair on face and body
Curvature of the spine
Spontaneous bone fractures
Osteoporotic changes in bones
Fluid retention in the body
Edema
Cardiovascular disorders
Neurological disorders.

What treatment measures are prescribed to patients?

Used to treat hypercortisolism integrated approach. The main goal of treatment is to relieve the clinical manifestations of the syndrome and restore the physiological rhythm of hormone synthesis. Prescribe medications that can suppress excess synthesis of cortisol and corticotropin. In the case of adrenal hyperplasia or pituitary adenoma, surgery or radiation therapy is indicated.

Drug treatment with inhibitors of corticotropin and corticoliberin production is prescribed when central hypercortisolism is detected. Patients are usually prescribed Peritol, a serotonin inhibitor, for a course of 4 weeks. It reduces the production of corticoliberin in the hypothalamus. Also dopamine agonists, such as Abergin and Bromergon (Parlodel), for a course of 6 to 10 months.

They reduce the release of corticotropin. Additionally, inhibitors of the formation of corticosteroids in the adrenal cortex are prescribed. These are the drugs Mamomit and Metapirone. You should not think that a disorder such as adrenal hyperfunction can be treated quickly. It will take time for all processes to return to normal. Usually treatment is delayed for 6 months or more.

Symptomatic therapy is aimed at adjusting the metabolism of carbohydrates, electrolytes and proteins. Prescribed drugs that lower blood pressure and normalize the functioning of the heart and blood vessels. A common complication Hyperfunction of the adrenal glands is osteoporosis, therefore, in the treatment of this syndrome, the prevention of bone fractures is important. To normalize protein metabolism, doctors prescribe anabolic steroid, for example, Nerobolil and Retabolil. Carbohydrate metabolism I regulate by correcting nutrition if there is a violation of tolerance to carbohydrates, as well as by prescribing insulin or sulfonylurea derivatives in case of diabetes mellitus.

Since adrenal hyperfunction syndrome is accompanied by hypoxia, patients should not take biguanides, and correction electrolyte metabolism carried out with potassium preparations. With increased blood pressure appoint antihypertensive therapy, and in case of disorders of the cardiovascular system - cardiac glycosides and diuretics. To prevent osteoporosis, it is recommended to take drugs that accelerate the absorption of calcium in the intestines: vitamin D derivatives. Calcitonin and Calcitrin are prescribed to fix calcium in the bones. For the prevention of fractures and other unpleasant complications osteoporosis therapy should be carried out for at least 1 year.