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The British physician Thomas Addison in 1855 first described the clinical manifestations of the disease caused by damage to the adrenal cortex. It is called Addison's disease. According to modern data, this is an endocrine pathology caused by the loss of the ability of the adrenal glands to synthesize the required amount of hormones. The main role is played by the lack of cortisol.

The prevalence of reported cases is about 1 per 100,000 population. But doctors do not consider these numbers reliable, because patients with mild symptoms may not seek medical help, and the level of detection in different countries of the world is too different in their capabilities.

So, in Denmark, the USA revealed 4-6 cases per 100,000 population, in the UK - 3.9. Some scientists argue that Addison's disease most often develops in women aged 30-50 years. Others insist that there is no connection with age, gender and race. General opinion: women are much more severely ill than men.

The pathology should not be confused with the well-known Addison-Birmer anemia. Thomas Addison described it 6 years earlier and considered it one of the manifestations of chronic adrenal insufficiency. By its nature, hematopoietic disease can be part of the signs of hypocorticism or develop as an independent disease.

Classification

The functioning of the peripheral endocrine glands is necessarily associated with the organ where they are located, and the "orders" of the hypothalamic-pituitary system. According to this principle, the disruption of the adrenal cortex is divided into:

• on the primary - the adrenal cortex is affected;
• secondary - all initial changes occur in the pituitary gland (anterior lobe) or hypothalamus (brain stem region), and then disrupt the regulation of adrenal hormone production.

How does the adrenal cortex work in normal and pathological conditions?

In the cortical layer of the adrenal glands, the following types of hormones are formed:

• glucocorticoids (cortisol, cortisone, deoxycortisol, corticosterone and dehydrocorticosterone);
• mineralcorticoids (aldosterone);
• dehydroepiandrosterone (precursor of androgens).

Each type of hormones of the adrenal cortex is responsible for its function.

The role of glucocorticoids

Of all the glucocorticoids, cortisol is the most active. The effect on the body is very multifaceted. The anti-stress effect in case of injuries, shock, massive blood loss is provided by:

• adaptation of blood pressure, vascular wall, myocardium to stress factors;
• regulation of erythrocyte production by the bone marrow.

Effect on metabolism

Cortisol is involved:

• in the biochemical process of synthesis in the liver of glucose from amino acids, creates a protein "depot" in the muscles to maintain energy balance;
• blocks the breakdown of sugars;
• replenishes glycogen stores (for energy extraction) in the muscles and liver;
• accumulates fats;
• supports aldosterone in sodium and water retention.

Anti-inflammatory protection

Provided through:

• blocking enzymes and autoantibodies involved in the inflammatory response;
• decrease in capillary permeability;
• reduction of oxidative processes;
• scar growth disorders;
• inhibition of cells that create conditions for allergies;
• reducing the susceptibility of tissues to histamine and serotonin, with an increase in adrenaline sensitivity.

The effect on immunity depends on the concentration in the blood: at low concentrations - stimulate, at high - suppress.

In addition, glucocorticoids:

• increase the secretion of acid and pepsin by the glands of the gastric mucosa;
• affect the functioning of the brain (information processing, evaluation of taste, smell).

The most significant in case of insufficiency of the adrenal cortex is the loss by the body of the ability to "extract" and replenish the energy balance. Patients develop severe weakness. The symptom often leads to a late diagnosis, as people associate it with age and do not consider it important.

With a lack of glucocorticoids in the body develops:

• a change in the sensitivity of cells to insulin, followed by a violation of all types of metabolism;
• hypoglycemia and a drop in the energy reserves of glycogen in the liver;
• reduced immunity to infectious pathogens;
• any kind of stress reactions proceed violently;
• due to the weakness of the myocardium, cardiac output falls, the development of heart failure is possible;
• an increase in the synthesis of ACTH increases the level of β-lipotropin in the blood, this substance has a melanocyte-stimulating effect, the property is manifested by the formation of such a sign as skin pigmentation (hence another name for the pathology - bronze disease).

Photo of pigmentation on the cheekbones of a woman with bronze disease

Mineralocorticoids, role in the mechanism of development

Aldosterone is an activator of the synthesis of a protein carrier of sodium molecules. Under the influence of the hormone, it undergoes reabsorption in the tubules of the kidneys and is retained in the blood. Sodium is always followed by water. At the same time, potassium is excreted into the urine. This mechanism maintains and raises blood pressure in the event of shock, is extremely important for bleeding, loss of fluid through sweat, profuse vomiting and diarrhea.

The synthesis of aldosterone is stimulated by:

• renin-angiotensin system of the kidneys;
• pituitary adrenocorticotropic hormone;
• sodium and potassium ions, with accumulation in the epithelium of the tubules.

Induced hypotension is important in the pathogenesis of cortical insufficiency in Addison's disease. Mineralocorticoid deficiency contributes to increased sodium and water excretion, potassium retention. A pronounced imbalance of electrolytes leads the body to a state of dehydration (dehydration). The volume of circulating blood decreases, blood pressure drops.

In secondary adrenal insufficiency associated with impaired ACTH synthesis, a normal electrolyte balance in the blood test is often observed.

Androgen deficiency leads to impaired synthesis of sex hormones. This is especially important in the development of the disease in adolescence. In adult men and women, productive function is impaired.

Possible causes and mechanism for the development of disorders

For primary insufficiency, the causes may be:

• autoimmune effects (idiopathic atrophy of the adrenal cortex), US researchers believe that this includes up to 70% of cases, there have been reports of the significance of AIDS;
• tuberculous inflammation, syphilis;
• amyloidosis;
• underdevelopment of the glandular apparatus (hypoplasia);
• tumor of the adrenal gland or metastases in it;
• destruction of glandular tissue by toxic substances;
• genetic disorders in the process of synthesis of hormonally active substances;
• decrease in the sensitivity of the tissue of the adrenal glands to "orders" from higher centers transmitted by adrenocorticotropic hormone of the pituitary gland (ACTH).

The tumor of the left adrenal gland compresses the glandular cells, causing their destruction

In secondary adrenal insufficiency (called hypothalamic-pituitary insufficiency), the main factor in pathogenesis is damage to the anterior pituitary gland with a lack of adrenocorticotropic hormone. Its concentration in the blood is not enough to stimulate the glandular cells of the adrenal glands.

The reasons are due to:

• a local tumor in the brain stem or pituitary gland;
• consequences of ischemic attack, stroke;
• prolonged stressful situations;
• head injury;
• radiation therapy of the brain in certain diseases;
• birth trauma in children during the first days of life;
• hormonal changes in women during pregnancy, during menopause.

Addison's disease in such cases is often combined with a decrease in thyroid function, diabetes mellitus, polyglandular insufficiency syndrome (of all endocrine glands).

What determines the development of the iatrogenic form?

Doctors are forced to isolate the iatrogenic form of the disease, depending on the treatment used. Modern therapy of many systemic diseases is not complete without corticosteroids. They are prescribed, for example, to patients with psoriasis, lupus erythematosus, asthma, ulcerative colitis, autoimmune thyroiditis and other pathologies of internal organs.

Patients have to take drugs for long courses according to vital indications. In this case, the own glandular cells of the adrenal glands atrophy, the connection with the hypothalamic-pituitary system of regulation is broken. If you stop taking the drugs, a "withdrawal syndrome" develops with severe insufficiency. Dosage reduction should be done in stages.

Symptoms

Symptoms of Addison's disease develop gradually, go unnoticed for a long time until a person has a sharp need for increased production of hormones to fight stress, a severe infection. Here it becomes clear that the body is not able to organize the fight against damaging factors and compensate for losses.

Areas of pigmentation may be combined with white spots (vitiligo)

The following signs of disturbed hormonal balance appear:

• increasing fatigue, gradually worsening over time;
• muscle weakness;
• trembling in the hands, tremor of the head;
• possible cramps in the limbs (often associated with eating dairy products);
• lack of appetite, impaired swallowing, weight loss;
• constant desire for salt and thirst;
• frequent nausea, diarrhea, vomiting, sometimes abdominal pain;
• hypotension is orthostatic in nature (pressure drops when standing), sometimes accompanied by fainting;
• areas of hyperpigmentation of the skin appear in open places, on the face, hands, neck, lips, nipples become bluish-black;
• the patient notices deviations in the psyche: irritability, anxiety, irascibility, followed by depression;
• women and girls note the irregularity or cessation of menstruation;
• for men, the occurrence of impotence is typical;
• excess potassium in the blood contributes to such manifestations as paresthesia and paralysis.

Patients are characterized by an exacerbation of symptoms in the spring-summer season.

How does an Addisonian crisis occur?

Against the background of the gradual course of the disease, the patient may develop a clinic of acute adrenal insufficiency. The pathology is called the Addisonian crisis. The reason is:

• prolonged lack of treatment;
• insufficient dosage of drugs;
• meeting a patient with a severe stressful situation;
• the need for surgical intervention;
• injury;
• infection.

A similar condition develops with the "withdrawal syndrome" of glucocorticoid drugs in patients with healthy adrenal glands due to functional disorders in the secreting cells.

The patient's condition is regarded as serious:

• sudden severe pain in the abdomen, lower back or legs;
• continuous vomiting, diarrhea;
• shock develops;
• arterial pressure is sharply reduced;
• consciousness is confused;
• possible acute psychosis;
• the expressed tachycardia, arrhythmias is registered;
• a significant amount of urine is excreted;
• there are signs of dehydration (dry skin, mucous membranes);
• possible fever.

The crisis lasts from several hours to three days. Treatment of Addison's disease during a crisis course requires immediate professional assistance: fluid administration, normalization of the electrolyte composition, compensatory dosage of hormones.

A brown coating is visible on the patient's tongue and teeth due to the addition of erythrocyte hemolysis, iron deficiency

Diagnostics

Diagnosis of Addison's disease is based on a combination of clinical and laboratory findings. Initial manifestations in the form of increased fatigue, weakness are often mistaken for neurasthenia. But further changes suggest increasing adrenal insufficiency.

• asthenia;
• neuropsychic changes;
• gastroenterological disorders;
• predisposition to oncology;
• cardiovascular signs;
• melasma manifestations;
• anemia.

The presence of a combination of these syndromes indicates Addison's disease. If they are allocated each separately, then the diagnosis is considered unreliable or erroneous.

The classic laboratory findings are electrolyte shifts:

• hyponatremia;
• hyperkalemia;
• hypercalcemia;
• hyperphosphatemia.

Especially if they are detected against the background of reduced hematocrit, glucose and high levels of urea in the blood. Perhaps an increase in the number of eosinophils, normo- and hyperchromic anemia. Special studies on hormones are to determine the level of cortisol and ACTH in plasma, their ratio:

• if the level of cortisol is low, and ACTH is elevated, one can assume the primary nature of adrenal insufficiency;
• with a simultaneously low level of ACTH and cortisol, the condition is regarded as a secondary insufficiency.

In case of urgent need for surgical treatment, the dosage of hydrocortisone administered is determined theoretically. Under the conditions of planned preparation of the patient for surgery, if Addison's disease is suspected, but hormone levels are normal, a provocative test is performed. Its meaning: to introduce ACTH to the patient and check the cortisol content. If there is no reaction, primary adrenal insufficiency is diagnosed.

To diagnose secondary insufficiency, tests are carried out simultaneously:

• on the effect of ACTH stimulation - after intramuscular administration of a prolonged drug with ACTH during the day, intermittently, the blood is examined for cortisol, its level rises after the first hour;
• insulin resistance;
• the effect of glucagon.

When making a diagnosis, the manifestations of Addison's disease are compared with Conn's disease, Itsenko-Cushing's disease (hyperaldosteronism, excessive production of ACTH in the anterior pituitary gland with hypercortisolism).

Aldosteronism refers to changes caused by an increase in the production of aldosterone. The disease is primary and secondary.

Conn's syndrome (primary aldosteronism) is associated with hyperproduction of the adrenal tumor. Its symptoms are characterized by:

• muscle weakness;
• hypertension;
• seizures;
• polyuria;
• no edema;
• in the blood test - hypokalemia;
• in urine - increased excretion of aldosterone.

Itsenko-Cushing's syndrome is pathogenetically associated with increased production of glucocorticoids. Occurs under the influence of a tumor that synthesizes ACTH (pituitary, lungs, adrenal glands) or in people who have been treated with hormones for a long time for autoimmune diseases.

Treatment

Treatment of Addison's disease requires the use of hormone replacement therapy.
For primary deficiency:

• to compensate for the loss of cortisol, hydrocortisone is prescribed;
• with a decrease in aldosterone - Fludrocortisone (Kortineff, Florinef), you may have to switch to a salt-free diet or reduce intake.

Cortineff has a 100 times stronger mineralocorticoid, 10 times the anti-inflammatory effect of Hydrocortisone (not all pharmaceutical companies retain the second letter "F")

Patients with secondary adrenal insufficiency do not require replacement of mineral corticosteroids. These substances continue to be synthesized normally. All dosages of drugs are selected individually.

Adequate therapy is indicated by sufficient fluid intake and the cessation of orthostatic hypotension. Some patients have to use drugs to lower blood pressure, because fludrocortisone causes hypertension in them.

Difficulties are caused by simultaneous concomitant diseases. If activation of the infection is observed, the dosage of Hydrocortisone is doubled. It is important for concomitant diabetes to revise the dosage of insulin if necessary. In the presence of severe nausea, vomiting, prescribing drugs in tablets does not make sense. Only injections are used.

Patients with chronic adrenal insufficiency are taught self-management for unexpected manifestations. They are advised to always have a special bracelet or card with them so that strangers know which drug to administer in case of unconsciousness.

In the picture of the Addisonian crisis, the patient's life is threatened by a drop in blood pressure, arrhythmias caused by an increase in potassium in the blood, and hypoglycemia. Therefore, on an emergency basis, intravenously administered:

• Hydrocortisone;
• saline (0.9% sodium chloride);
• Dextrose (instead of sugar).

Hydrocortisone is infused continuously drip for 24 hours

Usually there is an improvement. Then they switch to tablet forms of Hydrocortisone preparations, if necessary, Fludrocortisone. The recovery of the patient also depends on the treatment of the cause that provoked the crisis. If the culprit was stress, then the liquids are poured much less.

1. At high temperatures against the background of dehydration, drugs of the Aspirin group are used very carefully.
2. Antipsychotics will be required to affect the nervous system. Drugs with a short-term effect are preferred.
3. Symptomatic agents should be coordinated with the level of electrolytes in the plasma, the response of blood pressure.
4. Vitamins C and B 1 are shown. You can use folk remedies to strengthen the immune system, since most often the adrenal glands suffer from autoimmune reactions.

Patients are advised to protect themselves from any infections, more often to be checked for infection with tuberculosis. Addison's disease with compensated drug support does not reduce active life. The presence of any symptoms requires a full diagnosis.

The most common cause of primary adrenal insufficiency (hypocorticism, Addison's disease) is an autoimmune lesion of the adrenal cortex. There are two autoimmune deficiency syndromes. The first includes: chronic insufficiency of the adrenal cortex, chronic hypoparathyroidism and chronic mucocutaneous candidiasis. The second syndrome includes chronic adrenal insufficiency, autoimmune thyroiditis, and type 1 diabetes mellitus. Less commonly, both syndromes include autoimmune ovarian failure. The combination of autoimmune Addison's disease, autoimmune thyroiditis, and type 1 diabetes is called Schmidt's syndrome.

Addison's disease can be combined with autoimmune diseases of a non-endocrine nature: alopecia, chronic hepatitis, vitiligo. The second most common cause is adrenal tuberculosis, which can be combined with damage to other organs - the lungs, kidneys, intestines, urogenital system. Other causes of Addison's disease include: amyloidosis, sarcoidosis, effects of radiation therapy, fungal infection, metastases to both adrenal glands, condition after bilateral adrenalectomy. Rarely, the cause may be a congenital decrease in the sensitivity of the fascicular and reticular zones of the adrenal cortex to the stimulating effect of ACTH. As a result, the synthesis of cortisol decreases and the adrenal cortex atrophies.

The basis of all clinical manifestations of Addison's disease is the lack of cortisol and aldosterone, and in women - and adrenal androgens.

With a lack of cortisol:

• energy homeostasis. Decreased glycogen synthesis in the liver. The level of glucose in the blood decreases. Patients complain of weakness, weight loss, there is a tendency to hypoglycemia.
• Gastrointestinal tract. The secretory activity of the glands of the stomach, intestines, and pancreas decreases. Patients complain of loss of appetite, nausea, vomiting, diarrhea,.
• The cardiovascular system. The strength of heart contractions decreases, hypotension develops.
• Mental activity. There is a decrease in memory, drowsiness, apathy, psychosis appear.
• Pituitary. The secretion of ACTH increases, which leads to hyperpigmentation of the skin and mucous membranes.
• Reaction to stress. Decreased resistance to stressful situations.

With a lack of aldesterone: with a lack of aldesterone, there is a decrease in the amount of sodium in the body and an increase in potassium.

• With a lack of sodium, there is a decrease in extracellular fluid, cardiac output, heart size, hypotension, a decrease in glomerular filtration and, ultimately, this leads to shock. Clinically, this is manifested by weakness, weight loss, dizziness, fainting.
• An increase in the amount of potassium is manifested by acidosis, a violation of the heart rhythm.

With a lack of adrenal androgens: manifested only in women by a decrease in growth or the absence of axillary and pubic hair. Typically, Addison's disease progresses slowly. This is due to the gradual destruction of the adrenal cortex, the development of cortisol and aldosterone deficiency. The earliest symptoms of the disease are expressed in a tetrad: weakness, loss of appetite, weight loss, hypotension.

Addison's disease is characterized by anemia, leukopenia, neutropenia, eosinophilia, and lymphocytosis. The level of potassium in the blood serum is increased (more than 5.5-6.0 mmol / l), and the level of sodium is reduced. The level of cortisol in the blood serum is below 3 μg / dl (0.08 μmol / l), aldesterone is below 7.6 ng / dl (212 pmol / l). The concentration of ACTH is higher than normal, sometimes dozens of times (above 250 pg / ml (55 pmol / l). In case of latent insufficiency of the adrenal cortex, the level of cortisol in the blood may be normal. In such cases, a quick ACTH stimulation test is performed to confirm the diagnosis.

Treatment of primary chronic insufficiency of the adrenal cortex is carried out throughout the patient's life and consists of replacement therapy with glucocorticoids, if necessary, in combination with mineralocorticoids.

Content

Hypocorticism or Addison's disease is a disease of the endocrine system, in which the secretion (excretion process) of the hormones of the adrenal cortex decreases. The disease can affect people of all ages, but more often the pathology is diagnosed in women after 20 years. Often the disease is called bronze disease because of the yellow spots that occur on the body.

What is Addison's disease

Bronze disease is a rare disease of the endocrine system, the development of which is based on the destruction of the tissues of the outer layer of the adrenal glands. In this case, there is a deficiency of glucocorticoid hormones (aldosterone, cortisol), which protect the body from stress and are responsible for metabolism, water-salt metabolism. Hypocorticism was first described by British physician Thomas Addison in 1855. The disease disrupts the functioning of the whole organism. If treatment is not started on time, this can lead to serious complications:

• paralysis of the limbs;
• thyrotoxicosis (hyperfunction of the thyroid gland);
• ovarian dysfunction;
• swelling of the brain;
• paresthesia (impaired sensitivity);
• thyroiditis (inflammatory lesion of the thyroid gland);
• anemia (decreased hemoglobin concentration);
• chronic candidiasis (fungal infection).

Reasons for development

Approximately 70% of all cases of Addison's disease are caused by an autoimmune lesion of the adrenal cortex. At the same time, the body's defense system fails and it recognizes the cells of the endocrine glands as foreign. As a result, antibodies are produced that attack the adrenal cortex and damage it. Hypocorticism can cause harmful bacteria, fungi, viruses, immune, genetic disorders. Factors contributing to the occurrence of pathology:

• overweight;
• physical, emotional stress;
• hypofunction (weakening) of the thyroid gland;
• polycystic ovary syndrome;
• allergic reaction;
• prolonged depression;
• hypoglycemia (decrease in glucose levels due to nutritional deficiencies in the diet);
• severe form of diabetes.

Pathology has a primary, secondary form:

1. Reasons for the development of the primary lesion:

• adrenal tuberculosis;
• autoimmune processes;
• hypoplasia (underdevelopment of the organ);
• congenital anomalies;
• surgical removal of the adrenal gland;
• hereditary diseases;
• cancerous tumors, metastases;
• syphilis;
• AIDS;
• fungal diseases;
• decreased sensitivity of the adrenal glands.

1. The secondary form of the disease may appear due to:

• mechanical injury;
• meningitis (inflammation of the membranes of the brain);
• ischemia (reduced blood supply);
• benign, malignant tumor;
• brain irradiation.

If, after confirmation of bronze disease and a full course of treatment, the patient refuses further use of drugs, adrenal iatrogenic insufficiency may occur. This condition provokes a rapid drop in the level of endogenous glucocorticoids against the background of prolonged replacement therapy and inhibition of the activity of one's own glands.

Symptoms

The clinical picture of Addison's disease develops slowly. Symptoms for many years may be mild and manifest themselves only when an Addisonian crisis occurs. This is a life-threatening condition in which the level of glucose drops sharply. As a rule, important symptom complexes of pathology are:

• skin pigmentation;
• asthenia and adynamia;
• disorders of the gastrointestinal tract (gastrointestinal tract);
• hypotension (lowering blood pressure).

In addition, Addison's disease has the following manifestations:

• darkening of the skin;
• muscle weakness;
• weight loss, loss of appetite;
• cravings for sour, salty foods;
• increased thirst;
• stomach ache;
• vomiting, nausea, diarrhea;
• dysphagia (impaired swallowing);
• tremor (trembling) of the hands;
• dehydration;
• tachycardia (rapid heartbeat);
• irritability, irascibility, depression;
• impotence in men, amenorrhea (absence of menstruation) in women;
• dizziness;
• decrease in working capacity;
• the appearance of yellow spots;
• drying of mucous membranes, skin;
• convulsions.

Asthenia and adynamia

Physical, mental fatigue (asthenia, adynamia) and impotence are considered the earliest and permanent symptoms of bronze disease. Often the onset of the disease cannot be precisely determined. At the very beginning of the development of pathology, rapid fatigue appears from work that was previously performed without serious labor costs. In addition, there is a general weakness that develops with a normal lifestyle. Such sensations progress, intensify and lead the patient to a state of complete physical impotence.

Skin pigmentation

Violation of the uniform color of the skin or the appearance of pigmentation is the most important, conspicuous symptom. Abundant deposition of melanin (a pigment that does not contain iron) in the cells of the malpighian layer of the epidermis contributes to the appearance of brown, bronze or smoky spots on the skin. Starting on the face, pigmentation can capture the entire surface of the skin or be localized in certain places: forehead, interphalangeal joints, neck, nipples, scrotum, around the navel, etc.

Sometimes large dark spots appear on the face. The bluish color stains the lips, nipples, mucous membranes of the vagina and intestines in women. Along with a strong violation of pigmentation, the patient has areas of skin that are poorly pigmented or even completely devoid of melanin, which stand out sharply against the background of the surrounding dark skin - the so-called vitiligo, or leukoderma. In the primary form of Addison's disease, this symptom appears one of the first, while it can be several years ahead of other signs of the disease.

Addison syndrome in women

When Addison's disease occurs in women, there is a decrease in muscle mass due to loss of appetite. In addition, the patient gradually loses hair on the pubis and in the armpits, and the skin loses its elasticity. The lack of estrogen and testosterone leads to the cessation of monthly menstruation, a decrease in libido. Other distinctive features of the course of the disease in women:

• Gastrointestinal disorders (nausea, diarrhea, vomiting) are noted. A stomach ulcer, gastritis develops, because. glucocorticoids no longer protect the intestinal mucosa from the effects of aggressive factors.
• Pigmentation of the skin of large folds and open areas is characteristic. Dark spots may appear on the inside of the cheeks and gums.
• The risk of gynecological diseases (mastopathy, fibroids, endometriosis) increases.
• The water-salt metabolism in the body is disturbed, as a result of which dehydration occurs, the skin becomes dry, depressions appear on the cheeks, fainting occurs, and blood pressure (blood pressure) decreases.
• The brain and nervous system also suffer from dehydration, which is manifested by numbness of the limbs, sensory disturbances, and muscle weakness.
• Reproductive abilities are reduced up to miscarriage, infertility.

Treatment

Only an endocrinologist can establish an accurate diagnosis for Addison's disease based on the results of the diagnosis. To distinguish hypocorticism from Conn's disease, Itsenko-Cushing's, the specialist prescribes the patient to do a biochemical analysis of blood, urine, and an x-ray of the skull. Magnetic resonance and computed tomography are performed to detect signs of adrenal tuberculosis. The most important diagnostic method that confirms the disease is the electrocardiogram. After all, a violation of the water-salt balance often negatively affects the work of the heart.

The main treatment for hypocorticism is lifelong hormonal replacement therapy, i.e. taking glucocorticosteroid drugs - analogues of cortisol and aldosterone (Cortisone). The specialist selects the dosage individually. The duration of treatment depends on the form and severity of the disease. To prevent the occurrence of an Addisonian crisis against the background of an injury, an infectious disease, an upcoming operation, the dosage of hormonal agents should be reviewed by a doctor. How to treat:

1. The intake of glucocorticosteroids begins with physiological doses, then the amount of the drug used is gradually increased until the level of hormonal levels is normalized.
2. After 2 months of hormone treatment, a control blood test is performed to assess the effectiveness of therapy. If necessary, the dosage of drugs is adjusted.
3. With the tuberculous nature of the disease, therapy is carried out with the help of Rifampicin, Streptomycin, Isoniazid. The patient's condition is assessed by a phthisiatrician and an endocrinologist.
4. Compliance with a special diet. It is necessary to exclude from the diet: bananas, nuts, peas, coffee, potatoes, mushrooms. It is useful to eat liver, carrots, eggs, beans, legumes, fresh fruits. You should eat in small portions 6 times a day.

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