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Addison's disease occurs when the adrenal cortex malfunctions. This disease is diagnosed in both men and women, mainly of middle age (from 30 to 40 years). This is a fairly rare disease, which is registered in one person per 100 thousand population. Addison Birmer's disease can develop as a result of infectious diseases (syphilis, adrenal tuberculosis and typhus), as well as amyloidosis and malignant tumors. In 70% of patients, the disease occurs due to disruptions in the immune system (antibodies begin to mistake body cells for foreign bodies, attack and destroy them). When adrenal cortex cells are destroyed, the synthesis of gluco- and mineralocorticoids (cortisol, 11-deoxycorticosterone, aldosterone) decreases. Scientists have proven that glucocorticoids regulate various biochemical processes in the body (regulates blood pressure, insulin concentration, participates in the regulation of the synthesis of proteins, lipids and carbohydrates).

Hypocortisolism is often observed in patients taking adrenal hormones. In most cases, the etiology of the disease remains unclear. classified into primary and secondary. Primary failure develops when adrenal tissue is damaged, and secondary failure is caused by insufficient stimulation of them by adrenocorticotropic hormone.

Addison's disease: symptoms

Clinical signs of the disease are caused by a lack of mineral and glucocorticoids in the body. Most characteristic features are adynamia, hypotension, dysfunction of the gastrointestinal tract (nausea, loss of appetite, vomiting, constipation, which is often replaced by diarrhea). Some patients experience hypochlorhydria.

Addison's disease is accompanied by increased irritability or depression, frequent headaches and insomnia. X-ray examination of the chest organs shows a decrease in the size of the heart. The electrocardiogram records ( increased concentration potassium in the blood). Skin pigmentation does not reflect the severity of the disease, but its increase or decrease during treatment indicates the effectiveness of therapeutic actions.

Addison's disease of secondary origin is characterized by less severe symptoms. Very evident without skin pigmentation (so-called “Addison’s white”). The main cause of this disease is adrenal tuberculosis. Without appropriate treatment, Addison's disease becomes more complicated. Clinical signs intensify: nausea, vomiting, diarrhea, blood pressure drops sharply, and the concentration of potassium in the blood increases. In the peripheral blood, the amount of residual nitrogen, the number of red blood cells, and the hemoglobin content increase. Therefore, if timely assistance is not provided to the patient during the Addisonian crisis, he will die with signs of renal and

The most significant laboratory indicators for making a diagnosis are the content of 17-OX in the blood plasma and 17-KS in the urine, as well as a decrease in blood glucose levels. Morphological examination of the blood indicates lymphocytosis, eosinophilia and slow ESR.

Addison's disease is differentiated from the following diseases: bronze diabetes, pellagra, poisoning with arsene, bismuth and argentum. This disease, as a rule, has a chronic course with periodic exacerbation. The severity of Addison Birmer's disease is determined by the severity of the main symptoms of the disease, as well as by the number of medications that are necessary to compensate for adrenal insufficiency.

Addison's disease is a disease of the adrenal cortex. It is characterized by partial or complete inhibition of the functions of the glands for the synthesis and release of glucocorticoid hormones. The pathology has a wide variety of symptoms, since glucocorticoids affect many processes occurring in the body. The diagnosis of the disease is carried out by an endocrinologist. Treatment depends on the causes of the pathology.

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General characteristics of the pathology

The prevalence of the disease is estimated at 25-50 cases per 100 thousand people. Moreover, in women it occurs 3 times less often. It was first described in the 19th century (1855) by the English physician Addison. He initially called it bronze disease because of the characteristic skin tone of the patients, and he also correctly noted changes in the human constitution under the influence of a lack of adrenal hormones.

There are 3 main forms of adrenal insufficiency:

1. Primary - develops when the activity of the glands decreases due to internal pathologies.
2. Secondary - the result of a decrease in the production of ACTH (adrenocorticotropic hormone) by the pituitary gland.
3. Iatrogenic pathology - occurs with normal adrenal glands and the hypothalamic-pituitary system under the influence of exogenous hormones (entering the body from the outside).

Reasons for the development of pathology

Addison-Birmer syndrome develops for a number of reasons, which are conventionally divided into 3 groups:

1. Pathologies affecting the adrenal glands. These include autoimmune damage to the glands, their tuberculosis, scleroderma, syphilis, brucellosis, blastomycosis, coccidioidomycosis, tumor metastases (most often their primary focus is in the kidneys, mammary glands, and lungs).
2. Diseases and pathological conditions of the hypothalamic-pituitary region. This includes tumors and metastases, traumatic brain injuries, lacunar stroke at the location of these organs.
3. Medicinal and therapeutic measures: long-term use of adrenal hormones (especially glucocorticoids), removal of part of the gland tissue (carried out for the treatment of pheochromocytoma), therapy with cytostatic drugs, irradiation of the lumbar region and/or brain.

It is possible to detect the causes of Addison's disease in 7 out of 10 patients.

Pathogenesis of the disease

Adrenal insufficiency often goes silent for several months or even years. Only some iatrogenic cases of Addison's disease develop relatively quickly - within a few days.

The key link in the pathogenesis of the pathology is a disruption of the adrenal glands. Degradation of gland cells occurs, which leads to a decrease in its functions. As a result, hormone synthesis decreases.

The duration of the asymptomatic period is explained by the compensatory capabilities of the adrenal glands and the whole body. It is believed that the first clinical manifestations of the disease are observed when at least 90% of all gland cells stop working. Only glucocorticoid and mineralocorticoid deficiency occurs. The low production of catecholamines is compensated by their synthesis outside the adrenal glands.

Clinic

Often, the disease can be suspected only when there is extensive necrosis of the adrenal glands, when a noticeable decrease in hormone levels begins. The most typical option is the onset of symptoms after the so-called triggers. This type of clinic occurs in 9 out of 10 cases.

The disease develops most quickly in children. This is explained by their body’s high need for adrenal hormones.

The trigger mechanism for the appearance of symptoms of the disease is stress, illness, and injury.

Classic signs of pathology are:

weakness;
weight loss;
pigmentation of the skin and mucous membranes.

The weakness is not constant, it increases very quickly with movement, but decreases for a long time at rest. This is explained by a lack of muscle cell reserves and the lack of an impulse (in the form of glucocorticoids) to stimulate one’s own metabolism.

Weight loss develops due to two main reasons. The first is associated with a slowdown in metabolic processes in all cells. The second is dyspepsia, which is accompanied by decreased appetite, nausea, and stool disorders.

Pigmentation in 100% of cases is characteristic of primary adrenal insufficiency. It occurs due to the high production of adrenocorticotropic hormone, which stimulates the formation of melanin in all epithelial cells. Therefore, pigmentation increases not only on the skin, but also on the mucous membranes. The patient's color is tan. There is a brown stripe on the gums in the area of the dental border. With secondary adrenal insufficiency, pigmentation is not observed. This is the only difference between it and the primary form of the disease.

The following symptoms are more rare:

Muscle pain. Caused by the accumulation of lactic acid ( natural product cell functioning) due to the slow functioning of the enzymes that break it down.
Need for salt and salty foods. Occurs in a quarter of all patients. Associated with mineralocorticoid deficiency, which leads to excessive sodium excretion by the kidneys.

Diagnosis of pathology

To identify Addison's disease, a combination of several methods is necessary:

inspection;
complaints;
anamnesis (history of the onset and development of pathology);
blood tests for adrenal and pituitary hormones.

Other laboratory and instrumental diagnostic methods play a supporting role.

Inspection

When examining a patient, you should pay attention to the color of his skin and oral mucosa. Signs of weight loss and muscle atrophy are important. In some cases, a change in the color of the skin and mucous membranes for many years is the only symptom of the pathology that appears earlier than the others. Often pigmentation is local.

First of all, areas with initially pigmented skin become darker. These are the areolas of the mammary glands, genitals, lips. Then natural folds and areas of the skin that experience additional pressure are subjected to pigmentation. For example, places that are pressed by a belt, a scarf, and so on.

Complaints

The patient himself complains of decreased appetite, weakness and pigmentation of the oral mucosa in the classic course of the pathology.

In most cases, changes in the oral mucosa and skin for a long time(up to 10-15 years) are the only symptoms of the development of pathology. Therefore, such patients rarely see a doctor.

Anamnesis

A detailed questioning of the patient makes it possible to link the complaints and the clinic with the provoking factor only in half of the cases. Most often, after significant stress to the body (trauma, illness and psycho-emotional stress), signs of pathology begin to develop. In other situations, it is not possible to identify the provoking factor.

It is more important in the anamnesis to notice the appearance of the first signs of pathology after previous diseases of the lumbar region, tuberculosis, oncology, sepsis or against the background of HIV infection. All of these conditions can lead to damage to the adrenal glands.

Blood tests for hormones

The most reliable research. They make it possible to identify the morphological substrate of the disease (its immediate mechanisms).

The most important indicators are the following hormones:

cortisol;
17-hydroxycorticosterone (the main product of corticosteroid metabolism);
aldosterone;
ACTH (adrenocorticotropic hormone).

The first 3 hormones are reduced in all forms of adrenal insufficiency. High ACTH levels are observed only in primary Addison's disease.

General clinical studies

They are performed for any pathology, as they are included in the mandatory standard of patient examination. The following symptoms are characteristic of any form of the disease:

Anemia. Hemoglobin decreases to 50-40 g/l. The analysis shows anisocytosis and initial forms of red blood cells. The color indicator remains within the normal range (1-0.9), since the total number of red blood cells does not fall below the normal value (3.3 × 10 to the 12th power).
Leukopenia with relative lymphocytosis. The total number of leukocytes is below normal, but the number of lymphocytes in percentage becomes more than standard values.
Hypoglycemia and impaired carbohydrate tolerance. Associated with a slowdown in insulin synthesis and the liver’s ability to convert glycogen into glucose.
Reducing the amount of sodium and chlorine ions in the blood. At the same time, the concentration of potassium increases.
Low amount of T-suppressors. This is a system that suppresses the activity of leukocytes.

Of the instrumental methods, ultrasound and tomography are useful. Both show hypotrophy and atrophy of adrenal cells. On tomography you can see calcifications (salt deposits) formed due to tuberculosis of the glands.

Treatment of the disease

Treatment protocol for primary adrenal insufficiency:

1. Elimination of the cause that caused the pathology.
2. Medical nutrition and daily routine. The patient's diet should be 25-35% higher in calories than normal for his age. Proteins should predominate in the diet (at least 40%). It is recommended to consume carbohydrates in fractions, dividing the daily intake into 4-5 equal portions.
3. Multivitamins. Any drugs are suitable. The most important are vitamin complexes containing sufficient doses of vitamins C and group B.
4. Glucocorticoids and mineralocorticoids. Drugs such as Hydrocortisone, Methylprednisolone, Dexamethasone, Prednisolone, Aldosterone, DOXA, Deoxycorticosterone are used.
5. Anabolic agents (steroids and adaptogens). One of the the following drugs: Methandrostenolone, Retabolil, Phenobolil, Methylandostrendiol.
6. Transplantation of the cortex. It is carried out if there is convincing evidence that the causes of adrenal insufficiency have been eliminated and the hormonal background is stable (for 6 months). Otherwise, lifelong use of drugs containing hormones is indicated.

In the secondary form, transplantation is not performed, but lifelong hormonal replacement therapy is prescribed. Iatrogenic adrenal insufficiency requires temporary use of hormones to gradually restore gland function.

Hypocortisolism or Addison's disease is a disease endocrine system, in which the secretion (process of release) of hormones from the adrenal cortex decreases. The disease can affect people of different ages, but more often the pathology is diagnosed in women after 20 years. The disease is often called bronze disease because yellow spots appearing 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 appears a deficiency of glucocorticoid hormones (aldosterone, cortisol), which protect the body from stress and are responsible for metabolism and water-salt metabolism. Hypocorticism was first described by British physician Thomas Addison in 1855. The disease disrupts the functioning of the entire body. If treatment is not started in time, this can lead to serious complications:

paralysis of limbs;
thyrotoxicosis (hyperfunction of the thyroid gland);
ovarian dysfunction;
cerebral edema;
paresthesia (impaired sensitivity);
thyroiditis (inflammatory damage to 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 autoimmune damage to the adrenal cortex. At the same time, a failure occurs in the body’s defense system 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. Hypocortisolism can be caused by harmful bacteria, fungi, viruses, immune, and 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 (low glucose levels due to nutritional deficiencies in the diet);
severe form of diabetes.

Pathology has a primary and secondary form:

Reasons for the development of primary lesions:

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

The secondary form of the disease may appear due to:

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

If, after confirmation of bronze disease and a full course of treatment, the patient refuses further application medications, iatrogenic adrenal 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 throughout for long years can be mild and manifest themselves only when Addisonian crisis occurs. This is a life-threatening condition in which glucose levels drop sharply. As a rule, the following are considered important symptom complexes of pathology:

skin pigmentation;
asthenia and adynamia;
gastrointestinal (gastrointestinal) disorders;
hypotension (decreased blood pressure).

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

darkening of the skin;
muscle weakness;
weight loss, loss of appetite;
craving for sour, salty foods;
increased thirst;
stomach ache;
vomiting, nausea, diarrhea;
dysphagia (impaired swallowing);
tremor (shaking) of hands;
dehydration;
tachycardia (rapid heartbeat);
irritability, short temper, depression;
impotence in men, amenorrhea (lack of menstruation) in women;
dizziness;
decreased ability to work;
appearance of spots yellow color;
drying of mucous membranes and skin;
convulsions.

Asthenia and adynamia

Physical and mental fatigue (asthenia, adynamia) and impotence are considered the earliest and most persistent symptoms of bronze disease. Often the onset of the disease cannot be accurately 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 powerlessness.

Skin pigmentation

Violation of uniform skin color 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 cover the entire surface of the skin or be localized in certain places: forehead, interphalangeal joints, neck, nipples, scrotum, around the navel, etc.

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

Addison's syndrome in women

When Addison's disease appears 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 armpits, and the skin loses elasticity. Lack of estrogen and testosterone leads to the cessation of monthly menstruation and decreased libido. Other distinctive features course of the disease in women:

Gastrointestinal disorders (nausea, diarrhea, vomiting) are noted. Stomach ulcers and gastritis develop because... glucocorticoids no longer protect the intestinal mucosa from the effects of aggressive factors.
Characterized by pigmentation of the skin of large folds and open areas. Dark spots may appear on inside cheeks and gums.
The risk of gynecological diseases (mastopathy, fibroids, endometriosis) increases.
Water-salt metabolism in the body is disrupted, resulting in dehydration, the skin becomes dry, hollows appear on the cheeks, fainting occurs, and blood pressure (BP) decreases.
The brain and nervous system also suffer from dehydration, which is manifested by numbness of the limbs, sensitivity disorders, and muscle weakness.
Reproductive abilities decrease, up to miscarriage and infertility.

Treatment

Install accurate diagnosis In case of Addison's disease, only an endocrinologist can do so based on the diagnostic results. To distinguish hypocortisolism from Conn's disease, Itsenko-Cushing's disease, the specialist prescribes the patient to do a biochemical test of blood, urine, and an X-ray of the skull. Magnetic resonance imaging and computed tomography are performed to identify signs of adrenal tuberculosis. The most important diagnostic method that confirms the disease is an electrocardiogram. After all, a violation of the water-salt balance often negatively affects the functioning of the heart.

The main treatment method for hypocortisolism is lifelong hormone 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 Addisonian crisis due to trauma, infectious disease, upcoming surgery, the dosage of hormonal drugs should be reviewed by the doctor. How to treat:

Taking glucocorticosteroids begins with physiological doses, then gradually increases the amount of the drug used until hormonal levels normalize.
After 2 months of hormone treatment, benchmark analysis blood to assess the effectiveness of therapy. If necessary, the dosage of medications is adjusted.
If the disease is tuberculous in nature, therapy is carried out with the help of Rifampicin, Streptomycin, Isoniazid. The patient's condition is assessed by a phthisiatrician and an endocrinologist.
Following 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, and fresh fruits. You should eat small portions 6 times a day.

Video

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

The prevalence of registered cases is about 1 per 100 thousand population. But doctors don't consider these numbers reliable because patients with mild symptoms may not seek treatment. medical care, and the level of detection in different countries the world is too different in its capabilities.

Thus, in Denmark and the USA, 4–6 cases per 100,000 population were detected, in the UK – 3.9. Some scientists argue that Addison's disease most often develops in women aged 30–50 years. Others insist there is no connection with age, gender and race. The general consensus is that women get sick much more severely than men.

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

Classification

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

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

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

The following types of hormones are formed in the adrenal cortex:

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

Each type of adrenal hormone is responsible for its own function.

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 ensured due to:

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

Effect on metabolism

Cortisol is involved:

in the biochemical process of synthesis of glucose from amino acids in the liver, creates a protein “depot” in the muscles to maintain energy balance;
blocks the breakdown of sugars;
replenishes glycogen stores (for energy extraction) in 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;
reducing capillary permeability;
reducing oxidative processes;
disturbances in scar growth;
inhibition of cells that create conditions for allergies;
reducing tissue susceptibility to histamine and serotonin, while increasing adrenaline sensitivity.

The effect on the immune system depends on the concentration in the blood: at low concentrations it stimulates, at high concentrations it suppresses.

In addition, glucocorticoids:

help 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 thing with adrenal cortex insufficiency is the body’s loss of the ability to “extract” and replenish the energy balance. Patients experience severe weakness. The symptom often leads to a late diagnosis because people associate it with age and do not consider it important.

With a lack of glucocorticoids in the body, the following develops:

changes in cell sensitivity to insulin with subsequent disruption of all types of metabolism;
hypoglycemia and a decrease in glycogen energy reserves in the liver;
immunity to infectious pathogens decreases;
any types of stress reactions occur violently;
due to myocardial weakness, cardiac output decreases, and heart failure may develop;
an increase in ACTH synthesis 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 feature 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 development mechanism

Aldosterone is an activator of the synthesis of sodium transport protein. Under the influence of the hormone, it is reabsorbed in the kidney tubules and retained in the blood. Sodium is always followed by water. At the same time, potassium is excreted into the urine. This mechanism maintains and increases blood pressure when shock occurs, and is extremely important during bleeding, loss of fluid through sweat, excessive vomiting and diarrhea.

Aldosterone synthesis is stimulated by:

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

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

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

Androgen deficiency leads to impaired synthesis of sex hormones. This is especially important when the disease develops in adolescence. Productive function is impaired in adult men and women.

Possible causes and mechanism of development of disorders

For primary failure, the reasons may be:

autoimmune effects (idiopathic atrophy of the adrenal cortex), researchers from the USA believe that this includes up to 70% of cases of the disease, reports have appeared on the significance of AIDS;
tuberculosis, syphilis;
amyloidosis;
underdevelopment of the glandular apparatus (hypoplasia);
adrenal tumor or metastases to it;
destruction of glandular tissue by toxic substances;
genetic disorders in the process of synthesis of hormonally active substances;
decreased sensitivity of adrenal tissue to “orders” from higher centers transmitted by adrenocorticotropic hormone of the pituitary gland (ACTH).

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

In secondary adrenal insufficiency (called hypothalamic-pituitary), 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 arise due to:

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

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

What determines the development of the iatrogenic form?

Doctors are forced to identify an iatrogenic form of the disease, depending on the treatment used. Modern therapy for many systemic diseases cannot do 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 long-term courses of drugs for health reasons. In this case, the adrenal gland’s own glandular cells atrophy, and the connection with the hypothalamic-pituitary regulatory system is broken. If you stop taking the drugs, a “withdrawal syndrome” develops with severe deficiency. The dosage reduction must be carried out in stages.

Symptoms

Symptoms of Addison's disease develop gradually and remain unnoticed for a long time until a person has a sharp need for increased production of hormones to combat stress or severe infection. Here it becomes clear that the body is unable 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 hands, head tremor;
possible cramps in the limbs (often associated with eating dairy products);
lack of appetite, impaired swallowing, weight loss;
constant desire for salty foods and thirst;
frequent nausea, diarrhea, vomiting, and occasional abdominal pain;
hypotension is orthostatic in nature (pressure drops when standing), sometimes accompanied by fainting;
areas of skin hyperpigmentation occur in open places, on the face, hands, neck, lips, nipples become bluish-black;
the patient notices mental abnormalities: irritability, anxiety, irascibility, followed by depression;
women and girls note irregularity or cessation of menstruation;
impotence is typical for men;
Excess potassium in the blood contributes to such manifestations as paresthesia and paralysis.

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

How does Addisonian crisis occur?

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

long-term 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 during “withdrawal syndrome” of glucocorticoid drugs in patients with healthy adrenal glands due to functional disorders in the secreting cells.

The patient's condition is assessed as serious:

sudden severe pain appears in the abdomen, lower back or legs;
continuous vomiting, diarrhea;
shock develops;
blood pressure is sharply reduced;
consciousness is confused;
acute psychosis is possible;
Severe tachycardia and arrhythmias are recorded;
a significant amount of urine is released;
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 requires immediate professional assistance: fluid administration, normalization of electrolyte composition, compensatory dosage of hormones.

A brown coating is visible on the patient’s tongue and teeth due to the addition of hemolysis of red blood cells and iron deficiency

Diagnostics

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

asthenization;
neuropsychic changes;
gastroenterological disorders;
propensity for oncology;
cardiovascular signs;
melasma manifestations;
anemia.

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

Classic laboratory data are electrolyte shifts:

hyponatremia;
hyperkalemia;
hypercalcemia;
hyperphosphatemia.

Especially if they are detected against the background of reduced hematocrit, glucose and high level urea in the blood. An increase in the number of eosinophils, normo- and hyperchromic anemia is possible. Special studies on hormones consist of determining the level of cortisol and ACTH in plasma, their ratio:

if cortisol levels are low and ACTH is elevated, primary adrenal insufficiency can be assumed;
with simultaneously low levels of ACTH and cortisol, the condition is regarded as secondary deficiency.

In case of emergency need for surgical treatment, the dosage of administered Hydrocortisone is determined theoretically. In conditions of planned preparation of the patient for surgery, if there is a suspicion of Addison's disease, but normal hormone levels, a provocative test is performed. Its meaning: administer ACTH to the patient and check the cortisol level. If there is no response, primary adrenal insufficiency is diagnosed.

To diagnose secondary failure, the following tests are performed simultaneously:

on the effect of ACTH stimulation - after intramuscular administration of a prolonged drug with ACTH, the blood is examined for cortisol intermittently throughout the day, its level increases after the first hour;
insulin resistance;
influence 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 increased production of aldosterone. The disease can be primary or secondary.

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

muscle weakness;
hypertension;
seizures;
polyuria;
no swelling;
blood test shows hypokalemia;
in urine – increased secretion of aldosterone.

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

Treatment

Treatment of Addison's disease requires the use of hormone replacement therapy.
In case of primary failure:

Hydrocortisone is prescribed to compensate for the loss of cortisol;
if aldosterone decreases - Fludrocortisone (Cortineff, Florinef), you may have to switch to a salt-free diet or reduce your intake.

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

In cases of secondary adrenal insufficiency, patients do not need to replace mineralcorticosteroids. These substances continue to be synthesized normally. All dosages of drugs are selected individually.

Adequate therapy is indicated by sufficient fluid intake and cessation of orthostatic hypotension. Some patients need to take blood pressure medications because fludrocortisone causes hypertension in them.

Difficulties are caused by simultaneous concomitant diseases. If infection activation is observed, the dosage of Hydrocortisone is doubled. It is important to review the dosage of Insulin if necessary if there is concomitant diabetes mellitus. In the presence of severe nausea and vomiting, it makes no sense to prescribe drugs in tablets. Only injections are used.

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

In the picture of an 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, as an emergency, the following is administered intravenously:

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

Hydrocortisone is infused continuously by drip for 24 hours.

Usually there is an improvement in the condition. Then they switch to tablet forms of Hydrocortisone, and, if necessary, Fludrocortisone. The patient’s recovery also depends on the treatment of the cause that provoked the crisis. If the culprit is stress, then significantly less fluid is transfused.

At high temperature against the background of dehydration, drugs from the Aspirin group are used very carefully.
To influence nervous system antipsychotic medications will be required. Drugs with a short-lasting effect are preferred.
Symptomatic agents should be coordinated with plasma electrolyte levels and blood pressure response.
Vitamins C and B1 are shown. Can be used 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 and be checked more often for tuberculosis infection. Addison's disease with compensated support medicines does not reduce the active life span. The presence of any symptoms requires a full diagnosis.