Do people die from Addison's disease and how to survive. Addison's disease: photos, causes, symptoms and treatment Bronze disease hormone

The clinical symptoms of Addison's disease depend on the severity of the disease, which in turn is determined by the degree of hormonal insufficiency of the adrenal cortex, age-related characteristics of the body, the presence of concomitant diseases and, to a certain extent, its etiology (primarily tuberculosis intoxication). With primary autoimmune, hypoplastic processes, atrophy of the adrenal cortex, the disease often develops gradually without a clear anamnestic connection with previous diseases.

One of the characteristic symptoms of Addison's disease is increased fatigue and muscle weakness. Initially, muscle weakness occurs towards the end of the day. Older people usually associate it with overwork at work, increased physical or mental stress, and age. Over time, muscle weakness increases and occurs not only at the end of the day, but also at an earlier time. General asthenia is characteristic. Sleep does not bring vigor, general physical and mental lethargy, severe muscle weakness are constantly noted, which makes it difficult to move, especially climb stairs, in severe cases even speak, and eat food independently. In other words, muscle weakness takes on the character of adynamia, which is one of the classic symptoms of Addison's disease. The severity of asthenia and muscle weakness can serve as one of the criteria for the severity of the disease.

An early sign of chronic hypocortisolism is a gradually progressive loss of body weight (100% of cases), associated not only with dehydration, a decrease in anabolic processes, but also a decrease in appetite (70-90% of cases), as well as tuberculosis intoxication. Loss of body weight can range from insignificant - 3-5 kg, to severe - 25-30 kg or more, and develop relatively quickly (over 2-3 months) or slowly (over many months and years).

At the beginning of the disease, appetite is reduced for any food, with the exception of salty food, and later it is completely absent. Against the background of decreased appetite, some patients sometimes experience a feeling of hunger, accompanied by headache, dizziness, increasing general weakness, and sometimes trembling, which indicates the phenomena of hypoglycemia associated with relative hyperinsulinism. The hypoglycemic nature of the listed disorders is indicated by their reduction or elimination after eating, especially sweets, a glass of tea, a piece of sugar or candy.

With severe symptoms of hypocortisolism, patients also complain of nausea, abdominal pain, vomiting, which does not bring significant relief. Stools are often irregular and there is a tendency to diarrhea. Abdominal pain of varying intensity and localization usually indicates a severe course of the disease, its decompensation; When sufficient doses of hormones are prescribed, it usually decreases quickly.

One of the early complaints of patients is dizziness when quickly changing body position, especially when getting out of bed, noise in the head, even to the point of fainting. This is due to impaired vascular tone, arterial hypotension as a result of a deep disturbance of water-electrolyte, primarily sodium, metabolism - hyponatremia. In severe cases of the disease and the development of Addisonian crisis, arterial hypotension reaches an extreme degree - collapse. Typically, systolic blood pressure is less than 13.3 kPa (100 mm Hg), reaching in severe cases 9.3-8 kPa (70-60 mm Hg), diastolic - 8-4 kPa (60-30 mm Hg), usually 8-5.7 kPa (60-50 mm Hg). The level of blood pressure depends on the degree of corticosteroid deficiency, however, a normal blood pressure does not exclude chronic insufficiency of the adrenal cortex, which may be due to concomitant hypertension in such patients or secondary symptomatic, often renal, arterial hypertension.

Hypocorticism helps reduce blood pressure, sometimes to normal levels, that is, relative arterial hypotension occurs. It is important to remember this, since the reference point in diagnosing Addison’s disease to the obligatory presence of arterial hypotension can lead to serious consequences, including the death of patients due to the lack of adequate hormone replacement therapy. It is very important in these cases to measure blood pressure not only in a horizontal position (it can be normal or even elevated), but also in a vertical position.

One of the symptoms of Addison's disease is neuropsychic disorders (mental fatigue, memory loss, irritability, sleep disturbance, depression), which occur in 55-70% of cases. The threshold for perception of taste, olfactory, visual and auditory stimuli is reduced, which normalize only after glucocorticoid replacement therapy. One of the early signs of Addison's disease in men is a decrease in potency and libido, in women - oligo- and opsomenorrhea, and in severe cases - amenorrhea.

Noteworthy is the change in skin color - hyperpigmentation, which appears some time after the onset of the first signs of the disease (weakness, increased fatigue) or simultaneously with other manifestations of the disease. At the beginning of the disease, exposed parts of the body exposed to insolation (face, neck, back of the hands), places of friction of clothing, mechanical influence of various factors (area of wearing a belt, anterior and posterior skin-muscular folds surrounding the axillary region, elbows, anterior surface of the knee joints) become pigmented. , places of physiological pigment deposition (mammary nipples, skin of the scrotum, penis, labia, anal opening) are more intensely stained.

Pigmentation of skin scars (postoperative scars, sites of former boils and other purulent-inflammatory skin diseases) is characteristic. Skin pigmentation is bronze, golden brown, or less often an earthy dirty brown. Gradually, pigmentation spreads over the entire surface of the skin, remaining more pronounced in the indicated areas. Enhanced pigmentation of the dorsum of the hands and especially the dorsal surface of the interphalangeal joints is very characteristic: the palmar and plantar surfaces remain light while the pigmentation of the palmar folds is preserved. In 40-60% of cases, along with skin pigmentation, there is local pigmentation of the mucous membranes (inner surfaces of the cheeks in the area of the closure of the teeth, gums, lips, hard and soft palate, posterior wall of the pharynx, vaginal mucosa, rectum). The color of the mucous membranes is bluish-gray or bluish-gray. Bluish-brown pigmentation can be found on the conjunctival membrane, and brown spots are often found on the fundus.

In some patients, against the background of pigmented skin, depigmented spots of various sizes and shapes appear (vitiligo and leucoderma), which was first noticed by Addison. There is no clear relationship between the severity of the disease and the severity of pigmentation, although more severe forms of hypocortisolism are often accompanied by more intense pigmentation. In some patients, skin pigmentation precedes the appearance of other symptoms of the disease, which is associated with increased secretion of corticotropin (based on the feedback principle). Subsequently, due to the depletion of the reserve capacity of the adrenal cortex, absolute hormone deficiency occurs, which is manifested by the corresponding clinic. Much less often, as a rule, with secondary (adenopituitary) hypocortisolism, hyperpigmentation is absent despite the presence of pronounced symptoms of the disease (adynamia, anorexia, weight loss, arterial hypotension).

Along with hyperpigmentation, Addison's disease often (in 25% of cases) causes darkening of hair and hair loss (on the pubis, in the armpit). The absence of hyperpigmentation in such cases causes certain difficulties in diagnosing not only early, but also severe forms of the disease.

What is Addison's disease? Bronze disease is a pathological condition of the adrenal cortex. Pathology occurs with bilateral organ damage and leads to a decrease (or even absence) of hormone secretion. The disease begins to develop when there is a pathological change in 90% of the adrenal tissue. The main causes of Addison's are an autoimmune process (working against the body's own immune system) and tuberculosis. Women are usually affected more often than men; the syndrome is rare in children. The syndrome was first described by the famous English physician Thomas Addison in the mid-19th century.

A little about Addison's disease

The adrenal glands produce essential hormones. The paired organ consists of 2 zones: the cortex and medulla, which synthesize different hormones. The medulla produces adrenaline and norepinephrine (stress hormones), the cortex produces corticosterone, deoxycorticosterone, androgens. The work of the adrenal glands is controlled by the pituitary gland, which produces, acting on the cortex of the organ and stimulating its synthesis of hormones.

A distinction is made between primary and secondary cortical failure. Addison's disease is the primary form, that is, direct adrenal dysfunction that develops due to negative factors. Secondary is the response of the adrenal glands to a decrease in ACTH, leading to a decrease in hormone production. When the lack of ACTH supply continues for a long time, degenerative processes develop in the cortical tissue.

Causes of Addison's disease

The primary form of Addison's disease occurs quite rarely. Initial symptoms of the disease may begin to appear between 30 and 50 years. In 80% of cases, the disease begins to develop as a result of an autoimmune lesion. Another 10% become ill due to previous tuberculosis. For another 10% the reasons vary:

gland dysfunction due to long-term hormone therapy;
mycotic pathologies;
injuries;
removal of the adrenal glands;
sarcoidosis;
amyloidosis;
tumors;
gland infections with reduced immunity;
pituitary dysfunction;
heredity - the presence of chronic insufficiency of the adrenal cortex of an autoimmune nature and relatives of the 1st and 2nd lines of kinship;
AIDS;
syphilis.

What are the risks of developing Addison's disease without timely treatment? As a result, it may develop Addisonian crisis, occurring due to a sharp decrease in the amount of hormones.

Possible causes of the crisis:

deep stress - infectious disease, surgery, emotional distress;
error in dosing of hormone therapy;
acute infectious lesion;
gland injury;
circulatory pathologies: blood clots, arterial embolism, hemorrhage;
lack of replacement therapy after organ removal.

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Symptoms

Symptoms are directly related to insufficient production of hormones and depend on the duration of the disease and the degree of adrenal insufficiency. Regular A is a disorder of pigmentation of the skin and mucous membranes. The second name of the disease is bronze, which is associated precisely with the characteristic change in the color of the skin. In the absence of problems with pigmentation, the disease is very difficult to diagnose and is often detected only with the development of Addisonian crisis.

How does this happen. The pituitary gland receives a signal from the lack of adrenal hormones in the body and increases the synthesis of ACTH to activate the secretory function of the glands. ACTH, in turn, acts on skin cells, stimulating melanocytes to produce melanin. Because of this, it develops hyperpigmentation- the first symptom of the primary form of the disease. First, the areas of the body most exposed to sunlight darken, so the onset of the disease can easily be confused with prolonged tanning. Subsequently, the mucous membranes and friction points begin to darken. The shade can vary from smoky to very pronounced.

For a long time, only hyperpigmentation and dry skin on the hands are the only symptoms of the disease. Hyperpigmentation may be accompanied by vitiligo (appearance of lighter areas on the skin). The secondary form of pathology does not lead to pigmentation disorders.

After a long time, the following symptoms may appear:

hypotension leads to dizziness and cold sensitivity;
general weakness, fatigue, loss of appetite, active weight loss;
gastrointestinal dysfunction - nausea, vomiting, diarrhea (gastritis and ulcers are often diagnosed);
problems of the psycho-emotional spectrum - depression, increased anxiety;
receptor sensitivity - sensitivity to taste, auditory, olfactory stimuli increases;
muscle pain develops due to an increase in potassium levels in the blood; a person craves salty foods;
as a result of a violation of the water-salt balance, dehydration develops, expressed by numbness of the legs and arms, and fingertips.

In men, it affects sexual life up to the development of impotence. In women, there is no menstruation and hair growth in the pubic area and armpits decreases.

The extreme degree of manifestation of the pathology of Addison's disease is Addisonian crisis: a sharp lack of glucocorticoids or mineralocorticoids. Its signs: abdominal pain, drop in blood pressure, confusion, vomiting, salt imbalance, acidosis. The duration of Addisonian crisis varies - from several hours to several days. To remove a person from this condition, immediate hormone replacement therapy is performed.

The manifestation of the clinical picture depends on the degree of development of Addison's disease. The most common concomitant diseases include: thyroiditis, hypoparathyroidism, hypercalcemia, B12-deficiency anemia, chronic candidiasis.

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Diagnosis of Addison's disease

If a change in skin pigmentation occurs, you must immediately undergo diagnostics of the condition of the adrenal cortex.

First, the ability of the glands to increase the synthesis of cortisol after the administration of ACTH is determined. The level of cortisol in the blood is measured first before the administration of ACTH, and then half an hour after (short test). When the glands are in normal condition, the concentration of cortisol increases. With deficiency, cortisol levels do not change. A similar study is carried out with urine.

A standard test is more accurate - the study is carried out within 8 hours. ACTH is administered at 21-22 pm, and cortisol levels are measured at 8 am.

Additionally, OAC and OAM are performed and a blood biochemistry test is taken. Hypoglycemia, hyponatremia, hyperkalemia and metabolic acidosis are diagnosed.

Also shown:

CT scan of the abdominal organs and ultrasound measure the size of the organ;
X-ray of the abdominal cavity - detection of adrenal calcification;

With the disease, a change in the size of the adrenal glands is recorded. In the early stages of various infectious processes, iron increases. In the later stages of Addison's disease, the size of the gland decreases as a result of organ degeneration.

Treatment of Addison's disease

Treatment for Addison's disease is carried out on an outpatient basis. When diagnosing a disease, immediately hormone replacement therapy is prescribed hydrocortisone and fludrocortisone. Hydrocortisone dosage: 10 mg in the morning and 5 mg in the afternoon orally every day (in adults, the dosage can reach 20–30 mg per day). You can divide the drug intake into 3 times: the largest dose is taken in the morning, a smaller dose at lunch, the smallest in the evening (4 hours before bedtime to avoid problems falling asleep. Fludrocortisone is prescribed 0.1–0.2 mg once a day If blood pressure rises, the dosage is reduced, and if an acute illness develops, the dosage is doubled until you feel better.

Hydrocortisone

Cortineff

The course of therapy involves normalizing the water-salt balance. The patient is given intravenous saline. The patient is recommended to consume enough salt. If the blood glucose level is low, 5% glucose is prescribed intravenously.

If Addison's disease is caused by an infectious disease, the course of therapy is aimed at curing it. Treatment in this case is carried out by an endocrinologist, phthisiatrician and infectious disease specialist.

Treatment is lifelong. Regular medical monitoring is necessary to assess the adequacy of the therapy.

Folk recipes

Treatment of Addison's disease with folk remedies should be aimed at stimulating the work of the adrenal cortex. Decoctions and infusions of licorice root, snowdrop and geranium flowers, horsetail and lungwort herbs, string, echinata, mulberry, broom, and rose hips are used. Mustard perfectly stimulates the adrenal glands.

Addison's disease prognosis

The prognosis for the course of the disease with timely treatment is favorable. The disease does not affect life expectancy; the quality of life improves significantly with the start of treatment. Only a state of Addisonian crisis can lead to the death of a patient.

Among the many diseases affecting the adrenal glands, a rare pathology with a chronic, protracted course - Addison's disease, or hypocortisolism - deserves special attention. The disease affects the adrenal cortex, and as a result, a deficiency of vital hormones develops. The name of the pathology is associated with the name of the British physician Thomas Addison, who in the 19th century first described the symptoms of a serious illness.

Addison's disease can affect all age groups, but the main risk group is in the age range of 20–40 years. Hypocortisolism is rarely diagnosed - there is one patient per 100 thousand people. However, establishing the exact number of sick people is problematic - many patients do not suspect the course of the pathology due to mild symptoms and do not consult a doctor.

The adrenal glands are paired glands located in the retroperitoneal space above the kidneys and closely adjacent to them. They have different shapes - the left one is in the form of a hemisphere, the right one is in the form of a pyramid. The adrenal glands have two independent parts - the cortex and the medulla - and play a primary role in the regulation of endocrine processes.

The adrenal glands produce hormones:

adrenaline and norepinephrine;
cortisol and corticosterone;
aldosterone;
testosterone, estrogen.

The activity of the adrenal glands in producing hormones is regulated by the main endocrine organs - the hypothalamus, pineal gland and pituitary gland. When the concentration of hormones in the body decreases, a corresponding signal is sent to the brain - in response, the pituitary gland releases adrenocorticotropic hormone, under the influence of which the adrenal glands produce hormones.

The role of hormones produced by the adrenal glands is great. They are responsible for:

maintaining optimal metabolism;
establishing water-salt balance;
lipid metabolism;
optimization of the body's immune response;
stabilization of blood pressure;
stimulation of sexual desire, development of secondary sexual characteristics.

Etiology of the disease

The pathogenesis of Addison's disease is based on the development of persistent dysfunction of the adrenal cortex, as a result of which the synthesis of hormones gradually slows down. A failure in the production of hormones occurs against the background of the preservation of the functionality of the pituitary gland and the production of sufficient volumes of adrenocorticotropic hormone. Pathophysiology identifies a group of causes that cause disruption of the endocrine functions of the adrenal glands:

An important factor that increases the likelihood of the disease occurring is tuberculosis damage to the organ. With tuberculosis, not only the adrenal medulla is destroyed, but the entire structure is destroyed. The course of the tuberculosis process negatively affects other organs - the lungs, the esophagus;
adrenal dysfunction caused by surgery to remove an organ;
long-term use of certain medications that can block the production of hormones;
the presence of oncological processes - directly in the adrenal glands or caused by metastasis;
state of immunodeficiency due to HIV infection;
severe systemic infectious and specific diseases - syphilis, amyloidosis, rheumatism;
extensive hemorrhages in the medulla of the organ;
fungal infections (blastomycosis).

Pathophysiology assigns a special role in the development of bronze disease to autoimmune processes in the body. In case of autoimmune damage, adrenal antibodies have a detrimental effect on the organ itself. The process of autoimmune damage has not been fully studied, but it has been established that genetic predisposition plays an important role in the development of bronze disease - Addison's disease is transmitted from parents to children.

Clinical manifestations

Addison's disease has a rich clinical picture, which is due to the negative impact of hormone deficiency on all organ systems. There is a characteristic feature inherent in the pathology - the patient’s skin, as it progresses, acquires a bronze tint, hence Addison’s disease is sometimes called bronze. Changes in the color of the skin and mucous membranes are caused by increased synthesis of adrenocorticotropic and alpha-melanocyst-stimulating hormones. But this symptom is typical for primary forms of the disease; the secondary form of Addison's disease is not accompanied by darkening of the skin.

The variety of clinical manifestations is divided into pathological disorders:

from the skin, mucous membranes;
in the cardiovascular system;
in the reproductive system;
from the gastrointestinal tract;
other systemic disorders.

The cardiovascular system

A disorder in the functioning of the heart and blood vessels is associated with a decrease in the frequency of contractions of the heart muscle, the heart rhythm is upset, and the blood circulation process slows down. Thus, during the course of bronze disease in children, the heart is not fully developed, up to a severe degree of failure. Most people suffering from Addison's disease, due to dysfunction of the heart, look pale, swelling appears in the legs, and the limbs feel cold to the touch.

With hypocortisolism, the rate of transmission of nervous reactions necessary to stimulate contractions of the heart muscle decreases. Persistent arrhythmia occurs against the background of the accumulation of potassium ions in the myocardial tissue with simultaneous active leaching of sodium ions. An imbalance in the ratio of microelements causes disruption of the heart rhythm and a disorder of nerve transmission in third-party organs.

An uncontrolled decrease in blood pressure is another typical sign of pathology. Hypotension develops due to a weakening of the tone of the veins and arteries, a decrease in heart rate and cardiac rhythm. Accelerated excretion of sodium ions with urine leads to dehydration of the body and a drop in blood pressure.

Reproductive system

The adrenal glands produce sex hormones that the body needs for puberty and the appearance of libido. With Addison's disease, the synthesis of estrogen and testosterone decreases, which leads to negative reactions:

Women experience irregularities in the menstrual cycle up to amenorrhea; the skin loses its elasticity; pubic and armpit hair loss; the risk of developing gynecological diseases increases - fibroids, mastopathy, endometriosis;
in men, sexual desire decreases and impotence develops;
Reproductive abilities decrease, up to infertility and miscarriage in women.

Stomach and intestines

Hormone deficiency negatively affects the gastrointestinal tract, leading to a decrease in the secretory functions of the pancreas, stomach, and intestines. With prolonged hormonal deficiency, atrophy of the villi occurs, lining the inner lining of the large and small intestine. As a result, the process of nutrient absorption is completely disrupted. Gastritis, gastric and duodenal ulcers, and pancreatitis develop. The mechanism of disease occurrence is simple - a lack of hormones leads to a lack of protection of the gastrointestinal mucosa from aggressive factors.

In addition to classic gastrointestinal diseases, dyspeptic symptoms appear. Attacks of nausea and vomiting are characteristic of long-term Addison's disease. Stool disorder often occurs in the form of episodic diarrhea. Poor appetite is observed in almost all patients.

Other symptoms

Dehydration occurs due to a lack of the hormone aldosterone. Symptoms of dehydration are noticeable to the naked eye - patients have dry, wrinkled skin, the cheeks sag and fall into the cheek area, the lower eyelids droop, the patient’s face takes on a “martyrdom” expression. The stomach becomes retracted.

Dehydration affects the brain and central nervous system, leading to serious consequences:

muscle weakness develops, limbs may lose sensitivity up to parasthesia and paralysis;
the risk of thrombosis increases due to blood thickening and decreased pumping function of the heart muscle;
oxygen starvation of all organs develops due to sluggish blood circulation and slowing metabolic processes.

With bronze disease, the immune system is negatively affected. The body's natural defenses fall - the patient becomes more susceptible to viral and bacterial diseases. Those suffering from hypocortisolism are twice as likely to be diagnosed with bronchitis, pneumonia, and pneumonia.

As the disease progresses, severe neurological disorders occur. Typical symptoms appear in the form of lethargy, lethargy, and all types of reflexes fade in patients. The long-term course of hypocortisolism leads to persistent depression - interest in the environment is lost, periods of apathy are abruptly replaced by outbreaks of irritability and dissatisfaction with everything. The situation is aggravated by constant fatigue, weakness, and drowsiness.

Addisonian crisis

Addison's disease develops gradually, the clinical picture appears progressively. But in medicine there are cases of sudden appearance of signs of hypocortisolism. In acute adrenal insufficiency, a life-threatening condition occurs - Addisonian crisis. Crises more often develop in patients who are unaware of the presence of the disease, or in the absence of an inadequate dose of hormones as part of replacement therapy.

Crises in bronze disease can occur against the background of acute catarrhal processes, injuries, operations or infectious lesions - adrenal insufficiency sharply worsens and the patient's condition becomes critical. Crises may occur in patients treated with individual doses of corticosteroids. However, with a sudden withdrawal of hormones, a decrease in dosage, or an increase in the body's needs, there is a risk of developing a crisis.

Symptoms of a crisis:

sharp intolerable pain in the lower extremities, back or abdomen;
attacks of nausea combined with uncontrollable vomiting, which leads to dehydration and shock;
lowering blood pressure to critical levels;
severe anxiety, panic, confusion;
a sharp drop in the concentration of sodium ions with simultaneous hyperkalemia and hypercalcemia in the blood;
drop in blood glucose levels;
the appearance of brown plaque in the oral cavity.

The patient's condition during a crisis is severe; without providing urgent medical care by administering increased doses of hormones, death may occur due to increasing dehydration and disruption of the functioning of all vital organ systems.

Course of the disease in childhood

Addison's disease in children is most often diagnosed in primary school and adolescence. There are rare cases of confirmation of pathology in infants and preschoolers. Bronze disease in children in most cases is primary - the mechanism for the formation of adrenal insufficiency is genetically determined and transmitted from parents. The reasons leading to the secondary formation of the disease do not differ from the factors that provoke the development of the disease in adults:

autoimmune disorders;
tuberculosis lesion;
surgical operations on the adrenal glands;
previous catarrhal diseases;
oncology.

The initial signs of the disease in children are associated with defects in appearance and retardation in physical development:

the appearance of “bronze” skin and vitiligo (white spots);
unnatural thinness and haggard appearance;
asthenic syndrome (weakness, impotence);
dizziness and fainting;
gastrointestinal problems - diarrhea, nausea, vomiting, lack of appetite.

Secondary signs develop against the background of long-term hormone deficiency (after 1–3 years of illness):

constant thirst and desire to eat only salty foods;
reduced blood sugar;
amenorrhea in girls, absence of secondary sexual characteristics;
slow blood flow, bluish skin;
seizures;
difficulty swallowing;
depressive syndrome.

The disease in children is difficult, causing a lot of suffering physically and mentally. Children with bronze disease stand out from others - they are characterized by abnormal thinness, an atypical dark skin tone, pallor and weakness, a discrepancy between age and general development, and the impossibility of prolonged exposure to the sun. Therefore, early diagnosis and prescription of replacement therapy are of paramount importance.

Survey tactics

The diagnosis of “hypocortisolism” is established based on the results of laboratory tests and special tests. Instrumental examination methods play a secondary role in establishing the degree of damage to the adrenal glands in long-term illness.

Laboratory research

If adrenal insufficiency is suspected, blood and urine must be tested. Diagnostic tests are also indicative.

A general blood test in those suffering from bronze disease contains a lot of deviations from the normal variant: the hematocrit (the quantitative ratio of leukocytes, red blood cells and plasma) increases; the concentration of hormones (cortisol, aldosterone, testosterone) decreases with an increase in the content of adrenocorticotropic hormone.
Biochemistry will show disturbances in the ionic balance of the blood - a lack of sodium with an excess of potassium.
Urine analysis is informative in terms of studying the concentration of metabolic products of glucocorticoids and testosterone.
Diagnostic tests - with synacthen depot and ACTH - allow you to most reliably determine the level of endocrine disorders. Testing is aimed at identifying the target organ.

Instrumental examination includes:

ECG and EchoCG - to identify the degree of disorders in the cardiovascular system.
CT and MRI - to identify pathological processes in the adrenal glands, heart, nervous and digestive systems; The root cause of Addison's disease depends on the established size of the adrenal glands - with tuberculosis, the organ is enlarged and contains layers of calcium salts, with an autoimmune process the organ shrinks.
X-ray of the cranial bones is necessary when the cause of adrenal insufficiency lies in the pituitary gland or hypothalamus.

After a complete examination, the results are summarized. It is necessary to collect anamnesis, study heredity, and objectively examine the patient. The combination of complaints, external signs and diagnostic data makes it possible to differentiate Addison’s disease from other chronic pathologies and confirm the diagnosis.

Treatment

Timely and adequate treatment can optimize the patient’s condition. Therapy for Addison's disease is complex and includes:

basic treatment by selecting the optimal dose of hormones of synthetic origin (replacement therapy);
symptomatic treatment to relieve disturbing symptoms (pain, gastrointestinal disorders, depression, dehydration);
rational caloric nutrition.

Replacement therapy

Regular intake of synthetic hormones is necessary to maintain a stable condition of the patient. This is due to the fact that vital hormones - aldosterone, cortisol - are not synthesized anywhere except the adrenal glands. Those suffering from bronze disease are prescribed Cortisone as the main drug. Cortisone has long proven positive in the treatment of endocrine dysfunction.

When selecting an individual dose, it is important to consider the following rules:

the prescribed amount of medication should be identical to the level of hormones that is synthesized physiologically in healthy people;
replacement therapy begins with taking low doses (in order to adapt the body), the dosage is gradually increased until an adequate state of the body is achieved;
Hormone-containing drugs are taken on a decreasing basis - the maximum dose is taken in the morning, a reduced dose in the daytime, and a minimum dose in the evening; compliance with the principle is based on the natural activity of the adrenal glands, which are most active in the early morning and passive in the evening;
during Addisonian crises, intravenous or intramuscular infusion of hormones with increasing dosage is indicated.

Removing negative symptoms

Symptomatic treatment includes the prescription of medications to maintain optimal functioning of the body. For prolonged dehydration and electrolyte imbalance, intravenous administration of saline is indicated. A sharp drop in blood sugar requires the introduction of glucose at a 5% concentration.

If the course of hypocortisolism is complicated by the tuberculosis process, special drugs are prescribed - primary and reserve antibiotics (Isoniazid). In this case, the dose is selected by a phthisiatrician, who, together with an endocrinologist, controls the treatment process.

Diet

Diet plays an important role in complex treatment. Patients with hypocopticism need increased caloric nutrition with an optimal balance of proteins, carbohydrates, fats and vitamins. Basic principles of nutrition:

meals are divided into fractions, at least 4–5 meals, a light dinner before bed in the form of protein products (milk) is required to prevent hypoglycemia;
increasing the daily amount of salt consumed to 2 tbsp. l.;
daily consumption of meat and boiled vegetables;
strict limitation in the consumption of foods high in potassium - potatoes in all types, dried fruits, nuts, chocolate;
mandatory consumption of foods containing ascorbic acid and vitamin B in high doses (decoction of rose hips, citrus fruits, brewer's yeast).

Forecast and preventive measures

Patients with hypocortisolism are subject to lifelong observation by an endocrinologist to monitor their general condition, assess the effectiveness of therapy and prevent the development of crises. The supervising doctor keeps records of:

heart rhythm indicators - heart rate, pulse;
blood parameters - ions, coagulability, hematocrit;
weight and loss of appetite;
fasting blood sugar level.

The doctor is obliged to inform the patient about the first manifestations of Addison's crisis to prevent serious complications and sudden death. If you follow the right lifestyle, nutrition and supportive hormone therapy, the average life expectancy does not differ from that of ordinary people.

To prevent crises, persons with Addison's disease must follow a number of preventive measures:

avoid intense physical activity and stressful situations;
Do not cancel or adjust the dose of hormones on your own;
promptly treat infectious and viral diseases.

For general prevention of hypocortisolism, it is important to prevent the development of diseases that negatively affect the adrenal glands - tuberculosis, autoimmune and oncological diseases, fungal and systemic pathologies. At the slightest suspicion of adrenal insufficiency - sudden weight loss, changes in the cardiovascular system, surges in blood pressure - you should consult an endocrinologist.

Addison's disease, despite its progressive chronic course, is not a death sentence. Early detection and long-term supportive treatment allow those suffering from hypocortisolism to live a full life without experiencing discomfort. The main thing is to strictly follow medical recommendations and adhere to a calm, psycho-emotional and healthy lifestyle. When planning children for those suffering from Addison's disease, it makes sense to contact special reproduction centers to identify the risk of transmitting the pathology and minimize it.

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. The most characteristic signs 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 registers (increased concentration of 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 or bronze disease is a pathological lesion of the adrenal cortex. As a result, the secretion of adrenal hormones decreases. Addison's disease can affect both men and women. The main risk group is people in the age group 20–40 years. Addison's disease is characterized as a progressive disease with a severe clinical picture.

Etiology

In Addison's disease, the functioning of the adrenal cortex is disrupted. At this point in medicine there is no exact etiology of the disease. But, as medical practice shows, the following may be provoking factors:

autoimmune damage to the adrenal cortex;
severe infectious and viral diseases (most often);
oncological diseases (cancer tumors);
adrenal insufficiency;
wrong treatment.

As for tumors and insufficiency, such factors are quite rare in medical practice. According to statistics, for the total number of patients, this is no more than 3%.

In 70% of cases, the provoking factor for the development of Addison's disease is a severe infectious or viral disease. Most often it is tuberculosis.

Addison's disease (bronze disease) is characterized by a fairly rapid development. The initial stage quickly becomes chronic and relapse cannot be ruled out. Depending on the degree of damage and developmental characteristics, primary and secondary forms are distinguished.

Pathogenesis

The above etiological factors lead to complete or partial atrophy of the adrenal cortex. As a result, the production of necessary hormones - corticosteroid and aldosterone - sharply decreases. As a consequence of this, ailments of the gastrointestinal tract, cardiovascular system and general disruptions in the functioning of the body can occur.

General symptoms

Since the hormones produced by the adrenal cortex affect the body's metabolism, the symptoms of the disease are quite varied. This is what makes diagnosis somewhat difficult. It is quite difficult to make a diagnosis even preliminary based on symptoms alone.

In the first stages of the development of Addison's disease, the following symptoms are observed:

skin is pale, dry;
the skin on the hands loses elasticity;
low blood pressure;
disturbances in the functioning of the heart;
gastrointestinal diseases develop;
neurological disorders.

There are also more specific symptoms in women and men.

In men, insufficient testosterone production affects intimate life. Sexual desire is significantly reduced. In some cases it is possible.

In women, symptoms are more pronounced:

menstruation stops;
hair growth stops in the pubic area and armpits.

It is worth noting that such symptoms in women (especially with regard to the menstrual cycle) may indicate other disorders of the genitourinary system. Therefore, you need to contact a competent specialist for an accurate diagnosis.

From the gastrointestinal tract, not only symptoms in the form of diarrhea and nausea can be observed, but also the occurrence of other underlying diseases. Most often these are the following ailments:

In addition to the above symptoms, the patient may have changes in the functioning of the central nervous system. This is due to the fact that with Addison's disease, the water-salt balance is disturbed and dehydration occurs. As a result, the following clinical picture is observed:

numbness of the fingertips, sensitivity worsens;
numbness of legs and arms;
muscle weakness;
reflexes worsen.

At the same time, the appearance of the sick person also changes - he looks very tired.

The manifestation of such a clinical picture depends on the general condition of the patient and the degree of development of Addison's disease.

Diagnostics

Diagnosis of suspected Addison's disease is carried out through laboratory and instrumental tests. The history and general condition of the patient and his lifestyle are also taken into account.

Diagnosis through laboratory tests includes the following:

test samples for hormone production.

Instrumental diagnostic methods in this case are as follows:

Only based on the results of a comprehensive diagnosis can a doctor confirm or refute the diagnosis.

Treatment

If Addison's disease is diagnosed at an early stage, treatment will not only significantly improve the patient's condition, but also avoid serious complications.

In addition to drug treatment, the patient should adhere to a special diet. The main course of treatment is replacement therapy. In view of this, drugs with the following spectrum of action are prescribed:

glucocorticosteroids;
mineralocorticosteroids.

The treatment program also provides for the restoration of water-salt balance. To do this, the patient is injected intravenously with a saline solution of sodium chloride. If there is a low level of glucose in the blood, then a 5% glucose solution is prescribed intravenously.

The dosage and procedure for taking medications is prescribed only by the attending physician. Self-medication is unacceptable.

If the disease is caused by an underlying infectious disease, then the course of treatment includes drugs to eliminate it. In this case, the endocrinologist carries out treatment together with a phthisiatrician or infectious disease specialist.

Diet

In addition to drug treatment, you need to adhere to a special diet. Foods rich in potassium should be eliminated or minimized.

The patient’s daily diet should contain the following products:

apples, citrus fruits;
food with B vitamins (liver, carrots, egg yolk);
foods that are rich in minerals, fats, carbohydrates.

Alcohol is completely excluded. In the patient’s body, it is very important to maintain optimal metabolism and prevent weight loss (if there is no excess weight).

Such complex treatment will significantly improve the patient’s condition, relieve symptoms and prevent the development of complications.

Possible complications

Most often, patients may develop another underlying disease. Most often this is chronic insufficiency of the adrenal cortex. It is worth noting that the secondary form of this disease can also occur outside of Addison's disease.

Chronic adrenal insufficiency is very similar in symptoms to bronze disease:

craving for salty foods (due to a violation of the water-salt balance);
disturbances in the gastrointestinal tract;
apathy, irritability;
impaired memory, concentration;
sudden weight loss.

Diagnosis is carried out through laboratory and instrumental tests:

general blood and urine analysis;
blood chemistry;
hormonal tests;

Based on the results obtained, the endocrinologist prescribes treatment.

Forecast

With timely treatment, the disease proceeds without significant complications and does not affect life expectancy. Patients with this disease are strictly prohibited from physical and emotional stress.

Prevention

Preventive measures are aimed at generally strengthening the immune system and preventing infectious and viral diseases.

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Diseases with similar symptoms:

Diabetes mellitus is a chronic disease in which the functioning of the endocrine system is affected. Diabetes mellitus, the symptoms of which are based on a prolonged increase in the concentration of glucose in the blood and on the processes accompanying an altered state of metabolism, develops in particular due to a deficiency of insulin, a hormone produced by the pancreas, due to which the body regulates the processing of glucose in the tissues of the body and in his cells.