Addison disease (bronze disease). Addison disease or "bronze" disease bronze disease hormone

Addison's disease is a rare disease of the endocrine system, which lies in the loss of the ability to produce adrenal hormones in sufficient quantity.

First of all, the amount of cortisol produced is reduced. Addison disease is also known as "Bronze Disease".

Such a name occurred due to hyperpigmentation of body sites opened by the sunshine.

What is this disease and why Addison? Addison disease is, which is provoked by the understated indicators of a certain secret, which produces an adrenal gland.

Similar insufficiency may have primary and secondary character.

Insufficiency of the primary type

Insufficiency of primary adrenal glands was determined as a separate disease. The described violation was named after a person who posted the beginning of his research - Addison disease.

Such a form is formed due to the fact that the bark of adrenalities is damaged. After damage and changes in the adrenal structure, it becomes more incapable to the production of cortisol (F-compound 17-hydrocortisone) and, often - aldesterone, in normal amounts.

Failure deficiency

The insufficiency of the adrenalities of a secondary nature is formed under the condition of violation of the amount of adrenocorticotropin produced by the secret.

ACTH is produced by a pituitary gland and is responsible for stimulating the system for producing cortisol adrenal glands.

In the case when adrenocorticotropin is synthesized too slowly, blood indicators are rapidly falling.

With a long lack of regulating ACT, the gland may not lose the possibilities for the production of secrecy.

Secondary insufficiency is more frequent violation of the secretion of hormones than Addison disease.

Changes occurring in the body

Addison's disease is characterized by dysfunction of not the entire volume of gland tissues, and for the most part of the violations of the adrenal cortex.

Changes concern both functions such as mineralocorticoid and gluchorticoid. The first manifestations of Addison's disease are manifested only in cases where disorders arise by more than 90% of adrenal tissues from two sides.

Features of the illness Addison

According to international information, Addison's disease has a frequency of emergence equal to 1 person per 100,000 each of the age categories.

The number of registered clinical cases between women and men is approximately equal.

Thus, it makes sense to talk about the fact that it does not have a clear severity on sexual sign. Also identified dependence according to the racial affiliation of patients.

There is a so-called idiopathic form of a disease that does not have visible reasons.

Such syndrome often occurs in children and women. The age framework of the idiopathic form of syndrome in adults is a period of 30 to 50 years.

The main reasons according to which the syndrome leads to a fatal outcome, are:

1. Involvedly established diagnosis or delivered erroneously.
2. Invalid calculation of the required dosage of mineralocorticoid and glucocorticoid hormones.
3. Acute Addison Crisis, which was not in a timely manner.
4. Hidden course of the disease and a suddenly developed threatening symptomatic life.

Even with the truth of the diagnosis and its timely establishment, adequate therapy for the risks of death is two times higher than the average.

Diseases of the cardiovascular system, malignant neoplasms and viral diseases may also contribute to an increase in the risks of fatal outcome.

How exactly progresses the disease?

Patients who have the described disease can feel different manifestations. In the primary failure of the adrenal glands there is a dependence on the duration of the flow and its gravity.

At the initial stage, when Addison's disease is not yet running, symptoms do not seem threatening.
Provocates the beginning of the progress of pathology, its manifestation in most registered clinical cases is stressful factors:

• virus disease;
• injuries;
• medical surgery of surgical nature;
• steroid overdose.

The first symptoms of the Addison Disease, which at this stage fully justifies one of its own names - "Bronze Disease", as follows:

1. Hyperpigmentation of body cover - leather and mucous membranes change their own shade on the bronze. Skin color is changed earlier than any additional symptoms arise - the so-called "Addison Melasms".
2. Sometimes hyperpigmentation is not clearly pronounced - it is explained in a timely manner identified violation and the right assigned therapy.
3. Along with hyperpigmentation and in conjunction with it, the manifestations of vitiligo - the complete absence of a pigment of the skin may be present. It is most often manifested in the idiopathic form of the disease.
4. Almost all patients feel the increased level of fatigue, dizziness, overall progressive weakness, soreness of the joints and muscles, weakening appetite against the background of a sharp decrease in body weight.
5. The main gastroenterological manifestations are in the attacks of nausea, urges towards vomiting and diarrhea.
6. In men, there is a fuss of libido and signs of impotence arise. Menstruation failures occur in women.

Occasionally, adrenal insufficiency manifests itself extremely acute - Addison crisis.

The acute beginning of pathology is characterized by the following symptomatics:

• confusion of consciousness;
• vascular collapse, rapidly expanding vessels and a decrease in blood pressure indicators;
• the body temperature sharply reaches 40 ° C and higher;
• comatous states can be provoked;
• cutting pain in the abdomen.

When the sharp beginning is accompanied by opened hemorrhage into adrenal glands, collapse is provoked - strong nausea without changing the body temperature in a large side and sharp pain in the side and abdomen.

Root causes provoking this endocrine disease

About 80% of clinical cases are provoked by the gradual degradation of adrenal cortex, which is an outer cover of adrenal glands.

Destruction occurs due to the effect of antibodies of the body's immune system. In case of autoimmune diseases, the intrinsic antibodies of the body begin the systematic attack of cells and tissues, which is inevitably destroying them.

Sometimes damage concerns not exclusively adrenal glands, but also of other glands. In such a development, polyvory failure arises and progresses.

Polyvory insufficiency

Polyvory failure, otherwise, is divided into two types.

The type of first refers to hereditary diseases that arise due to violations of the genetics of one of the parents.
In addition to adrenal failure, the following symptoms may appear:

• slowness of the process of sexual formation;
• severe and malignant anemia;
• the inactivity of glands producing hormones-regulators of phosphate exchange (and calcium);
• candidiasis chronic or other fungal lesions;
• liver pathology, often hepatitis.

The second type of occasionally is referred to as Schmidt syndrome and manifests itself, for the most part, in people of young people.
They are characterized by the following list of symptomatic manifestations:

1. The passivity of the thyroid gland, which is responsible for the development of the secret regulating the organism metabolic processes.
2. Sexual development slowed down, as at the first type.
3. There may be symptoms of diabetes, or directly diabetes.
4. Skin covers in separate sites are completely devoid of pigment - vitiligo.

Scientists are inclined to the fact that the second type is also hereditary in nature, as several blood relatives suffer from him quite often.

Tuberculosis and other factors

About 20% of clinical cases of the occurrence of Addison's disease is provoked by tuberculosis, since tuberculosis mycobacteria violate the integrity of the adrenal glands.

During the description of the disease in 1849, Dr. Thomas Addison Tuberculosis performed the main reason for the provocateur of adrenal insufficiency in humans.

After the methods of effective combating mycobacterial infection have been developed, tuberculosis has ceased to be considered the main source of primary insufficient insufficiency.

Other reasons that can potentially become provocatives of Addison Diseases, the following triggers are:

• chronic viral diseases, often - fungal;
• malignation processes and the formation of cancer cells;
• excessive reproduction of proteins by the organism - amyloidosis;
• surgical interventions aimed at excision of adrenal glands;
• deviations of genetic nature, which include anomalies for the formation of adrenal glands;
• immunity to the ACST produced;
• hemorrhage into adrenal glands;
• secretion of inactive hormones.

The indicated causes account for an extremely small number of cases of Addison's disease. Therefore, it is extremely difficult.

Tactics used in diagnosis

Addison's disease, the diagnosis of which is produced in the early stages, is extremely difficult to identify.

An exclusively close and comprehensive consideration by the medical specialist of the patient's history and symptoms described by them can contribute to the appearance of suspicion at the doctor's disease.

Like the adrenal insufficiency syndrome, confirm the preliminary diagnosis and approve its truth in the illness of Addison can only after a series of surrendered analyzes and a certain spectrum of research.

The purpose of the tests conducted is to determine the insufficiency of the level of cortisol. The following is the search for true root cause.

The most effective methodology for clarifying the diagnosis is the radiological examination of the pituitary area and adrenal glands.

Emergency diagnosis

With the suspicions of adrenal insufficiency during the prescription crime, doctors need to produce intravenous administration of glucose-containing and saline solutions with an admixture of glucocorticoid hormones.

If it is impossible to make a diagnosis to the introduction of glucocorticoids, blood sample is closed on cortisol and ACTG indicators. Crisis is determined according to the following laboratory response:

• understated sodium indicators;
• reduced glucose content;
• hurried potassium level.

After the patient's condition stabilizes, an ATG test is performed.

Other studies

When the diagnosis was determined, an ultrasound and radiological study of the peritoness are required. The main factors of the presence of the illness of Addison are the immutability of the structure of adrenal glands and calcium deposits.

Calcifications may occur after hemorrhages, or - with adrenal tuberculosis.

As additional studies are manufactured:

• skin tuberculin test;
• check on the autoimmune blood antibodies.

As diagnostic measures in the secondary insufficiency of adrenal glands, comprehensive techniques of hardware analysis of parameters and the structure of the damaged organ are produced.

The main postulates of treatment

The adrenal insufficiency is treated when using compensating the lack of hormones therapy.

Cortisol is replaced with a synthesized analogue - glucocorticoid. The most commonly applied the following glucocorticoid preparations:

• Dexamethasone;
• Hydrocortisone;
• Prednisolone.

These drugs are applied throughout the day several times. At the same time, in addition to drug therapy, patients are encouraged to adhere to a certain diet.

Therapeutic diet is based on the preparation of a daily diet, which contains nutrient components and nutrients needed for the patient's body.

The main principles of the formation of the menu is the presence of the following components:

1. The content of fats, carbohydrates, proteins, vitamins (C, B - especially) should be optimal. Recommended for currant consumption black, decoction of rosehip.
2. Sol.and it should be extremely high - the daily rate is 20 grams.
3. Daily diet Must contain as little bean, potatoes, caffery-containing products and mushrooms as possible.
4. Eating meat productsFish and vegetables are allowed only in boiled or baked version.
5. Food is fractionalAnd before going to bed, you should refrain from solid food. The preferred product before bedtime is milk.

Subject to adequate therapy, Addison's disease forecast is favorable.

The life expectancy of patients with adrenal insufficiency is practically no different from the norm and close to the indicators of healthy people.

Addison's disease (hypocorticism, bronze disease) is a rare disease of the endocrine system, in which the secretion of hormones (primarily, cortisol) of the adrenal cortex decreases.

The disease was first described in 1855 by the British physician Thomas Addison. It is with the same frequency of men and women; More often diagnosed in people of young and middle age.

Causes and risk factors

The development of addison's disease leads to damage to the cells of the adrenal cortex or pituitary, caused by various pathological conditions and diseases:

• autoimmune defeat of adrenal cortex;
• adrenal tuberculosis;
• removal of adrenal glands;
• hemorrhages in adrenal tissue;
• adrenoleykodistrophy;
• sarcoidosis;
• long-term substitution hormone therapy;
• fungal infections;
• syphilis;
• amyloidosis;
• AIDS;
• tumors;
• irradiation.

Around 70% of cases, the cause of Addison's disease is an autoimmune lesion of adrenal cortex. Due to various reasons, the immune system fails, and it begins to recognize adrenal cells as alien. As a result, antibodies are produced, attacking adrenal kour and damaging it.

Addison Syndrome accompanies a number of hereditary pathologies.

Forms of the disease

Depending on the cause of the disease Addison happens:

1. Primary. Due to insufficient functioning or damage directly to the adrenal cortex.
2. Secondary. The front proportion of the pituitary is secreted by an insufficient amount of adrenocorticotropic hormone, which leads to a decrease in the secretion of hormones with adrenal cortex.
3. Yatrogenic. The long-lasting intake of corticosteroid drugs entails adrenal atrophy, in addition, disrupts the relationship between the hypothalamus, the pituitary gland and adrenal glands.

Addison's disease with the same frequency affects men and women; More often diagnosed in people of young and middle age.

Symptoms

Addison's disease has the following manifestations:

• darkening of skin and mucous membranes;
• muscle weakness;
• hypotension;
• ortostatic collaps (a sharp decrease in blood pressure when changing the position);
• decline in appetite, weight loss;
• thrust to acidic and (or) salted food;
• increased thirst;
• abdominal pain, nausea, vomiting, diarrhea;
• dysphagia;
• tremor hands and head;
• parrestzia limbs;
• tetany;
• polyuria (increased urine release), dehydration, hypovolemia;
• tachycardia;
• irritability, hot temper, depression;
• violations of sexual function (cessation of menstruation in women, impotence in men).

In the blood, the decrease in the level of glucose and eosinophilia is determined.

The clinical picture develops slowly. Over the years, the symptoms are expressed weakly and can remain unrecognized, attracting attention only when against the background of stress or any other disease there is an addisonic crisis. This is an acute state for which it is characteristic:

• sharp drop in blood pressure;
• vomiting, diarrhea;
• sudden acute pain in the abdomen, lower back and lower limbs;
• confused or acute psychosis;
• fainting due to a sharp decline in blood pressure.

The most dangerous complication of Addison's illness is the development of an addisonic crisis - a state of threatening life.

With addisonic crime, a pronounced violation of the electrolyte balance arises, in which the sodium content in sodium is significantly reduced, and phosphorus, calcium and potassium increases. The level of glucose is also sharply reduced.

Diagnostics

The diagnosis is assumed on the basis of the study of the clinical picture. For its confirmation, a number of laboratory research is carried out:

• stimulation test with ACTH;
• determining the level of ACTH in the blood;
• determining the level of cortisol in the blood;
• determining the level of electrolytes in the blood.

Treatment

The main method of treating the illness of Addison is a lifelong replacement hormone therapy, that is, the reception of drugs that replace hormones produced by the adrenal cortex.

To prevent the development of an addisonic crime against the background of infectious disease, injury or upcoming surgery, the dosage of hormonal drugs should be revised by an endocrinologist.

With adequate replacement hormone therapy, the life expectancy of patients is the same as in people who do not suffer from this disease.

In the case of an addisonic crisis, the patient needs emergency hospitalization into the separation of endocrinology, and in serious condition - in the separation of resuscitation and intensive therapy. Crisis stop, introducing intravenous hormones of adrenal cortex. In addition, the correction of the existing disorders of the water and electrolyte balance and hypoglycemia is carried out.

Possible complications and consequences

The most dangerous complication of Addison's illness is the development of an addisonic crisis - a state of threatening life.

The reasons for its occurrence may be:

• stress (surgical intervention, emotional overvoltage, injury, acute infectious diseases);
• removal of both adrenal glands without adequate replacement hormone therapy;
• bilateral thrombosis of adrenal veins;
• bilateral embolism of adrenal arteries;
• bilateral hemorrhage in adrenal fabrics.

Forecast

Forecast for Addison's disease is favorable. With adequate replacement hormone therapy, the life expectancy of patients is the same as in people who do not suffer from this disease.

Prevention

Addison's prevention measures include preventing all those states that lead to its development. Specific prevention measures do not exist.

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Addison disease (synonym Bronze disease) is a clinical syndrome caused by chronic insufficiency of adrenal cortex. The causes of insufficiency of adrenal cortex are most often, primary adrenal glands, tumors of adrenal cortex, treatment with cytostatic means (myelosan, derivatives of Iprit). At the heart of the pathogenesis of symptoms at Addison Disease lies a decrease in Cortizon and Aldosterone products. With a disadvantage of the first bind disorders of the gastrointestinal tract, cardiovascular disorders, low blood sugar levels of an empty stomach; With a second deficit - impaired saline exchange, dehydration ,.

The development of the disease is gradual. At first, weakness appear, fast fatigue, weight loss. Then join the symptoms of the disorder function of the digestive tract: the complete absence, alternating, with time, severe abdominal pain. Arterial pressure is significantly reduced. Develops. The most vivid symptom of the disease is the bronze skin painting, depending on the accumulation of the pigment in it (Fig. 1). It appears to a greater degree in places, not covered with clothing (face, neck, hand brushes). Pigmented on the nature of the place (nipples of the mammary glands, anal folds) stain stronger. It also applies to mucous membranes (soft, mucous membrane of the cheek).

Characteristic for Addison Disease Low sodium content and chlorides in the blood, as well as sugar on an empty stomach and increased content. The course of the disease is chronic. Complications - suddenly or attended the advancing attacks of adrenal insufficiency, sometimes leading to a coma (see). Significantly improved due to the use of modern and hormonal means.

Treatment. Therapy is anti-tuberculosis (,) and hormonal (, deoxyactorosterone acetate intramuscularly, curtains subcutaneously or intramuscularly).

Treatment of adrenal coma - see coma. The nutrition of the patient by Addison disease should be varied, food must contain a large amount of sodium chloride and a small number of potassium salts; Vitamins are prescribed in large doses, especially (0.4-0.6 g per day). It is recommended to maximize peace; The work associated with significant neuropsychic and physical tension is contraindicated. Hospitalization is shown in the primary identification of Addison disease, with severe forms of the disease with a tendency to crisis.

Addison disease (synonyms: hypocorticalism, bronze disease, hypocorticism) - chronic lack of adrenal cortex.

Addison disease occurs as a result of the primary decrease in the function of the cortical layer of adrenal glands or the regulation of the adrenal cortex, which ultimately leads to the fallout of their function. Named by the name of the English dermatologist and the pathoanate of Thomas Addison (1793-1860), which described this disease in 1855 and the occurrence of the disease with the defeat of the adrenal glands. It is observed equally often in men and women usually aged 30 to 50 years old, less often in children and old people.

Etiology. Most often, the disease causes tuberculosis (in 80% of cases) and a diancephaal-pituitary lesion of adrenal glands. Much less often the causes of the disease are toxicosis of adrenal glands in infectious diseases, amyloidosis, adrenal tumors or tumor metastases in adrenal glands, syphilis, hemochromatosis, sclerodermia.

Tuberculosis of adrenal glands usually occurs as a result of hematogenic metastasis. For the occurrence of clinical signs of Addison disease, it is necessary that at least 90% of the substance of the cortical layer of the adrenal glands may be destroyed, therefore the beginning of the disease is difficult to recognize.

Pathogenesis. The disease is a sharp decrease in the products of the hormones of the adrenal cortex. Corticosteroid products decreases. The lack of mineralocorticoids causes a violation of the electrolyte equilibrium (increasing the release of sodium urine and chlorine, lowering their blood content: lowering the selection of potassium urine, increase it in the blood), dehydration, hypotension. Violation of the production of glycocorticosteroids leads to a drop in blood sugar, increased sensitivity to insulin, inclinations to spontaneous hypoglycemias, increase the number of lymphocytes and eosinophils in the blood and maintaining their amount in the blood after the introduction of ACTH.

The selection of 17-ketosteroids and 17-hydrooxysteroids decreases. ACTH products are disturbed - the number of basophilic cells is reduced in the front share of the pituitary.

Pathological anatomy. There is an increase in melanin in a malpigayy skin layer, atrophy fat, muscles, myocardials, tubules, stomach ulceration, bilateral atrophy of the cortical layer of adrenal glands. The number of the basophilic cells of the front lobe of the pituitary is reduced.

Complaints. Complained complaints of strong fatigue and weakness, poor well-being. Fatigue is celebrated in the morning and intensifying in the evening. Often, the patient's attention is attracted to the darkness of the skin, which is often regarded as the result of solar irradiation. A significant weight loss is combined with the lack of appetite, while with thyrotoxicosis and diabetes mellitus, the appetite is saved or even enhanced.

Signs. Melanomium lies in brown color of the skin of various shades: golden-brown, dirty-brown, earthy, lemon yellow. Pigmentation is most expressed in places of natural pigmentation exposed to sunlight or intensive friction. Darken finger bends, palm furrows, the back of the brushes and stop; On the gums, lips, mucous cheeks, in the area of \u200b\u200bthe rear pass and external genital bodies, the smoky-blue color in the form of spots acquires the smoke-blue color in the form of spots. Often dark hair patients.

Melanomium is not obligatory at Addison Disease.

Patients lose weight up to 10-15 kg, which is connected not so much with
tuberculosis (in the case of specific origin of the disease), as with dehydration, destruction of muscle tissue as a result of the violation of the exchange of creatine and creatinine, the absence of appetite and disruption of digestion.

Heart sizes are reduced, which is often visible when x-ray. The backup power of the heart decreases. Even after a minor physical tension, shortness of breath and tachycardia occur, although it rarely arises severe heart failure as a result. When X-ray study, occasionally can be detected by the ordinary manners.

On the electrocardiogram, a decrease in the voltage is detected due to diffuse myocardial damage, the distance PQ and ST are extended, the ST of the ST interval is observed.

Teeth T are compacted or becomes negative in all leads. There may be atrial or ventricular extrasystole.

For the disease, hypotension is characterized. Systolic pressure from 100 to 80 mm Hg. Art., and diastolic 70-40 mm Hg. Art.

If the patient earlier was hypertensive, blood pressure is normal or slightly elevated, but in the future it gradually decreases. In the emotional excitation of hypotension can be changed by hypertension. Orthodatic hypotension is observed. At the same time there are dizziness, tachycardia, stupid pain in the heart area and a faint condition.

Due to the fact that the tuberculosis of the adrenal glands does not exist, it is necessary to search for the primary hearth tuberculosis. Often detects the ulcer of the stomach and duodenum. In addition to anorexia, meteorism, diarrhea, ahilia, pain in the go of the intestine are noted.

Patients are sensitive to cold and painful irritation, their resistance to infections, various adverse effects, is reduced. Body temperature is often lowered. Sexual function is most often dropped.

Early sign of the disease is a sharp asthenia, which is often preceded. Patients become apathetic, forgetful, unable to concentrate their thoughts, act. Violated sleep rhythm, sometimes the state of psychosis with disorientation and hallucinations is developing.

Flow. Addison disease is a chronically occurring disease, which begins to be sophisticated. It is often about the same disease of the disease without a noticeable deterioration or with a minor deterioration.

It is noted that the disease occurs easier when the part of the adrenal cortex is maintained. Addison disease occurs more hard with tuberculosis and adrenal tumors.

The division of the disease on the melanodermic, astheno-adamic, hypotonic, gastrointestinal, cardiovascular types on the predominance of signs is very conditional, since with the Addison Disease, the isolated damage to any system is not observed.

It is more expedient to the division of the disease according to the general condition of the patient and the severity of signs on the shape of light, moderate gravity and severe, non-separated from each other with clear boundaries.

With a light form of illness to achieve good well-being, there is enough changes of the diet (adding a cooking salt and ascorbic acid and potassium limitations).

With the disease of the average gravity, which occurs most often, it is necessary to use cortisone, hydrocortisone, prednisone, prednisone, and with severe forms, it is necessary to constantly maintain a satisfactory condition of the patient with said hormones and deoxyticosterone-acetate. In this form, the course of the disease is complicated.

Laboratory data. Mix hyponatremia, hypochloremia and hypercalemia. Isolation of sodium and chlorine with urine increased, and potassium lowered. The organism of patients with Adddison disease loses the ability to quickly release the injected fluid (Robinson - Power - Kepler).

Blood sugar is reduced due to a decrease in glyconegenesis. Glycemic curve flat. With a worsening of the disease, the sugar curve is becoming more flat, and even if it seems normal, it is returned to the norm not after 2, but only after 3-4 hours.

There is an increased insulin sensitivity, but insulin load is not recommended due to the risk of heavy hypoglycemia. The main exchange is reduced by no more than 20%.

Creatinuria with the disease reflects the destruction of muscle fibers. Blood creatine is increased. The number of blood albumines is reduced, the albumin-globulin coefficient is reduced accordingly. The number of erythrocytes (up to 3 million) and hemoglobin decreases. Due to the hyperplasia of lymphoid tissue, relative lymphocytosis is observed. Roe slowed down. The absolute amount of eosinophils increases, which does not decrease and when the ACTH is introduced (Torn). In a healthy person, the introduction of ACTH causes an increase in creatinine, and this is not observed during Addison Disease.

The amount of 11-oxycisterans drops. The technique with the use of formaldehydogen in the disease gives 30 in 11-oxycisterans per day (norm 300-800 y), and the use of reducing techniques gives 120 y (norm 240 y).

If the patient corticoids are allocated normally, then their number does not increase under the action of ACTH.

Aldosterone and 17-ketosteroids decreases. If the selection of steroids increases after the introduction of ACTH, then the lack of adrenal glands is associated with the front fraction of the pituitary gland, but if the release does not change after the introduction of ACTH, then we are talking about the primary insufficiency of the adrenal cortex.

Worsen renal function. Reducing blood pressure up to 50 mm Hg. Art. Accompanied by Anuria, and before that the clearance of creatine, urea and inulin is reduced.

Diagnosis and Differential Diagnosis. The diagnosis of Addison Disease is made on the basis of the characteristic clinical signs - adamis, melanomy, hypotension, hypoglycemia, weight loss, disorders from the digestive tract and laboratory data. In order to cause a hidden melanomy, mustard pieces are put on the skin. The disease is distinguished from thyrotoxicosis, in which adynamia may be, weight loss, pigmentation. However, with Addison disease, weight loss is accompanied by a decrease in appetite, and with thyrotoxicosis, the appetite is increased.

In contrast to the hypothyroidism, in which weakness is also noted, a decrease in the main exchange and release of 17-ketosteroids, a flat sugar curve, with addison disease there is no mucous edema, dry skin, kettle sample is positive, there is melanodermia.

The uterine stains of pregnancy in contrast to pigmentation under Addison disease are located on the forehead, around the mouth and eye, and not on the mucous cover and in places exposed to mechanical irritation.

Differentiate Addison disease with a number of states and diseases accompanied by pigmentation of skin and mucous covers. With racial and national pigmentation there are no other signs of Addison disease, unevenness of melanomy, bluish pigment spots on the mucous membrane.

Solar tan with fatigue and hypotension is recognized on the basis of the history and laboratory data.

With a malignant melanoma, pigmentation unlike Addison disease is heterogeneous, located in the form of "black freckles", and melanin is found in the urine.

From Addison Disease Melanose Rile, manifested in merging spots on the skin of the face, neck, chest, back, is distinguished by the absence of adamisia, hypotension, hypoglycemia.

With sclerodermia, abdominal tumors, malaria, chronic renal failure, melanomy is also observed. With these diseases, the functional study of the adrenal cortex makes it possible to reject the diagnosis of Addison disease.

With arsenic poisoning on the gums, dark spots appear, combined with hyperkeratosis of palms and soles; Similar stains on the gums are noted in pioneering lead, bismuth, mercury, nitric acid silver.

At Pellagra, there is a darkening of the stop, brushes and nearby parts of the limbs. Diarrhea and dementia testify against Addison Disease.

Pigmentation can also cause multiple X-ray irradiation of the skin; Pigment cirrhosis of the liver, in which the liver is increasing and its function is disturbed; Malignant anemia at which the composition of the red blood changes and increases the color indicator.

Hemochromatosis differs from Addison Disease with accumulation in the skin of iron-containing hemosidere and hemopuscin pigments. The diagnosis of hemochromatosis is often based on the presence of ascite and "bronze" diabetes patients.

The development of adamisia, weight loss, the falling of blood pressure without pigmentation can be observed in a sharp supply of nutrition as a result of chronic infections of non-propellate localization (for example, with a kidney tuberculosis).

With neurality, an increased irritability is noted, fast mental and physical fatigue and hypotension, but orthostatic hypotension is not observed, the kettle sample is negative, and 17-ketosteroids remain normal.

During myasthenia, which occurs with increased fatigue, functional adrenal tests are negative.

When jade with loss of salt, mineralocorticoids lose the opportunity to influence the channel epithelium of the kidneys, and the result of which the body loses many sodium and chlorine. The introduction of the docta in this case does not bring relief, which occurs only after receiving large quantities of the table salt.

Treatment. Bed regime. A diet is appointed, poor potassium (without peas, canned, potatoes, dry fruits, meat, caviar). Give 10 g of cook salt per day, in the form of Elixir Addison with 5 g sodium citrate in a liter of water with fruit juice.

When edema appear, the amount of salt should be reduced. DOCCES is introduced at 5-10 mg in the muscles once a day or in the form of tablets subcutaneously at 25-50 mg (for 2-3 months), so that 0.3 mg is absorbed per day.

Cortisone gives 12.5-25 mg 2-3 times a day, vitamin C - 300-500 mg per day.

With crises, coma and collapse, cortisone is 100 mg after 12 hours, doxa - up to 15 mg, camphor, caffeine, Cordiamine, adrenaline. It is necessary to overflow hypertensive solutions, to give abundant drink, to introduce streptomycin 0.5-1.0 g per day (rate 50 g), futvazide, PASK, even if there is a suspicion of adrenal tuberculosis.

Adrenal transplant or their bark is ineffective.

Addison's disease has another name - bronze disease. Under this implies a violation of adrenal functioning. In turn, it disrupts the hormonal balance, as a result, the synthesis of glucocorticoids is reduced or completely disappears.

Addison-Birmer's disease has a large number of symptoms that mainly arise due to the defeat of most of the crust. The reason for the occurrence of this disease can be different. In 8 out of 10 cases, Addison-Birmer disease develops due to an autoimmune process in the body.

But sometimes the disease can be accompanied by tuberculosis, which influence the adrenal glands. Pathology can be inherited and transmitted by inheritance. An autoimmune type of disease is most often found in the female half of the population.

The most common symptoms of Addison's disease are painful sensations, disorders in the functioning of the gastrointestinal tract and hypotension. Pathology can lead to disorders in metabolism. Such a disease can be treated and with the help of traditional medicine, which will strengthen the work of the adrenal glands, and will also help in the fight against microbes and inflammation.

General characteristics of the disease

Addison's disease, whose photo shows the lesion area, can be both primary and secondary failure. As many know, pathology is striking the urban secretion gland responsible for the production of one of the most important hormones in the human body. These organs have 2 zones:

• crust;
• brain substance.

Each zone is responsible for the synthesis of different types of hormones. In the cerebral substance is the production of norepinephrine and adrenaline. They are especially necessary for a person in a stressful situation, these hormones will help to use all reserves of the body.

And other hormones are synthesized in the cortical substance.

• Corticosterone. It is necessary for the balance of water and salt metabolism in the body, and is also responsible for the regulation of electrolytes in blood cells.
• Deoxikorticosterone. Its synthesis is also required for water-salt metabolism, besides, it affects the efficiency and duration of the use of muscles.
• Cortisol is responsible for regulating carbon exchanges, as well as to generate energy resources.

A great influence on adrenal cortical substance has a pituitary gland, it is iron that is located in the brain area. The pituitary glands produces a special hormone that stimulates the work of the adrenal glands.

As mentioned above, Addison-Birmer's disease has two types. Primary this is the very disease when the work of the adrenal glands is completely violated due to negative factors. Secondary implies a decrease in the number of the synthesized ACTG, which, in turn, worsens the work of the internal secretion glands. In that situation, when the hypophysis produces an insufficient number of hormones a long period - dystrophic processes in the cortical substance of adrenal glands can begin to develop.

Causes of disease

The primary form of the illness of Addison-Burmer is quite rare. It can be found in both men and a woman with the same share of probability. In most cases, the diagnosis is made by people whose age is from 30 to 50.

There is a chronic form of the disease. Such a development of pathology is possible with various negative processes. Almost in all cases, namely, in 80%, the cause of the occurrence of Addison-Burmer's disease is the autoimmune state of the body. In 1 out of 10 cases, the cause of pathology is the defeat of the screw substance of the adrenal glands of the infectious disease, for example, tuberculosis.

For the remaining 10% patients, the causes of occurrence may have a different character:

• this can affect the long-term reception of drugs, in particular, glucocorticoids;
• varieties of fungal infection;
• injury to the internal secretion gland;
• amyloidosis;
• tumors of both benign and malignant;
• bacterial infections with a weakened immune system of a person;
• pituitary dysfunction;
• genetic predisposition to the disease.

Because of the Addison Disease, other syndromes may also develop, for example, adrenal crisis, which occurs at a low concentration of adrenal hormones.

There are the most likely causes of crisis:

• severe stressful condition;
• disorders in the dosage in the preparation of the course of treatment with hormonal drugs;
• aggravate the disease can infectious damage to the screw of the adrenal glands;
• injury injury;
• disorders in blood circulation, such as blood clots.

Symptomatics of the disease

The symptoms of Addison's disease directly depend on the impairment of the synthesis of some types of hormones. Clinical manifestations of the disease may be different. Defining factors are a form of pathology and its duration.

The most common clinical manifestations of pathology are as follows:

• His name of the bronze disease Addison pathology has not just like that. The most obvious sign of this disease is a violation of pigmentation. Cleaning changes its color. Changes the shade of mucous membranes. It's all about too big pigmentation. When lacking for adrenal hormones, much more ATG is produced, it is explained by this necessity to stimulate the work of the internal secretion glands.
• One of the common clinical manifestations of the disease is chronic hypotension. This can lead to dizziness and a fainting state, the sensitivity to low temperatures increases.
• With insufficient work glands of the internal secretion weakens the entire body as a whole. If you have a constant fatigue, fast fatigue should consult with a medical specialist.
• With this pathology, disorders often arise in the work of the gastrointestinal tract, this can manifest itself in the form of vomiting, constant nausea and diarrhea.

• The disease may affect the emotional component. Depressive condition is one of the clinical manifestations of Addison's disease.
• Patients have noted increased sensitivity to stimuli. Exacerbate smell, rumor, man better feels food. In most cases, patients prefer to use salted food.
• Painful sensations in muscle tissues can also be a symptom of Addison pathology. This is explained by an increase in potassium concentration in blood vessels.
• As was said above, one of the clinical manifestations of the disease is an adrenal crisis, which occurs as a result of a sharp decrease in the level of hormones of the domestic secretion. The most popular symptoms of the crisis are painful sensations in the abdomen, low blood pressure, disturbed saline balance.

Diagnosis of the disease

First of all, patients pay their attention to changes in the shade of the skin. Such a phenomenon signals the insufficient activity of adrenal hormones. When contacting a medical specialist in this situation, it determines the ability of adrenal glands to increase hormone synthesis.

The diagnosis of addison's disease occurs by the introduction of ACTH and the cortisol content measurements in the blood vessels before the introduction of the drug and 30 minutes after vaccination. If a potential patient has no problems with adrenal functions - the level of cortisol will increase. If the concentration of the substance under study has not changed - a person has violations in the work of the internal secretion glands. In some cases, for more accurate diagnosis, the content of hormone in urea is measured.

Treatment of pathology

In the course of treatment, special attention should be paid to the diet. It should be diverse, there should be a necessary amount of proteins, fats and carbohydrates to provide the body. It is especially worth paying attention to the vitamins of the B and C group. They can be found in Bran, wheat, fruits and vegetables. In addition, the patient is recommended to drink more drinks on the basis of rosehip or black currant.

With Addison Disease in the body decreases the content of sodium, for this reason it is recommended to focus on salty food. In addition, pathology is characterized by an increased concentration of potassium in blood vessels, it is recommended not to include products that are rich in potassium. These include potatoes and nuts. Patients are recommended to eat as often as possible. Before going to bed, medical professionals recommend dinner, it will reduce the chance of hypoglycemia in the morning.

Almost all folk recipes are aimed at stimulating adrenal cortical substances. Folk medicine has a soft effect, the side effects are practically absent. The use of folk recipes will not only improve the work of the adrenal glands, but also will have a positive effect on the state of the whole organism as a whole. With the help of this approach, you can normalize the work of the gastrointestinal tract, to oppose the inflammatory processes of a chronic nature. It is recommended to use several recipes in turn, it will avoid addiction to the body.

Prevention and forecasting

If the therapy has begun in a timely manner and complyed with all the recommendations of the medical specialist, the outcome of the disease will be favorable. The disease will not affect the duration of life. In some cases, the Addison disease is accompanied by a complication - adrenal crisis. In such a situation, it is necessary to immediately seek advice with a medical specialist. Crisis can lead to a fatal outcome. Addison's disease is accompanied by rapid fatigue, weight loss and deterioration of appetite.

Changes in the shade of the skin occurs in all cases, deterioration in the work glands of the internal secretion occurs gradually, so it is difficult for a person it's hard to detect. In such a situation, the critical condition develops sharply and unexpectedly for the patient. Most often, the reason in a negative factor, for example, stress, infection or injury.

Since Addison's disease often has an autoimmune character - prevention measures practically does not exist. It should be followed by your immune system, avoid drinking alcoholic beverages, smoking. Medical professionals recommend paying attention to the manifestations of infectious diseases, especially tuberculosis.

Alexandra Warschal about the syndrome, describing who, Thomas Addison became the "father of endocrinology"

In 1849, Thomas Addison described the primary chronic insufficiency of adrenal glands (otherwise, the bronze disease) and allocated the main signs of the disease: "lethargy and weakness, heartbeat, abdominal pain and a change in skin color."

Prevalence

Primary adrenal insufficiency is rarely found: according to domestic authors, in 1 at 4000-6,000 hospitalized patients. American endocrinologists lead data on 39-60 cases of adrenal insufficiency per 1 million population. Chronic adrenal insufficiency (HNH) is more common in men; The ratio of men and women suffering from this disease - 2: 1. According to German doctors - Oelkers and his colleagues - the average age in which the disease is diagnosed is 40 years (from 17 to 72).

Etiology and pathogenesis

The clinical manifestations of the CHNN occur when the functional tissue of adrenal cortex is violated by a pathological process by 90%. Occasionally this takes place in bilateral metastases of carcinoma of light, mammary glands and intestines, cytomegalovirus adrenalites in HIV-infected or with HIV-adrenalites (which develop in 5% of patients in the late stages of the disease against the background of opportunistic infections) with antiphospholipid syndrome.

The main causes of chronic adrenal insufficiency are autoimmune adrenage (60-65% of cases); tuberculosis infection; Deep myoses, amyloidosis, histoplasmosis, hemochromatosis (10% of cases).

With autoimmune adrenalitis, there is an intense lymphoid infiltration of adrenal cortex and the growth of fibrous tissue with expressed functional cell atrophy. In the serum, such patients are found at the microsomal and mitochondrial antigens of the cells of adrenal cortex. Like other autoimmune diseases, such a defeat occurs more often in women. An autoimmune adrenalitis is often a component of autoimmune polyglandular syndrome I and II type.

The autoimmune polyglandular type I syndrome is developing in childhood (about 10-12 years) and includes hypoparathyroidism, adrenal insufficiency and candidomicosis. It is often combined with hypogonadism, pernicious anemia, alopecia, vitiligo and chronic active hepatitis. An autoimmune polyglandular type II syndrome is observed in adults and is characterized by triad: diabetes mellitus, autoimmune diseases of the thyroid gland and adrenal insufficiency.

In tuberculous lesion, adrenal glands can be increased, but more often wrinkled, fibroids changed. The pathological process is involved in the brain layer of the adrenal gland (synthesizing adrenaline and norepinephrine), which is almost always completely resolved. The active tuberculosis process in the adrenal glands is extremely rare. As a rule, tuberculosis infection extends to the adrenal glands of hematogenically from foci localized in the lungs, bones, urogenital system and other organs.

In the primary HNF, the number of secreted mineralocorticoids and glucocorticoids is reduced and, according to the reverse negative communication system, the secretion of ACTH increases and the secretion associated with its secretion of the β-melanocyate immuling hormone increases, which causes hyperpigmentation with Addison syndrome.

Glucocorticoids (cortisol) are synthesized in the bundle zone of adrenal cortex under the influence of ACTH, insulin antagonists. They increase blood glucose levels increase the gluchegenesis of amino acids in the liver, inhibit the capture and utilization of glucose cells of peripheral tissues, increase the synthesis of glycogen in the liver and skeletal muscles, strengthen the catabolism of proteins and reduce their synthesis, increase the catabolism of fats in subcutaneous fatty tissue and other tissues. . Glucocorticoids also have a certain mineralocorticoid effect.

Symptoms of Addison syndrome

Most of the symptoms of Addison's disease are relatively nonspecific. Almost all patients complain of weakness, increased fatigue and weight loss. Ortostatic hypotension, arthralgia, Malgia and an increased desire to eat salt may also be observed. In some cases, gastrointestinal symptoms may be predominant and as a result make it difficult to identify adrenal insufficiency. Mental symptoms vary from a minor impairment of memory to a pronounced psychosis, so some patients are mistakenly made a diagnosis of depression or nervous anorexia.

Patients, as a rule, cannot determine the time of the beginning of the disease and indicate the constantly progressive general and muscular weakness, increasing by the end of the day, in contrast to patients with neurasthenia, whose general weakness decreases by the evening. As the adrenal insufficiency progressing, weakness goes to adamise, speech slows down, the voice becomes quiet. Often, unusual weakness is detected during intercurrent infections or during the period of disorders of the gastrointestinal tract. Muscular weakness develops as a result of a violation of carbohydrate and electrolyte metabolism. Along with the general weakness marks reducing body weight. These two symptoms are available in all patients suffering from HNH. The weight loss is due to dehydration, the decline in appetite and the subsequent attachment of nausea and vomiting.

Mineralocorticoids (aldosterone, deoxykorticosterone) are synthesized in the glomerular zone of adrenal cortex under the influence of angiotensin II, cause enhancing the tubular reabsorption of sodium and chlorine ions, water and at the same time enhance the canaline excretion of potassium and increase the hydrophilicity of tissues, contribute to the transition of liquid and sodium from the vascular channel in the tissue. Mineralocorticoids increase the volume of circulating blood and increase blood pressure.

Hyperpigmentation Observed in 90% of patients. The deposition of melanin primarily increases in places of skin friction, in areas exposed to sunlight, nipples of the mammary glands, as well as on mucous membranes (lips, cheeks, etc.). In the future, generalized hyperpigmentation is developing associated with an excess of secretion of ACTH and β-melanocytimulatory hormone. Fresh scars are often pigmented, the amount of freckles increases. In some patients, on the background of general hyperpigmentation of the skin there are areas of depigmentation - vitiligo, which serves as a marker of the autoimmune process.

Arterial hypotension It is detected in 88-90% of patients. Systolic blood pressure 90 or 80 mm Hg, diastolic - below 60 mm Hg. In rare cases, diastolic pressure may be normal. Reducing the volume of plasma leads to a decrease in the minute and impact volume of the heart. Pulse soft, small, slow. Dehydration and reducing the total amount of sodium in the body lead to a decrease in the extracellular volume of the fluid and are one of the factor of hypotension. Another factor is reduced tone of the vascular wall due to lowering the level of cortisol and catecholamines.

Remarkable feature - calcification of ears cartilage - May accompany a long-term insufficiency of adrenal glands of any origin.

The functions of the gastrointestinal tract are disturbed. Most often there are nausea, vomiting, anorexia, constipation, changing diarrhea. The stomach decreases the secretion of hydrochloric acid and pepsin. The pathogenesis of gastrointestinal symptoms is associated with increased secretion of sodium chloride into the intestinal lumen. Vomiting and diarrhea enhance sodium loss and lead to the development of acute adrenal insufficiency. Patients with primary HNL have an increased need for salt.

Hypoglycemia It develops as a result of a decrease in cortisol secretion (counterinsular hormone), reduction of gluconeogenesis, glycogen reserves in the liver. The attacks of hypoglycemia are developing in the morning (empty stomach) or after a long break between meals and are accompanied by weakness, irritability, feeling of hunger, sweating.

Nicturia It is one of the frequent symptoms of the CHNN.

Changing the CNS function It is manifested in reducing mental activity and memory, concentration of attention, sometimes states of depression and acute psychosis. Replacement therapy normalizes the function of the central nervous system and the listed symptoms are reduced directly proportional to the normalization of the level of cortisol in the blood. In women suffering from HNH, there is a hair loss (exhaustion on the pubis, in the armpits) due to the fact that they have adrenal glands are the main place of the synthesis of androgen (in men they are synthesized mainly by the testicles).

In patients with Addison syndrome can be reduced libido and potency, Women have amenorrhea.

Laboratory finds

The most frequent violations in blood test - increase potassium levels (above 5 mmol / l) and creatinine with a decrease in sodium level (up to 110 mmol / l) and chlorine (below 98.4 mmol / l). Calcium content in serum occasionally increased. Hypercalcemia in such cases is combined with hypercalciuria, thirst, polyuria and hypoxenuria. Patients may also develop normocitar normschromic anemia, in the smears of peripheral blood, are noted eosinophilia and relative lymphocytosis. Often fix a slight increase in the content of TSG (as a rule,< 15 мкЕд/мл). Остается неясным, обусловлено ли это повышение ТТГ сопутствующим аутоиммунным заболеванием щитовидной железы, отсутствием подавления ТТГ эндогенными стероидами или развитием эутиреоидного патологического синдрома.

Disorders of the kidney function are observed: the speed of glomerular filtration and renal blood flow decreases.

Metabolic disorders and electrolyte exchange disorder lead to a change in the ECG. An enlarged and pointed teeth of T, which in separate leads may even exceed the QRS complex in the height. It is possible to slow down the atrocadic or intraventricular conductivity.

The diagnosis is based not only on the data of the clinical picture and laboratory research, but also on direct confirmation of the reduction in the functional activity of adrenal glands. If the level of corticosteroids in the blood taken at 8-10 hours in the morning, less than 170 nmol / l (6 μg / 100 ml), then the diagnosis of adrenal insufficiency is no doubt. The presence or absence of pigmentation indicates the primary or secondary nature of the disease. With primary HNH, the level of ACTH is usually increased, and at the secondary - reduced. Also, to clarify the diagnosis, a number of pharmacodynamic samples are carried out - cortisol oscillations are recorded when an ACTH or insulin is introduced. The sample with insulin allows to differentiate the tuberculous lesion of the adrenal cortex from the destruction of its autoimmune process. Tuberculosis lesion is accompanied by the destruction of the brain layer (in which catecholamines are synthesized), whereas with the damage to the autoimmune process, changes occur only in the cortical layer of adrenal gland. Therefore, by defining in the period of insulin test, along with glucocorticoids, the content of adrenaline in serum can be determined, caused by chronic adrenal failure.

For the diagnosis of hypoaldosteroneism, the concentration of aldosterone in the blood plasma or its excretion with urine is determined. And here, preference should be given to pharmacodynamic tests. Angiotensin is a specific stimulant of the secretion of aldosterone. If the concentration of aldosterone at the end of the angiotensin infusion does not increase, it indicates hypoaldosteronism.

Treatment

How to treat Addison syndrome? Patients with Addison syndrome need permanent intake of corticosteroids. In most cases, it is enough to introduce only glucocorticoids for full compensation; Sometimes additional appointment is required and mineralocorticoids. Hydrocortisone (cortisol) is a selection preparation and is assigned to 30 mg per day (15-20 mg early in the morning and 5-10 mg at noon). Cortisone is usually used in a daily dose of 40-50 mg. Other synthetic glucocorticoids (prednisolone, dexamethasone, triamcinolone, etc.) are less desirable, as they do not have mineralocorticoid action. With pronounced mineralocorticoid insufficiency, the dox is additionally recommended (5 mg 1 time per day intramuscularly), deoxyticosterone trimethyl acetate (1 ml of 2.5% solution of parenteral 1 time in 2-3 weeks) or fluorohydrocortisone / cortinef (0.05-0 , 1 mg per day).

Excess mineralocorticoids are fraught with edema, headache, increased blood pressure, hypokalemic alkalosis and muscle weakness. In these cases, it is necessary to cancel mineralocorticoids and assign potassium chloride.

In women suffering from HNH, pregnancy and normal childbirth are possible. As a rule, during pregnancy, the need for mineralocorticoids is reduced due to improving the secretion of progesterone. However, the reception of glucocorticoids should be increased, and in some cases the parenteral administration of hydrocortisone is required. During the birth, glucocorticoids are administered intravenously.

In case of infectious diseases of light or moderate severity, the dose of glucocorticoids is doubled or lost. If the disease proceeds with vomiting, as well as when the symptoms of the adrenal crisis appear, intensive therapy of the patient in the hospital is necessary. Surgical interventions in patients with HNR are produced under the condition of intravenous administration of hydrocortisone (100-200 mg, depending on the type of operation). In the postoperative period, the shock doses of glucocorticoids are reduced quickly - 2-3 days after the liquidation of the stressful situation.

Forecast

Prior to the use of glucocorticoids, life expectancy in patients with adrenal failure was less than 6 months. Today, with timely diagnosis and adequate substitution therapy, in patients with autoimmune adrenalitis, life expectancy is not different from such a healthy person. With the adrenal insufficiency of other etiology, the forecast is determined by the main disease.

Mode

Addison syndrome does not allow patients to engage in severe physical labor. Any stressful state (infection, physical or mental overvoltage, etc.) requires an increase in glucocorticoid reception. The principle of dispensary observation regarding these patients should be observed strictly. All patients with Addison syndrome are supplied with a special memo, which indicates a rational schedule for taking corticosteroids and optimal for this patient a single and daily dose of various corticosteroid drugs. In case of an urgent situation, glucocorticoids for parenteral administration should be ready. Warning information should also be prepared for physicians in case the patient will not be able to independently state information about its illness. Patients should be aware that they need to immediately consult a doctor when weakness, malaise, increasing the temperature, pain in the abdomen, diarrhea and other signs of deterioration. Alcohol, the use of barbituric sleeping pills, as well as the use of alkaline mineral waters to pick up corticosteroids containing corticosteroids is prohibited.

1. Balabolkin M. I. Endocrinology, 1998 2. McDemmott M. Secrets of Endocrinology, 2001 3. Wolfgang Oelkers M. Adrenal Issuficiency. THE NEW ENGLAND JOURNAL OF MEDICINE, VOL. 335, No. 16, p. 1206-1212 http://www.temple.edu/imReports/reading/endo%20%20-adrenal%20insuff.pdf 4. May M., Vaughn E., Carey R. ADRENOCORTICAL INSUFFICIENCY - CLINICAL ASPECTS. In: Adrenal Disorders, 1989, p. 171-189 5. Oelkers W., Diederich S., Bähr V. Recent Advances in Diagnosis and Therapy of Addison's Disease. Journal of Endocrinology Vol. 1. 1994, p. 69-80