Content

The oscillations of aldosterone - one of the most important hormones produced by the adrenal glands - leads to a violation of the work of the whole organism. Pathology has several forms, so the tactics of the treatment of patients depends on the observed symptoms.

Development mechanism

Aldosterone is responsible for saving water electrolyte balance, adjusting the ratio of sodium and potassium ions in the body.

With excessive hormone generation in response to an increase in the number of the first element and the decrease in the second kidney begin the secretion of renin. As a result, the pH of blood serum is disturbed and magnesium deficiency is developing.

There are three types of disorders of the kidneys, leading to increased mining of the hormone:

• Primary idiopathic hyperaldosteroneism - the bark of adrenal glands highlights a lot of aldosterone.
• Secondary - a violation of other organs provokes an increase in hormone content.
• Pseudoaldosteroneism is a rare disease in which the aldosterone is reduced, hypertension is observed, hypokalemia, and the activity of renin is normal.

Primary aldosteronism

Such a form of the disease is more often observed in adult patients, and about 70% of cases occur in women aged thirty to fifty years. According to the principle of nosology, it is classified as follows:

• the presence of adenoma (aldoster);
• idiopathic hyperaldosteroneism;
• adrenal hyperplasia (primary or bilateral congenital);
• carcinoma or adenoma secreting corticosterone;
• hyperaldosteroneism of the family type of first and second form;
• incenko-Kushing syndrome, Gydelman, Liddle;
• immunity to the means containing corticosteroids;
• aldosteroctopopted syndrome.

Secondary

Highlynaine secondary hyperaldosteroneism is observed in excessive activation of the renin-angiotensin-aldosterone system. It imitates the primary shape and is caused by cirrhosis of the liver, impaired heart, nephrosis and other pathologies. Secondary hormone increase cause certain reasons:

• dehydration due to excessive sweating;
• polyuria;
• loss of sodium ions against the background of the high flow of potassium;
• edems, due to which large vessels are not filled completely;
• pregnancy.

Symptoms

With the primary form of hyperaldosteroneism, the symptoms of the disease are more pronounced. Secondary accompanies the pathology of any organs and is compensatory, therefore it is characterized by their clinic, but in some cases additional signs are possible. The main symptoms of hypeldosteroneism of two types:

Special forms of pathology

There are special types of hyperaldosteroneism, under which a pronounced unusual clinic is observed:

1. Conne syndrome in the primary form - in this case there is a benign adenoma of adrenal glands, producing aldosterone. This formation has a size of about 2.5 cm, contains a large amount of cholesterol and the enzyme of aldosteronsonttase. The syndrome is manifested by all signs of the primary form.
2. Barter Syndrome at the secondary - for patients with this disease with children's age Characterized convulsions, myopathy, abundant, frequent urinationleading to loss of electrolytes and liquid. In most cases, kids suffering from such pathology are lagging behind in developing from their peers.

What is hyperaldosteroneism secondary

it is an increase in the level of aldosterone, developing as a result of the activation of the renin angiotensin-aldosterone system with various impaired water-electrolyte exchange, due to increasing renin production.

What provokes hyperaldosteroneism secondary

Secondary hyperaldosteronismobserved at:

• heart failure
• liver cirrhosis
• chronic jade (contributes to the development of edema).

The speed of aldosterone products in patients with secondary aldosteroneism is often higher than with primary aldosteroneism.

Secondary aldosteroneism is combined Usually S. fast development Hypertension or arises due to edema states. During pregnancy, secondary aldosteronism is a normal physiological response to the estrogen caused by estrogen, an increase in the level of renin substrate in the blood and the activity of renin plasma.

With hypertensive statessecondary aldosteronism develops due to the primary hyperproduction of renin (primary reninism) or on the basis of such hyperproduction, which is due to a decrease in the renal blood flow or renal perfusion pressure. The secondary hypercecration of renaine is a consequence of the narrowing of one or both of the main renal arteries caused by atherosclerotic blushing or fibrous muscular hyperplasia.

Renin hyperproduction with both kidneys occurs in severe arterilation nephrosclerosis (malignant hypertension) or due to the narrowing of deep renal vessels (the phase of acceleration of hypertension).

Pathogenesis (what happens?) During the secondary hyperaldosteroneism

Secondary aldosteroneism is characterized by hypokalemic alkalosis, an increase in the activity of renin plasma and an increase in the level of aldosterone.

Secondary aldosteroneism with hypertension also occurs with rare renin-product tumors. In such patients there are vasorenal hypertension, the primary impairment consists in secretion of renin tumor emanating from YuCstaglomelar cells. The diagnosis is established on the basis of the lack of changes in the renal vessels or with the x-ray detection of the volumetric process in the kidney and one-sided increase in the activity of renin in the blood from the renal vein.

Secondary aldosteronism accompanies many types of edema. An increase in the secretion of aldosterone in the conditions of moving intravascular sodium and water into intercellular spaces to an even greater degree contributes to the fluid delay and sodium in the body, in connection with which the edema develops with. The decrease in oncotic pressure leads to the movement of intravascular sodium and water into intercellular spaces. Due to hypovolemia and decrease in sodium concentration in vascular bed, baroreceptors are irritated (in the left ventricle, aorta, the right of atrium, hollow veins). They reflectically through the hypothalamic area cause compensatory increase in the secretion of aldosterone. Other factors causing secondary hyperaldosteroneism are also promoted by the development of edema: an increase in the activity of a renin angiotensin system and a decrease in the inactivation of aldosterone in the liver. An increase in edema leads to an increase in the content of antidiuretic hormone in the blood. This, on the one hand, is due to the increase in the secretion of the hormone under the influence of aldosterone, and on the other - with a decrease in its inactivation in the liver. An increase in penetration of capillaries also contributes to an increase in capillaries as a result of enhancing the activity of the enzyme hyaluronidase. In patients with edema on the basis of cirrhosis of the liver or nephrotic syndrome, an increase in the speed of the aldosterone secretion is observed.

In case of diseases accompanied by edema (heart failure, nephrotic syndrome, liver cirrhrosis, etc.), the pathogenesis of secondary hyperaldosteroneism is mainly due to hypovolemia, a decrease in oncotic pressure and hyponatremia.

With stagnation of heart failure The degree of increase in the secretion of aldosterone depends on the severity of the decompensation of blood circulation, the cause is arterial hypovolemia or a decrease in blood pressure.

The reception of diuretics enhances secondary aldesteronism, hypokalemia and alkalosis are performed on the fore.

Secondary hyperaldosteroneism is sometimes found in the absence of edema or hypertension (Barter syndrome). This syndrome is characterized by signs of severe hyperaldosteroneism (hypokalemic alkalosis) with a moderate or increasing activity of renin, but normal arterial pressure and lack of edema. In the biopsy of the kidneys, the hyperplasia of the YUCSTAGLOMERARUAL complex is detected. A pathogenetic role plays a violation of kidney ability to delay sodium or chloride. Loss of sodium through the kidneys stimulates the secretion of renin and then the products of aldosterone.

The role of the factors involved in the pathogenesis of secondary hyperaldosteroneism, largely depends on the pathogenesis of the main disease. With hypertension and renal hypertension, the renal and ischemcekpi factor appears to the fore. The occasion of the kidney ischemia leads to an increase in the activity of its YUKSTAGLOMEROLANIC apparatus with reinforced Renin products and an increased formation of angiotensin II. The latter stimulates the glomerious zone of adrenal cortex with enhanced Aldosterone secretion.

Symptoms of hyperaldosteroneism secondary

Secondary hyperaldosteronism it does not have specific clinical manifestations, since it is a compensatory phenomenon in many diseases and states, while the electrolyte changes are characteristic of the primary hyperaldosteroneism.

The diagnostics of hyperaldosteroneism is secondary

The diagnosis of hyperaldosteroneism is based on the results biochemical analyzes (Increased removal of aldosterone with urine with the normal removal of 17-oxycorticosteroids, low content in the blood plasma of potassium ions, elevated potassium removal with urine, alkalosis).

Treatment of hyperalosteroneism secondary

With secondary hyperaldosteroneism, symptomatic therapy is carried out, aimed at increasing the removal of sodium with urine (Veroshpiron, etc.), as well as the treatment of the main disease that caused the cause of hyperaldosteroneism.

With secondary hyperaldosteroneism, the forecast depends on the severity of the main disease and the success of its treatment.

Prevention of hyperalosteroneism of secondary

Hyperldosteroneism prevention is regular dispensary observation patients with arterial hypertension, liver disease and kidney disease, compliance with the recommendations of the doctor regarding the nature of nutrition and reception of diuretic and laxatives.

What doctors should be addressed if you have a secondary hyperaldosteroneism

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Conna syndrome (Kona) is a complex of symptoms due to aldosterone hyperproduction with adrenal crusts. The cause of pathology is a tumor or hyperplasia of the glomerular zone of the cortical layer. In patients raised arterial pressureThe number of potassium is reduced and the sodium concentration in the blood increases.

Syndrome has several equivalent items: primary hyperaldosteronism, aldosteroma. These medical terms combine a number of close on clinical and biochemical features, but various diseases of the disease. Conna syndrome is the pathology of the endocrine glands, manifested by a combination of myasthenia, unnaturally strong, non-fatty thirst, increased blood pressure and an increased volume of urine allocated per day.

Aldosterone performs vital functions in the human body. Hormone contributes:

• suction sodium in blood,
• development of hypernatremia,
• remove potassium with urine,
• latching blood,
• renin hypoproduks.

When the level of aldosterone in the blood increases, the functioning of blood, urinary and neuromuscular systems is disturbed.

Syndrome is extremely rare. For the first time, he was described by scientists from America Konn in 1955, thanks to which he received its name. Endocrinologist described the main clinical manifestations of the syndrome and proved that the most effective method The treatment of pathology is surgical. If patients monitor their health and regularly attend doctors, the disease is detected on time and is well treatable. Removal of adenoma of adrenal cortex leads to the complete recovery of patients.

Pathology is more common in women aged 30-50 years. In men, the syndrome develops 2 times less frequently. It is extremely rarely rarely affected by children.

Etiology and pathogenesis

Ethiopathogenetic factors of Conne syndrome:

1. The main cause of Konna syndrome is an excess allocation of aldosterone hormone adrenal glands, due to the presence in the outer cortical layer of hormonally active tumor - aldoster. In 95% of cases, this neoplasm is benign, does not give metastases, has a one-sided course, is characterized only by an increase in the level of aldosterone in the blood and causes serious impaired water and salt metabolism in the body. Adenoma has a diameter of less than 2.5 cm. On a cut, it is yellowish due to the high cholesterol content.
2. Bilateral hyperplasia of adrenal cortex leads to the development of idiopathic hyperaldosteroneism. The cause of the development of diffuse hyperplasia is hereditary predisposition.
3. It is less likely to be a malignant tumor-carcinoma of adrenal glands, which synthesizes not only aldosterone, but also other corticosteroids. This tumor is larger - in diameter up to 4.5 cm and more, capable of invasive growth.

Pathogenetic syndrome links:

• hypersection of aldosterone,
• reducing renin and angiotensin activity,
• vanalis excretion of potassium,
• hypercaliuria, hypokalemia, lack of potassium in the body,
• development of Miasthenia, Parentesies, Transient Muscular Palsy,
• enhanced suction sodium, chlorine and water,
• fluid delay in the body
• hypervolemia
• swelling of the walls and narrowing of vessels,
• an increase in OPS and BCC,
• raising blood pressure
• hypersensitivity of vessels for pressing influences,
• hypomagnation
• strengthening neuromuscular excitability,
• impairment of mineral exchange,
• dysfunction of internal organs,
• intermediate inflammation of the renal fabric with the immune component,
• nephrosclerosis
• appearance renal symptoms - polyuria, polydipsy, niccountura,
• development of renal failure.

Stubborn hypokalemia leads to structural and functional disorders in organs and tissues - in the tubular kidney channels, smooth and skeletal muscles, nervous systemse.

Factors promoting the development of syndrome:

1. cardiovascular disease vascular system,
2. accompanying chronic pathologies,
3. reducing the protective resources of the body.

Symptomatics

Clinical manifestations of primary hyperaldosteroneism are very diverse. For some of them patients simply do not pay attention to what makes it difficult early diagnosis pathology. Such patients fall to the doctor with a launched form of syndrome. This forces specialists to limit oneself to palliative treatment.

Symptomatics of Conne syndrome:

• weakness and fatigue muscles,
• ticket tachycardia,
• tonic-clonic convulsions
• headache,
• constant thirst
• polyuria with low urine relative density,
• parrestzia limbs
• laryngospasm, choking,
• arterial hypertension.

Conne syndrome is accompanied by signs of heart lesions and vessels, kidneys, muscle tissue. Arterial hypertension is malignant and resistant to hypotensive therapy, as well as moderate and soft, well-leaning treatment. It may have a crisis or stable flow.

1. Increased arterial pressure is usually normalized with hypotensive drugs. This leads to the appearance of characteristic clinical signs - dizziness, nausea and vomiting, shortness of breath, cardialgia. Each second patient hypertension is critical.
2. In severe cases, they observe the attacks of Tutania or the development of a sluggish paralysis. Parables arise suddenly and can be saved for several hours. The hypoxicia in patients are combined with diffuse motor deficits, which is manifested by myoclonic twitching in the study.
3. Resistant hypertension leads to the development of complications from the heart and nervous systems. Hypertrophy of the left heart cameras ends with progressive coronary failure.
4. Arterial hypertension violates the work of the body: changes the eye bottom, swells disk spectator nerve, the acuity of vision is falling until full blindness.
5. Muscular weakness reaches extreme degree of severity, not allowing patients to move. Constantly feeling the weight of your body, they can not even get out of bed.
6. In severe cases, nephrogenic not diabetes.

There are three variants of the course of the disease:

1. Conna syndrome with the rapid development of symptoms - dizziness, arrhythmia, violation of consciousness.
2. Monosimptomic course of illness - an increase in blood pressure in patients.
3. Primary hyperaldosteroneism with low-rise clinical signs - ailment, fatigue. The syndrome is revealed by chance during a vulture. In patients with time, secondary inflammation of the kidneys is developing against the background of the available electrolyte disorders.

When signs of Conne syndrome, you need to visit the doctor. In the absence of proper and timely therapy dangerous complications are developing, representing a real threat to the patient's life. Due to long hypertension, severe diseases of the cardiovascular system can develop, up to strokes and heart attacks. It is possible to develop hypertensive retinopathy, expressed myasthenia and malignancy of the tumor.

Diagnostics

Diagnostic measures in suspected Conna syndrome are to carry out laboratory tests, hormonal studies, functional trials and topical diagnostics.

• Blood research on biochemical indicators - hypernatremia, hypokalemia, blood grid, hypocalcemia, hyperglycemia.
• Hormonal examination is an increase in the level of aldosterone in plasma.
• The overall urine analysis is determining its relative density, calculating the daily diurea: iso- and hypoxenuria, nicricacy, alkaline urine reaction.
• Specific tests - determination of the level of renin in the blood, the ratio of the activity of aldosterone plasma and renin, determining the level of aldosterone in the daily portion of urine.
• To increase the activity of renin in the blood plasma, it is stimulated by a long walking, a hypontatrium diets and diuretic reception. If the activity of renin does not change even after stimulation, it means that in patients with KONNN syndrome.
• To identify urinary syndrome, a sample with "Veroshpiron" is carried out. The drug is accepted 4 times a day for three days with the restriction of the daily consumption of salt up to six grams. Elevated level Potassium in the blood for the 4th day - a sign of pathology.
• CT and MRI abdominal cavity - Detection of aldoster or bilateral hyperplasia, its type and size, determination of the volume of operation.
• Scintigraphy - Detection of adrenal neoplasm, secreting aldosterone.
• Oxisopraneography allows you to determine the localization and magnitude of the adrenal tumors.
• Ultrasound of adrenal glands with color doppler mapping has a high sensitivity, low cost and is carried out for visualization of aldoster.
• On ECG - metabolic changes in myocardium, signs of hypertension and left ventricular overload.
• Molecular genitic analysis - identification of family forms of aldosteroneism.

Topical methods - CT and MRI - with great accuracy reveal new formation in the adrenal gland, but do not give information about its functional activity. It is necessary to compare the identified changes on the tomogram with data of hormonal analyzes. The results of a comprehensive patient examination allow specialists to properly diagnose and assign competent treatment.

Special attention deserves persons with arterial hypertension. Experts pay attention to the presence of clinical symptoms of the disease - severe hypertension, polyuria, polydipsy, muscle weakness.

Treatment

Therapeutic measures in the Conne syndrome are aimed at the correction of hypertension and metabolic disorders, as well as to prevent possible complicationsConditioned by high arterial pressure and a sharp decline in blood potassium. Conservative therapy is not able to radically improve the condition of the patients. They can completely recover only after removing aldoster.

adrenalctomy

Operational intervention is shown in patients with aldoster adrenal gland. One-sided adrenalectomy is a radical method consisting in partial or complete resection of an affected adrenal gland. Most patients show a laparoscopic operation, the advantage of which is insignificant pain and trauma of tissues, a short recovery period, small cuts that leaving small scars. 2-3 months before surgery, patients should start receiving diuretics and hypotensive tools of different pharmacological groups. After spent surgical treatment The recurrence of Konna syndrome is usually not observed. The idiopathic shape of the syndrome is not subject to operational treatment, since even the total adrenal resection will not help bring pressure to normal. Such patients showed lifelong treatment of aldosterone antagonists.

If the cause of the syndrome is hyperplasia of adrenal glands or there is an idiopathic form of pathology, shown conservative therapy. Patients prescribe:

1. Potassiabelling diuretics - "Spironolactone",
2. Glucocorticosteroids - "dexamethasone",
3. Hypotensive drugs - Nifedipin, Metoprolol.

For the treatment of primary hyperaldosteroneism, it is necessary to observe the diet and limit the use of a cook salt up to 2 grams per day. Gentle mode, moderate physical exercise And maintaining the optimal body weight significantly improve the patient's condition.

Strict adherence to the diet reduces the severity of clinical signs of syndrome and increases the chances of patients to recovery. Patients should be powered by home food that does not contain amplifiers of taste, flavors and other additives. Doctors do not recommend moving. It is better to eat in small portions every 3 hours. The basis of the diet should be fresh fruits and vegetables, coarse products, lean meat, potassium-containing products. At least 2 liters of water should be used. Diet eliminates any kind of alcohol, strong coffee, tea, products that increase blood pressure. Patients need to use products with a diuretic effect - watermelons and cucumbers, as well as special decoction and tincture.

• fresh outdoor walks,
• sports,
• fighting smoking and rejection of alcoholic beverages,
• fastfund refusal.

Forecast for diagnosed horseback syndrome is usually favorable. It depends on the individual characteristics of the organism of the patient and the professionalism of the attending physician. It is important - to apply for medical help, Before the development of nephropathy and persistent hypertension. High blood pressure is a serious and dangerous health problem associated with primary hyperaldosteronism.

Video: Aldosteroma - the cause of the horse's syndrome, the program "live great!"

Aldosteronism - clinical syndromeassociated with excessively secretion of aldosterone in adrenal cortex. The most powerful, produced adrenal glands, is considered that he designed to detain sodium in the body.

The process is due to sodium transfer from distal tubules into the tubular cells and its exchange with potassium and hydrogen. Such processes are also noted in sweat glands and in the intestine.

Controls the secretion of renin-angiotensin mechanism. Thanks to the proteolytic enzyme, localized in kidney cells, it is possible to identify a sharp decrease in blood volume, which circulates in renal arteriols. The hypersecretion of this enzyme can be associated with a decrease in blood flow rate.

The enhanced production of aldosterone causes a delay in sodium and hydrogen, which normalizes the amount of blood in the kidneys, while maintaining the secretion of renin minor.

From what causes affect the excessive formulation of aldosterone, the diagnosis is determined - primary or secondary aldosteroneism.

In medical practice, it is also called Conne syndrome, associated with the appearance. The disease is due to disruption endocrine system and meets quite often. Hormonally active tumor is localized in the glomerular zone of adrenal cortex.

Renal arrhythmia, a decrease in the blood volume in the kidneys, the narrowing of the renal vessels may affect the hypersection of the hormone, which also contributes to the development of this disease. It should be known that the swelling and hypertension do not always accompany the aldosteroneism, with barter syndrome, these symptoms may be completely absent, but hypokalemia, alkalosis and renin activity in plasma are preserved.

Causes of occurrence

Excessive mining of hormone bark of adrenal leads to the formation of a tumor, in most cases we are talking about aldoster or bilateral, less often occurs carcinoma. It is noted that the disease is more susceptible to the weak floor representative.

Male body transfers this disease lighter, in rare cases requires the help of medical personnel.

The reasons for the occurrence of secondary aldosteroneism can be diseases with kidney ischemia, various liver diseases, heart failure, diabetes, myocardial infarction, pneumonia.

Often, nozzles arises against the background of long diets, at which the daily diet is not enriched with sodium. Violation of hormonal balance arises with prolonged therapy in combination with.

Nargin mechanism

Primary aldosteroneism is due to the strengthened aldosterone secretion, which contributes to the significant release of potassium and hydrogen from the body. The lack of potassium is characterized by muscle weakness, which can develop into muscular paralysis.

One of the main symptoms is considered to be the kidney channels are subjected to a dystrophic change and loss of sensitivity to antidiuretic hormone. As a result, intracellular acidosis develops and extracellular alkalosis, which are the first step in the development of hypertension. The symptoms of increased blood pressure are migraines, changes in the eye dna and hypertrophy of the heart muscle.

Speaking about the pathogenesis of secondary aldosteroneism should take into account the primary role of the underlying disease. In some cases, we are talking about excessive reinforcement, in others - on oncotical pressure and hypovolemia. In this connection, hypertensive syndrome, sweeping syndrome and forms without the appearance of swelling and hypertension are distinguished.

Clinical picture

Signs of primary aldosteroneism:

• enhance arterial pressure
• migraine
• permanent thirst
• and abundant urination
• major pain in the heart
• dyspnea
• tachycardia
• weakness in muscles
• causes
• blood test demonstrates a sharp decrease in potassium content

The critical stage of the disease is characterized by the following symptoms:

• muscular paralysis
• loss of view
• nausea
• vomot
• retina edema or optic nerve

Signs of secondary aldosteroneism:

• heart failure
• chronic jade
• botkin's disease
• chronic hepatitis
• cirrhosis of the liver
• elevated swelling

Diagnostic methods

To identify primary aldosteroneism with signs of hypokalemia, a diagnostic sample is used based on the introduction of an aldactone. For the diagnosis of aldoster, the radioisotope visualization of adrenal glands is used, the radioisotope drug is pre-intravenously administered and only a week is carried out a visualization procedure.

X-ray diagnostics are also used with pneumosupendaranography and angiography, this method is observed as one of the most efficient.

As practice shows, diagnose secondary aldosteroneism is quite difficult. For a long time, the excretion of urine with aldosterone, the balance of electrolytes, as well as the ratio of sodium and potassium is studied.

Methods of therapy

After conducting careful diagnosis and diagnosis, methods of treating aldosteroneism are determined. Surgical intervention is recommended for the treatment of primary. The tumor formed in the adrenal glands is removed operational method, after which the patient's guaranteed recovery occurs.

Removal of the neoplasm is accompanied by pressure normalization and recovery of the electrolyte balance. The patient's rehabilitation passes into the shortest time, unpleasant symptoms are completely passing.

The treatment of secondary aldosteroneism has a fundamental difference and is associated with the elimination of all the reasons that cause additional hormone stimulation. The doctor appoints the most effective therapy in combination with blockers of excess hormone.

IN complex treatment Provided application. Diuretics remove all excess fluid from the body, which guarantees the disappearance of edema. The elimination of the underlying disease is the key to the recovery of the patient, correctly selected therapy, which will be successfully combined with the hormone blockers and diuretics, and is determined by the degree of development of the disease ..

The treatment of secondary aldosteroneism, occurs in parallel with the main treatment, the most popular schemes are considered to use prednisolone with diuretics or aldactone.

Forecasts

With a timely handling of the patient, the treatment of primary aldosteroneism on forecasts is defined as favorable. But only subject to the absence of irreversible changes in the kidneys and the vascular system. Operational intervention and removal of education is not accompanied by a sharp decrease in blood pressure or collapse. After the operation, there is a complete disappearance of the symptom, the secretion of hormones is gradually restored.

Without treatment, the fatal outcome occurs, due to progressive concomitant diseases. Malignant aldoster does not have favorable forecasts.

Fine treatment and operational treatment in a later period in most cases is due to the disability loss and assignment of the disability 1 of the group, the duration of the body's restoration in the postoperative period is determined by the degree of reversibility of changes in the body.

Forecasts for the treatment of secondary aldosteroneism depend on the severity of the concomitant diseases, it is important and how striking the kidneys are. Often, the pathology of the kidneys is accompanied by the formation of malignant tumors ().

Primary aldosteronism (Konna syndrome) is aldosteroneism caused by autonomous products of aldosterone with adrenal crusts (due to hyperplasia, adenoma or carcinoma). Symptoms and features include episodic weakness, an increase in blood pressure, hypokalemia. Diagnostics includes the determination of the level of the aldosterone plasma and the activity of renin plasma. Treatment depends on the cause. The tumor is deleted if possible; For hyperplasia, spirironolactone or close drugs can normalize blood pressure and cause the disappearance of other clinical manifestations.

Aldosterone is the most potent mineralocorticoid produced by adrenal glands. It regulates sodium delay and potassium loss. In the kinders, aldosterone causes sodium transfer from the lumen of the distal tubules into the tubular cells in exchange for potassium and hydrogen. The same effect is observed in salivary, sweat glands, the cells of the intestinal mucosa, the exchange between inside and the extracellular fluid.

The secretion of aldosterone is regulated by a renin-angiotensin system and to a lesser extent - ACTG. Renin, proteolytic enzyme accumulates in YuCstaglomelar kidney cells. Reducing the volume and velocity of blood flow in afferent renal arteriols induces the secretion of renin. Renin turns the angiotensinogen of the liver into angiotensin I, which, with the help of an angiotensin-shift enzyme, is transformed into angiotensin II. Angiotenzine II causes the secretion of aldosterone to a lesser extent to the secretion of cortisol and deoxyticosterone, also possessing pressing activity. Sodium and water delays caused by the increased secretion of aldosterone increase the volume of circulating blood and reduce the release of renin.

The primary hyperaldosteroneism syndrome described J. Conn (1955) due to the aldosterontocating adenoma adrenal cortex (aldoster), the removal of which led to the complete recovery of the patient. Currently, the collective concept of primary hyperaldosteroneism combines a number of clinical and biochemical signs, but various diseases of the disease, which are based on excessive and independent (or partially dependent) from the Renin-angiotensin system, Aldosterone products of adrenal cortex.

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Code of the ICD-10

E26.0 Primary hyperaldosteronism

What causes primary aldosteronism?

Primary aldosteroneism can be caused by adenoma, usually unilateral, cells of the glomerular layer of adrenal cortex or less frequent carcinoma or adrenal hyperplasia. With hyperplasia of adrenal glands, which is more often observed in older men, both adrenal glasses are hyperactive, there is no adenoma. The clinical picture can also be observed with congenital hyperplasia due to the deficiency of 11-hydroxylase and with dominently inherited dexamethane fluorescent hyperalosteroneism.

Symptoms of primary aldosteroneism

Clinical case of primary hyperalosteroneism

Patient M., Woman, 43 years old, entered the endocrinological department of the Republic of Kazakhstan, Kazan 01/31/12 with complaints about headaches, dizziness when lifting blood pressure, up to 200/100 mm MM. Art. (with a comfortable pressure of 150/90 mm Hg. Art.), generalized muscular weakness, cramps in the legs, general weakness, Fast fatigue.

Anamnesis of the disease. The disease developed gradually. For five years, the patient notes an increase in blood pressure, regarding which was observed by the therapist at the place of residence, received hypotensive therapy (Enalapril). About 3 years ago began to disturb periodic pain In the legs, convulsions, muscle weakness arising without visible provoking factors passing on their own within 2-3 weeks. Since 2009, 6 times received inpatient treatment in neurological departments of various LPUs with a diagnosis: chronic demyelinizing polyneuropathy, subaclately developing generalized muscle weakness. One of the episodes was with the weakness of the muscles of the neck and the hanging of the head.

Against the background of the infusion of prednisolone and the polarizing mixture, the improvement has occurred within a few days. According to blood tests, potassium - 2.15 mmol / l.

From 12/26/11 to 01/25/12 was inpatient treatment in the RKB, where he entered complaints into generalized muscle weakness, periodically arising cramps in the legs. A survey was conducted: Blood test 27.12.11: Alt - 29 UR \\ L, AST - 14 URS / L Creatine - 53 μmol / l, potassium 2.8 mmol / l, urea - 4.3 mmol / l, Society. Protein 60 g / l, bilirubin total. - 14.7 μmol / l, KFK - 44.5, LDH - 194, phosphorus 1.27 mmol / l, calcium - 2.28 mmol / l.

Urine analysis of 12/17/11; HSE-1002, protein traces, leukocytes - 9-10 V p / s, epit. PL - 20-22 in p / s.

Hormones in the blood: T3SV - 4.8, T4 SV - 13.8, TTH-1.1 μM / L, cortisol - 362.2 (NMOL 230-750 NMOL / L).

Ultrasound: Kidney Lion: 97x46 mm, parenchyma 15 mm, echogenicity increased, CHL-20 mm. Echogenicity is increased. The cavity is not expanded. Right 98x40 mm. Parenchima 16 mm, echogenicity is raised, chls 17 mm. Echogenicity is increased. The cavity is not expanded. Around the pyramids on both sides is visualized by a hyperheogenic rim. Based on the physical inspection and data of laboratory research to eliminate the endocrine pathology of the adrenal genesis, a further survey was recommended.

Ultrasound of adrenal glands: In the projection of the left adrenal gland, an isochogenic rounded formation 23x19 mm is visualized. In the projection of the right adrenal gland of pathological formations is not significantly visualized.

Watering on catecholamines: diuresis - 2.2 l, adrenaline - 43.1 nmol / day (norm 30-80 nmol / day), norepinephrine - 127.6 nmol / l (norm 20-240 nmol / day). These results excluded the presence of feochromocytoma as possible cause Unmanaged hypertension. Renin dated 13.01.12-1.2 μM / ml (N vert- 4.4-46,1 ;,, Goriz 2.8-39.9), aldosterone 1102 pg / ml (norm: lying 8-172, sitting 30 -355).

ABC of 18.01.12: RT-signs of the formation of the left adrenal gland (in the medial leg of the left adrenal gland, the isogenic formation of oval shape with dimensions of 25 * 22 * \u200b\u200b18 mm, uniform, 47 NU density is determined.

On the basis of anamnesis, clinical picture, data laboratory and tool methods Studies are installed clinical diagnosis: Primary hyperaldosteroneism (left adrenal aldosterome), first identified in the form of hypokalemic syndrome, neurological symptoms, sinus tachycardia. Hypologiamic periodic seizures with generalized muscle weakness. Hypertonic disease 3 degrees, stage 1. Xsn 0. Sinus tachycardia. Infection urinary tract In the resolution stage.

Hyperldosteroneism syndrome proceeds with clinical manifestationsdue to the three main symptomsomplexes: arterial hypertension, which can have both the critical flow (up to 50%) and persistent; violation of neuromuscular conductivity and excitability, which is associated with hypokalemia (in 35-75% of cases); Disruption of the function of the renal tubules (50-70% of cases).

The patient was recommended for operational treatment in order to remove the hormone-producing adrenal tumor - laparoscopic adrenaliactomy on the left. Operation was carried out - laparoscopic adrenaliactomy on the left under the conditions of separation of Abdominal Surgery of the RKB. Postoperative period Became without features. On the 4th day after surgery (02/12/12), the level of potassium blood was 4.5 mmol / l. Hell 130/80 mm Hg. Art.

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Secondary aldosteronism

Secondary aldosteroneism is an increased product of aldosterone adrenal glands in response to nonhyraphizar, extraadrenal incentives, including renal artery stenosis and hypovolemia. Symptoms are similar to those of primary aldosteroneism. Treatment includes correction caused by the cause.

Secondary aldosteronism is caused by a decrease in the renal blood flow, which stimulates the renin angiotensin mechanism with the final hypersection of aldosterone. For reasons, renal blood flow reasons include obstructive renal artery diseases (for example, atheroma, stenosis), renal vasoconstriction (with malignant hypertension), diseases accompanied by edema (for example, heart failure, cirrhosis with ascites, nephrotic syndrome). Secrecy can be normal in heart failure, but the hepatic blood flow and the aldosterone metabolism are reduced, so the levels of the circulating hormone are high.

Diagnosis of primary aldosteroneism

The diagnosis is suspected of patients with hypertension and hypokalemia. Laboratory study consists of determining the level of the aldosterone plasma and the activity of renin plasma (ARP). Tests should be carried out in the patient's refusal of drugs affecting the renin angiotensin system (for example, tiazide diuretics, aPF inhibitors, angiotensin antagonists, blockers), within 4-6 weeks. An ARP is usually measured in the morning in the patient's lying position. Usually in patients with primaryldosteronism, the plasma aldosterone level is greater than 15 ng / dl (\u003e 0.42 nmol / l) and low levels ARP, with aldosterone plasma ratio (in nanograms / dL) to armp [in nanograms / (MLHH)] more than 20.