Primary hyperaldosteronism. Hormonal examination and diagnostic signs

Content

According to statistics, primary (idiopathic) hyperaldosteronism (IHA) occurs in women 3 times more often than in men. The manifestation of the disease falls on the age of over 30 years. Of all types of hyperaldosteronism, primary is considered predominant. It is detected in 1% of patients with arterial hypertension.

What is idiopathic hyperaldosteronism

The term "hyperaldosteronism" refers to several syndromes in which too much of the hormone of the adrenal cortex (aldosterone) is secreted. Depending on the cause, there are 2 forms of the disease:

• Primary, or idiopathic. It develops due to increased activity of the glomerular zone of the adrenal cortex, which provokes excessive production of aldosterone.
• Secondary. Associated with disorders in the work of other internal organs, which also lead to excessive secretion of aldosterone.

Reasons for development

The main cause of the development of idiopathic hyperaldosteronism is an excess of the mineralocorticosteroid hormone of the adrenal cortex. It is responsible for the transition of sodium and fluid from blood vessels to body tissues.

With an increased level of aldosterone, the volume of circulating blood increases, which leads to an increase in blood pressure. Idiopathic aldosteronism develops for the following reasons:

Symptoms

Primary hyperaldosteronism is often asymptomatic. In such cases, in addition to an increase in blood pressure, no other abnormalities are detected in patients. Sometimes the disease proceeds without any symptoms. The clinical picture is characterized by a triad of syndromes:

• cardiovascular;
• neuromuscular;
• renal.

Cardiovascular Syndrome

One of the constant symptoms of IHA is arterial hypertension. Against the background of hypokalemia, it causes electrocardiographic disturbances. Hypertension can also be malignant, i.e. not respond to traditional treatment. In half of the patients, arterial hypertension occurs in the form of crises. Other symptoms of cardiovascular syndrome:

• headache;
• dizziness;
• heart rhythm disturbances;
• the appearance of flies before the eyes;
• cardialgia - aching pain in the region of the heart.

Neuromuscular

Due to hypokalemia, patients with hyperaldosteronism develop neuromuscular conduction and excitability disorders. They are indicated by the following symptoms:

• paresthesia;
• convulsions and paralysis affecting the neck, legs, fingers (differ in sudden onset and end);
• muscle weakness (typical for 73% of patients);
• bradycardia;
• severe weakness, which sharply increases suddenly or during physical exertion;
• tetany is an involuntary painful muscle contraction.

Renal

Excess aldosterone leads to the development of electrolyte disturbances, which negatively affects the function of the renal tubules. Dystrophic changes in the tubular apparatus of the kidneys cause kaliepenic nephropathy. The following symptoms indicate its development:

• nocturia - the predominance of nocturnal diuresis;
• polyuria - an increase in the daily volume of urine;
• polydipsia - intense thirst, which is observed in 46% of patients.

Diagnostic methods

In the process of diagnosis, the presence of idiopathic aldosteronism is revealed and its form is determined. For this, the following procedures are carried out:

Treatment

The choice of a specific treatment regimen depends on the cause of the development of hyperaldosteronism and the nature of its course. The main methods of treating the disease:

• taking potassium-sparing diuretics;
• adherence to a diet with restriction of table salt and the use of products containing potassium;
• injections of potassium preparations;
• surgery to excise the affected segment of the adrenal glands;
• conducting bilateral adrenalectomy (removal of the adrenal glands) in the hyperplastic form of the disease;
• prescription of Dexamethasone for glucocorticoid-suppressed aldosteronism.

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Hyperaldosteronism is a pathology of the adrenal cortex, characterized by excessive production of the mineralocorticoid hormone - aldosterone. Previously, the disease was considered rare, now it occurs in every tenth patient with arterial hypertension.

Disease classification

Hyperaldosteronism can be primary or secondary. Primary, in turn, is divided into:

• Adenoma of the adrenal cortex;
• carcinoma of the adrenal cortex;
• Glucocorticoid suppressed hyperaldosteronism;
• Primary adrenal hyperplasia.

Each of these conditions is characterized by increased production of aldosterone, in some cases - several steroid hormones.

Primary hyperaldosteronism

The pathogenesis and symptoms of primary and secondary hyperaldosteronism are different, so there is a separation of their symptoms and causes.

Causes

The most common causes of aldosteronism are:

• Adenoma of the adrenal cortex is a benign neoplasm that produces an excessive amount of aldosterone. In 75% of cases, it is the adenoma that causes primary aldosteronism.
• In 20% of cases, the disease is caused by bilateral aldosteromas.
• Only in 5% of cases the disease develops as a result of carcinoma of the adrenal cortex.

In medicine, a hereditary cause is also distinguished, which leads to a family disease with excessive production of aldosterone. And if in one member of the family the pathology can be caused by a neoplasm of any nature, then in the rest it is simply transmitted in the form of a syndrome. Hereditary transmission is realized in autosomal dominant inheritance.

Symptoms

The main symptoms of hyperaldosteronism are manifested by the cardiovascular and autonomic nervous systems. This is chronic stable arterial hypertension, overload of the left ventricle of the myocardium, sometimes hypertension reaches crises.

Other symptoms of the disease:

• Lethargy, fatigue;
• Weakness in the muscles;
• convulsions;
• Numbness of the limbs;

• Twitching in the muscles;
• Headache;
• Thirst and polyuria;
• Feeling of numbness of the limbs;
• Decreased concentration of vision.

Developing against the background of the disease, arterial hypertension also manifests its own symptoms, expressed in migraines, stress on the heart, hypokalemia. Every fourth patient develops a pre-diabetic condition. May be associated with osteoporosis.

Conn syndrome

Doctors call primary hyperaldosteronism Conn's syndrome in cases where excessive concentrations of aldosterone are produced by an adrenal adenoma.

This is a benign neoplasm, reaching a maximum diameter of 25 mm, filled with cholesterol and therefore having a yellowish color. Inside the adenoma there is also a high content of aldosterone synthetase.

Idiopathic hyperplasia

Bilateral idiopathic hyperaldosteronism occurs in half of the cases in patients over the age of 45 and is more common than adrenal adenoma.

In essence, hyperplasia is an increase in the cells of the adrenal cortex, while the volume of the cortex increases. Hyperplasia more than other types of primary hyperaldosteronism refers to hereditary pathologies.

Carcinoma is a malignant formation that synthesizes not only, but also estrogen, cortisol, androgens. Severe hypokalemia is noted.

The neoplasm reaches 45 mm in diameter and shows signs of growth. When neoplasms of unknown etiology are detected, with a diameter of more than 25 mm, it is customary to consider the patient's condition as a syndrome of increased risk of carcinoma formation.

Secondary form of the disease

Secondary hyperaldosteronism is a separate diagnosis, although it occurs against the background of already existing diseases of the systems of internal organs of a person.

Reasons for development

Secondary hyperaldosteronism is associated with the following pathologies:

• Reactivity, which manifests itself during pregnancy, with an excess of potassium in food, with the loss of sodium from the body during diets, diarrhea, long-term drug treatment with diuretics, large blood loss.
• With tumors or stenosis of the vessels, organic secondary hyperaldosteronism is noted.
• Violation of metabolic processes with the participation of aldosterone, which is observed in chronic pathologies of the kidneys and adrenal glands, heart failure.
• Long-term treatment with hormonal drugs based on estrogen, as well as during menopause, accompanied by hormonal imbalance.

The principal difference from primary hyperaldosteronism is that primary hyperaldosteronism entails an electrolyte imbalance, while secondary hyperaldosteronism is a natural reaction to renin-angiotensin-aldosterone complex reactivity.

Symptoms

Secondary hyperaldosteronism does not show its own symptoms, as it is a compensatory pathology. Therefore, its symptoms manifest themselves precisely in those diseases or conditions against which it manifests itself. Unlike the primary, the secondary form is not accompanied by a violation of the water-salt balance, high blood pressure and cardiac pathologies.

The only symptom with which a secondary form of aldosteronism can be associated is edema. Sodium accumulation and fluid accumulation lead to excess secretion of aldosterone, but sodium accumulation is caused by comorbidities.

Diagnostic methods

Diagnosis of primary or secondary hyperaldosteronism can only be carried out using a biochemical blood test. When an excess of aldosterone is detected, they proceed to the diagnosis of diseases that accompany or cause excessive secretion of aldosterone.

CT and MRI

Computed and magnetic resonance imaging can detect neoplasms from five millimeters in diameter. With the help of computer diagnostics, the following pathologies can be diagnosed:

• An increase in the size of the adrenal glands indicates bilateral hyperplasia, or unilateral if only one adrenal gland is changed in size.
• The presence of nodes in the adrenal cortex can be regarded as macronodular hyperplasia.
• If neoplasms larger than 30 mm are found, especially in the body of the adrenal gland, a carcinoma is suspected.
• Detection of a hormonally inactive tumor may indicate essential hypertension.

It should be understood that computer diagnostic methods examine morphological changes, and not functional ones, therefore additional methods are always required to clarify the suspected diagnosis.

Secondary hyperaldosteronism is an increase in aldosterone production in response to activation of the renin-aldosterone-angiotensin system. The intensity of aldosterone production in patients with secondary hyperaldosteronism in most cases is not lower than with, and the level of renin activity is increased.

Etiology and pathogenesis

The main pathogenetic features of secondary hyperaldosteronism include the rapid development of arterial hypertension, edematous syndrome of various origins, liver and kidney pathology with impaired metabolism and excretion of electrolytes and aldosterone.

During pregnancy, secondary hyperaldosteronism develops in response to the normal physiological response of increased blood renin levels and plasma renin activity to excess estrogens and the antialdosterone effect of progestins.

In arterial hypertension, secondary aldosteronism develops as a result of primary hyperproduction of renin or its hyperproduction due to a decrease in renal blood flow and renal perfusion. Secondary renin hypersecretion may result from narrowing of one or both major renal arteries caused by an atherosclerotic process or fibromuscular hyperplasia.

Secondary hyperaldosteronism can also occur with rare renin-producing tumors originating from juxtaglomerular cells, or hyperplasia of the juxtaglomerular complex (Barter's syndrome), which is accompanied by the absence of changes in the renal vessels and verification of a volumetric process in the kidney with a unilateral (with tumor genesis) increase in renin activity in the blood taken selectively from the renal veins. To confirm Bartter's syndrome, a kidney biopsy is performed (detect hyperplasia of the juxtaglomerular complex).

An increase in the rate of aldosterone secretion is typical for patients with edema of various origins. At the same time, certain differences are noted in the pathogenesis of secondary hyperaldosteronism. So, for example, in congestive heart failure, arterial hypovolemia and/or a decrease in blood pressure serve as triggers for excessive secretion of aldosterone, and the degree of increase in aldosterone secretion depends on the severity of circulatory decompensation. Diuretics may exacerbate secondary hyperaldosteronism by reducing the volume of circulating blood, which is manifested by hypokalemia and the subsequent development of alkalosis.

Symptoms

Clinical manifestations are determined by the cause that caused the indicated pathology (renal arterial hypertension, edema of various origins). There are difficulties in the correction of arterial hypertension due to resistance to standard therapy. Clinical manifestations of Bartter's syndrome include dehydration and severe myopathic syndrome, which develop in childhood. Seizures may occur as a result of hypokalemic alkalosis and the child's lag in physical development. Blood pressure does not rise.

Diagnostics

The disease is familial, so a careful family history is necessary.

Diagnosis is based on the identification of a pathology that causes secondary hyperaldosteronism, a decrease in potassium levels, an increase in aldosterone levels, and an increase in plasma renin activity. Possible hypochloremic alkalosis, as well as hypomagnesemia. Samples intended to verify the autonomous secretion of aldosterone are negative in secondary hyperaldosteronism.

The examination complex includes measures aimed at confirming the cause of secondary hyperaldosteronism (renal angiography, sonography or computed tomography for visualization of the kidneys, liver biopsy, biochemical blood test, etc.).

Confirmation of the diagnosis of Bartter's syndrome is based on the results of a puncture biopsy and the detection of hyperplasia of the juxtaglomerular apparatus of the kidney. The familial nature of the disease and the absence of severe arterial hypertension are also characteristic.

Treatment

Treatment includes measures aimed at eliminating and minimizing the manifestations of the underlying disease. In addition, dietary sodium restriction and the use of an aldosterone antagonist, spironolactone, are recommended. Hypertension and hypokalemia can be stopped by the appointment of spironolactone in doses of 25-100 mg every 8 hours. Long-term use of spironolactone in men can lead to the development of gynecomastia, decreased libido and the appearance of impotence. If a renin-producing tumor is detected, surgical treatment is indicated.

Aldosterone is one of the important hormones with synthesis in the adrenal glands, without which the coordinated work of the endocrine system as a whole is indispensable. Fluctuations of this hormone (deficiency, excess) lead to a failure of functions, the development of a whole complex of symptoms that are unfavorable for patients at once. This - hyperaldosteronism, mechanism and provoking factors, which can be very different.

The endocrinologist is engaged in the study of pathology, the appointment of effective treatment. The choice of tactics directly depends on the type, origin, severity of the course of the pathology, existing problems in patients with the urinary, cardiovascular system.

What is hyperaldosteronism?

Hyperaldosteronism is a combination of syndromes with different pathogenesis and symptoms or a disease caused by hypersecretion, increased production (metabolic disorders) of the mineralocorticoid aldosterone of the adrenal cortex.

Patients often have Conn's syndrome, a benign tumor of the adrenal cortex. The risk group includes women over 40 years of age.

Clinically, the pathology manifests itself as arterial hypertension, which accounts for up to 70% of all known cases. In a complicated course against the background of severe hypokalemia, the development of arrhythmia with a fatal outcome is possible.

The main method of exposure is an operation (adrenalectomy) to remove the affected adrenal gland. If there are tumor-like formations produced by aldosterone, then stenting of the artery is performed. In secondary hyperaldosteronism, endovascular balloon dilatation is performed.

If the aldosterone-producing formation is benign and adrenal cancer is not confirmed during the diagnosis, then the prognosis is quite favorable. After drug treatment, patients quickly recover.

Causes

The reasons for the development of pathology- a bunch of. Main:

• adenoma of the adrenal cortex caused by hypersecretion of aldosterone;
• bilateral hyperplasia of endocrine gland tissues
• hypertension;
• cirrhosis of the liver due to increased production of renin;
• dehydration of the body;
• abuse of a number of medicines (laxatives, diuretics);
• the use of oral contraceptives by women, which can lead to the development of a secondary form of the disease;
• carcinoma of the adrenal cortex;
• hereditary factor in case of detection of excessive production of aldosterone against the background of autosomal dominant inheritance;
• violation of metabolic processes involving aldosterone;
• abuse of hormonal drugs in the composition with estrogen;
• menopause in women with hormonal imbalance.

Secondary hyperaldosteronism develops due to:

• abuse of medicines (diuretics, hormones in the composition with estrogen);
• overproduction syndrome, ACTH;
• heart failure (congestion);
• arterial, renal hypertension;
• essential hypertension of the hyperrenin form.

Provoking factors for the development of the condition

A disease such as hyperaldosteronism often provokes the development of diseases aggravated by heredity, adrenal adenoma, leading to primary aldosteronism in 70% of cases. The provoking factors of the disease are systemic. As a rule, this is the development of pathologies in the thyroid gland, intestines, ovaries in women.

Symptoms

Symptoms directly depend on the type of pathology. With hyperaldosteronism, there are signs characteristic of Conn's syndrome (photo above), especially at an early stage of uncontrolled production of the hormone aldosterone against the background of dystrophic changes in the adrenal cortex. Main symptoms:

• arterial hypertension;
• persistently elevated diastolic pressure;
• decreased vision;
• vascular lesions of the fundus;
• dysfunction of the nervous, muscle tissue due to a lack of potassium in the body;
• weakness, rapid fatigue;
• pseudo-paralytic states;
• headache;
• violation of water and electrolyte balance;
• hypochondria;
• asthenia syndrome (psycho-emotional disorder);
• cephalgia;
• cardialgia;
• tachycardia;
• myasthenia gravis;
• paresthesia, numbness of the upper limbs;
• convulsive twitching of muscles;
• sagging head syndrome;
• polyuria against the background of changes in the renal tubules with urine output of not more than 3 liters per day.

Diagnostically revealed:

• low concentration of potassium and an overestimated concentration of sodium ions in the urine;
• a high level of PH against the background of the accumulation of alkaline metabolic products in the blood;
• high aldosterone levels;
• low unregulated level of renin in the blood even with medications;
• left ventricular hypertrophy during ECG.

Secondary hyperaldosteronism is a kind of compensation for the primary one and it often happens that there are no characteristic symptoms. In case of fluid retention and accumulation of sodium in the kidneys, patients experience:

• puffiness;
• hypernatremia;
• frequent urge to go to the toilet at night;
• increased anxiety;
• sweating;
• hypochondria;
• high pressure indicators;
• low levels of potassium in the blood;
• signs of alkalosis.

A feature of secondary aldosteronism is an excess of sodium in the urinary system, which provokes an increase in pressure indicators, an increase in the volume of circulating blood. While potassium in the body is sorely lacking. This leads to weakening of the muscles, chronic constipation in patients.

With the development of primary pathology, stagnation of sodium ions and fluids in the body is observed. Due to what blood pressure rises, it hurts in the heart area, vision decreases, the volume of urine excreted per day increases. May occasionally be observed convulsions, pseudo-paralysis in one or another muscle group. Episodes - psychoemotional instability, heart failure. At the same time, pressure indicators are consistently high, which can cause oxygen starvation of tissues, chronic renal failure.

REFERENCE! It happens that with hyperaldosteronism, pressure indicators are absolutely normal. Although at the same time a secondary form develops - Barter's syndrome. The secondary form of pathology is considered a compensatory mechanism under the influence of various pathologies.

Symptoms of the main provoking disease are clinically manifested:

• kidney dysfunction;
• neuroretinopathy;
• fundus hemorrhage;
• atrophy of the heart muscle;
• nephrogenic diabetes.

It happens that the symptoms are practically absent or hypertension is expressed in Bartter's syndrome. Most often, with secondary hyperaldosteronism, diseases of the heart, liver and kidneys begin to progress, manifesting themselves in the form of heart failure, arterial hypertension, nephrotic syndrome, cirrhosis of the liver.

On a note! Secondary hyperaldosteronism does not lead to electrolyte imbalance.

Types and stages of the disease

Hyperaldosteronism is divided into:

• primary aldosteronism in case of increased activity of cellular structures of the glomerular zone, excessive production of aldosterone in the adrenal cortex;
• secondary aldosteronism, complicated by excessive secretion of aldosterone production against the background of disorders occurring in neighboring organs (kidneys, liver, heart).

Varieties of the primary form of the disease, according to the classification:

• diffuse, focal hyperplasia.
• aldosterone-producing adenoma.
• Conn's syndrome.
• glucocorticoid-dependent form.
• pseudohyperaldosteronism in case of non-perception of aldosterone by the renal tubules.
• Itsenko-Cushing's syndrome.
• familial type 1,2, not amenable to the effects of glucocorticoids.
• aldosterone-producing carcinoma of the adrenal cortex.

Less common, but found adrenal, idiopathic hyperaldosteronism.

Diagnostics

Examination of patients begins with the identification of provoking causes that led to the development of the disease. In most cases, patients have a clearly overestimated excoriation of aldosterone in the blood or urine, and renin (a component of the renin-angiotensin system) is practically inactive. Although this is not a factor in confirming the pathology, since in elderly patients suffering from hypertension, these are quite acceptable phenomena.

At the initial stage, the state of the renin-angiotensin-aldosterone system is examined to identify renin and aldosterone concentrate in urine, blood after exercise or at rest in patients.

Examines the anamnesis, medical history, draws up a protocol for the subsequent development of a treatment program, an endocrinologist. Conducts a physical examination of the condition of the skin, measures blood pressure. Further, patients are redirected to an ophthalmologist for an examination of the fundus.

Diagnosis for the detection of primary hyperaldosteronism is differential in order to give an etiology, a form of pathology. The basis is a blood test, urine for biochemistry. Samples are taken in the laboratory:

• spironolactone with the introduction of the drug Spironolactone for 3 days or Captopril to determine the rhythm of aldosterone at rest or when walking in patients;
• with the introduction of Dox (10 mg) every 12 hours for 3 days;
• PCR - tests for suspected familial form of pathology;
• duplex scanning of blood vessels;
• angiography.

Patients are referred to a neurologist, a cardiologist. If a familial form of pathology is suspected, a genetic examination is performed.

Additional measures to identify the localization of the focus of the disease:

• MRI for suspected adenoma;
• CT to detect aldosterone-producing adenoma;
• scintigraphy of the adrenal glands as an informative method for adenoma, large nodular hyperplasia;
• phlebography to study the concentration of renin, aldosterone.

Treatment

The treatment regimen is compiled on the basis of the reasons that caused the increase in the level of aldosterone in the adrenal glands. If the pathology is not burdened and blood pressure jumps are caused by Conn's syndrome, then the therapy is based on drugs. If, after undergoing a course of therapy, there is no improvement, then the endocrinologist may suggest surgical intervention. The main goal of exposure, if primary hyperaldosteronism is established, is to prevent the development of a hypertensive crisis, the manifestation of complications from neighboring organs (heart, kidneys, liver).

When making a diagnosis - for patients, regardless of the identified form of hyperaldosteronism, a sparing diet with the inclusion of foods rich in potassium is included in the mandatory treatment program. Salt intake will need to be limited.

The detection of elevated testosterone levels in women must be stabilized by hormonal agents. If congestion in the kidneys is observed, then potassium preparations.

Treatment features:

• stabilization of pressure indicators;
• restoration of water-salt balance.

REFERENCE! Surgical correction is inevitable in case of ineffective use of potassium-containing, diuretic drugs. With Liddle's syndrome or a tumor-like neoplasm in the adrenal glands, the best option for getting rid of is transplantation of a diseased kidney.

Medical treatment

Conservative therapy for hyperaldosteronism includes the following medication prescriptions:

• diuretics ( Spironolactone, Amiloride);
• glucocorticoids ( Hydrocortisone, Dexamethasone) to eliminate signs of metabolism, normalize blood pressure;
• ACE inhibitors in case of diagnosing bilateral hypoplasia of the adrenal cortex;
• calcium channel antagonists;
• diuretic potassium-sparing drugs (injections) to restore the level of potassium in the body.

Treatment for secondary hyperaldosteronism is symptomatic. If the pressure jumps, then for normalization, patients are shown to receive cardiovascular drugs. If the level of potassium in the blood predominates, then drugs to stabilize the indicators - Triamterene.

When a glucocorticoid-dependent form of pathology is detected, the treatment is based on Dexamethasone and diuretics (spironolactone) with the provision of antiandrogenic action, the dose is 150-200 mg per day.

REFERENCE! Many drugs cause side effects. In men - the development and decrease in libido, in women - a manifestation of menstrual disorders. Doses are selected exclusively by the attending physician. Possible combinations are beta-blockers + calcium antagonists or the appointment of Spironolactone in small doses.

Surgery

Surgery for this disease, in particular Conn's syndrome, allows patients to prolong life by almost 5-6 times, prevent the development of complications from target organs (heart, kidneys, brain and fundus vessels). This is the best option for therapeutic effects, especially if medications become powerless in advanced cases, and the tumor has reached a large size and compresses the peripheral vessels in nearby organs.

Surgery is a tough method, therefore, before removing neoplasms in the adrenal glands, a number of preparatory procedures are expected. It is important for patients:

• refuse to take carcinogenic, fatty, fried, salty foods for 3-4 days;
• put an enema in the evening to cleanse the intestines;
• take a laxative.

The main methods of surgical intervention, taking into account weight, age, concomitant diseases in patients:

1. The traditional option with opening the peritoneal cavity, excision of the neoplasm together with metastases.
2. Laparoscopy is a low-traumatic method by introducing a laparoscope through a small puncture into the walls of the peritoneum to remove the affected lesion.
3. Adrenalectomy to remove the adrenal gland when a bilateral hyperplastic form of pathology is detected, followed by hypokalemia.
4. Focal artery stenting
5. Endovascular balloon dilatation.

If hyperplasia of the adrenal gland is detected, then bilateral removal of the organ is possible, followed by the restoration of the normal concentration of potassium in the blood, the appointment of medications in addition - Spironolactone, Amiloride, Aminoglutethimide but at higher doses.

After surgery, patients are indicated for replacement therapy. with the introduction of intravenous Hydrocortisone (30-40 mg) every 6-8 hours

On a note! Not every form of hyperaldosteronism is amenable to surgery to remove the affected adrenal gland. For example, with bilateral hyperplasia, an operation is prescribed only if the effects of medications are ineffective. With carcinoma, chemotherapy can not be dispensed with additionally.

If the form of the disease is glucocorticoid-dependent, then the operation is not performed. The main goal is to comply with clinical recommendations for patients to normalize pressure indicators using Dexamethasone, administered intravenously. The course of treatment is 1 month. Further - the passage and the recovery period of up to 5 days under the strict guidance of an endocrinologist with measurements of aldosterone and renin by blood donation.

In order to restore the activation of the body's defenses and support immunity, in addition, all patients are prescribed:

• physiotherapy after the operation, which proved to be highly effective in combination with drugs to enhance regenerative processes in tissues, providing a stimulating (anti-inflammatory) effect;
• UHF with heat on the body of different temperatures to form the body's resistance to infectious diseases;
• electrophoresis with the influence of different voltage frequencies to stimulate the functions of the nervous system, stabilize the production of the necessary hormones by the endocrine glands, normalize the water and electrolyte balance;
• magnetotherapy with the influence of frequency alternating current on the composition of cells and tissues to stabilize the liquid medium with the provision of a sedative, antispasmodic effect;
• ultrasound with a beneficial effect on tissues and cellular structures.

In the secondary form of pathology, the development of therapy as such is not carried out. It is important to direct measures to eliminate provoking factors and the underlying disease.

Alternative methods at home

If the disease is mild, and also after surgery with the permission of the attending physician to help - alternative folk methods for a beneficial effect on the structures of tissues (cells) of the thyroid gland. Home recipes will help:

• stabilization of blood pressure;
• restoration of hormonal levels;
• having a positive effect on the adrenal glands;
• improvement of blood supply;
• regeneration of processes in cells, tissues of the adrenal gland.

The best means:

• fresh burdock, crush the leaves in a blender, pour water (3 cups), insist, take 1/4 cup 2 times a day;
• medicinal lungwort (30g) pour boiled water (1 l), insist, take 1-2 tbsp. before meals 3 times a day;
• geranium (leaves), 2-3 pcs. crush into gruel, pour boiling water (1 cup), take 1/3 cup 2 times a day.

Nutrition and supplements

Patients are shown a salt-free diet with the inclusion of potassium-rich foods in the diet:

• prunes;
• beans;
• beans;
• pine nuts;
• mustard;
• raisin;
• dried apricots;
• seaweed.

It is important to limit salt intake, exclude spicy, fatty and specific foods from the diet.

Herbs

To reduce the pronounced symptoms of the disease, to stabilize the general well-being, you can use infusions, decoctions of medicinal herbs: lungwort, geranium, fresh burdock.

With hyperaldosteronism, there is a high synthesis of aldosterone in the blood. If there are suspicions of thyroid dysfunction, then of course, one should not hesitate to contact an endocrinologist, it is necessary to undergo diagnostics at an early stage of the disease.

Prevention measures

It is always better to protect yourself from a disease than to treat it. Measures are simple:

• treat hypertension of 1-2 degrees in a timely manner;
• undergo a scheduled medical examination at least once a year;
• lead a healthy lifestyle;
• follow a diet with the inclusion of potassium-containing foods;
• plan pregnancy for women if there is hyperaldosteronism in close relatives, since it is often inherited.

Prognosis for patients

Hyperaldosteronism is a progressive disease. Can lead to serious consequences:

• decreased vision up to the complete development of blindness;
• ischemia of the heart;
• paresthesia;
• arterial hypertension;
• oncology;
• hypertrophy of the left ventricle, heart;
• bilateral hyperplasia of the adrenal cortex.

If the secondary form of the pathology often goes away on its own, one has only to recover from the underlying disease, then with the primary form, the prognosis is ambiguous. It will directly depend on the degree of damage to important systems: urinary, cardiovascular, and the severity of the underlying disease.

The prognosis is unfavorable for adrenal cancer, carcinoma. An adenoma is considered a benign tumor. Successfully treated with chemotherapy. The main thing for patients is not to let the pathology progress, not to start the process. If metastases are detected, then one can hardly count on a long life without constantly painful symptoms, because a severely affected adrenal gland is practically not restored. With diffuse-nodular hyperplasia, in order to achieve a long-term stable remission, patients should be constantly examined by doctors, treated with drugs: steroidogenesis inhibitors, Spironolactone.

Related videos

- a pathological condition caused by increased production of aldosterone - the main mineralocorticoid hormone of the adrenal cortex. With primary hyperaldosteronism, arterial hypertension, headaches, cardialgia and cardiac arrhythmia, blurred vision, muscle weakness, paresthesia, convulsions are observed. With secondary hyperaldosteronism, peripheral edema, chronic renal failure, changes in the fundus develop. Diagnosis of various types of hyperaldosteronism includes a biochemical analysis of blood and urine, functional stress tests, ultrasound, scintigraphy, MRI, selective venography, a study of the state of the heart, liver, kidneys and renal arteries. Treatment of hyperaldosteronism in aldosteroma, adrenal cancer, kidney reninoma - surgical, in other forms - medication.

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General information

Hyperaldosteronism includes a whole complex of syndromes that are different in pathogenesis, but similar in clinical signs, occurring with excessive secretion of aldosterone. Hyperaldosteronism can be primary (due to the pathology of the adrenal glands themselves) and secondary (due to renin hypersecretion in other diseases). Primary hyperaldosteronism is diagnosed in 1-2% of patients with symptomatic arterial hypertension. In endocrinology, 60-70% of patients with primary hyperaldosteronism are women aged 30-50; few cases of detection of hyperaldosteronism among children are described.

Causes of hyperaldosteronism

Depending on the etiological factor, there are several forms of primary hyperaldosteronism, of which 60-70% of cases are Conn's syndrome, the cause of which is aldosteroma - an aldosterone-producing adenoma of the adrenal cortex. The presence of bilateral diffuse-nodular hyperplasia of the adrenal cortex leads to the development of idiopathic hyperaldosteronism.

There is a rare familial form of primary hyperaldosteronism with an autosomal dominant type of inheritance, caused by a defect in the 18-hydroxylase enzyme, which is out of control of the renin-angiotensin system and corrected by glucocorticoids (occurs in young patients with frequent cases of arterial hypertension in a family history). In rare cases, primary hyperaldosteronism can be caused by adrenal cancer that can produce aldosterone and deoxycorticosterone.

Secondary hyperaldosteronism occurs as a complication of a number of diseases of the cardiovascular system, pathology of the liver and kidneys. Secondary hyperaldosteronism is seen in heart failure, malignant arterial hypertension, cirrhosis of the liver, Bartter's syndrome, renal artery dysplasia and stenosis, nephrotic syndrome, renal reninoma, and renal failure.

To increase the secretion of renin and the development of secondary hyperaldosteronism leads to sodium loss (with diet, diarrhea), a decrease in circulating blood volume during blood loss and dehydration, excessive potassium intake, long-term use of certain drugs (diuretics, COCs, laxatives). Pseudohyperaldosteronism develops when the reaction of the distal renal tubules to aldosterone is disturbed, when, despite its high level in the blood serum, hyperkalemia is observed. Extra-adrenal hyperaldosteronism is noted quite rarely, for example, in the pathology of the ovaries, thyroid gland and intestines.

Pathogenesis

Primary hyperaldosteronism (low-reninated) is usually associated with a tumor or hyperplastic lesion of the adrenal cortex and is characterized by a combination of increased secretion of aldosterone with hypokalemia and arterial hypertension.

The basis of the pathogenesis of primary hyperaldosteronism is the effect of excess aldosterone on the water-electrolyte balance: an increase in the reabsorption of sodium and water ions in the renal tubules and an increased excretion of potassium ions in the urine, leading to fluid retention and hypervolemia, metabolic alkalosis, and a decrease in the production and activity of blood plasma renin. There is a violation of hemodynamics - an increase in the sensitivity of the vascular wall to the action of endogenous pressor factors and the resistance of peripheral vessels to blood flow. In primary hyperaldosteronism, a pronounced and prolonged hypokalemic syndrome leads to degenerative changes in the renal tubules (kaliepenic nephropathy) and muscles.

Secondary (high-renin) hyperaldosteronism occurs as a compensatory response to a decrease in renal blood flow in various diseases of the kidneys, liver, and heart. Secondary hyperaldosteronism develops due to the activation of the renin-angiotensin system and increased production of renin by the cells of the juxtaglomerular apparatus of the kidneys, which provide excessive stimulation of the adrenal cortex. The pronounced electrolyte disturbances characteristic of primary hyperaldosteronism do not occur in the secondary form.

Symptoms of hyperaldosteronism

The clinical picture of primary hyperaldosteronism reflects water and electrolyte imbalance caused by hypersecretion of aldosterone. Due to the retention of sodium and water in patients with primary hyperaldosteronism, severe or moderate arterial hypertension, headaches, aching pains in the region of the heart (cardialgia), cardiac arrhythmias, changes in the fundus of the eye with deterioration in visual function (hypertonic angiopathy, angiosclerosis, retinopathy) occur.

Potassium deficiency leads to fatigue, muscle weakness, paresthesia, seizures in various muscle groups, periodic pseudo-paralysis; in severe cases - to the development of myocardial dystrophy, kaliepenic nephropathy, nephrogenic diabetes insipidus. With primary hyperaldosteronism in the absence of heart failure, peripheral edema is not observed.

With secondary hyperaldosteronism, a high level of blood pressure is observed (with diastolic blood pressure> 120 mm Hg), gradually leading to damage to the vascular wall and tissue ischemia, deterioration of kidney function and the development of chronic renal failure, changes in the fundus (hemorrhages, neuroretinopathy). The most common sign of secondary hyperaldosteronism is edema, hypokalemia occurs in rare cases. Secondary hyperaldosteronism can occur without arterial hypertension (for example, with Bartter's syndrome and pseudohyperaldosteronism). Some patients have an asymptomatic course of hyperaldosteronism.

Diagnostics

Diagnosis involves the differentiation of various forms of hyperaldosteronism and the determination of their etiology. As part of the initial diagnosis, an analysis of the functional state of the renin-angiotensin-aldosterone system is carried out with the determination of aldosterone and renin in the blood and urine at rest and after stress tests, potassium-sodium balance and ACTH, which regulate aldosterone secretion.

Primary hyperaldosteronism is characterized by an increase in the level of aldosterone in the blood serum, a decrease in plasma renin activity (ARP), a high aldosterone / renin ratio, hypokalemia and hypernatremia, low relative density of urine, a significant increase in the daily excretion of potassium and aldosterone in the urine. The main diagnostic criterion for secondary hyperaldosteronism is an increased rate of ARP (with reninoma - more than 20-30 ng / ml / h).

In order to differentiate individual forms of hyperaldosteronism, a test with spironolactone, a test with a hypothiazide load, and a “marching” test are carried out. In order to identify the familial form of hyperaldosteronism, genomic typing is carried out by PCR. In case of hyperaldosteronism corrected by glucocorticoids, trial treatment with dexamethasone (prednisolone) is of diagnostic value, in which the manifestations of the disease are eliminated and blood pressure normalizes.

To determine the nature of the lesion (aldosteroma, diffuse nodular hyperplasia, cancer), topical diagnostic methods are used: ultrasound of the adrenal glands, scintigraphy, CT and MRI of the adrenal glands, selective venography with simultaneous determination of the levels of aldosterone and cortisol in the blood of the adrenal veins. It is also important to establish the disease that caused the development of secondary hyperaldosteronism using studies of the state of the heart, liver, kidneys and renal arteries (EchoCG, ECG, ultrasound of the liver, ultrasound of the kidneys, ultrasound and duplex scanning of the renal arteries, multispiral CT, MR angiography).

Treatment of hyperaldosteronism

The choice of method and tactics for the treatment of hyperaldosteronism depends on the cause of aldosterone hypersecretion. Examination of patients is carried out by an endocrinologist, cardiologist, nephrologist, ophthalmologist. Drug treatment with potassium-sparing diuretics (spirolactone) is carried out in various forms of hyporeninemic hyperaldosteronism (hyperplasia of the adrenal cortex, aldosterone) as a preparatory stage for surgery, which helps to normalize blood pressure and eliminate hypokalemia. A low-salt diet with an increased content of potassium-rich foods in the diet, as well as the introduction of potassium preparations, is shown.

Treatment of aldosteroma and adrenal cancer is surgical, it consists in removing the affected adrenal gland (adrenalectomy) with a preliminary restoration of water and electrolyte balance. Patients with bilateral adrenal hyperplasia are usually treated conservatively (spironolactone) in combination with ACE inhibitors, calcium channel antagonists (nifedipine). In hyperplastic forms of hyperaldosteronism, complete bilateral adrenalectomy and right-sided adrenalectomy in combination with subtotal resection of the left adrenal gland are ineffective. Hypokalemia disappears, but there is no desired hypotensive effect (BP normalizes only in 18% of cases) and there is a high risk of developing acute adrenal insufficiency.

With hyperaldosteronism, which can be corrected by glucocorticoid therapy, hydrocortisone or dexamethasone is prescribed to eliminate hormonal and metabolic disorders and normalize blood pressure. In secondary hyperaldosteronism, combined antihypertensive therapy is carried out against the background of pathogenetic treatment of the underlying disease under the mandatory control of ECG and potassium levels in blood plasma.

In the case of secondary hyperaldosteronism due to stenosis of the renal arteries, it is possible to perform percutaneous X-ray endovascular balloon dilatation, stenting of the affected renal artery, and open reconstructive surgery to normalize blood circulation and functioning of the kidney. When a kidney reninoma is detected, surgical treatment is indicated.

Forecast and prevention of hyperaldosteronism

The prognosis of hyperaldosteronism depends on the severity of the underlying disease, the degree of damage to the cardiovascular and urinary systems, timeliness and treatment. Radical surgical treatment or adequate drug therapy provide a high probability of recovery. The prognosis for adrenal cancer is poor.

In order to prevent hyperaldosteronism, constant dispensary observation of persons with arterial hypertension, diseases of the liver and kidneys is necessary; compliance with medical recommendations regarding the intake of medications and the nature of nutrition.