Primary secondary aldosteronism. Primary hyperaldosteronism - overview of information

- 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 arrhythmias, 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, examination of the state of the heart, liver, kidneys and renal arteries. Treatment of hyperaldosteronism in aldosteroma, adrenal cancer, kidney reninoma is surgical, in other forms it is medication.

ICD-10

E26

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; described a few cases of detection of hyperaldosteronism among children.

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 (during 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 mmHg), gradually leading to damage to the vascular wall and tissue ischemia, deterioration of kidney function and the development of CRF, 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, multislice 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 cancer of the adrenal glands 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.

In 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 the 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.

An increase in aldosterone levels (hyperaldosteronism) is one of the causes of high blood pressure, cardiovascular complications, decreased kidney function, and changes in electrolyte ratios. Classify primary and secondary hyperaldosteronism, which are based on different etiological factors and pathogenetic mechanisms. The most common cause of the development of the primary type of pathology is Conn's syndrome.

Show all

Conn syndrome

Conn syndrome- a disease that occurs due to increased production of aldosterone by a tumor of the adrenal cortex. In the structure of primary aldosteronism (PHA), the incidence of this pathology reaches 70% of cases, so some combine these concepts. According to the latest data, among patients with arterial hypertension that is difficult to treat with medication, Conn's syndrome occurs in 5-10% of cases. Women get sick 2 times more often, while the onset of the pathology is gradual, symptoms appear after 30-40 years.

The concept and causes of primary and secondary hyperaldosteronism:

	Primary hyperaldosteronism	Secondary hyperaldosteronism
Definition	A syndrome that develops as a result of excessive production of aldosterone by the adrenal cortex (rarely an aldosterone-producing tumor of extra-adrenal localization), the level of which is relatively autonomous from the renin-angiotensin-aldosterone system (RAAS) and is not suppressed by sodium loading	A syndrome resulting from a decrease in colloid osmotic blood pressure and stimulation of the RAAS (as a complication of a number of diseases)
Causes	The disease is associated with the pathology of the adrenal glands: aldosterone-producing adenoma (Conn's syndrome) - 70%; bilateral hyperplasia of the glomerular zone of the adrenal cortex (idiopathic hyperaldosteronism) - up to 30%; rare diseases (aldosterone-producing carcinoma, unilateral hyperplasia of the glomerular zone of the adrenal cortex, familial hyperaldosteronism types I, II, III, MEN - I).	Associated with the pathology of other organs and systems: kidney disease (nephrotic cider, renal artery stenosis, kidney tumors, etc.); heart disease (congestive heart failure); other causes (hypersecretion of ACTH, diuretics, liver cirrhosis, starvation)

Etiology

The most common localization of aldosterone-producing adenoma is in the left adrenal gland. The tumor is solitary, does not reach large sizes (up to 3 cm), is benign in nature (malignant aldosteromas occur extremely rarely).



CT scan of the abdomen. adrenal adenoma



Pathogenesis

Aldosterone is a mineralocorticoid hormone produced by the adrenal cortex. Its synthesis occurs in the zona glomeruli. Aldosterone plays a leading role in the regulation of water and electrolyte balance in the body. Its secretion is controlled mainly by the RAA system.

Excess aldosterone plays a major role in the pathogenesis of Conn's syndrome. It promotes increased excretion of potassium by the kidneys (hypokalemia) and sodium reabsorption (hypernatremia), leads to alkalization of the blood (alkalosis). Sodium ions accumulate fluid in the body, increasing the volume of circulating blood (BCC), which leads to an increase in blood pressure. High BCC inhibits the synthesis of renin by the kidney. Prolonged loss of potassium ions further leads to nephron dystrophy (kalipenic kidney), arrhythmias, myocardial hypertrophy, and muscle weakness. It was noted that in patients the risk of sudden death from cardiovascular accidents sharply increases (10–12 times on average).






Clinic

Symptoms of primary hyperaldosteronism develop gradually. Patients with Conn's syndrome have:

• persistent increase in blood pressure, resistant to medical treatment in the history of the disease;
• headaches;
• heart rhythm disturbances due to a lack of potassium, bradycardia, the appearance of a U wave on the ECG;
• neuromuscular symptoms: weakness (especially in the calf muscles), cramps and paresthesias in the legs, tetany may occur;
• renal dysfunction (hypokalemic nephrogenic diabetes insipidus): an increase in urine volume per day (polyuria), the predominance of nighttime diuresis over daytime (nocturia);
• thirst (polydipsia).

Secondary aldosteronism is expressed in the manifestations of the underlying disease, arterial hypertension and hypokalemia may not be, the presence of edema is characteristic.

Diagnostics

Diagnosis of Conn's syndrome is recommended in individuals with arterial hypertension that is not amenable to drug therapy, with a combination of increased blood pressure and hypokalemia (identified by clinical symptoms or blood tests), with the onset of hypertension up to 40 years, with a aggravated family history of cardiovascular diseases , as well as in the presence of a confirmed diagnosis of PHA in relatives. Laboratory diagnosis is quite difficult and requires confirmation with the help of functional tests and instrumental research methods.

Laboratory research

After the formation of a risk group, patients are determined:

• plasma aldosterone level (increase in 70%);
• blood potassium (decrease in 37-50% of patients);
• plasma renin activity (ARP) or its direct concentration (RCR) (decrease in most patients);
• aldosterone-renin ratio (ARC) is a mandatory screening method.

Obtaining reliable results of the level of APC depends on the preparation of the patient before the analysis and compliance with the conditions for blood sampling according to the protocol. The patient should exclude Veroshpiron and other diuretics, licorice drugs and about 2 weeks in advance other drugs that affect the level of aldosterone and renin: b-blockers, ACE inhibitors, AR I blockers, central a-adrenergic agonists, NSAIDs, inhibitors renin, dihydropyridines. Control of hypertension should be carried out using drugs with a minimal effect on the level of aldosterone (Verapamil, Hydralazine, Prazosin hydrochloride, Doxazosin, Terazosin). If a patient has a malignant course of hypertension and the abolition of antihypertensive drugs can lead to serious consequences, APC is determined against the background of their use, taking into account the error.

Drugs affecting the result of ARS:

In addition to taking various medications, there are other factors that affect the interpretation of the results. :

• age > 65 years (renin levels decrease, leading to an increase in APC values);
• time of day (the study is carried out in the morning);
• the amount of salt consumed (usually not limited);
• dependence on the position of the body (when waking up and moving to a vertical position, the level of aldosterone rises by a third);
• pronounced decrease in kidney function (ARS increases);
• in women: the phase of the menstrual cycle (the study is carried out in the follicular phase, since physiological hyperaldosteronemia occurs in the luteal phase), taking contraceptives (decrease in plasma renin), pregnancy (decrease in APC).

If APC is positive, one of the functional tests is recommended. If the patient has spontaneous hypokalemia, no renin is detected, and the aldosterone concentration is above 550 pmol / l (20 ng / dl), the diagnosis of PHA does not need to be confirmed by exercise tests.

Functional tests to determine the level of aldosterone:

Functional trials	Methodology	Interpretation of test results
Sodium Load Test	Within three days, salt intake is increased to 6 g per day. It is necessary to control the daily excretion of sodium, to normalize the content of potassium with the help of drugs. Daily excretion of aldosterone (SEA) is determined on the third day of the study in the morning	PGA is unlikely - SEA< 10 мг или 27,7 нмоль (исключить ХПН); PHA is highly likely - SEA >12 mg (>33.3 nmol)
Test with 0.9% sodium chloride solution	In the morning, carry out an intravenous infusion of 2 liters of 0.9% solution for 4 hours (subject to the supine position one hour before the start). Blood test for aldosterone, renin, cortisone, potassium at the beginning of the test and after 4 hours. Control blood pressure, pulse rate. Option 2: the patient takes a sitting position 30 minutes before and during the infusion	PHA is unlikely with post-infusion aldosterone< 5 нг/дл; Doubtful - 5 to 10 ng/dl; PHA is likely at > 10 ng/dL (sitting > 6 ng/dL)
Captopril test	Captopril at a dose of 25-50 mg an hour after waking up. Aldosterone, ARP and cortisol are determined before taking Captopril and after 1-2 hours (all this time the patient must be in a sitting position)	The norm is a decrease in the level of aldosterone by more than a third of the initial value. PHA - aldosterone remains elevated at low ARP
Suppressive test with fludrocortisone	Fludrocortisone 0.1 mg qid for 4 days, potassium supplements qid (target level 4.0 mmol/l) with unlimited salt intake. On the 4th day at 7.00 cortisol is determined, at 10.00 - aldosterone and ARP while sitting, cortisol is repeated	With PHA - aldosterone> 170 pmol / l, ARP< 1 нг/мл/ч; Cortisol at 10.00 is not lower than at 7.00 (excluding the influence of cortisol)

Instrumental Research

Conducted to all patients after receiving the results of laboratory tests:

• Ultrasound of the adrenal glands - detection of tumors more than 1.0 cm in diameter.
• CT of the adrenal glands - with an accuracy of 95% determines the size of the tumor, shape, topical location, differentiates benign neoplasms and cancer.
• Scintigraphy - with aldosteroma there is a unilateral accumulation of 131 I-cholesterol, with hyperplasia of the adrenal cortex - accumulation in the tissue of both adrenal glands.
• Adrenal vein catheterization and comparative selective venous blood sampling (SSVZK) - allows you to clarify the type of primary aldosteronism, is the preferred method of differential diagnosis of unilateral aldosterone secretion in adenoma. The lateralization gradient is calculated from the ratio of aldosterone and cortisol levels on both sides. The indication for carrying out is the clarification of the diagnosis before surgical treatment.
Differential Diagnosis

Differential diagnosis of Conn's syndrome is carried out with idiopathic hyperplasia of the adrenal cortex, with secondary hyperaldosteronism, essential hypertension, endocrine diseases accompanied by an increase in blood pressure (Itsenko-Cushing's syndrome, pheochromocytoma), with hormonally inactive neoplasm and cancer. A malignant aldosterone-producing tumor on CT scan can reach a large size, is characterized by high density, inhomogeneity, blurred contours.

Differential diagnosis:

	Conn's syndrome (aldosterone-producing adenoma)	Idiopathic hyperaldosteronism	Secondary hyperaldosteronism
Laboratory indicators		aldosterone, ↓↓renin, ARS, ↓potassium	aldosterone, renin, -ARS, ↓potassium
Orthostatic (marching) test - study of the level of aldosterone upon awakening in a horizontal position, re-examination after staying in an upright position (walking) for 3 hours	High aldosterone initially, some decrease on follow-up, or at the same level	Increased aldosterone levels (preservation of sensitivity to AT-II)	Increase in aldosterone levels
CT	a small mass in one of the adrenal glands	adrenal glands are not changed, or there are small nodular formations on both sides	The adrenal glands are not enlarged, the size of the kidneys may be reduced
Adrenal vein catheterization with selective blood sampling	Lateralization	-	-

Treatment

With aldosteroma, laparoscopic adrenalectomy is performed (after 4 weeks of preoperative preparation at an outpatient level). Drug treatment is carried out with contraindications to surgery or with other forms of hyperaldosteronism:

• The main pathogenetic treatment is aldosterone antagonists - Veroshpiron 50 mg 2 r / d with an increase in dose after 7 days to 200-400 mg / day in 3-4 doses (maximum up to 600 mg / day);
• To lower the level of blood pressure - Dihydropyridines 30–90 mg / day;
• Correction of hypokalemia - potassium preparations.



Spironolactone is used to treat idiopathic GA. To reduce blood pressure, the addition of saluretics, calcium antagonists, ACE inhibitors and angiotensin II antagonists is necessary. If during the differential diagnosis glucocorticoid-suppressed hyperaldosteronism is detected, dexamethasone is prescribed.

Primary hyperaldosteronism (PHA, Conn's syndrome) is a collective concept that includes pathological conditions that are similar in clinical and biochemical signs and differ in pathogenesis. The basis of this syndrome is autonomous or partially autonomous from the renin-angiotensin system, excessive production of the hormone aldosterone, which is produced by the adrenal cortex.

ICD-10	E26.0
ICD-9	255.1
DiseasesDB	3073
Medline Plus	000330
eMedicine	med/432
MeSH	D006929

Leave a request and within a few minutes we will select a trusted doctor for you and help you make an appointment with him. Or choose a doctor yourself by clicking on the "Find a doctor" button.

General information

For the first time, a benign unilateral adenoma of the adrenal cortex, which was accompanied by high arterial hypertension, neuromuscular and renal disorders, manifested against the background of hyperaldosteronuria, was described in 1955 by the American Jerome Conn. He noted that the removal of the adenoma led to the recovery of a 34-year-old patient, and called the identified disease primary aldosteronism.

In Russia, primary aldosteronism was described in 1963 by S.M. Gerasimov, and in 1966 by P.P. Gerasimenko.

In 1955, Foley, studying the causes of intracranial hypertension, suggested that the violation of water and electrolyte balance observed in this hypertension is caused by hormonal disorders. The connection between hypertension and hormonal changes was confirmed by studies by R. D. Gordone (1995), M. Greer (1964) and M. B. A. Oldstone (1966), but the causal relationship between these disorders has not been finally identified.

Conducted in 1979 by R. M. Carey et al., studies of the regulation of aldosterone by the renin-angiotensin-aldosterone system and the role of dopaminergic mechanisms in this regulation showed that these mechanisms control the production of aldosterone.

Thanks to the experimental studies conducted in 1985 by K. Atarachi et al. on rats, it was found that atrial natriuretic peptide inhibits the secretion of aldosterone by the adrenal glands and does not affect the level of renin, angiotensin II, ACTH and potassium.

The research data obtained in 1987-2006 suggest that the hypothalamic structures have an effect on hyperplasia of the glomerular zone of the adrenal cortex and hypersecretion of aldosterone.

In 2006, a number of authors (V. Perrauclin et al.) revealed that cells containing vasopressin are present in aldosterone-producing tumors. Researchers suggest the presence in these tumors of V1a receptors, which control the secretion of aldosterone.

Primary hyperaldosteronism is the cause of hypertension in 0.5 - 4% of cases of the total number of patients with hypertension, and among hypertension of endocrine origin, Conn's syndrome is detected in 1-8% of patients.

The frequency of primary hyperaldosteronism among patients with arterial hypertension is 1-2%.

Aldosteromas account for 1% of incidentally diagnosed adrenal masses.

Aldosteromas are 2 times less common in men than in women, and are extremely rare in children.

Bilateral idiopathic adrenal hyperplasia as the cause of primary hyperaldosteronism in most cases is detected in men. Moreover, the development of this form of primary hyperaldosteronism is usually observed at a later age than aldosteromas.

Primary hyperaldosteronism is usually seen in adults.

The ratio of women and men 30 - 40 years old is 3: 1, and in girls and boys the incidence of the disease is the same.

Forms

The most common is the classification of primary hyperaldosteronism according to the nosological principle. In accordance with this classification, there are:

• Aldosterone-producing adenoma (APA), which was described by Jerome Conn and called Conn's syndrome. It is detected in 30 - 50% of cases of the total number of the disease.
• Idiopathic hyperaldosteronism (IHA) or bilateral small- or large-nodular hyperplasia of the glomerular zone, which occurs in 45-65% of patients.
• Primary unilateral adrenal hyperplasia, which occurs in approximately 2% of patients.
• Familial hyperaldosteronism type I (glucocorticoid-suppressed), which occurs in less than 2% of cases.
• Familial hyperaldosteronism type II (glucocorticoid-non-suppressed), which is less than 2% of all cases of the disease.
• Aldosterone-producing carcinoma, found in approximately 1% of patients.
• Aldosteronectopic syndrome, which occurs with aldosterone-producing tumors located in the thyroid gland, ovary, or intestines.

Reasons for development

The cause of primary hyperaldosteronism is excessive secretion of aldosterone, the main mineralocorticosteroid hormone of the human adrenal cortex. This hormone promotes the transfer of fluid and sodium from the vascular bed to the tissues due to increased tubular reabsorption of sodium cations, anions of chlorine and water and tubular excretion of potassium cations. As a result of the action of mineralocorticoids, the volume of circulating blood increases, and systemic arterial pressure rises.

1. Conn's syndrome develops as a result of the formation in the adrenal glands of aldosteroma - a benign adenoma that secretes aldosterone. Multiple (solitary) aldosteromas are detected in 80-85% of patients. In most cases, aldosteroma is unilateral, and only in 6 - 15% of cases bilateral adenomas are formed. The size of the tumor in 80% of cases does not exceed 3 mm and weighs about 6-8 grams. If the aldosteroma increases in volume, there is an increase in its malignancy (95% of tumors larger than 30 mm are malignant, and 87% of tumors of a smaller size are benign). In most cases, the adrenal aldosteroma mainly consists of cells of the glomerular zone, but in 20% of patients the tumor consists mainly of cells of the zona fasciculata. Damage to the left adrenal gland is observed 2-3 times more often, since anatomical conditions predispose to this (compression of the vein in the "aorto-mesenteric forceps").
2. Idiopathic hyperaldosteronism is presumably the last stage in the development of low-renin arterial hypertension. The development of this form of the disease is caused by bilateral small- or large-nodular hyperplasia of the adrenal cortex. The glomerular zone of hyperplastic adrenal glands produces an excess amount of aldosterone, as a result of which the patient develops arterial hypertension and hypokalemia, and the level of plasma renin decreases. The fundamental difference of this form of the disease is the preservation of sensitivity to the stimulating effect of angiotensin II of the hyperplastic glomerular zone. The formation of aldosterone in this form of Conn's syndrome is controlled by adrenocorticotropic hormone.
3. In rare cases, the cause of primary hyperaldosteronism is adrenal carcinoma, which is formed during the growth of an adenoma and is accompanied by increased urinary excretion of 17-ketosteroids.
4. Sometimes the cause of the disease is genetically determined glucocorticoid-sensitive aldosteronism, which is characterized by increased sensitivity of the glomerular zone of the adrenal cortex to adrenocorticotropic hormone and suppression of aldosterone hypersecretion by glucocorticoids (dexamethasone). The disease is caused by an unequal exchange of sections of homologous chromatids during meiosis of the 11b-hydroxylase and aldosterone synthetase genes located on the 8th chromosome, resulting in the formation of a defective enzyme.
5. In some cases, the level of aldosterone rises due to the secretion of this hormone by extraadrenal tumors.

Pathogenesis

Primary hyperaldosteronism develops as a result of excessive secretion of aldosterone and its specific effect on the transport of sodium and potassium ions.

Aldosterone controls the cation exchange mechanism by binding to receptors located in the tubules of the kidneys, intestinal mucosa, sweat and salivary glands.

The level of potassium secretion and excretion depends on the amount of sodium reabsorbed.

With hypersecretion of aldosterone, sodium reabsorption is increased, resulting in the induction of potassium loss. In this case, the pathophysiological effect of the loss of potassium overlaps the effect of reabsorbed sodium. Thus, a complex of metabolic disorders characteristic of primary hyperaldosteronism is formed.

A decrease in the level of potassium and the depletion of its intracellular reserves causes universal hypokalemia.

Potassium in the cells is replaced by sodium and hydrogen, which, in combination with the excretion of chlorine, provoke the development of:

• intracellular acidosis, in which there is a decrease in pH less than 7.35;
• hypokalemic and hypochloremic extracellular alkalosis, in which there is an increase in pH greater than 7.45.

With potassium deficiency in organs and tissues (distal renal tubules, smooth and striated muscles, central and peripheral nervous system), functional and structural disorders occur. Neuromuscular excitability is aggravated by hypomagnesemia, which develops with a decrease in magnesium reabsorption.

In addition, hypokalemia:

• inhibits the secretion of insulin, so patients have reduced tolerance to carbohydrates;
• affects the epithelium of the renal tubules, so the renal tubules are exposed to antidiuretic hormone.

As a result of these changes in the work of the body, a number of renal functions are disturbed - the concentration ability of the kidneys decreases, hypervolemia develops, and the production of renin and angiotensin II is suppressed. These factors increase the sensitivity of the vascular wall to a variety of internal pressor factors, which provokes the development of arterial hypertension. In addition, interstitial inflammation with an immune component and interstitium sclerosis develop, therefore, the long course of primary hyperaldosteronism contributes to the development of secondary nephrogenic arterial hypertension.

The level of glucocorticoids in primary hyperaldosteronism caused by adenoma or hyperplasia of the adrenal cortex, in most cases, does not exceed the norm.

In carcinoma, the clinical picture is complemented by impaired secretion of certain hormones (glucocorticoids or mineralocorticoids, androgens).

The pathogenesis of the familial form of primary hyperaldosteronism is also associated with hypersecretion of aldosterone, but these disorders are caused by mutations in the genes responsible for encoding adrenocorticotropic hormone (ACTH) and aldosterone synthetase.

Normally, the expression of the 11b-hydroxylase gene occurs under the influence of adrenocorticotropic hormone, and the aldosterone synthetase gene - under the influence of potassium ions and angiotensin II. During a mutation (unequal exchange during meiosis of sections of homologous chromatids of the 11b-hydroxylase and aldosterone synthetase genes localized on the 8th chromosome), a defective gene is formed that includes the 5ACTH-sensitive regulatory region of the 11b-hydroxylase gene and the 3′-sequence of nucleotides that encode the synthesis of the aldosterone synthetase enzyme . As a result, the fascicular zone of the adrenal cortex, whose activity is regulated by ACTH, begins to produce aldosterone, as well as 18-oxocortisol, 18-hydroxycortisol from 11-deoxycortisol in large quantities.

Symptoms

Conn's syndrome is accompanied by cardiovascular, renal and neuromuscular syndromes.

Cardiovascular syndrome includes arterial hypertension, which may be accompanied by headaches, dizziness, cardialgia and cardiac arrhythmias. Arterial hypertension (AH) may be malignant, refractory to traditional antihypertensive therapy, or corrected even with small doses of antihypertensive drugs. In half of the cases, hypertension is of a crisis nature.

The diurnal profile of AH demonstrates an insufficient decrease in blood pressure at night, and if the circadian rhythm of aldosterone secretion is disturbed, an excessive increase in blood pressure is observed at this time.

With idiopathic hyperaldosteronism, the degree of nocturnal decrease in blood pressure is close to normal.

Sodium and water retention in patients with primary hyperaldosteronism also causes hypertensive angiopathy, angiosclerosis and retinopathy in 50% of cases.

Neuromuscular and renal syndromes manifest themselves depending on the severity of hypokalemia. Neuromuscular syndrome is characterized by:

• attacks of muscle weakness (observed in 73% of patients);
• convulsions and paralysis affecting mainly the legs, neck and fingers, which last from several hours to a day and are distinguished by a sudden onset and end.

Paresthesias are observed in 24% of patients.

As a result of hypokalemia and intracellular acidosis in the cells of the renal tubules, dystrophic changes occur in the tubular apparatus of the kidneys, which provoke the development of kaliepenic nephropathy. Renal syndrome is characterized by:

• decrease in the concentration function of the kidneys;
• polyuria (an increase in daily diuresis, detected in 72% of patients);
• (increased urination at night);
• (strong thirst, which is observed in 46% of patients).

In severe cases, nephrogenic diabetes insipidus may develop.

Primary hyperaldosteronism can be monosymptomatic - in addition to increased blood pressure, patients may not show any other symptoms, and the level of potassium does not differ from the norm.

In aldosterone-producing adenoma, myoplegic episodes and muscle weakness are observed more frequently than in idiopathic hyperaldosteronism.

AH with a familial form of hyperaldosteronism manifests itself at an early age.

Diagnostics

Diagnosis primarily includes the identification of Conn's syndrome among individuals with arterial hypertension. The selection criteria are:

• The presence of clinical symptoms of the disease.
• Blood plasma test data to determine the level of potassium. The presence of persistent hypokalemia, in which the content of potassium in the plasma does not exceed 3.0 mmol / l. It is detected in the vast majority of cases with primary aldosteronism, but normokalemia is observed in 10% of cases.
• ECG data that allows you to detect metabolic changes. With hypokalemia, there is a decrease in the ST segment, inversion of the T wave, the QT interval is lengthened, an abnormal U wave and conduction disturbance are detected. The changes detected on the ECG do not always correspond to the true concentration of potassium in the plasma.
• The presence of urinary syndrome (a complex of various disorders of urination and changes in the composition and structure of urine).

To identify the relationship between hyperaldosteronemia and electrolyte disorders, a test with veroshpiron is used (veroshpiron is prescribed 4 times a day, 100 mg for 3 days, with at least 6 g of salt included in the daily diet). Elevated by more than 1 mmol / l potassium level on the 4th day is a sign of hyperproduction of aldosterone.

To differentiate various forms of hyperaldosteronism and determine their etiology, the following is carried out:

• a thorough study of the functional state of the RAAS system (renin-angiotensin-aldosterone system);
• CT and MRI, allowing to analyze the structural state of the adrenal glands;
• hormonal examination, which allows to determine the level of activity of the identified changes.

In the study of the RAAS system, stress tests are carried out aimed at stimulating or suppressing the activity of the RAAS system. Since a number of exogenous factors influence the secretion of aldosterone and the level of plasma renin activity, drug therapy that can affect the result of the study is excluded 10-14 days before the study.

Low plasma renin activity is stimulated by hourly walking, hyposodium diet and diuretics. With unstimulated plasma renin activity in patients, aldosteroma or idiopathic adrenal hyperplasia is suspected, since this activity is subject to significant stimulation in secondary aldosteronism.

Tests that suppress excess aldosterone secretion include a high sodium diet, deoxycorticosterone acetate, and intravenous isotonic saline. When conducting these tests, aldosterone secretion does not change in the presence of aldosterone, autonomously producing aldosterone, and with hyperplasia of the adrenal cortex, suppression of aldosterone secretion is observed.

As the most informative X-ray method, selective venography of the adrenal glands is also used.

To identify the familial form of hyperaldosteronism, genomic typing is used using the PCR method. In familial hyperaldosteronism type I (glucocorticoid-suppressed), a trial treatment with dexamethasone (prednisolone) that eliminates the signs of the disease has a diagnostic value.

Treatment

Treatment of primary hyperaldosteronism depends on the form of the disease. Non-drug treatment includes limiting the intake of table salt (less than 2 grams per day) and a sparing regimen.

Treatment of aldosteroma and aldosterone-producing carcinoma involves the use of a radical method - subtotal or total resection of the affected adrenal gland.

For 1-3 months before the operation, patients are prescribed:

• Aldosterone antagonists - the diuretic spironolactone (the initial dose is 50 mg 2 times a day, and later it increases to an average dose of 200-400 mg / day 3-4 times a day).
• Dihydropyridine calcium channel blockers that help lower blood pressure until potassium levels normalize.
• Saluretics, which are prescribed after the normalization of potassium levels to reduce blood pressure (hydrochlorothiazide, furosemide, amiloride). It is also possible to prescribe ACE inhibitors, angiotensin II receptor antagonists, calcium antagonists.

In idiopathic hyperaldosteronism, conservative therapy with spironolactone is justified, which, when erectile dysfunction occurs in men, is replaced with amiloride or triamterene (these drugs help normalize potassium levels, but do not reduce blood pressure, so it is necessary to add saluretics, etc.).

With glucocorticoid-suppressed hyperaldosteronism, dexamethasone is prescribed (the dose is selected individually).

In the event of a hypertensive crisis, Conn's syndrome requires emergency care in accordance with the general rules for its treatment.

Liqmed reminds: the sooner you seek help from a specialist, the more chances you have to maintain your health and reduce the risk of complications.

Found an error? Select it and click Ctrl+Enter

print version

Conn's syndrome is a disease of the endocrine system, which is characterized by a large amount of aldosterone production. In medicine, it is referred to as primary aldosteronism. This ailment can be called a consequence of the main disease, which, progressing, causes complications. The main diseases include a tumor of the adrenal glands, cancer of the adrenal glands, neoplasm of the pituitary gland, adenoma and carcinoma.

General information

Aldosteronism is divided into primary and secondary. Both types occur due to excessive production of the hormone aldosterone, which is responsible for retaining sodium in the body and excreting potassium through the kidneys. This hormone is also called the hormone of the adrenal cortex and mineralocorticoid. The most common and severe companion of this disease is arterial hypertension. Primary and secondary aldosteronism are not two stages of the same disease, but two completely different diseases. They differ in the causes of appearance, the effect on the body and, accordingly, the method of treatment.

Primary (Conn's syndrome) aldosteronism

Opened by the city of Conn in 1955. Women are 3 times more likely to suffer from aldosteronism. In the risk zone, the fair sex at the age of 25-45 years. Primary aldosteronism occurs due to neoplasms of the adrenal cortex (unilateral adenoma). Much less often, the cause is hyperplasia or cancer of the adrenal glands. With increased production of aldosterone, there is an increase in the amount of sodium in the kidneys, and potassium, in turn, decreases.

The study is carried out by a pathologist who diagnoses a tumor of the adrenal cortex. It can be single or multiple and involve one or both of the adrenal glands. In more than 95% of cases, the tumor is benign. Also, as a study, doctors often prescribe an enzyme immunoassay, where venous blood is used as a biomaterial. An ELISA is prescribed to determine the amount of aldosterone in the body and to screen for primary hyperaldosteronism.

Conn's syndrome occurs with the pathology of the adrenal glands, tumor neoplasms.

The indications for the study are most often high blood pressure, which does not return to normal during therapeutic manipulations, suspicion of the development of renal failure. Getting ready to donate blood is essential. First, limit the consumption of foods rich in carbohydrates for 2-4 weeks. Also for this period to exclude diuretics, estrogens, oral contraceptives, steroids. Stop therapy with renin inhibitors for 1 week, remove for 3 days, in extreme cases - limit moral and physical overstrain. Do not smoke for three hours before the procedure. Having the results on hand, taking into account the amount of renin, aldosterone and cortisone hormones, the attending physician will be able to correctly diagnose and prescribe an effective drug treatment.

Secondary compensatory (symptomatic)

Unlike primary aldosteronism, secondary aldosteronism is not triggered by diseases associated with the adrenal glands, but by problems with the liver, heart, and kidneys. That is, it acts as a complication of some serious diseases. At risk are patients diagnosed with:

• adrenal cancer;
• a number of heart diseases;
• abnormalities in the work of the thyroid gland, intestines;
• idiopathic hyperaldosteronism;
• adrenal adenoma.

Also to the list should be added a tendency to bleeding, prolonged exposure to medications. But this does not mean that all patients who suffer from these ailments will add the diagnosis of “secondary aldosteronism” to their medical history, they just should be more attentive to their health.

Symptoms of the disease

Persistent arterial hypertension is a characteristic symptom of Conn's syndrome.

Primary and secondary aldosteronism are associated with the manifestation of such symptoms:

1. swelling that appears due to fluid retention in the body;
2. weakening of muscle strength, fatigue;
3. frequent urination, especially at night (pollakiuria);
4. hypertension (increased blood pressure);
5. thirst;
6. vision problems;
7. feeling unwell, headache;
8. muscle paralysis for short periods of time, numbness of body parts, mild tingling;
9. an increase in the size of the ventricles of the heart;
10. rapid weight gain - more than 1 kg per day.

The evacuation of potassium contributes to the appearance of weakness in the muscles, paresthesia, sometimes muscle paralysis and many other kidney diseases. The symptoms of aldosteronism are quite dangerous, but the consequences are no less dangerous. Therefore, do not hesitate, you need to contact the doctor for help as soon as possible.

Complications and consequences

Primary aldosteronism, in case of ignoring symptoms and refusing therapy, leads to a number of complications. First of all, the heart begins to suffer (ischemia), heart failure develops, intracranial bleeding develops. In rare cases, the patient has a stroke. Since the amount of potassium in the body decreases, hypokalemia develops, which provokes arrhythmia, and that, in turn, can lead to death. Secondary hyperaldosteronism itself is a complication of other serious ailments.

Diagnosis and differential diagnosis

Urine and blood tests are prescribed for the correct and accurate diagnosis of the disease.

If the attending physician suspects aldosteronism, a number of studies and analyzes are prescribed to confirm or refute the alleged diagnosis, as well as for the correct further drug therapy. First of all, urine and blood tests are performed. The laboratory establishes or refutes the presence of polyuria or analyzes its urine density. In the blood, the concentration of aldosterone, cortisol and renin is studied. In primary hyperaldosteronism, renin is low, cortisol is normal, and aldosterone is high. For secondary aldosteronism, a somewhat different situation is inherent, the presence of renin must be significant. For more accurate results, ultrasound is often used. Rarely - MRI and CT of the adrenal glands. Additionally, the patient should be examined by a cardiologist, ophthalmologist, nephrologist.

Treatment of aldosteronism

Treatment of primary or secondary aldosteronism should be comprehensive and include not only drug therapy, but also proper nutrition, and in some cases surgical intervention. The main goal of curing Conn's syndrome is to prevent complications after The diet for Crohn's disease depends on the severity of the disease's symptoms.

In parallel, you should follow a diet. It is based on an increase in potassium-containing foods and additional potassium-containing drugs. Eliminate or limit salt intake. Foods rich in potassium include:

• dried fruits (raisins, dried apricots, prunes);
• fresh fruits (grapes, melon, apricots, plums, apples, banana);
• fresh vegetables (tomatoes, potatoes, garlic, pumpkin);
• greenery;
• meat;
• nuts;
• Black tea.

Conn's (Kohn's) syndrome is a complex of symptoms caused by hyperproduction of aldosterone by the adrenal cortex. The cause of the pathology is a tumor or hyperplasia of the glomerular zone of the cortical layer. In patients, blood pressure rises, the amount of potassium decreases and the concentration of sodium in the blood increases.

The syndrome has several equivalent names: primary hyperaldosteronism, aldosteroma. These medical terms unite a number of diseases similar in clinical and biochemical characteristics, but different in pathogenesis. Conn's syndrome is a pathology of the endocrine glands, manifested by a combination of myasthenia gravis, unnaturally strong, unquenchable thirst, high blood pressure and an increased volume of urine excreted per day.

Aldosterone performs vital functions in the human body. The hormone contributes to:

• absorption of sodium into the blood
• development of hypernatremia
• excretion of potassium in the urine
• alkalization of blood
• underproduction of renin.

When the level of aldosterone in the blood rises, the functioning of the circulatory, urinary and neuromuscular systems is disrupted.

The syndrome is extremely rare. It was first described by the American scientist Conn in 1955, which is how it got its name. The endocrinologist characterized the main clinical manifestations of the syndrome and proved that the most effective method of treating pathology is surgery. If patients monitor their health and regularly visit doctors, the disease is detected on time and responds well to treatment. Removal of an adenoma of the adrenal cortex leads to a complete recovery of patients.

Pathology is more common in women aged 30-50 years. In men, the syndrome develops 2 times less often. Very rarely, the disease affects children.

Etiology and pathogenesis

Etiopathogenetic factors of Conn's syndrome:

1. The main cause of Conn's syndrome is the excessive secretion of the hormone aldosterone by the adrenal glands, due to the presence in the outer cortical layer of a hormonally active tumor - aldosteroma. In 95% of cases, this neoplasm is benign, does not give metastases, has a unilateral course, is characterized only by an increase in the level of aldosterone in the blood and causes serious disturbances in the water-salt metabolism in the body. The adenoma has a diameter of less than 2.5 cm. On the cut, it is yellowish in color due to the high cholesterol content.
2. Bilateral hyperplasia of the adrenal cortex leads to the development of idiopathic hyperaldosteronism. The cause of the development of diffuse hyperplasia is a hereditary predisposition.
3. Less commonly, the cause can be a malignant tumor - adrenal carcinoma, which synthesizes not only aldosterone, but also other corticosteroids. This tumor is larger - up to 4.5 cm in diameter or more, capable of invasive growth.

Pathogenetic links of the syndrome:

• hypersecretion of aldosterone
• decreased activity of renin and angiotensin,
• tubular excretion of potassium,
• hyperkaliuria, hypokalemia, lack of potassium in the body,
• development of myasthenia gravis, paresthesia, transient muscle paralysis,
• increased absorption of sodium, chlorine and water,
• fluid retention in the body
• hypervolemia,
• swelling of the walls and vasoconstriction,
• increase in OPS and BCC,
• increase in blood pressure,
• vascular hypersensitivity to pressor influences,
• hypomagnesemia,
• increased neuromuscular excitability,
• violation of mineral metabolism,
• dysfunction of internal organs,
• interstitial inflammation of the renal tissue with an immune component,
• nephrosclerosis,
• the appearance of renal symptoms - polyuria, polydipsia, nocturia,
• development of renal failure.

Persistent hypokalemia leads to structural and functional disorders in organs and tissues - in the tubules of the kidneys, smooth and skeletal muscles, and the nervous system.

Factors contributing to the development of the syndrome:

1. diseases of the cardiovascular system,
2. concomitant chronic diseases,
3. decrease in the protective resources of the body.

Symptoms

The clinical manifestations of primary hyperaldosteronism are very diverse. Patients simply do not pay attention to some of them, which makes it difficult to diagnose pathology early. Such patients come to the doctor with an advanced form of the syndrome. This forces specialists to limit themselves to palliative care.

Symptoms of Conn's syndrome:

• muscle weakness and fatigue,
• paroxysmal tachycardia,
• tonic-clonic convulsions,
• headache,
• constant thirst
• polyuria with low relative density of urine,
• paresthesia of the limbs
• laryngospasm, dyspnoea,
• arterial hypertension.

Conn's syndrome is accompanied by signs of damage to the heart and blood vessels, kidneys, and muscle tissue. Arterial hypertension is malignant and resistant to antihypertensive therapy, as well as moderate and mild, well treatable. It can have a crisis or a stable course.

1. Elevated blood pressure is usually normalized with great difficulty with the help of antihypertensive drugs. This leads to the appearance of characteristic clinical signs - dizziness, nausea and vomiting, shortness of breath, cardialgia. In every second patient, hypertension is of a crisis nature.
2. In severe cases, they experience tetany attacks or the development of flaccid paralysis. Paralysis occurs suddenly and may persist for several hours. Hyporeflexia in patients is combined with diffuse motor deficits, which is manifested by myoclonic twitches during the study.
3. Persistent hypertension leads to the development of complications from the heart and nervous systems. Hypertrophy of the left chambers of the heart ends with progressive coronary insufficiency.
4. Arterial hypertension disrupts the functioning of the organ of vision: the fundus of the eye changes, the optic nerve disc swells, visual acuity decreases up to complete blindness.
5. Muscle weakness reaches an extreme degree of severity, not allowing patients to move. Constantly feeling the weight of their body, they cannot even get out of bed.
6. In severe cases, nephrogenic diabetes insipidus may develop.

There are three options for the course of the disease:

1. Conn's syndrome with the rapid development of symptoms - dizziness, arrhythmia, impaired consciousness.
2. The monosymptomatic course of the disease is an increase in blood pressure in patients.
3. Primary hyperaldosteronism with mild clinical signs - malaise, fatigue. The syndrome is discovered by chance during a physical examination. In patients with time, secondary inflammation of the kidneys develops against the background of existing electrolyte disturbances.

If signs of Conn's syndrome appear, you should visit a doctor. In the absence of correct and timely therapy develop dangerous complications that pose a real threat to the life of the patient. Due to prolonged hypertension, severe diseases of the cardiovascular system, up to strokes and heart attacks, can develop. Perhaps the development of hypertensive retinopathy, severe myasthenia gravis and malignancy of the tumor.

Diagnostics

Diagnostic measures for suspected Conn's syndrome include laboratory tests, hormonal studies, functional tests and topical diagnostics.

• Blood test for biochemical parameters - hypernatremia, hypokalemia, alkalization of blood, hypocalcemia, hyperglycemia.
• Hormonal examination - an increase in the level of aldosterone in plasma.
• General analysis of urine - determination of its relative density, calculation of daily diuresis: iso- and hypostenuria, nocturia, alkaline urine reaction.
• Specific tests - determination of the level of renin in the blood, the ratio of plasma aldosterone and renin activity, determination of the level of aldosterone in the daily portion of urine.
• To increase the activity of renin in the blood plasma, stimulation is carried out by long walking, a hyposodium diet and the intake of diuretics. If renin activity does not change even after stimulation, then patients have Conn's syndrome.
• To identify the urinary syndrome, a test with "Veroshpiron" is carried out. The drug is taken 4 times a day for three days with a restriction of daily salt intake to six grams. An elevated level of potassium in the blood on the 4th day is a sign of pathology.
• CT and MRI of the abdominal cavity - detection of aldosteroma or bilateral hyperplasia, its type and size, determination of the volume of the operation.
• Scintigraphy - detection of a neoplasm of the adrenal gland that secretes aldosterone.
• Oxysuprarenography allows you to determine the location and size of the tumor of the adrenal glands.
• Adrenal ultrasound with color Doppler imaging has high sensitivity, low cost, and is performed to visualize aldosteroma.
• On the ECG - metabolic changes in the myocardium, signs of hypertension and overload of the left ventricle.
• Molecular genetic analysis - identification of familial forms of aldosteronism.

Topical methods - CT and MRI - with great accuracy reveal a neoplasm in the adrenal gland, but do not provide information about its functional activity. It is necessary to compare the revealed changes on the tomogram with the data of hormonal tests. The results of a comprehensive examination of the patient allow specialists to correctly diagnose and prescribe competent treatment.

Persons with arterial hypertension deserve special attention. Specialists pay attention to the presence of clinical symptoms of the disease - severe hypertension, polyuria, polydipsia, muscle weakness.

Treatment

Therapeutic measures for Conn's syndrome are aimed at correcting hypertension and metabolic disorders, as well as preventing possible complications caused by high blood pressure and a sharp decrease in potassium in the blood. Conservative therapy is not able to radically improve the condition of patients. They can fully recover only after removal of the aldosteroma.

adrenalectomy

Surgery is indicated for patients with adrenal aldosteroma. Unilateral adrenalectomy is a radical method consisting in partial or complete resection of the affected adrenal gland. Most patients are indicated for laparoscopic surgery, the advantage of which is a slight soreness and tissue trauma, a short recovery period, small incisions that leave small scars. 2-3 months before surgery, patients should start taking diuretics and antihypertensive drugs of various pharmacological groups. After the surgical treatment, recurrence of Conn's syndrome is usually not observed. The idiopathic form of the syndrome is not subject to surgical treatment, since even a total resection of the adrenal glands will not help normalize the pressure. Such patients are shown lifelong treatment with aldosterone antagonists.

If the cause of the syndrome is adrenal hyperplasia or an idiopathic form of pathology occurs, conservative therapy is indicated. Patients are prescribed:

1. Potassium-sparing diuretics - Spironolactone,
2. Glucocorticosteroids - "Dexamethasone",
3. Antihypertensive drugs - Nifedipine, Metoprolol.

For the treatment of primary hyperaldosteronism, it is necessary to follow a diet and limit the intake of table salt to 2 grams per day. A sparing regimen, moderate physical activity and maintaining optimal body weight significantly improve the condition of patients.

Strict adherence to the diet reduces the severity of the clinical signs of the syndrome and increases the chances of patients to recover. Patients should eat homemade food that does not contain flavor enhancers, flavorings and other additives. Doctors do not recommend overeating. It is better to eat small meals every 3 hours. The basis of the diet should be fresh fruits and vegetables, cereals, lean meat, potassium-containing foods. Drink at least 2 liters of water per day. The diet excludes 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 decoctions and tinctures.

• frequent walks in the fresh air,
• sports,
• smoking cessation and abstinence from alcohol,
• giving up fast food.

The prognosis for diagnosed Conn's syndrome is usually favorable. It depends on the individual characteristics of the patient's body and the professionalism of the attending physician. It is important to seek medical help in time, 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 Conn's syndrome, the program “Live healthy!”