Home Coated tongue Conn's syndrome is primary aldosteronism. Primary hyperaldosteronism (Conn's syndrome)

Coated tongue

Conn's syndrome is primary aldosteronism. Primary hyperaldosteronism (Conn's syndrome)

– 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 heart rhythm disturbances, blurred vision, muscle weakness, paresthesia, and convulsions are observed. With secondary hyperaldosteronism, peripheral edema, chronic renal failure, and fundus changes develop. Diagnostics various types hyperaldosteronism includes biochemical analysis blood and urine, functional stress tests, ultrasound, scintigraphy, MRI, selective venography, examination of the condition of the heart, liver, kidneys and renal arteries. Treatment of hyperaldosteronism in aldosteroma, adrenal cancer, and renal reninoma is surgical; in other forms, it is medicinal.

ICD-10

E26

General information

Hyperaldosteronism includes a whole complex of syndromes, different in pathogenesis, but similar in clinical signs, occurring with excessive secretion of aldosterone. Hyperaldosteronism can be primary (caused by pathology of the adrenal glands themselves) and secondary (caused by hypersecretion of renin in other diseases). Primary hyperaldosteronism diagnosed in 1-2% of patients with symptomatic arterial hypertension. In endocrinology, 60-70% of patients with primary hyperaldosteronism are women aged 30-50 years; A few cases of hyperaldosteronism among children have been 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 goes beyond the control of the renin-angiotensin system and is corrected by glucocorticoids (occurs in patients young with a frequent family history of hypertension). In rare cases, primary hyperaldosteronism may be caused by adrenal cancer, which can produce aldosterone and deoxycorticosterone.

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

Increased renin secretion and the development of secondary hyperaldosteronism are caused by sodium loss (due to diet, diarrhea), a decrease in circulating blood volume due to blood loss and dehydration, excessive potassium intake, long-term intake of certain medicines(diuretics, COCs, laxatives). Pseudohyperaldosteronism develops when the response of the distal renal tubules to aldosterone is impaired, when, despite its high level in the blood serum, hyperkalemia is observed. Extra-adrenal hyperaldosteronism is observed quite rarely, for example, in pathologies of the ovaries, thyroid gland and intestines.

Pathogenesis

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

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

Secondary (high aldosteronism) hyperaldosteronism occurs compensatory, in response to a decrease in the volume of renal blood flow in various diseases of the kidneys, liver, and heart. Secondary hyperaldosteronism develops due to 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. Severe electrolyte disturbances characteristic of primary hyperaldosteronism do not occur in the secondary form.

Symptoms of hyperaldosteronism

The clinical picture of primary hyperaldosteronism reflects disturbances in water and electrolyte balance caused by hypersecretion of aldosterone. Due to sodium and water retention, patients with primary hyperaldosteronism experience severe or moderate arterial hypertension, headaches, aching pain in the heart (cardialgia), heart rhythm disturbances, changes in the fundus with worsening visual function(hypertensive angiopathy, angiosclerosis, retinopathy).

Potassium deficiency leads to the appearance fatigue, muscle weakness, paresthesia, seizures in various groups muscles, periodic pseudoparalysis; in severe cases - to the development of myocardial dystrophy, kalipenic nephropathy, nephrogenic diabetes insipidus. In 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). Most a common symptom secondary hyperaldosteronism are edema, hypokalemia occurs in rare cases. Secondary hyperaldosteronism can occur without arterial hypertension (for example, with Barter syndrome and pseudohyperaldosteronism). Some patients experience asymptomatic hyperaldosteronism.

Diagnostics

Diagnostics involves differentiation various forms hyperaldosteronism and determination of their etiology. Within 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 the secretion of aldosterone.

Primary hyperaldosteronism is characterized by an increase in the level of aldosterone in the blood serum, a decrease in plasma renin activity (PRA), 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 increased rate ARP (for reninoma - more than 20–30 ng/ml/h).

For the purpose of differentiation separate forms hyperaldosteronism, a test with spironolactone, a test with a hypothiazide load, and a “marching” test are performed. In order to identify the familial form of hyperaldosteronism, genomic typing is performed using PCR. With hyperaldosteronism corrected by glucocorticoids, diagnostic value has a trial treatment with dexamethasone (prednisolone), which eliminates the manifestations of the disease and normalizes arterial pressure.

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, liver ultrasound, kidney ultrasound, ultrasound and duplex scanning renal arteries, multislice CT, MR angiography).

Treatment of hyperaldosteronism

The choice of method and tactics for treating hyperaldosteronism depends on the cause of aldosterone hypersecretion. Patients are examined by an endocrinologist, cardiologist, nephrologist, and ophthalmologist. Drug treatment potassium-sparing diuretics (spirolactone) are carried out with different forms hyporeninemic hyperaldosteronism (adrenal cortical hyperplasia, aldosterome) as preparatory stage before surgery, which helps 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 administration of potassium supplements, is indicated.

Treatment of aldosteroma and adrenal cancer is surgical and consists of removing the affected adrenal gland (adrenalectomy) with 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 adrenalectomy in combination with subtotal resection of the left adrenal gland are ineffective. Hypokalemia disappears, but the desired hypotensive effect is absent (BP is normalized only in 18% of cases) and there is a high risk of developing acute adrenal insufficiency.

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

In the case of secondary hyperaldosteronism due to renal artery stenosis, to normalize blood circulation and kidney function, percutaneous x-ray endovascular balloon dilation, stenting of the affected renal artery, or open reconstructive surgery are possible. If renal 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 provides a high probability of recovery. Adrenal cancer has a poor prognosis.

In order to prevent hyperaldosteronism, constant clinical monitoring of persons with arterial hypertension, liver and kidney diseases is necessary; compliance medical recommendations regarding medication and diet.

Aldosteronism is a clinical syndrome associated with increased production of the adrenal hormone aldosterone in the body. There are primary and secondary aldosteronism. Primary aldosteronism (Conn's syndrome) occurs with a tumor of the adrenal gland. It is manifested by increased blood pressure, changes in mineral metabolism (the content in the blood sharply decreases), muscle weakness, seizures, and increased excretion of aldosterone in the urine. Secondary aldosteronism is associated with increased production of aldosterone by the normal adrenal glands due to excessive stimuli regulating its secretion. It is observed in heart failure, some forms of chronic nephritis and cirrhosis of the liver.

Disturbances of mineral metabolism in secondary aldosteronism are accompanied by the development of edema. With kidney damage, aldosteronism increases. Treatment of primary aldosteronism is surgical: removal of the adrenal tumor leads to recovery. In case of secondary aldosteronism, along with the treatment of the disease that caused aldosteronism, aldosterone blockers (aldactone 100-200 mg 4 times a day orally for a week) and diuretics are prescribed.

Aldosteronism is a complex of changes in the body caused by increased secretion of aldosterone. Aldosteronism can be primary or secondary. Primary aldosteronism (Conn's syndrome) is caused by overproduction of aldosterone by a hormonally active tumor of the adrenal gland. Clinically manifested by hypertension, muscle weakness, seizures, polyuria, a sharp decrease in potassium content in the blood serum and increased excretion of aldosterone in the urine; As a rule, there is no swelling. Removal of the tumor leads to a decrease in blood pressure and normalization of electrolyte metabolism.

Secondary aldosteronism is associated with dysregulation of aldosterone secretion in the zona glomerulosa of the adrenal glands. A decrease in the volume of the intravascular bed (as a result of hemodynamic disorders, hypoproteinemia or changes in the concentration of electrolytes in the blood serum), an increase in the secretion of renin, adrenoglomerulotropin, ACTH leads to hypersecretion of aldosterone. Secondary aldosteronism is observed in heart failure (congestion), liver cirrhosis, edematous and edematous-hypertensive forms of chronic diffuse glomerulonephritis. The increased aldosterone content in these cases causes increased sodium reabsorption in the renal tubules and thereby may contribute to the development of edema. In addition, increased aldosterone secretion during hypertensive form diffuse glomerulonephritis, pyelonephritis or occlusive lesions of the renal arteries, as well as hypertension in late stages its development and malignant course leads to the redistribution of electrolytes in the walls of arterioles and to increased hypertension. Suppression of the action of aldosterone at the level of the renal tubules is achieved by using its antagonist, aldactone, 400-800 mg per day per os for a week (under the control of the excretion of electrolytes in the urine) in combination with conventional diuretics. To suppress aldosterone secretion (in edematous and edematous-hypertensive forms of chronic diffuse glomerulonephritis, liver cirrhosis), prednisolone is prescribed.

Aldosteronism. There are primary (Conn's syndrome) and secondary hyperaldosteronism. Primary hyperaldosteronism was described by J. Conn in 1955. In the occurrence of this clinical syndrome The leading role belongs to the production of excess aldosterone by the adrenal cortex.

In the majority of patients (85%), the cause of the disease is an adenoma (synonymous with “aldosteroma”), less commonly, bilateral hyperplasia (9%) or carcinoma of the adrenal cortex of the zona glomerulosa and zona fasciculata.

More often the syndrome develops in women.

Clinical picture (symptoms and signs). With the disease, periodic attacks of cramps in various muscle groups are observed with normal levels of calcium and phosphorus in the blood, but with the presence of alkalosis outside the cells and acidosis inside the cells, positive Trousseau and Chvostek signs, sharp headaches, sometimes attacks of muscle weakness lasting from several hours to three weeks. The development of this phenomenon is associated with hypokalemia and depletion of potassium reserves in the body.

The disease develops arterial hypertension, polyuria, polydipsia, nocturia, severe inability to concentrate urine during dry eating, resistance to antidiuretic drugs, etc. The level of antidiuretic hormone is normal. Hypochloremia, achylia, alkaline urine reaction, periodic proteinuria, and decreased levels of potassium and magnesium in the blood are also noted. The sodium content increases, less often remains unchanged. As a rule, there is no swelling. The ECG shows myocardial changes characteristic of hypokalemia (see Hegglin's syndrome).

Urinary 17-hydroxycorticoid and 17-ketosteroid levels are normal, as are plasma ACTH levels.

Children with Conn's syndrome have growth retardation.

The oxygen content in arterial blood is reduced. The content of uropepsin in patients is increased.

Diagnostic methods. Suprapneumoreno-radiography and tomography, determination of aldosterone and potassium in urine and blood.

Treatment is surgical, adrenalectomy is performed.

The prognosis is favorable, but only until malignant hypertension develops.

Secondary hyperaldosteronism. The symptoms are the same as in Conn's syndrome, which develops in a number of conditions in the form of hypersecretion of aldosterone in response to stimuli originating outside the adrenal glands and acting through physiological mechanisms that regulate aldosterone secretion. Secondary hyperaldosteronism associated with edematous conditions leads to: 1) congestive heart failure; 2) nephrotic syndrome; 3) cirrhosis of the liver; 4) “idiopathic” edema.

Loss of significant amounts of fluids due to untreated diabetes insipidus and diabetes mellitus, salt-losing nephritis, sodium restriction in the diet, use of diuretics, and excessive physical stress also cause secondary hyperaldosteronism.

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

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

Leave a request and within a few minutes we will find you a trusted doctor and help you make an appointment with him. Or select 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, were described in 1955 by the American Jerome Conn. He noted that removal of the adenoma led to the recovery of the 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 intracranial hypertension, suggested that the disturbance 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 cause-and-effect relationship between these disorders was not finally identified.

Research conducted in 1979 by R. M. Carey et al. on the regulation of aldosterone by the renin-angiotensin-aldosterone system and the role of dopaminergic mechanisms in this regulation showed that aldosterone production is controlled by these mechanisms.

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

Research data obtained in 1987 -2006 suggest that hypothalamic structures influence hyperplasia of the zona glomerulosa of the adrenal cortex and hypersecretion of aldosterone.

In 2006, a number of authors (V. Perrauclin and others) revealed that vasopressin-containing cells are present in aldosterone-producing tumors. Researchers suggest the presence of V1a receptors in these tumors, 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 incidence of primary hyperaldosteronism among patients with arterial hypertension is 1-2%.

1% of incidentally detected adrenal tumors are aldosteromas.

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

Bilateral idiopathic adrenal hyperplasia as the cause of primary hyperaldosteronism is detected in most cases in men. Moreover, the development of this form of primary hyperaldosteronism is usually observed in more late age than aldosteromes.

Primary hyperaldosteronism is usually observed in adults.

The ratio of women to men aged 30-40 years 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 nosological principle. In accordance with this classification, the following are distinguished:

Aldosterone-producing adenoma (APA), which was described by Jerome Conn and called Conn's syndrome. Is detected in 30–50% of cases from total number diseases.
Idiopathic hyperaldosteronism (IHA) or bilateral small- or large-nodular hyperplasia of the zona glomerulosa, which is observed 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-unsuppressible), which accounts for less than 2% of all cases of the disease.
Aldosterone-producing carcinoma, detected in approximately 1% of patients.
Aldosteronectopic syndrome, which occurs with aldosterone-producing tumors located in 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 transition of fluid and sodium from the vascular bed to the tissues by enhancing the tubular reabsorption of sodium cations, chlorine anions and water and the tubular excretion of potassium cations. As a result of the action of mineralocorticoids, circulating blood volume increases and systemic blood pressure increases.

Conn's syndrome develops as a result of the formation of an aldosteroma, a benign adenoma that secretes aldosterone, in the adrenal glands. Multiple (solitary) aldosteromas are detected in 80 - 85% of patients. In most cases, aldosteroma is unilateral, and only in 6–15% of cases do bilateral adenomas form. 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 exceeding 30 mm are malignant, and 87% of tumors of smaller size are benign). In most cases, adrenal aldosteroma consists primarily of cells of the zona glomerulosa, but in 20% of patients the tumor consists primarily 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”).
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 zona glomerulosa of hyperplastic adrenal glands produces excess amounts of aldosterone, as a result of which the patient develops arterial hypertension and hypokalemia, and plasma renin levels decrease. The fundamental difference between this form of the disease is the preservation of sensitivity to the stimulating influence of angiotensin II in the hyperplastic zona glomerulosa. The formation of aldosterone in this form of Conn's syndrome is controlled by adrenocorticotropic hormone.
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 excretion of 17-ketosteroids in the urine.
Sometimes the cause of the disease is genetically determined glucocorticoid-sensitive aldosteronism, which is characterized by increased sensitivity zona glomerulosa of the adrenal cortex to adrenocorticotropic hormone and suppression of hypersecretion of aldosterone 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 chromosome 8, resulting in the formation of a defective enzyme.
In some cases, aldosterone levels increase due to the secretion of this hormone by extra-adrenal 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 through communication with receptors located in the kidney tubules, 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 enhanced, resulting in induced potassium loss. In this case, the pathophysiological effect of potassium loss overrides the effect of reabsorbed sodium. Thus, a complex of metabolic disorders characteristic of primary hyperaldosteronism is formed.

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

Potassium in 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 above 7.45.

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

In addition, hypokalemia:

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

As a result of these changes in the functioning of the body, a number of renal functions is disrupted - the concentrating ability of the kidneys decreases, hypervolemia develops, and the production of renin and angiotensin II is suppressed. These factors help to 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 interstitial sclerosis develop, so a 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 (gluco- 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 occurs under the influence of potassium ions and angiotensin-P. When mutation (unequal exchange during the process of meiosis of sections of homologous chromatids of the 11b-hydroxylase and aldosterone synthetase genes localized on chromosome 8), a defective gene is formed, including the 5ACTH-sensitive regulatory region of the 11b-hydroxylase gene and a 3′-nucleotide sequence that encodes the synthesis of the enzyme aldosterone synthetase . As a result, the zona fasciculata 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 heart rhythm disturbances. Arterial hypertension (AH) can be malignant, resistant to traditional antihypertensive therapy, or correctable even with small doses of antihypertensive drugs. In half of the cases, hypertension is of a crisis nature.

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

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 characterized by a sudden onset and end.

Paresthesia is 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 kaliopenic nephropathy. Renal syndrome is characterized by:

decreased concentration function of the kidneys;
polyuria (increased daily diuresis, detected in 72% of patients);
(increased urination at night);
(extreme thirst, which is observed in 46% of patients).

In severe cases, nephrogenic diabetes insipidus may develop.

Primary hyperaldosteronism can be monosymptomatic - in addition to elevated blood pressure, patients may not show any other symptoms, and potassium levels may not differ from normal.

With aldosterone-producing adenoma, myoplegic episodes and muscle weakness are observed more often than with idiopathic hyperaldosteronism.

Hypertension in the familial form of hyperaldosteronism manifests itself at an early age.

Diagnostics

Diagnosis primarily involves identifying Conn's syndrome among individuals with arterial hypertension. The selection criteria are:

Availability clinical symptoms diseases.
Blood plasma test data to determine potassium levels. The presence of persistent hypokalemia, in which the potassium content in 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 can detect metabolic changes. With hypokalemia, a decrease in the ST segment, inversion of the T wave is observed, the QT interval is prolonged, a pathological U wave and conduction disturbances are detected. Changes detected on the ECG do not always correspond to the true concentration of potassium in the plasma.
Availability urinary syndrome(a complex of various urination disorders and changes in the composition and structure of urine).

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

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, which allow us to analyze the structural state of the adrenal glands;
hormonal examination to determine the level of activity of the identified changes.

When studying the RAAS system, stress tests are carried out aimed at stimulating or suppressing the activity of the RAAS system. Since the secretion of aldosterone and the level of renin activity in the blood plasma is influenced by a number of exogenous factors, 10-14 days before the study exclude drug therapy, which can affect the results of the study.

Low plasma renin activity is stimulated by walking for an hour, a hyposodium diet, and diuretics. With unstimulated plasma renin activity in patients, aldosteroma or idiopathic adrenal hyperplasia is assumed, since with secondary aldosteronism this activity is subject to significant stimulation.

Tests to suppress excess aldosterone secretion include a high-sodium diet, deoxycorticosterone acetate, and intravenous administration isotonic solution. When performing these tests, aldosterone secretion does not change in the presence of aldosterone, which autonomously produces aldosterone, and with adrenal hyperplasia, suppression of aldosterone secretion is observed.

Selective adrenal venography is also used as the most informative x-ray method.

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

Treatment

Treatment of primary hyperaldosteronism depends on the form of the disease. Non-drug treatment includes limiting the use of table salt (less than 2 grams per day) and a gentle 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 surgery, patients are prescribed:

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

In idiopathic hyperaldosteronism it is justified conservative therapy using spironolactone, 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.).

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

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

Liqmed reminds you: the sooner you seek help from a specialist, the greater your chances of maintaining health and reducing the risk of complications.

Found a mistake? Select it and click Ctrl + Enter

print version

Conn's syndrome (primary aldosteronism, Conn syndrome) is a syndrome caused by autonomous (that is, independent of the renin-aldosterone system) hypersecretion of aldosterone in the adrenal cortex.

Causes of Conn's syndrome

The most common direct causes of its development are aldosterone-producing adrenal adenoma or bilateral adrenal hyperplasia; much less often - unilateral hyperplasia, adrenal carcinoma, or familial hyperaldosteronism (types I and II are distinguished). In persons under the age of 40 years, the cause of Conn's syndrome is much more often an adrenal adenoma than a bilateral adrenal hyperplasia.

Causes of hypersecretion of mineralocorticoids:

Aldosterone-producing adrenal adenoma

Aldosterone-producing adenomas account for about 35-40% of cases in the structure of primary aldosteronism. Solitary benign adenomas are almost always unilateral (one-sided). In most cases they are small in size (in 20-85% of cases - less than 1 cm). Beyond the adenoma, focal or diffuse tissue hyperplasia may occur in the rest of the adrenal tissue, as well as in the contralateral adrenal gland (making differential diagnosis with bilateral hyperplasia difficult).

Bilateral adrenal hyperplasia
Primary unilateral adrenal hyperplasia (rare)
Familial hyperaldosteronism (types I and II), glucocorticoid controlled (rare)
Adrenal carcinoma (rare)

Most cases of aldosteronism (increased plasma aldosterone levels) that occur in clinical practice are secondary to increased activity of the renin-aldosterone system (in response to decreased renal perfusion, such as in renal artery stenosis or in some chronic conditions, accompanied by the development of edema). For differential diagnosis You can use the determination of plasma renin activity (PRA):

with secondary aldosteronism this indicator is increased,
in Conn's syndrome - reduced.

Previously, the dominant point of view was the relative rarity of primary aldosteronism. However, with the increasing use of the aldosterone-renin ratio (ARR) technique, which allows identifying more soft shapes This condition (usually in bilateral adrenal hyperplasia), previously existing ideas about the prevalence of Conn's syndrome have changed. It is currently believed that primary aldosteronism is one of the most common (if not the most common) causes of the development of symptomatic arterial hypertension. Thus, some reports indicate that the proportion of people with Conn's syndrome among the general population of patients with arterial hypertension can reach 3-10%, and among patients with arterial hypertension of the 3rd degree - up to 40%.

Conn's syndrome can be detected in any age group(most typical age- 30-50 years), more often in women. Classic clinical and laboratory symptoms of primary aldosteronism include:

arterial hypertension;
hypokalemia;
excessive excretion of potassium by the kidneys;
hypernatremia;
metabolic alkalosis.

Let's take a closer look at some of these manifestations.

Arterial hypertension

Arterial hypertension is present in almost all patients with Conn's syndrome.

Mechanisms of development of arterial hypertension

The pressor effects of an excess amount of aldosterone are predominantly associated with the development of sodium retention (this effect is realized through a complex of genomic mechanisms of the action of aldosterone on the sodium channels of tubular epithelial cells) and hypervolemia; a certain role is also assigned to increasing the overall peripheral resistance vessels.

Arterial hypertension in persons with Conn's syndrome is usually characterized by high levels of blood pressure, often occurring as resistant, malignant hypertension. Significant left ventricular hypertrophy may be detected, often disproportionate to the severity and duration of arterial hypertension. In its development important role attributed to increased processes of myocardial fibrosis due to the effect of excessive amounts of aldosterone on myocardial fibroblasts. The profibrotic effects of excessive concentrations of aldosterone (realized through its non-genomic mechanisms of action on target cells) can also be quite clearly represented in the vascular wall (with an acceleration of the rate of progression of atherosclerotic lesions) and in the kidneys (with an increase in the processes of interstitial fibrosis and glomerulosclerosis).

Hypokalemia

Hypokalemia is a common but not universal manifestation of Conn's syndrome. The presence and severity of hypokalemia may depend on a number of factors. Thus, it is almost always present and quite clearly expressed in aldosterone-producing adrenal adenoma, but may be absent in bilateral adrenal hyperplasia. Hypokalemia may also be absent or insignificant in severity in the early stages of the formation of Conn's syndrome, as well as with significant restriction of sodium intake from food (for example, during the restriction of table salt when changing the lifestyle recommended for a patient with arterial hypertension).

Experts indicate that potassium levels may increase (and hypokalemia may be eliminated/mask) when:

prolonged and painful venipuncture (mechanisms may include respiratory alkalosis during hyperventilation; release of potassium from muscle depots during repeated repeated clenching of the fist; venous stasis during prolonged compression with a tourniquet);
hemolysis of any nature;
the release of potassium from red blood cells in cases of delayed blood centrifugation and when the blood is kept in cold/ice.

Diagnosis of Conn's syndrome

Stages of diagnosing Conn's syndrome, establishing the type of adrenal lesion and choosing treatment tactics

Diagnosis of Conn's syndrome in people with arterial hypertension consists of several stages:

identification of primary aldosteronism itself, for which they use the study of blood and urine electrolytes, screening tests (primarily, determination of the aldosterone-renin ratio) and verification tests (with a sodium load, captopril, etc.);
establishing the type of adrenal gland lesion - uni- or bilateral (CT and separate study of the aldosterone content in the blood of each of the adrenal veins).

Detection of Conn's syndrome itself

Blood potassium and sodium levels are routine laboratory tests for hypertension. The detection of hypokalemia and hypernatremia already at the initial stage of the diagnostic search suggests the presence of Conn's syndrome. Diagnosis of primary aldosteronism is not very difficult in patients with a detailed picture of Conn's syndrome (primarily with clear hypokalemia not associated with other causes). However, over the past two decades, there has been a frequent possibility of primary aldosteronism among individuals with normokalemia. Taking this into account, it is considered necessary to carry out additional research to exclude Conn's syndrome in a fairly wide category of patients with arterial hypertension:

at a blood pressure level >160/100 mm Hg. Art. (and, especially, >180/110 mmHg and);
with resistant arterial hypertension;
in persons with hypokalemia (both spontaneous and induced by the use of a diuretic, especially if it persists after taking potassium supplements);
for arterial hypertension in persons with an increase in the size of the adrenal gland according to data instrumental studies(adrenal incidentaloma; however, it has been shown that only ~1% of all adrenal incidentalomas are the cause of primary aldosteronism).

Assessing the excretion of electrolytes (potassium and sodium) in urine

This study occupies a fairly important place in diagnosing the causes of hypokalemia. Potassium and sodium levels are tested in urine collected over a 24-hour period from a patient who is not receiving potassium supplements and who has abstained from taking any diuretics for at least 3-4 days. If sodium excretion exceeds 100 mmol/day (this is the level at which the degree of potassium loss can be clearly assessed), a potassium excretion level >30 mmol/day indicates hyperkaliuria. Along with primary aldosteronism, increased potassium excretion may be due to a number of reasons.

Causes of hypokalemia associated with increased excretion of potassium by the kidneys:

Increased potassium excretion by nephron collecting ducts:
1. increased sodium excretion (eg, when taking a diuretic)
2. increased urine osmolarity (glucose, urea, mannitol)
High potassium concentration in the nephron collecting duct:
- with an increase in intravascular blood volume ( low level plasma renin):
  - primary aldosteronism
  - Liddle syndrome
  - taking amphotericin B
- with a decrease in intravascular blood volume (high plasma renin level):
  - Bartter syndrome
  - Giletman syndrome
  - hypomagnesemia
  - increased bicarbonate excretion
  - secondary aldosteronism (eg, in nephrotic syndrome)

Once it has been established that the cause of the patient's hypokalemia is an increase in potassium excretion in the urine, it is considered advisable to attempt to correct the hypokalemia. In the absence of contraindications, potassium supplements are prescribed (potassium 40-80 mmol/day), and diuretics are discontinued. It may take from 3 weeks to several months to restore potassium deficiency after prolonged use of diuretics. After this period, potassium supplements are discontinued and blood potassium testing is repeated >3 days after discontinuation. If blood potassium levels return to normal, plasma renin and aldosterone levels should be re-evaluated.

Aldosterone-renin ratio assessment

This test is currently considered as the main screening method in the diagnosis of Conn's syndrome. Normal values for aldosterone levels when drawing blood with the patient in the supine position are 5-12 ng/dl (in SI units - 180-450 pmol/l), plasma renin activity is 1-3 ng/ml/h, aldosterone-renin ratio is up to 30 (in SI units - up to 750). It is important to note that the normal indicator values given are only approximate values; for each specific laboratory (and for specific laboratory kits) they may differ (comparison with indicators in healthy individuals and in individuals with essential arterial hypertension is required). Taking into account such insufficient standardization of the method, one can agree with the opinion that when interpreting the results of assessing the aldosterone-renin ratio, “flexibility of judgment is required from the clinician.” Below are the main recommendations for assessing the aldosterone-renin ratio.

Recommendations for assessing the aldosterone-renin ratio

Patient preparation:

Correction of hypokalemia if present.

Liberalization of table salt intake.

Discontinuing for at least 4 weeks drugs that increase renin levels and decrease aldosterone concentrations, which causes false results:
spironolactone, eplerenone, amiloride, triamterene;

products containing licorice.

Discontinuing for at least 2 weeks other drugs that may affect the test result:
β-AB, central α2-agonists (clonidine), NSAIDs (reduce renin levels);

ACE inhibitors, sartans, direct renin inhibitors, dihydropyridine calcium channel blockers (increase renin levels, reduce aldosterone levels).

If it is impossible to discontinue these medications in patients with stage 3 arterial hypertension, it is permissible to continue taking them with mandatory discontinuation of spironolactone, eplerenone, triamterene and amiloride for at least 6 weeks before the study.

Cancellation of estrogen-containing drugs.

Conditions for blood sampling:

Blood should be collected in the middle of the morning, approximately 2 hours after the patient wakes up and gets out of bed. Immediately before blood collection, the patient should sit for 5-15 minutes.

Blood must be collected carefully, avoiding stasis and hemolysis.

Before centrifugation, the blood sample should be at room temperature (not on ice, which will facilitate the conversion of inactive renin to active); After centrifugation, plasma should be quickly frozen.

Factors to consider when interpreting results

Age (in persons over 65 years of age, there is a greater age-related decrease in renin compared to aldosterone).

Time of day, recent dietary regimen, body position, length of stay in this position.

Medicines taken.

Details of the blood sample collection, including any difficulties encountered.

Blood potassium levels.

Decreased renal function (there may be an increase in aldosterone due to hyperkalemia and a decrease in renin secretion).

The recommendation of Kaplan N.M. seems important from a practical point of view:

“Recommendations for assessing the aldosterone-renin ratio should be followed as closely as possible. Next, the levels of aldosterone and plasma renin activity should be assessed separately, without yet calculating the relationship between them. If plasma renin activity is clearly low (<0,5 нг/мл/ч) и уровень альдостерона плазмы явно повышен (>15 mg/dl), then it is advisable to repeat this measurement again. If low values plasma renin activity and high levels aldosterone levels will be confirmed, we should proceed to verification tests.”

Studying the aldosterone-renin ratio, as well as conducting all further studies, requires discussing their purpose with the patient; A diagnostic search (with a cost of time and money) should be planned taking into account the patient’s readiness and desire to undergo a laparoscopic adrenalectomy in the future if an adrenal adenoma is detected.

Verification test - captopril test

Plasma aldosterone levels are assessed before and 3 hours after oral administration of captopril at a dose of 1 mg/kg body weight of the subject (in healthy people and in patients with essential and renovascular hypertension, aldosterone levels clearly decrease, but in Conn’s syndrome this does not happen). A normal response is considered to be a decrease in aldosterone levels by >30% of baseline values.

Treatment of Conn's syndrome

Long-term treatment using mineralocorticoid receptor antagonists (spironolactone or eplerenone), if they are intolerant - amiloride; Often, combination with a thiazide diuretic can be the treatment approach of choice in patients:

for whom surgical intervention is not possible;
who do not want to carry it out;
in whom arterial hypertension persists after surgery;
the diagnosis of Conn's syndrome, in which it remains not fully confirmed despite the examination.

The use of mineralocorticoid receptor antagonists in individuals with Conn's syndrome provides a fairly clear reduction in blood pressure and allows regression of left ventricular hypertrophy. At the initial stages of treatment, doses of 50-100 mg/day or more of spironolactone or eplerenone may be required; subsequently, lower dosages (25-50 mg/day) are quite effective. The dose of these drugs can be reduced by combining them with thiazide diuretics. For long-term treatment Conn's syndrome is a selective representative of the mineralocorticoid receptor antagonists eplerenone with its inherent frequency significantly lower than that of spironolactone side effects may be considered as the drug of choice.

If others are necessary, the initial choice includes calcium channel blockers (eg, amlodipine), since in high doses they have some ability to block aldosterone receptors. To control arterial hypertension, other classes of antihypertensive drugs can be used as components of treatment tactics.

In persons with adrenal carcinoma, drugs from the group of steroidogenesis antagonists can be used.

Conn's syndrome (Conn) is a complex of symptoms caused by overproduction of aldosterone by the adrenal cortex. The cause of the pathology is a tumor or hyperplasia of the glomerular zone of the cortex. In patients, blood pressure increases, 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 combine a number of diseases that are 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 released per day.

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

absorption of sodium into the blood,
development of hypernatremia,
excretion of potassium in urine,
alkalization of blood,
hypoproduction of renin.

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

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

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

Etiology and pathogenesis

Etiopathogenetic factors of Conn's syndrome:

The main cause of Conn's syndrome is the excessive secretion of the hormone aldosterone by the adrenal glands, caused by the presence of a hormonally active tumor in the outer cortical layer - aldosteroma. In 95% of cases, this neoplasm is benign, does not metastasize, has a unilateral course, is characterized only by an increase in the level of aldosterone in the blood and causes serious disorders water-salt metabolism in organism. 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.
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.
Less commonly, the cause may be 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, and is 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, paresthesias, transient muscle paralysis,
enhanced absorption of sodium, chlorine and water,
fluid retention in the body,
hypervolemia,
swelling of the walls and constriction of blood vessels,
increase in OPS and BCC,
increased blood pressure,
vascular hypersensitivity to pressor influences,
hypomagnesemia,
increased neuromuscular excitability,
disturbance of mineral metabolism,
dysfunction of internal organs,
interstitial inflammation of the kidney tissue with an immune component,
nephrosclerosis,
appearance kidney symptoms- polyuria, polydipsia, nocturia,
development renal failure.

Persistent hypokalemia leads to structural and functional disorders in organs and tissues - in the kidney tubules, smooth and skeletal muscles, nervous systems e.

Factors contributing to the development of the syndrome:

diseases of the cardiovascular system,
concomitant chronic pathologies,
reduction of the body's protective resources.

Symptoms

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

Symptoms of Conn's syndrome:

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

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

High blood pressure is usually difficult to normalize with 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.
In severe cases, they experience attacks of tetany or the development of flaccid paralysis. Paralysis occurs suddenly and can last for several hours. Hyporeflexia in patients is combined with diffuse motor deficits, which is manifested by myoclonic twitches during examination.
Persistent hypertension leads to the development of complications from the heart and nervous systems. Hypertrophy of the left chambers of the heart ends in progressive coronary insufficiency.
Arterial hypertension disrupts the functioning of the organ of vision: the fundus of the eye changes, the disc swells optic nerve, visual acuity decreases up to complete blindness.
Muscle weakness reaches extreme severity, preventing patients from moving. Constantly feeling the weight of their body, they cannot even get out of bed.
In severe cases, nephrogenic diabetes insipidus may develop.

There are three variants of the course of the disease:

Conn's syndrome with rapid development of symptoms - dizziness, arrhythmia, impaired consciousness.
The monosymptomatic course of the disease is an increase in blood pressure in patients.
Primary hyperaldosteronism with mild clinical signs - malaise, fatigue. The syndrome is discovered accidentally during a medical examination. Over time, patients develop secondary inflammation of the kidneys 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 are developing dangerous complications, representing real threat for the life of the patient. Due to prolonged hypertension, they can develop serious illnesses cardiovascular system, up to strokes and heart attacks. The development of hypertensive retinopathy, severe myasthenia gravis and tumor malignancy is possible.

Diagnostics

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

Blood test for biochemical indicators - hypernatremia, hypokalemia, blood alkalization, hypocalcemia, hyperglycemia.
Hormonal examination - increase in plasma aldosterone levels.
General urine analysis - determination of its relative density, calculation of daily diuresis: iso- and hyposthenuria, 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 a daily urine sample.
To increase the activity of renin in the blood plasma, stimulation is carried out by long walking, a hyposodium diet and diuretics. If renin activity does not change even after stimulation, then the patient has Conn's syndrome.
To identify urinary syndrome, a test with Veroshpiron is performed. The drug is taken 4 times a day for three days, limiting daily salt intake to six grams. Increased level potassium in the blood on the 4th day is a sign of pathology.
CT and MRI of the abdominal cavity - identifying aldosteroma or bilateral hyperplasia, its type and size, determining the extent of the operation.
Scintigraphy - detection of a tumor of the adrenal gland that secretes aldosterone.
Oxysuprarenography allows you to determine the location and size of an adrenal tumor.
Ultrasound of the adrenal glands with color Doppler mapping has high sensitivity, low cost and is performed to visualize aldosteroma.
The ECG shows metabolic changes in the myocardium, signs of hypertension and left ventricular overload.
Molecular genetic analysis - identification of familial forms of aldosteronism.

Topical methods - CT and MRI - detect tumors in the adrenal gland with great accuracy, but do not provide information about its functional activity. It is necessary to compare the detected changes on the tomogram with the data of hormonal tests. Results comprehensive examination patients allow specialists to correctly diagnose and prescribe competent treatment.

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

Treatment

Treatment 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 capable of radically improving 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 minor pain and tissue trauma, short recovery period, small incisions that leave small scars. 2-3 months before surgery, patients should start taking diuretics and antihypertensive drugs different 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 blood pressure. Such patients are indicated for lifelong treatment with aldosterone antagonists.

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

Potassium-sparing diuretics - Spironolactone,
Glucocorticosteroids – “Dexamethasone”,
Antihypertensive drugs - Nifedipine, Metoprolol.

To treat primary hyperaldosteronism, it is necessary to follow a diet and limit the consumption of table salt to 2 grams per day. Gentle mode, moderate physical exercise 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 patients' chances of recovery. Patients should eat home-cooked food that does not contain flavor enhancers, flavorings or other additives. Doctors do not recommend overeating. It is better to eat small portions every 3 hours. The basis of the diet should be fresh fruits and vegetables, cereals, lean meat, and potassium-containing products. You should drink at least 2 liters of water per day. The diet excludes any type of alcohol, strong coffee, tea, and foods that increase blood pressure. Patients need to consume foods with a diuretic effect - watermelons and cucumbers, as well as special decoctions and tinctures.

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

The prognosis for diagnosed Conn's syndrome is usually favorable. It depends on individual characteristics the patient’s body and the professionalism of the attending physician. It is important to apply for timely medical care, before the development of nephropathy and persistent hypertension. High blood pressure is a serious and dangerous problem health benefits associated with primary hyperaldosteronism.