Endocrine causes of hypertension. Endocrine hypertension. Instrumental examination methods

These hypertension account for up to 1% of all arterial hypertension (according to specialized clinics - up to 12%) and develop as a result of the hypertensive effect of a number of hormones.

Arterial hypertension in adrenal endocrinopathies. At least half of all cases of endocrine hypertension occur in adrenal arterial hypertension.

— Adrenal glands are the main endocrine organ that provides regulation of systemic blood pressure. All adrenal hormones normally have a more or less pronounced relationship to the regulation of blood pressure, and in pathology they participate in the formation and consolidation of high blood pressure.

+ Adrenal arterial hypertension are divided into catecholamine and corticosteroid, and the latter into mineralocorticoid and glucocorticoid.

— Mineralocorticoid arterial hypertension. In the pathogenesis of arterial hypertension, the excessive synthesis of the mineralocorticoid aldosterone (primary and secondary hyperaldosteronism) is of primary importance. Cortisol, 11-deoxycortisol, 11-deoxycorticosterone, corticosterone, although they have minor mineralocorticoid activity, are regarded as glucocorticoids (their total contribution to the development of arterial hypertension is small).

— Primary hyperaldosteronism. Arterial hypertension in primary hyperaldosteronism accounts for up to 0.4% of all cases of arterial hypertension. There are several etiological forms of primary hyperaldosteronism: Conn's syndrome (aldosterone-producing adenoma), adrenocortical carcinoma, primary adrenal hyperplasia, idiopathic bilateral adrenal hyperplasia. The main manifestations of primary hyperaldosteronism: arterial hypertension and hypokalemia (due to increased renal Na2+ reabsorption).

— Secondary aldosteronism. Develops as a consequence of pathological processes occurring in other organs and their physiological systems(for example, with cardiac, renal, liver failure). With these forms of pathology, hyperproduction of aldosterone can be observed in the zona glomerulosa of the cortex of both adrenal glands.

— Hyperaldosteronism of any origin is accompanied by an increase in blood pressure. The pathogenesis of arterial hypertension with hyperaldosteronism is shown in the figure.

General links in the pathogenesis of endocrine arterial hypertension.

+ Glucocorticoid arterial hypertension. They are the result of overproduction of glucocorticoids, mainly cortisol (17-hydrocortisone, hydrocortisone, which accounts for 80%; the remaining 20% is cortisone, corticosterone, 11-deoxycortisol and 11-deoxycorticosterone). Almost all arterial hypertension of glucocorticoid origin develops with Itsenko-Cushing's disease and syndrome.

+ Catecholamine arterial hypertension. They develop due to a significant increase in the blood content of catecholamines - adrenaline and norepinephrine, produced by chromaffin cells. In 99% of all cases of such hypertension, pheochromocytoma is detected. Arterial hypertension with pheochromocytoma occurs in less than 0.2% of cases of all arterial hypertension.

— Mechanism of hypertensive action excess catecholamines. Catecholamines simultaneously increase vascular tone and stimulate heart function.

— Norepinephrine stimulates mainly alpha-adrenergic receptors and, to a lesser extent, beta-adrenergic receptors. This leads to an increase in blood pressure due to the vasoconstrictor effect.

— Adrenalin affects both a- and beta-adrenergic receptors. In this regard, vasoconstriction (both arterioles and venules) and an increase in heart function (due to positive chrono- and inotropic effects) and blood release into the vascular bed are observed.

General links in the pathogenesis of arterial hypertension in hyperaldosteronism.

Taken together, these effects determine the development arterial hypertension.

— Manifestations pheochromocytomas varied but nonspecific. Arterial hypertension is noted in 90% of cases, headache occurs in 80% of cases, orthostatic arterial hypotension- in 60%, sweating - in 65%, palpitations and tachycardia - in 60%, fear of death - in 45%, pallor - in 45%, tremors of the limbs - in 35%, abdominal pain - in 15%, visual impairment - in 15% of cases. In 50% of cases, arterial hypertension can be constant, and in 50% it can be combined with crises. A crisis usually occurs out of connection with external factors. Hyperglycemia (as a result of stimulation of glycogenolysis) is often observed.

Endocrine arterial hypertension

Endocrine arterial hypertension accounts for approximately 0.1-1% of all arterial hypertension (up to 12% according to specialized clinics).

Pheochromocytoma

Arterial hypertension with pheochromocytoma occurs in less than 0.1 - 0.2% of cases of all arterial hypertension. Pheochromocytoma is a catecholamine-producing tumor, in most cases (85-90%) localized in the adrenal glands. In general, the “rule of ten” can be used to characterize it: in 10% of cases it is familial, in 10% it is bilateral, in 10% it is malignant, in 10% it is multiple, in 10% it is extra-adrenal, in 10% it develops in children .

Clinical manifestations of pheochromocytoma are very numerous, varied, but nonspecific. Arterial hypertension is noted in 90% of cases, headache occurs in 80% of cases, orthostatic arterial hypotension - in 60%, sweating - in 65%, palpitations and tachycardia - in 60%, fear - in 45%, pallor - in 45%, tremor of the limbs - in 35%, abdominal pain - in 15%, visual impairment - in 15% of cases. In 50% of cases, arterial hypertension can be constant, and in 50% it can be combined with crises. A crisis usually occurs without any connection with external factors. Hyperglycemia often occurs. It should be remembered that pheochromocytoma can appear during pregnancy and that it may be accompanied by other endocrine pathologies.
To confirm the diagnosis, laboratory and special research methods are used.

Ultrasound of the adrenal glands can usually detect a tumor when its size is more than 2 cm.

Determination of the content of catecholamines in blood plasma is informative only during a hypertensive crisis. Determining the level of catecholamines in urine during the day is of greater diagnostic importance. In the presence of pheochromocytoma, the concentration of adrenaline and norepinephrine should be more than 200 mcg/day. If the values are questionable (concentration 51-200 mcg/day), a test with clonidine suppression is performed. Its essence lies in the fact that at night there is a decrease in the production of catecholamines, and taking clonidine further reduces the physiological, but not autonomous (produced by the tumor) secretion of catecholamines. The patient is given 0.15 or 0.3 mg of clonidine before bedtime, and in the morning night urine is collected (for the period from 21 to 7 hours) provided that the subject is completely at rest. In the absence of pheochromocytoma, the level of catecholamines will be significantly reduced, and if it is present, the level of catecholamines will remain high, despite taking clonidine.

Primary hyperaldosteronism

Arterial hypertension in primary hyperaldosteronism accounts for up to 0.5% of all cases of arterial hypertension (up to 12% according to specialized clinics). There are several etiological forms of primary hyperaldosteronism: Conn's syndrome (aldosterone-producing adenoma), adrenocortical carcinoma, primary adrenal hyperplasia, idiopathic bilateral adrenal hyperplasia. In the pathogenesis of arterial hypertension, excessive production of aldosterone is of primary importance.

Main clinical signs: arterial hypertension, hypokalemia, ECG changes in the form of flattening of the T wave (80%), muscle weakness (80%), polyuria (70%), headache (65%), polydipsia (45%), paresthesia ( 25%), visual impairment (20%), fatigue (20%), transient convulsions (20%), myalgia (15%). As you can see, these symptoms are nonspecific and are of little use for differential diagnosis.
The leading clinical and pathogenetic sign of primary hyperaldosteronism is hypokalemia (90%). In this regard, it is necessary to remember about other causes of hypokalemia: taking diuretics and laxatives, frequent diarrhea and vomiting.

Hypothyroidism, hyperthyroidism

Hypothyroidism. A characteristic sign of hypothyroidism is high diastolic blood pressure. Other manifestations of the cardiovascular system are a decrease in heart rate and cardiac output.

Hyperthyroidism. Characteristic signs of hyperthyroidism are increased heart rate and cardiac output, predominantly isolated systolic arterial hypertension with low (normal) diastolic blood pressure. It is believed that an increase in diastolic blood pressure in hyperthyroidism is a sign of another disease accompanied by arterial hypertension, or a sign hypertension.

In both cases, to clarify the diagnosis, in addition to a general clinical examination, it is necessary to determine the functions of the thyroid gland.

Endocrine hypertension - Arterial hypertension - differential diagnosis

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Conn's syndrome (primary hyperaldosteronism). IN last years Hypertension caused by excessive activity of mineralocorticoids in the body is attracting more and more attention (see Appendix). Conn's syndrome is a classic example of this type of pathology. Its clinical manifestations consist of arterial hypertension, which is combined with increased secretion of aldosterone, leading to the development of hypokalemia with its characteristic nephropathy and muscle weakness.

The disease begins with minor and short-term increases blood pressure and is usually mistaken for benign hypertension. The potassium content in the blood remains normal over time, which has given some authors grounds to identify a special normokalemic stage of primary aldosteronism. In later stages of the disease, hypokalemia develops, and arterial hypertension takes a malignant course in about a quarter of cases.

It was found that out of 284 cases of the disease, primary aldosteronism was caused by adenoma in 84.5%, diffuse or small nodular hyperplasia in 11.3%, and adrenal cancer in 2.1% of cases. The adrenal glands in 2.1% of patients operated on for Conn's syndrome turned out to be unchanged. In 90% of cases of the disease, the adenoma was located in the left adrenal gland, in 10% of cases the adenomas were bilateral or multiple.

The severity of aldosteronism does not depend on the size of the adenoma, which is sometimes so small that it is difficult to detect during surgery.

Aldosterone levels in the blood and urinary excretion of aldosterone products are elevated in most, but not all cases of Conn's syndrome. It is possible that the secretion of aldosterone in adenoma of the adrenal cortex (similar to the secretion of catecholamines in pheochromocytoma) periodically increases and slows down. It follows from this that the diagnosis of Conn's syndrome should be made only based on the results of repeated determinations of aldosterone concentration in the blood. When making a diagnostic conclusion, it is necessary to take into account the existence of age-related fluctuations in the concentration of aldosterone in the blood. In old and senile age, the concentration of aldosterone in the blood is approximately 2 times less than in young people.

In typical cases, Conn's syndrome occurs with a decrease in renin activity in the blood. This is explained by the inhibitory effect of aldosterone on the function of the juxtaglomerular apparatus of the kidneys. The content of renin in the blood in Conn's syndrome remains low even after the prescription of a hyposodium diet and diuretics. It remains low even during pregnancy. These signs are widely used to distinguish Conn's syndrome from similar clinical manifestations of hypertension and arterial hypertension caused by renal artery stenosis.

The potassium content in the blood in the initial stages of Conn's syndrome remains normal, later periodic hypokalemia appears. In cases of severe illness, severe hypertension is combined with persistent hypokalemia and metabolic alkalosis. The consequence of hypokalemia is polyuria, which occurs in 72% of cases and is most pronounced at night, and weakening of muscle strength, especially in the muscles of the neck and proximal limbs. Antidiuretic hormone has no effect on the severity of polyuria, apparently due to the development of hypokalemic nephropathy. Muscle weakness is occasionally complicated by the development of temporary paresis and even paralysis.

Occasionally, patients with Conn's syndrome develop edema, which, like other signs of the disease, disappears soon after removal of the adenoma.

In order to distinguish symptomatic hypertension in primary aldosteronism from hypertension, it is necessary to pay attention to the severity of symptoms and signs of hypokalemic alkalosis when collecting anamnesis. In the clinic, it is most clearly manifested by dysfunction of the kidneys and striated muscles. As already indicated, hypokalemic nephropathy leads to the development of thirst and polyuria, which are especially pronounced at night. Muscle weakness is initially perceived by patients as fatigue, “weakness.” Characterized by intermittent muscle weakness. It always occurs in attacks, during which patients cannot raise their arms, cannot hold a glass, plate or other objects in their hands, the severity of which was not previously noticed. Sometimes they have difficulty speaking or lifting their head.

The use of aldosterone antagonists leads to the disappearance of hypokalemic alkalosis. Aldactone or veroshpiron is prescribed in a daily dose of 300-400 mg for 2-4 weeks. Before starting the test and during it, the content of total and exchangeable potassium in the body is re-determined. Simultaneously with the disappearance of hypokalemic alkalosis, arterial hypertension usually disappears, and renin and angiotensin appear in the patient’s blood (Brown et al. 1972). In some cases, with late initiation of therapy, blood pressure remains elevated, which is explained by the development of renal arteriolosclerosis. Blood pressure in such cases remains elevated even after tumor removal.

Conn's syndrome should be suspected in all cases of hypertension combined with polyuria and muscle weakness or with a rapidly developing decrease in the patient's physical endurance. Discussing differential diagnosis between Conn's syndrome and hypertension, it must be borne in mind that increased levels of aldosterone in the blood and increased excretion of its metabolic products in the urine occur in all cases of Conn's syndrome from the very beginning of the disease and that renin activity in the blood in all cases of this syndrome is either not at all determined or sharply reduced. It turns out to be low in 10-20% of patients with hypertension, but the aldosterone level in such cases is normal. Low renin activity in the blood in combination with hyperaldosteronemia occurs both in Conn's syndrome and in arterial hypertension, which is easily cured by the administration of dexamethasone.

Arterial hypertension caused by adrenal adenoma often disappears after therapy with aldosterone antagonists. The results of this trial therapy not only confirm the causal relationship of hypertension with increased aldosterone activity" but also predict the effect surgical treatment for hypertension. Hypothiazide therapy in such cases (at a daily dose of at least 100 mg for 4 weeks) is unsuccessful and only leads to a sharp increase in hypokalemia. In benign hypertension, hypothiazide therapy is usually accompanied by a prolonged and pronounced decrease in blood pressure. Hypokalemia usually does not develop. A rapidly progressive course distinguishes malignant hypertension from malignant hypertension syndrome with primary aldosteronism.

Adenocarcinoma of the adrenal gland. Adrenal cortical adenoma is only one cause of Conn's syndrome. Other causes include adenocarcinoma and adrenal hyperplasia. Cancer, like adenoma, in most cases affects one of the adrenal glands. Height malignant tumor accompanied by fever, usually of the wrong type, the appearance of abdominal pain, and microhematuria. Lack of appetite leads to emaciation of patients. In the later stages of the disease, metastases appear, often in the bones and lungs.

Results matter x-ray examination. By the time arterial hypertension appears, the cancerous tumor is usually much larger in size than the adenoma. Infusion urograms or nephrograms show displacement of the affected kidney. Retrograde pyelograms can detect deformation of the pyelocaliceal system. Pneumoren in combination with tomography allows you to obtain a good image of the kidneys and adrenal glands, localize the tumor and determine its size.

Adrenal adenoma is characterized by increased urinary excretion of aldosterone, with cancerous tumor adrenal gland in the urine there is an increased content of not only aldosterone and its metabolites, but also other corticosteroids.

Hypersecretion of other mineralocorticoids. Arterial hypertension caused by hypersecretion of aldosterone is closely related to hypertension, which develops as a result of hypersecretion of other mineralocorticoids. Having a less pronounced effect on the metabolism of sodium and potassium, these mineralocorticoids can still cause not only an increase in blood pressure, but also hypokalemia. Arterial hypertension caused by hypersecretion of deoxycorticosterone or its precursors is best known. Brown et al. (1972), Melby, Dale, Wilson (1971) and others described isolated hypersecretion of 18-hydroxydeoxycorticosterone and 11-deoxycorticosterone, which occurred with arterial hypertension, suppression of renin activity in the blood and severe hypokalemia. The amount of exchangeable sodium was increased, the content of aldosterone and 11-hydroxycorticosterone in the blood was normal.

According to Brown et al. (1972), a decrease in rhein activity in the blood is found in approximately 25% of patients with benign essential hypertension. The normal levels of aldosterone and deoxycorticosterone suggest that both hypertension and suppression of renin secretion in these patients are due to the activity of as yet unidentified mineralocorticoids. This assumption is confirmed by the results of trial therapy with spironolactones. The administration of aldactone or veroshpiron to these patients is accompanied, as in patients with primary aldosteronism, by a decrease in blood pressure.

From the above, however, it does not follow that all cases of arterial hypertension with reduced renin activity develop as a result of hypersecretion of mineralocorticoids. Spironolactones are effective in many, but not all cases of hypertension with reduced renin activity. Hypersecretion of mineralocorticoids is probably the cause of only one and not all forms of essential hypertension.

Hypertension caused by primary hypersecretion of unidentified mineralocorticoids can be benign or malignant in its clinical course. Its clinical picture at the onset of the disease may be no different from hypertension. Its symptomatic origin is indicated by the favorable results of a trial of spironolactone therapy at the dose indicated above. The widespread use of spironolactones for diagnostic purposes will make it possible to suspect this type of hypertension long before the appearance of its late clinical syndromes: hypokalemic nephropathy, hypokalemic paresis and paralysis. The final diagnosis is established by the content of mineralocorticoids in the blood or urine, by a decrease or complete disappearance of renin activity and by negative results of urological research methods.

Hypersecretion of glucocorticoids. Itsenko-Cushing syndrome occurs in many diseases. Currently, it is more common to encounter iatrogenic Itsenko-Cushing syndrome, which develops under the influence of corticosteroid therapy. Increased blood pressure occurs in 85% of patients with this syndrome. Sodium retention is sometimes accompanied by the development of slight edema and decreased renin activity. The characteristic appearance of patients, changes in the skin, neuropsychic sphere, signs of diabetes mellitus and osteoporosis make it easy to distinguish hypertension in Itsenko-Cushing syndrome from hypertension. Congenital anomalies The synthesis of corticosteroids also explains arterial hypertension in some cases of Shereshevsky-Turner syndrome.

Renin hypersecretion. Renin is one of the renal pressor factors. Its effect on vascular tone is not direct, but indirect through angiotensin. The rate of renin secretion by cells of the juxtaglomerular apparatus is controlled by nervous influences, the degree of irritation of the mechanoreceptors of the renal arterioles and the sodium content in the distal tubule of the nephron. Severe renal ischemia, regardless of its cause, leads to an increase in renin secretion.

Renin secretion increases markedly during hypertensive crises and malignant hypertension of any origin. It is believed that in all such cases, ischemia of one or both kidneys through the activation of one of the above mechanisms causes increased secretion of renin. The consequence of this is an increase in the activity of angiotensin II, under the influence of which there is a further increase in spasm of the renal vessels and an increase in the rate of aldosterone secretion. If this vicious circle does not break under the influence of renal depressor factors, then stable hypertension is established, characteristic feature which is increased excretion of aldosterone in the urine with increased renin activity in the blood.

The clinic of this type of arterial hypertension was studied in detail by N. A. Ratner, E. N. Gerasimova and P. P. Gerasimenko (1968), who established that high renin activity in malignant renovascular hypertension sharply decreases after a successful operation and that its decrease is always accompanied by normalization of blood pressure and a decrease in urinary aldosterone excretion. An increase in renin activity and an increase in urinary aldosterone excretion were also observed by them in malignant hypertension, chronic pyelonephritis, and in the terminal phase of chronic glomerulonephritis.

Blood pressure in most patients with chronic renal failure can be maintained at a normal level by removing excess sodium and associated water by repeated dialysis. These measures are ineffective in some patients. They develop severe hypertension, the characteristic signs of which are high content in the blood of renin, angiotensin II and I and aldosterone. Removal of water and electrolytes in these patients during dialysis is accompanied by an even greater increase in the activity of renin and angiotensin in the blood and a further increase in blood pressure. Angiotensin in these patients appears to have a direct pressor effect on the blood vessels. Immediately after bilateral nephrectomy, the content of renin and angiotensin in the blood drops sharply, and blood pressure drops to normal level(Morton, Waite, 1972).

The administration of spironolactones to these patients does not lead to a decrease in blood pressure, although it does allow hypokalemia to be corrected. Their ineffectiveness probably depends on the fact that hyperaldosteronism here is not the primary cause of hypertension, but develops secondary. The amount of metabolizable sodium in the body of these patients does not increase; under the influence of spironolactone therapy, they only experience a decrease in metabolizable sodium in the body and usually a slight decrease in blood pressure.

High renin activity in the blood is the only reliable laboratory sign that allows us to distinguish this form of arterial hypertension from hypertension with increased excretion of aldosterone in the urine and decreased renin activity in the blood. The results of spironolactone therapy are of value only as a preliminary diagnostic method, which does not replace the determination of renin activity in the blood. Arterial hypertension is observed both in the above-described aldosterone-secreting tumors of the adrenal cortex, and in primary kidney tumors secreting renin. Hypersecretion of renin (“primary reninism” by Kohn) is recognized as the main cause of arterial hypertension in hemangiopericytoma (a tumor arising from the cells of the juxtaglomerular cells of the nephron) and in Wilms tumor.

Arterial hypertension in such cases may be of vascular or endocrine origin. In the first case, it turns out to be a consequence of compression of the renal artery by a growing tumor, in the second - a consequence of the tumor secreting pressor substances into the blood. Conn, Cohen, Lucas (1972), Ganguly et al. (1973) found in the tissue of these tumors a large number of renina. The tumor explant in tissue culture continues to produce renin.

The diagnosis of hemangiopericytoma is extremely difficult, since the tumor is very small and grows extremely slowly. Wilms tumor grows much faster, and diagnosing it is not difficult. Removal of hemangiopericytoma or Wilms tumor leads to the disappearance of arterial hypertension. Hypersecretion of catecholamines. Tumors of the adrenal medulla are among the rare diseases. They account for 0.3-0.5% of all cases of arterial hypertension. The tumor grows from chromaffin tissue. In approximately 90% of cases it is localized in the adrenal glands. In 10% of cases, it is located in other organs - aortic paraganglia and especially often in the Zuckerkandl body, carotid bodies, ovaries, testicles, spleen, bladder wall.

Tumors located in the adrenal glands and in the wall of the bladder secrete adrenaline and norepinephrine. Tumors of other locations secrete only norepinephrine. Depending on the growth pattern, the tumor can be benign (pheochromocytoma) or malignant (pheochromoblastoma). Adrenal medulla tumors are usually unilateral and in the vast majority of cases benign.

The clinical picture of pheochromocytoma is formed under the influence of excess intake of adrenaline and norepinephrine into the blood. Periodic entry into the blood of large quantities of these amines is accompanied by paroxysmal attacks of palpitations, arterial hypertension, headaches, and profuse sweating. The paroxysmal form of arterial hypertension occurs in approximately 1/3-1/2 of all cases of pheochromocytoma. In other cases of this disease, arterial hypertension is permanent. It is based on the continuous flow of large quantities of catecholamines into the blood. In rare cases, an asymptomatic course of the disease is observed.

Paroxysms of arterial hypertension are among the most characteristic signs of pheochromocytoma. At first they occur rarely and are mild. As the tumor grows, paroxysms become more frequent and can become daily. Paroxysms in most cases occur for no apparent reason. Sometimes it is possible to establish their connection with emotional disorders, physical activity or other stressful situations. The clinical picture of paroxysm is especially pronounced in children.

The attacks occur suddenly. Initially, paresthesia, a feeling of anxiety and unreasonable fear, and profuse sweating appear. At the height of the attack, 55% of patients develop headaches. In approximately 15% of cases, dizziness occurs simultaneously with headaches. Palpitations are the second most common symptom of paroxysm. It is observed in 38% of patients. Simultaneously with an increase in blood pressure, sometimes up to 200-250 mm Hg. Art. chest pain occurs. During paroxysm, no serious disturbances are usually observed heart rate, nor the appearance of electrocardiographic signs of coronary insufficiency.

Often during an attack, abdominal pain develops, at the height of which vomiting sometimes occurs. At the height of the attack, hyperglycemia and moderate neutrophilic leukocytosis with a shift to the left regularly develop. Attack moderate severity continues for several hours. After blood pressure drops to normal levels, profuse sweating and polyuria are observed. General weakness at the end of the attack depends on its severity and can last from several hours to a day.

An extremely high rise in blood pressure during an attack can lead, especially in older people, to pulmonary edema and cerebral hemorrhage. In rare cases, hemorrhage occurs in the adrenal gland, which may be accompanied by spontaneous healing. Typical paroxysmal increases in blood pressure significantly facilitate the identification of the true cause of hypertension.

Persistent hypertension is observed in more than half of patients with pheochromocytoma. Sometimes blood pressure periodically increases, simulating hypertensive crises inherent in benign hypertension, sometimes it remains constantly high, as is observed in malignant hypertension. If hypertension appears in children or young people, then its symptomatic origin is beyond doubt. It is more difficult to notice the connection between arterial hypertension and pheochromocytoma in older people. The patient's tendency to faint may provide some assistance in this regard, especially

when quickly getting out of bed. Such fainting reactions in ordinary hypertensive patients develop only in cases where they take antihypertensive drugs. A certain importance should also be attached to the tendency of these patients to faint during anesthesia or, with minor surgical operations, for example tooth extraction. Sometimes these patients experience diffuse hyperpigmentation of the skin or the appearance of café-au-lait spots on the skin.

Urinary syndrome is manifested by proteinuria and microhematuria, which are detected initially only during paroxysms of hypertension, and in a later period become permanent. In severe cases, N. A. Ratner et al. (1975) observed constant proteinuria. To find out its causes, a complete urological examination is performed (pyelography, pneumoren, kidney tomography), during which signs of a tumor of one or both adrenal glands are detected.

Pharmacological tests using histamine, phentolamine, tropafen have no practical value. Great diagnostic importance is attached to the results of direct determination of the rate of secretion of catecholamines in the body of the test subject. Daily urinary excretion of catecholamines in pheochromocytoma always increases. It increases especially sharply on days of hypertensive crises. Great importance is also associated with increased excretion of dopamine, DOPA and vanillyl-mandelic acid.

Pheochromocytoma with paroxysms of hypertension often has to be differentiated from diencephalic syndrome, in which attacks also periodically appear autonomic disorders, occurring with general anxiety, increased blood pressure, headache, tachycardia, hyperglycemia. Increased urinary excretion of catecholamines or vanillyl-mandelic acid is a characteristic feature of pheochromocytoma. Disorders of carbohydrate, fat or water-electrolyte metabolism accompanying attacks, and increased intracranial pressure indicate a connection between attacks and diencephalic syndrome.

Tumor localization is determined according to data instrumental examination. Intravenous urography can detect no more than 1/2 of all tumors, since the compression of the upper pole of the kidney or displacement of the kidney that it detects is caused only by large tumors. More reliable diagnostic methods are pneumorenography, which is usually performed in combination with urography, and tomography. In recent years, aortography, thermography and adrenal scintigraphy have been successfully used.

Pheochromoblastoma accounts for approximately 10% of all adrenal tumors. It also occurs with an increase in the production of catecholamines, but its symptoms differ markedly from those of pheochromocytoma. Like any malignant neoplasm, it metastasizes to regional retroperitoneal The lymph nodes. The growth of the tumor into the surrounding tissue, as well as the growth of metastases, leads to pain in the abdomen or lumbar region. The growth of the tumor is accompanied by an increase in temperature, accelerated erythrocyte sedimentation, and emaciation of the patient. In later stages, metastases appear in the liver, bones, and lungs.

Drug-induced hypertension. By collecting anamnesis, the doctor finds out what medications the patient used. Despite the different mechanisms final result The effects of some drugs turn out to be the same: their systematic use leads to an increase in blood pressure. We have identified hypertension caused by these drugs as a separate group, giving preference to practical interest rather than academic rigor.

Nowadays, the most common cause of drug-induced hypertension is contraceptives. Regular and long-term use of them worsens the course of pre-existing hypertension and can even cause persistent hypertension in previously healthy women. Discontinuation of the drug is accompanied by the disappearance of hypertension.

Licorice powder is often used to treat peptic ulcers and to combat constipation. Long-term use of large doses of this drug leads to the development of hypertension, which develops against the background of hypokalemia. In severe cases, clinical manifestations of hypokalemia appear in the form of muscle weakness and polyuria. IN clinical picture This hypertension has many features reminiscent of Conn's syndrome, but urinary aldosterone excretion remains normal. Liquorice hypertension disappears soon after discontinuation of the drug.

Long-term use of steroid hormones sometimes leads to arterial hypertension, simultaneously with which centripetal obesity and other signs of Itsenko-Cushing syndrome usually develop. Arterial hypertension disappears soon after discontinuation of the drug. In order to avoid making a diagnostic error and not mistaking these essentially iatrogenic hypertension for hypertension, it is necessary to ask the patient every time whether he is taking medications that can cause an increase in blood pressure.

Failure of hormonal regulation of the tone of peripheral arteries, sodium and water retention in the body lead to increased blood pressure. Endocrine hypertension occurs with diseases of the pituitary gland, adrenal glands, damage to the thyroid and parathyroid glands. Treatment is carried out by eliminating the cause high pressure and prescription of antihypertensive drugs.

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What hormones increase blood pressure?

To maintain the desired tone of the arteries, the body produces and releases hormones into the blood. The glands of the endocrine system that are involved in the regulation of this process include:

adrenal glands (cortisol, aldosterone, adrenaline, norepinephrine and dopamine);
pituitary gland (growth hormone somatotropin, thyrotropin);
thyroid(thyroxine, triiodothyronine).

Adrenal hormones have the most significant effect on blood pressure. They increase the activity of the sympathetic nervous system.

The heart and blood vessels respond to excess stress hormones by accelerating and intensifying the heartbeat, narrowing the lumen of the arteries. All these factors increase the level of systemic blood pressure. The second mechanism of adverse effects in the hormonal form of hypertension is a delay in the excretion of sodium and water.

Signs of hypertension of endocrine origin

Hypertension or occurs in 95% of cases, but occupies only 5%. Of these, endocrine pathology accounts for only 0.5%. Therefore, doctors are often not wary about the hormonal nature of high blood pressure.

If the diagnosis is not made on time, then complications arise - damage to the retina, kidneys, cerebral vessels, changes in the heart. Signs that require the exclusion of endocrine diseases are:

the occurrence of hypertension before 20 years of age or after 60 years of age;
sudden increase in pressure to extremely high values;
rapid progression of complications;
weak response to antihypertensive drugs.

Pituitary gland diseases

A tumor of the pituitary gland leads to excessive production of growth hormone - somatotropin. It prevents the excretion of sodium from the body, retains water, which causes an increase in circulating blood volume and persistent hypertension. The disease that occurs is called acromegaly. TO external signs diseases include:

high growth;
proliferation of tissues of the lips, nose;
thickening of the brow ridges and cheek bones;
enlargement of hands and feet.

Patients complain of severe weakness, sexual dysfunction, headaches, and hearing loss. In many patients, acromegaly causes not only arterial hypertension, but also damage to the liver and lungs. Tumors often form in the thyroid gland, uterus and ovaries.

To make a diagnosis, determination of somatotropin in the blood and insulin-like growth factor is required. The tumor can be seen with skull radiography, CT and MRI. Treatment is carried out with somatotropic hormone analogues (Octreotide), dopamine antagonists (Parlodel), and irradiation of the pituitary gland. The best results can be obtained with early diagnosis and removal of the pituitary tumor.

Watch the video about the types of hypertension, causes of development and treatment:

Pathology of the adrenal glands

These glands produce a number of hormones that have a pressor (narrowing) effect on the arteries.

Excess cortisol

Cushing's syndrome occurs in patients with a tumor in the adrenal glands that releases large amounts of cortisol into the blood. In patients, blood pressure increases due to a sharp activation of sympathetic influences on the blood vessels. The result of an excess of this hormone is the following manifestations:

mental disorders;
cataract;
obesity localized in the abdomen, chest and neck;
moon-shaped face with a bright blush;
excessive hair growth on the arms, legs, face;
stretch marks (striae) on the abdomen and thighs;
loss of muscle strength;
frequent fractures;
sexual dysfunction.

The diagnosis is made based on a study of the concentration of cortisol in the blood, tests with dexamethasone, ultrasound or CT scan of the adrenal glands. Treatment involves removal of the tumor; other methods (radiation and drug therapy) have low effectiveness.

Increased aldosterone (Conn's syndrome)

In the adrenal glands, a tumor of the cortical layer can intensively produce aldosterone. This hormone removes potassium and retains sodium, while water remains in the vessels and tissues. This leads to the formation of the following symptoms:

arterial hypertension with severe crises that cannot be corrected with medications;
muscle weakness;
convulsive syndrome;
numbness of the limbs;
increased thirst;
predominantly nocturnal urine output;
circulatory failure and its consequences - cardiac asthma, pulmonary edema;
impaired blood flow in the brain;
paralysis of the heart muscle due to a severe lack of potassium.

Primary hyperaldosteronism can be detected using a blood test for electrolytes and aldosterone. To clarify the diagnosis, patients are prescribed an ultrasound scan of the adrenal glands.

Treatment - surgical removal tumors. Before surgery, a salt-free diet and Spironolactone are recommended.

Increased production of stress hormones

If stress hormones are produced uncontrollably in the adrenal glands, then most often the cause of this is a tumor of the medulla, which is called. The main feature of the disease is the occurrence of crises. They are accompanied by severe agitation, anxiety, sweating, trembling of the whole body, convulsions, a sharp increase in blood pressure, headache and heart pain, palpitations, nausea and vomiting.

The diagnosis can be made after determining catecholamines in urine and blood, ultrasound and CT scan of the adrenal gland. The only chance to get rid of pheochromocytoma is surgery to remove the tumor.

Thyroid diseases

If the release of thyroid hormones into the bloodstream increases, the pulse accelerates, the release of blood from the ventricles into the arterial network increases, and peripheral vascular resistance increases. These changes lead to a persistent increase in blood pressure.

Patients with thyrotoxicosis note irritability, anxiety, sleep disturbances, hot flashes, tremors in the limbs, weight loss with increased appetite.

The diagnosis is made after a blood test to check hormone levels. In the initial stages of the disease, medications may be recommended, radioisotope methods treatment, in severe cases the thyroid gland is removed.

The tendency to retain fluid in the body with low thyroid function (hypothyroidism) causes an isolated increase in diastolic blood pressure.

Such patients are apathetic, inhibited, their eyelids, face, and limbs swell. Characteristic changes in the cardiovascular system include blockade of impulse transmission through the myocardium.

Diagnosis involves identifying hormone deficiency through a blood test. Treatment is carried out with L-thyroxine.

Endocrine arterial hypertension occurs due to excessive production of hormones by the pituitary gland, adrenal glands, and changes in the function of the thyroid gland. The reason for the increase in pressure is the activation of sympathetic effects on the myocardium and arteries, fluid and sodium retention in the body.

They manifest themselves as persistent hypertension, which is not relieved by conventional antihypertensive drugs. To make a diagnosis, a study of hormones in the blood, ultrasound, CT and MRI are required. Treatment in most cases involves surgical removal of the tumor or gland, radiation and drug therapy.

Glands and hormones that interest us

The pituitary gland (synonym: pituitary gland) is a round-shaped gland located on the lower surface of the brain. The pituitary gland produces hormones that affect metabolism and, in particular, growth. If the pituitary gland is affected by a tumor, then this causes increased production of some hormone inside it, and then “along the chain” in the adrenal glands, which it controls. A pituitary tumor is often the endocrinological cause of hypertension. Read more below.

The adrenal glands are glands that produce various hormones, including catecholamines (adrenaline, norepinephrine and dopamine), aldosterone and cortisol. There are 2 of these glands in humans. They are located, as you might guess, on top of the kidneys.

If a tumor develops in one or both adrenal glands, it causes excessive production of a hormone, which in turn causes hypertension. Moreover, such hypertension is usually stable, malignant and cannot be treated with pills. The production of some hormones in the adrenal glands is controlled by the pituitary gland. Thus, there is not one, but two potential sources of problems with these hormones - diseases of both the adrenal glands and the pituitary gland.

Hypertension can be caused by excessive production of the following hormones in the adrenal glands:

Catecholamines - adrenaline, norepinephrine and dopamine. Their production is controlled by adrenocorticotropic hormone (ACTH, corticotropin), which is produced in the pituitary gland.
Aldosterone is produced in the zona glomerulosa of the adrenal cortex. Causes salt and water retention in the body, and also enhances the excretion of potassium. Increases circulating blood volume and systemic blood pressure. If there are problems with aldosterone, edema, hypertension, sometimes congestive heart failure, and weakness due to low potassium levels in the blood develop.
Cortisol is a hormone that has a multifaceted effect on metabolism, preserving the body's energy resources. Synthesized in the outer layer (cortex) of the adrenal glands.

The production of catecholamines and cortisol occurs in the adrenal glands under the control of the pituitary gland. The pituitary gland does not control the production of aldosterone.

Adrenaline is the hormone of fear. Its release occurs during any strong excitement or sudden physical activity. Adrenaline saturates the blood with glucose and fats, increases the absorption of sugar from the blood by cells, and causes vasoconstriction of the abdominal organs, skin and mucous membranes.

Norepinephrine is the rage hormone. As a result of its release into the blood, a person becomes aggressive, and muscle strength increases significantly. The secretion of norepinephrine increases during stress, bleeding, heavy physical work and other situations that require rapid restructuring of the body. Norepinephrine has a strong vasoconstrictor effect and plays a key role in regulating the speed and volume of blood flow.

Dopamine causes an increase in cardiac output and improves blood flow. From dopamine, under the action of enzymes, norepinephrine is produced, and from it adrenaline, which is the final product of catecholamine biosynthesis.

So, we’ve sorted out a little about hormones, now let’s list them directly endocrine causes of hypertension:

Pheochromocytoma is a tumor of the adrenal glands that causes increased production of catecholamines. In 15% of cases it occurs not in the adrenal glands, but in the abdominal cavity or chest.
Primary hyperaldosteronism is a tumor in one or both adrenal glands that causes too much aldosterone to be produced.
Itsenko-Cushing syndrome, also known as hypercortisolism, is a disease in which too much cortisol is produced. In 65-80% of cases it is due to problems with the pituitary gland, in 20-35% of cases it is due to a tumor in one or both adrenal glands.
Acromegaly is an excess of growth hormone in the body due to a tumor in the pituitary gland.
Hyperparathyroidism is an excess of parathyroid hormone (parathyroid hormone), which is produced by the parathyroid glands. Not to be confused with the thyroid gland! Parathyroid hormone increases the concentration of calcium in the blood by leaching this mineral from the bones.
Hyper- and hypothyroidism are increased or decreased levels of thyroid hormones.

If you do not treat the listed diseases, but simply give the patient pills for hypertension, then this usually does not sufficiently reduce the pressure. To bring blood pressure back to normal and avoid heart attack and stroke, you need to participate in the treatment of a whole team of competent doctors - not just an endocrinologist, but also a cardiologist and a surgeon with golden hands. The good news is that treatment options for hypertension due to endocrine causes have expanded significantly over the past 20 years. Surgeries have become much safer and more effective. In some situations, timely surgical intervention allows you to normalize the blood pressure so much that you can stop taking pills for hypertension.

The problem is that all the diseases listed above are rare and complex. Therefore, it is not easy for patients to find doctors who can treat them conscientiously and competently. If you suspect you have hypertension due to an endocrine cause, then keep in mind that the endocrinologist on duty at the clinic will probably try to kick you off. He doesn’t need your problems for money, much less for nothing. Look for a smart specialist based on reviews from friends. Surely it will be useful to go to the regional center, or even to the capital of your state.

Below is detailed information that will help you understand the course of treatment: why this or that activity is carried out, medications are prescribed, how to prepare for surgery, etc. Let us note that to date, not a single major serious study has been conducted among patients with endocrine hypertension. would meet the criteria evidence-based medicine. All information about treatment methods, which is published in medical journals and then in books, is collected “from around the world.” Doctors exchange experiences with each other, gradually generalize them, and thus universal recommendations appear.

Pheochromocytoma is a tumor that produces catecholamines. In 85% of cases it is found in the adrenal medulla, and in 15% of patients - in the abdominal cavity or chest. It is extremely rare that a catecholamine-producing tumor occurs in the heart, bladder, prostate, pancreas, or ovaries. In 10% of patients, pheochromocytoma is a hereditary disease.

Usually this is a benign tumor, but in 10% of cases it turns out to be malignant and metastasizes. IN? cases it produces adrenaline and norepinephrine, in? cases - only norepinephrine. If the tumor turns out to be malignant, it can also produce dopamine. Moreover, there is usually no relationship between the size of the pheochromocytoma and how abundantly it produces hormones.

Among all patients with arterial hypertension, approximately 0.1-0.4%, i.e., 1-4 patients out of 1000, are diagnosed with pheochromocytoma. In this case, the pressure may be elevated all the time or in attacks. The most frequent symptoms: headache, increased sweating and tachycardia (palpitations). If your blood pressure is elevated but these symptoms are not present, pheochromocytoma is unlikely to be the cause. There are also trembling hands, nausea, vomiting, visual disturbances, attacks of fear, sudden pallor or, conversely, redness of the skin. About y? Patients experience persistently or occasionally elevated levels of glucose in the blood and even sugar in the urine. At the same time, the person inexplicably loses weight. If the heart is affected due to increased levels of catecholamines in the blood, symptoms of heart failure develop.

Frequency of main symptoms in pheochromocytoma

It happens that pheochromocytoma occurs without pronounced symptoms. In such cases, the main complaints from patients are signs of tumor growth, i.e. pain in the abdomen or chest, a feeling of fullness, compression of internal organs. In any case, to suspect this disease, it is enough to simultaneously detect hypertension, high sugar in the blood and signs of accelerated metabolism against the background of normal levels of thyroid hormones.

Diagnostics

The symptoms of pheochromocytoma are not unambiguous; they vary from patient to patient. Therefore, it is impossible to make a diagnosis based solely on visual observation and listening to patient complaints. It is necessary to look for and identify biochemical signs of increased production of adrenaline and norepinephrine. These hormones are excreted in the urine in the form of vanilla-mandelic acid compounds, metanephrines (methylated products), and free catecholamines. The concentration of all these substances is determined in daily urine. This is a standard diagnostic procedure for suspected pheochromocytoma. Before undergoing tests, patients must first stop taking medications that increase or, on the contrary, inhibit the production of catecholamine hormones in the body. These are the following drugs: adrenergic blockers, adrenergic stimulants, including centrally acting ones, MAO inhibitors and others.

If possible, compare the content of catecholamine metabolic products in the urine in a normal situation and immediately after a hypertensive crisis. It would be good to do the same with blood plasma. But to do this, one would have to take blood through a venous catheter, which must be installed 30-60 minutes in advance. It is impossible to keep the patient in a state of rest all this time, and then have him have a hypertensive crisis on schedule. A blood test from a vein is a stress in itself, which increases the concentration of adrenaline and norepinephrine in the blood and thus leads to false positive results.

Also, to diagnose pheochromocytoma, functional tests are used, in which the secretion of catecholamines is inhibited or stimulated. The production of these hormones can be inhibited with the medication clonidine (clonidine). The patient donates blood for analysis, then takes 0.15-0.3 mg of clonidine, and then donates blood again 3 hours later. The content of adrenaline and norepinephrine in both tests is compared. Or they check how much clonidine suppresses the nighttime production of catecholamines. To do this, tests are performed on urine collected overnight. In a healthy person, after taking clonidine, the content of adrenaline and norepinephrine in night urine will significantly decrease, but in a patient with pheochromocytoma - not.

Stimulation tests are also described, in which patients receive histamine, thyramione, and best of all, glucagon. Taking stimulant drugs in patients with pheochromocytoma significantly increases blood pressure, and the content of catecholamines increases several times, much stronger than in healthy people. To avoid a hypertensive crisis, patients are first given alpha-blockers or calcium antagonists. These are drugs that do not affect the production of catecholamines. Stimulation tests can only be used with great caution, because there is a risk of provoking a hypertensive crisis and cardiovascular accident in the patient.

The next stage in diagnosing pheochromocytoma is identifying the location of the tumor. To do this, computed tomography or magnetic resonance imaging is performed. If the tumor is in the adrenal glands, it is usually easily detected, often even with the help of ultrasound, which is the most accessible examination. But if the tumor is located not in the adrenal glands, but somewhere else, then whether it can be identified largely depends on the experience and will to win that the doctor will show. As a rule, 95% of pheochromocytomas are found in the adrenal glands if their size is more than 1 cm, and in the abdominal cavity if their size is more than 2 cm.

If using computed tomography or magnetic resonance imaging failed to detect a tumor, then a radioisotope scan using a contrast agent has to be done. A substance that emits radioactivity is injected into the patient's blood. It spreads throughout the body, “illuminates” the vessels and tissues from the inside. Thus, the X-ray examination is more informative. Metaiodobenzylguanidine is used as a contrast agent. Radioisotope scans using contrast material may cause kidney failure and have other risks. Therefore, it is prescribed only in exceptional cases. But if the benefit is higher than the potential risk, then you need to do it.

They can also test for catecholamines in the blood that flows from the site of the tumor. If there was no mistake in identifying this location, then the concentration of hormones will be several times higher than in blood taken from other vessels. This analysis is prescribed if pheochromocytoma is found in the adrenal glands. However, this is a complex and risky analysis, so they try to do without it.

Treatment

To treat pheochromocytoma, surgery is performed to remove the tumor if there are no contraindications. The good news for patients is that in recent years, surgeons have adopted laparoscopy. This is a method of performing operations in which the incision on the skin is very small and minimal damage is caused inside. Thanks to this, recovery takes no more than 2 weeks, while previously it was an average of 4 weeks. After surgery, more than 90% of patients experience a persistent decrease or even complete normalization of blood pressure. Thus, the effectiveness of surgical treatment of pheochromocytoma is very high.

If it turns out that surgically It is impossible to remove the tumor, then it is irradiated, and chemotherapy is also prescribed, especially if there are metastases. Radiation and chemotherapy are called “conservative treatments,” that is, without surgery. As a result of their use, the size and activity of the tumor are reduced, due to which the condition of patients improves.

What blood pressure pills are prescribed for pheochromocytoma:

alpha-blockers (prazosin, doxazosin, etc.);
phentolamine - intravenously, if necessary;
labetalol, carvedilol - combined alpha and beta blockers;
calcium antagonists;
centrally acting drugs - clonidine (clonidine), imidazoline receptor agonists;
Methyltyrosine is a dopamine synthesis blocker.

The anesthesiologist is advised to avoid fentanyl and droperidol during surgery because these drugs may stimulate additional catecholamine production. The function of the patient's cardiovascular system should be carefully monitored at all stages of surgical treatment: during induction of anesthesia, then during the operation and the first day after it. Because severe arrhythmias, a strong decrease in blood pressure, or, conversely, hypertensive crises are possible. In order for the circulating blood volume to remain sufficient, the patient must receive enough fluid.

It is recommended to take a urine test for catecholamines 2 weeks after surgery. Sometimes, over time, the tumor recurs or additional pheochromocytomas are discovered, in addition to the one that was removed. In such cases, repeated surgical operations are recommended.

Primary hyperaldosteronism

Let us recall that aldosterone is a hormone that regulates water and mineral metabolism in the body. It is produced in the adrenal cortex under the influence of renin, an enzyme synthesized by the kidneys. Primary hyperaldosteronism is a tumor in one or both adrenal glands that causes too much aldosterone to be produced. These tumors can be of different types. In either case, excess aldosterone production causes blood potassium levels to drop and blood pressure to rise.

Causes and treatment of primary hyperaldosteronism

What is the renin-angiotensin-aldosterone system

To understand what primary hyperaldosteronism is, you need to understand how renin and aldosterone are related. Renin is an enzyme that the kidneys produce when they sense that blood flow to them is decreasing. Under the influence of renin, the substance angiotensin-I is converted into angiotensin-II and the production of aldosterone in the adrenal glands is also stimulated. Angiotensin-II has a powerful vasoconstrictor effect, and aldosterone increases sodium and water retention in the body. Thus, blood pressure rises rapidly simultaneously through several different mechanisms. At the same time, aldosterone suppresses further production of renin so that the pressure does not go off scale. The more aldosterone in the blood, the less renin, and vice versa.

This is called the renin-angiotensin-aldosterone system. It is a feedback system. Let us mention that some medications block its action so that blood pressure does not increase. ACE inhibitors interfere with the conversion of angiotensin I to angiotensin II. Angiotensin II receptor blockers prevent this substance from exerting its vasoconstrictor effect. And there is also the newest drug - the direct renin inhibitor Aliskiren (Rasilez). It blocks the activity of renin, i.e. it acts on more early stage than the medications we mentioned above. All this is not directly related to the endocrinological causes of hypertension, but it is useful for patients to know the mechanisms of action of drugs.

So, aldosterone in the adrenal glands is produced under the influence of renin. Secondary hyperaldosteronism is when there is too much aldosterone in the blood due to excess renin. Primary hyperaldosteronism - if the increased production of aldosterone by the adrenal glands does not depend on other reasons, and the activity of renin in the blood plasma is definitely not increased, but rather even decreased. For a correct diagnosis, it is important for a doctor to be able to distinguish between primary and secondary hyperaldosteronism. This can be done based on the results of tests and tests, which we will discuss below.

Renin production by the kidneys is inhibited by the following factors:

increased aldosterone levels;
excess volume of circulating blood;
high blood pressure.

Normally, when a person gets up from a sitting or lying position, he produces renin, which quickly increases blood pressure. If there is an adrenal tumor that produces excess aldosterone, the release of renin is blocked. Therefore, orthostatic hypotension is possible - dizziness and even fainting with a sudden change in body position.

Let's list other possible symptoms of primary hyperaldosteronism:

High blood pressure, can reach 200/120 mm Hg. Art.;
Excessive concentration of potassium in urine;
Low potassium levels in the blood, causing patients to feel weak;
Elevated levels of sodium in the blood;
Frequent urination, especially the urge to urinate in a horizontal position.

The symptoms observed in patients are common to many diseases. This means that it is difficult for a doctor to suspect primary hyperaldosteronism, and without testing it is generally impossible to make a diagnosis. Primary hyperaldosteronism should always be suspected if the patient has severe hypertension that is resistant to medication. Moreover, if the level of potassium in the blood turns out to be normal, this does not exclude that the production of aldosterone is increased.

The most significant test for diagnosis is determining the concentration of hormones of the renin-aldosterone system in the blood. In order for the test results to be reliable, the patient needs to carefully prepare for their delivery. Moreover, preparations begin very early, 14 days in advance. It is advisable at this time to stop taking all blood pressure pills, balance your diet, and protect yourself from stress. During the preparatory period, it is better for the patient to go to the hospital.

What blood tests are done:

Aldosterone;
Potassium;
Plasma renin activity;
Activity and concentration of renin before and after taking 40 mg of furosemide.

It is advisable to take a blood test for aldosterone early in the morning. At night, the level of aldosterone in the blood should decrease. If the concentration of aldosterone in the morning blood is increased, then this more clearly indicates a problem than if the test is taken in the afternoon or evening.

Of particular diagnostic importance is the calculation of the ratio of aldosterone content (ng/ml) and plasma renin activity (ng/(ml*h)). Normal value this ratio is below 20, the diagnostic threshold is above 30, and if it is more than 50, then the patient almost certainly has primary hyperaldosteronism. The calculation of this ratio has only recently been widely introduced into clinical practice. As a result, it turned out that every tenth patient with hypertension suffers from primary hyperaldosteronism. However, the level of potassium in the blood may be normal and decrease only after a salt load test is carried out for several days.

If the results of the blood tests listed above do not allow an unambiguous diagnosis, then additional salt or captopril load tests are performed. Salt load is when the patient eats 6-9 g table salt in a day. This increases the exchange of potassium and sodium in the kidneys and allows you to clarify the results of tests for aldosterone levels in the blood. If hyperaldosteronism is secondary, then salt loading will inhibit aldosterone production, but if it is primary, then not. Test with 25 mg captopril - the same. If a patient has hypertension due to kidney problems or other reasons, captopril will lower the level of aldosterone in the blood. If the cause of hypertension is primary hyperaldosteronism, then while taking captopril, the level of aldosterone in the blood will remain unchanged.

They try to identify a tumor in the adrenal glands using ultrasound. But even if ultrasonography does not show anything, then the presence of adenoma or adrenal hyperplasia still cannot be completely excluded. Because in 20% of cases the tumor is less than 1 cm in size, and in this case it will not be easy to detect. Computed tomography or magnetic resonance imaging is always advisable if primary hyperaldosteronism is suspected. There is also a method for determining the concentration of aldosterone in blood from the adrenal veins. This method allows you to determine whether the problem is in one adrenal gland or both.

Blood pressure in patients with primary hyperaldosteronism can literally go through the roof. Therefore, they are especially susceptible to the serious complications of hypertension: heart attacks, strokes, and kidney failure. Also low level Potassium in the blood provokes the development of diabetes in many of them.

Treatment

Above, at the beginning of the section devoted to this disease, we provided a table in which we showed that the choice of surgical or drug treatment for primary hyperaldosteronism depends on its cause. The physician must make the correct diagnosis to distinguish unilateral aldosterone-producing adenoma from bilateral adrenal hyperplasia. The latter is considered a milder disease, although it is less amenable to surgical treatment. If the damage to the adrenal glands is bilateral, then surgery can normalize blood pressure in less than 20% of patients.

If an operation is planned, then before it the aldosterone content in the blood that flows from the adrenal veins should be determined. Let's say a tumor of the adrenal gland is discovered as a result of an ultrasound, computer or magnetic resonance imaging. But according to the results of a blood test, it may turn out that it is not hormonally active. In this case, it is recommended to refrain from performing the operation. Hormonally inactive tumors of the adrenal cortex are found at any age in 0.5-10% of people. They don't cause any problems and you don't need to do anything about them.

Patients with primary hyperaldosteronism are prescribed spironolactone, a specific aldosterone blocker, for hypertension. Potassium-sparing diuretics are also used - amiloride, triamterene. Spironolactone is started immediately with high doses, 200-400 mg per day. If it is possible to stabilize blood pressure and normalize the level of potassium in the blood, then the dose of this drug can be significantly reduced. If the level of potassium in the blood is consistently normal, then thiazide diuretics are also prescribed in small doses.

If blood pressure control remains poor, the medications listed above are supplemented with long-acting dihydropyridine calcium antagonists. These drugs are nifedipine or amlodipine. Many practitioners believe that ACE inhibitors help well with bilateral adrenal hyperplasia. If the patient experiences side effects or intolerance to spironolacter, then eplerenone should be considered, this is a relatively new drug.

Itsenko-Cushing syndrome

First let's introduce the terminology:

Cortisol is one of the hormones produced in the adrenal glands.
The pituitary gland is a gland in the brain that produces hormones that affect growth, metabolism and reproductive function.
Adrenocorticotropic hormone (adrenocorticotropin) - produced in the pituitary gland, controls the synthesis of cortisol.
The hypothalamus is one of the parts of the brain. Stimulates or inhibits the production of hormones by the pituitary gland and thus controls the human endocrine system.
Corticotropin-releasing hormone, also known as corticorelin, corticotropin-releasing hormone, is produced in the hypothalamus, acts on the anterior pituitary gland and causes the secretion of adrenocorticotropic hormone there.
Ectopic - one that is located in an unusual place. Excessive production of cortisone is often stimulated by tumors that produce adrenocorticotropic hormone. If such a tumor is called ectopic, it means that it is not in the pituitary gland, but somewhere else, for example, in the lungs or in the thymus gland.

Itsenko-Cushing syndrome, also known as hypercortisolism, is a disease in which too much of the hormone cortisol is produced. Hypertension occurs in approximately 80% of patients with this hormonal disorder. Moreover, blood pressure is usually significantly increased, from 200/120 mm Hg. Art., and it cannot be normalized by any traditional medicines.

The synthesis of cortisol in the human body is controlled by a complex chain of reactions:

First, corticotropin-releasing hormone is produced in the hypothalamus.
It acts on the pituitary gland to produce adrenocorticotropic hormone.
Adrenocorticotropic hormone gives a signal to the adrenal glands to synthesize cortisol.

Itsenko-Cushing syndrome can be caused by the following reasons:

Due to problems with the pituitary gland, too much adrenocorticotropic hormone circulates in the blood, which stimulates the adrenal glands.
A tumor develops in one of the adrenal glands, while the levels of adrenocorticotropic hormone in the blood are normal.
An ectopic tumor that is not located in the pituitary gland and produces adrenocorticotropic hormone.
There are also rare causes, which are listed in the table below along with the main ones.

In approximately 65-80% of patients, excess cortisol production occurs due to increased secretion of adrenocorticotropic hormone. In this case, a secondary enlargement (hyperplasia) of the adrenal glands is observed. This is called Cushing's disease. In almost 20% of cases, the primary cause is an adrenal tumor, and this is not called a disease, but Cushing's syndrome. More often there is a unilateral tumor of the adrenal glands - adenoma or carcinoma. Bilateral adrenal tumor is rare and is called micro- or macronodular hyperplasia. Cases of bilateral adenoma have also been described.

Classification of causes of hypercortisolism

Type of disease	Detection rate, 5
Spontaneous hypercortisolism
Cushing's disease (pituitary hypercortisolism)
Ectopic production of adrenocorticotropic hormone
Ectopic production of corticotropin-releasing hormone	Very rarely
Cushing's syndrome (adrenal hypercortisolism)
Adrenal carcinoma
Adrenal hyperplasia
Hereditary forms (Carney, McClury-Albright syndromes)
Iatrogenic hypercortisolism
Taking adrenocorticotropic hormone
Taking glucocorticoids	Most often
Pseudo-Cushing's syndrome (alcoholism, depression, HIV infection)

Cushing's syndrome is more common in women, usually between the ages of 20 and 40. In 75-80% of patients, it is difficult to detect the location of the tumor, even with the use of modern methods of computed tomography and magnetic resonance imaging. However, the initial diagnosis of the disease is not difficult, because chronically elevated levels of cortisol in the blood cause typical changes in the appearance of patients. This is called Cushingoid type of obesity. Patients have a moon-like face, purplish-blue cheeks, and fat deposits in the neck, torso, shoulders, abdomen and thighs. At the same time, the limbs remain thin.

Additional symptoms of elevated cortisol levels in the blood:

Osteoporosis and brittle bones.
Low potassium concentration in the blood.
Tendency to bruise.
Patients lose muscle mass, look weak, and stoop.
Apathy, drowsiness, loss of intelligence.
The psycho-emotional state often changes from irritability to deep depression.
Skin stretch marks on the abdomen, purple, 15-20 cm long.

Symptoms of increased levels of adrenocorticotropic hormone in the blood and pituitary tumors:

Headaches caused by a tumor of the pituitary gland, which presses from the inside.
Body skin pigmentation.
In women - violations menstrual cycle, atrophy of the mammary glands, growth of unwanted hair.
In men - potency disorders, testicular hypotrophy, beard growth decreases.

Diagnostics

First of all, they try to determine the increased level of cortisol in the blood or daily urine. At the same time, one-time negative result analysis does not prove the absence of the disease, because the level of this hormone physiologically fluctuates widely. It is recommended to measure free cortisol in urine rather than 17-keto- and 17-hydroxyketosteroids. It is necessary to take measurements in at least two consecutive 24-hour urine samples.

It can sometimes be difficult to distinguish Cushing's syndrome from normal obesity, which often accompanies hypertension. To make a correct diagnosis, the patient is given the drug dexamethasone at a dose of 1 mg at night. If there is no Cushing's syndrome, then the level of cortisol in the blood will decrease the next morning, and if there is, then the level of cortisol in the blood will remain high. If a test with 1 mg of dexamethasone previously showed Cushing's syndrome, then a repeat test is performed using a larger dose of the drug.

The next stage is to measure the level of adrenocorticotropic hormone in the blood. If it turns out to be high, a pituitary tumor is suspected, and if it is low, then perhaps the primary cause is an adrenal tumor. It happens that adrenocorticotropic hormone is produced by a tumor not in the pituitary gland, but located somewhere else in the body. Such tumors are called ectopic. If the patient is given a dose of 2-8 mg of dexamethasone, the production of adrenocorticotropic hormone in the pituitary gland is suppressed, even despite the tumor. But if the tumor is ectopic, then dexamethasone in a high dosage will not affect its activity in any way, which will be evident from the results of a blood test.

To establish the cause of the disease - a pituitary tumor or an ectopic tumor - instead of dexamethasone, corticotropin-releasing hormone can also be used. It is administered in a dosage of 100 mcg. In Cushing's disease, this will lead to a decrease in the levels of adrenocorticotropic hormone and cortisol in the blood. And if the tumor is ectopic, then the hormone levels will not change.

Tumors that cause increased cortisol production are looked for using computed tomography and magnetic resonance imaging. If microadenomas with a diameter of 2 mm or more are found in the pituitary gland, then this is considered irrefutable evidence of the presence of Cushing’s disease. If the tumor is ectopic, then it is recommended to carefully, step by step, “enlighten” the chest and abdominal cavity. Unfortunately, ectopic tumors can be very small in size and still produce hormones in large doses. For such cases, magnetic resonance imaging is considered the most sensitive examination method.

Treatment

The cause of Cushing's syndrome is a tumor that produces “extra” hormone cortisol. Such a tumor may be located in the pituitary gland, adrenal glands, or somewhere else. In a real way A treatment that gives a long-term effect is surgical removal of the problematic tumor, wherever it is located. Neurosurgery methods for removing pituitary tumors have undergone significant development in the 21st century. In the world's best clinics, the rate of complete recovery after such operations is more than 80%. If the pituitary tumor cannot be removed in any way, then it is irradiated.

Varieties of Itsenko-Cushing syndrome

For six months after removal of the pituitary tumor, the patient’s cortisol level remains too low, so replacement therapy is prescribed. However, over time, the adrenal glands adapt and begin to function normally. If the pituitary gland cannot be cured, both adrenal glands are surgically removed. However, after this, the production of adrenocorticotropic hormone by the pituitary gland further increases. As a result, the patient’s skin color may darken significantly within 1-2 years. This is called Nelson's syndrome. If adrenocorticotropic hormone is produced by an ectopic tumor, then it is highly likely to be malignant. In this case, chemotherapy is necessary.

For hypercortisolism, the following medications can theoretically be used:

affecting the production of adrenocorticotropic hormone - cyproheptadine, bromocriptine, somatostatin;
inhibiting the production of glucocorticoids - ketoconazole, mitotane, aminoglutethimide, metyrapone;
blocking glucocorticoid receptors - mifepristone.

However, doctors know that these medications are of little use, and the main hope is surgical treatment.

Blood pressure in Cushing's syndrome is controlled with spironolactone, potassium-sparing diuretics, ACE inhibitors, and selective beta blockers. Try to avoid medications that negatively affect metabolism and reduce the level of electrolytes in the blood. Drug therapy for hypertension in in this case- This is only a temporary measure before radical surgery.

Acromegaly

Acromegaly is a disease that is caused by excessive production of growth hormone. This hormone is also called somatotropic hormone, somatotropin, somatropin. The cause of the disease is almost always a tumor (adenoma) of the pituitary gland. If acromegaly begins before the end of the growth period at a young age, then such people grow up to be giants. If it begins later, the following clinical signs appear:

coarsening of facial features, including massive lower jaw, developed brow ridges, prominent nose and ears;
disproportionately enlarged hands and feet;
There is also excessive sweating.

These signs are very characteristic, so any doctor can easily make a primary diagnosis. To determine the final diagnosis, you need to take blood tests for growth hormone, as well as insulin-like growth factor. The content of growth hormone in the blood in healthy people never exceeds 10 mcg/l, and in patients with acromegaly it exceeds. Moreover, it does not decrease even after taking 100 g of glucose. This is called a glucose suppression test.

Hypertension occurs in 25-50% of patients with acromegaly. Its cause is considered to be the property of growth hormone to retain sodium in the body. There is no direct relationship between blood pressure readings and the level of somatotropin in the blood. Patients with acromegaly often experience significant hypertrophy of the myocardium of the left ventricle of the heart. It is explained not so much by high blood pressure as by changes in hormonal levels. Because of her the level cardiovascular complications among patients is extremely high. Mortality rate is about 100% within 15 years.

For acromegaly, conventional first-line blood pressure medications are prescribed, alone or in combination. Efforts are directed towards treating the underlying disease by surgical removal pituitary tumors. After surgery, blood pressure in most patients decreases or completely normalizes. At the same time, the content of growth hormone in the blood decreases by 50-90%. The risk of death from all causes is also reduced several times.

There is research evidence that the use of bromocriptine can normalize the level of growth hormone in the blood in approximately 20% of patients with acromegaly. Also, short-term administration of octreotide, an analogue of somatostatin, suppresses the secretion of somatotropin. All of these measures can lower blood pressure, but the real long-term treatment is surgery or x-rays to the pituitary tumor.

Hyperparathyroidism

Parathyroid glands (parathyroid glands, parathyroid glands) are four small glands located along the back surface thyroid gland, in pairs at its upper and lower poles. They produce parathyroid hormone (parathyroid hormone). This hormone inhibits the formation of bone tissue, leaches calcium from bones, and increases its concentration in the blood and urine. Hyperparathyroidism is a disease that occurs when too much parathyroid hormone is produced. The most common cause of the disease is hyperplasia (overgrowth) or tumor of the parathyroid gland.

Hyperparathyroidism leads to the fact that in the bones bone is replaced by connective, and in urinary tract calcium stones are formed. The doctor should suspect this disease if the patient has hypertension combined with elevated calcium levels in the blood. In general, arterial hypertension is observed in approximately 70% of patients with primary hyperparathyroidism. Moreover, parathyroid hormone itself does not increase blood pressure. Hypertension occurs due to the fact that with a long course of the disease, kidney function is impaired, and the blood vessels lose the ability to relax. Parathyroid hypertensive factor is also produced - an additional hormone that activates the renin-angiotensin-aldosterone system and increases blood pressure.

Based on symptoms, without tests, it is impossible to immediately make a diagnosis. Manifestations from the bones - pain, fractures. From the kidneys - urolithiasis, renal failure, secondary pyelonephritis. Depending on which symptoms predominate, there are two forms of hyperparathyroidism - renal and bone. Tests show increased levels of calcium and phosphate in the urine, excess potassium and a lack of electrolytes in the blood. X-rays show signs of osteoporosis.
Blood pressure increases already in the initial stages of hyperparathyroidism, and target organ damage develops especially quickly. Normal indicators parathyroid hormone in the blood - 10-70 pg/ml, and with age upper limit increases. The diagnosis of hyperparathyroidism is considered confirmed if there is too much calcium in the blood and at the same time an excess of parathyroid hormone. Ultrasound and tomography of the parathyroid gland are also performed, and if necessary, a radiological contrast study.

Surgical treatment of hyperparathyroidism has been found to be safe and effective. After the operation, more than 90% of patients recover completely; blood pressure normalizes, according to various sources, in 20-100% of patients. Blood pressure pills for hyperparathyroidism are prescribed as usual - first-line medications alone or in combinations.

Hypertension and thyroid hormones

Hyperthyroidism is an increased production of thyroid hormones, and hypothyroidism is a lack of them. Both problems can cause drug-resistant hypertension. However, if the underlying disease is treated, then blood pressure will normalize.

A huge number of people have problems with the thyroid gland, especially often in women over 40 years of age. The main problem is that people with this problem do not want to go to an endocrinologist and take pills. If thyroid disease is left untreated, it greatly shortens life and worsens its quality.

Basic Symptoms of an overactive thyroid gland:

thinness, despite a good appetite and good nutrition;
emotional instability, anxiety;
sweating, heat intolerance;
attacks of heartbeat (tachycardia);
symptoms of chronic heart failure;
skin is warm and moist;
hair is thin and silky, early gray hair is possible;
The upper blood pressure is likely to be increased, while the lower blood pressure may be decreased.

Basic symptoms of thyroid hormone deficiency:

obesity, resistant to attempts to lose weight;
chilliness, cold intolerance;
puffy face;
swelling;
drowsiness, lethargy, memory loss;
hair is dull, brittle, falls out, grows slowly;
the skin is dry, the nails are thin and flaking.

You need to take blood tests:

Thyroid-stimulating hormone. If the function of the thyroid gland is reduced, then the content of this hormone in the blood is increased. Conversely, if the concentration of this hormone is below normal, it means that the thyroid gland is too active.
T3 free and T4 free. If the levels of these hormones are not normal, it means that the thyroid gland needs to be treated, even despite the good levels of thyroid-stimulating hormone. There are often hidden problems with the thyroid gland, in which the level of thyroid-stimulating hormone is normal. Such cases can only be detected using tests for free T3 and free T4.

Endocrine and cardiovascular changes in thyroid diseases

If the thyroid gland is too active, then hypertension occurs in 30% of patients, and if there is a deficiency of its hormones in the body, then the pressure is increased in 30-50% of such patients. Let's take a closer look.

Hyperthyroidism

Hyperthyroidism and thyrotoxicosis are the same disease, increased production of thyroid hormones, which accelerate metabolism. Cardiac output, pulse rate and myocardial contractility indicators increase. The volume of circulating blood increases, and peripheral vascular resistance decreases. The upper blood pressure is likely to be increased, while the lower blood pressure may be decreased. This is called systolic hypertension, or increased pulse pressure.

Let your endocrinologist prescribe therapy for hyperthyroidism. This is a broad topic that goes beyond the scope of the site about the treatment of hypertension. Beta blockers, both selective and non-selective, are considered the most effective as blood pressure pills. Some studies have shown that non-selective beta blockers may reduce excess production of the thyroid hormones T3 and T4. Non-dihydropyridine calcium antagonists, which slow the heart rate, may also be prescribed. If hypertrophy of the left ventricle of the heart is pronounced, then ACE inhibitors or angiotensin-II receptor blockers are prescribed. Diuretics complement the effects of all these drugs. It is undesirable to use dihydropyridine calcium channel blockers and alpha-blockers.

Hypothyroidism is a decreased production of thyroid hormones or problems with their availability to body tissues. This disease is also called myxedema. In such patients, cardiac output is reduced, pulse is reduced, circulating blood volume is also reduced, but peripheral vascular resistance is increased. Blood pressure increases in 30-50% of patients with hypothyroidism due to increased vascular resistance.

Tests show that those patients who have developed hypertension due to hypothyroidism have elevated levels of adrenaline and norepinephrine in the blood. Characterized by increased diastolic “lower” blood pressure. Upper blood pressure may not increase because the heart is working sluggishly. It is believed that the more elevated the lower pressure, the more severe the hypothyroidism, i.e., the more acute the lack of thyroid hormones.

Treatment of hypothyroidism - pills prescribed by an endocrinologist. When the therapy begins to work, your health improves and your blood pressure returns to normal in most cases. Get repeated blood tests for thyroid hormones every 3 months to adjust your pill dosage. In elderly patients, as well as those with a long history of hypertension, treatment is less effective. These categories of patients need to take blood pressure pills along with medications for hypothyroidism. ACE inhibitors, dihydropyridine calcium antagonists or alpha-blockers are usually prescribed. You can also add diuretics to enhance the effect.

conclusions

We looked at the main endocrine causes, other than diabetes, that cause severe increases in blood pressure. It is typical that in such cases they do not help traditional methods treatment of hypertension. It is possible to stably bring blood pressure back to normal only after taking control of the underlying disease. In recent years, doctors have made progress in solving this problem. Particularly encouraging is the development of the laparoscopic approach to surgical operations. As a result, the risk for patients has decreased, and recovery after surgery has accelerated by approximately 2 times.

If you have hypertension + diabetes type 1 or 2, then study.

If a person has hypertension due to endocrine causes, then usually the condition is so bad that no one hesitates to see a doctor. An exception is problems with the thyroid gland - deficiency or excess of its hormones. Tens of millions of Russian-speaking people suffer from thyroid diseases, but are lazy or stubbornly do not want to be treated. They do themselves a disservice: they shorten their own lives, suffer from severe symptoms, and risk a sudden heart attack or stroke. If you have symptoms of hyper- or hypothyroidism, get blood tests and go to an endocrinologist. Don't be afraid to take thyroid hormone replacement pills, they provide significant benefits.

The rarest endocrine causes of hypertension are beyond the scope of the article:

hereditary diseases;
primary hyperrenism;
endothelin-producing tumors.

The likelihood of these diseases is much lower than that of a lightning strike. If you have questions, please ask them in the comments to the article.

Galina
Thank you very much for the article!
I’ll get my hormones tested and try to treat my hypertension correctly.
Ella Stepina
Good afternoon I am 38 years old, height 158 cm, weight 40 kg, I have no chronic diseases, except for hemorrhoids (3 years) and migraines, the duration of which is 10 years, but its intensity is decreasing. More often the head and neck area hurt, work is immobile. Recently, there has been a steady increase in diastolic pressure against the background of a slight increase in systolic pressure. The difference is 20-25 mm, the lower one is about 90 and higher, rarely 130/100 (105). In the morning the pressure is 90/70, then it rises. I used to be hypotensive, but with age the pressure became a little higher, but if the upper level rose to 120, I felt bad and had nausea. Now I didn’t feel any increase in diastolic pressure, it just became clear during the measurement. Papazol 1 tablet reduces it to 75. I tested thyroid hormones a long time ago - within normal limits. Cholesterol is also elevated - 6.3. Other biochemical blood and urine tests are normal. 3 months ago I took them in the hospital during hospitalization with migraine status. There is nervousness, anxiety, periodic pain in the intestines and constipation and, possibly against the background of blood pressure control, pain in the heart. I have always been slim, my diet is very moderate and healthy, except for salt consumption (I love pickles). I do not take therapy with medications, including hormonal ones; I only take NSAIDs during migraine attacks. Tell me, please, what does an increase in diastolic pressure primarily indicate? Where to start the examination? Thank you!
flora(tsvetok)
I am 73 years old, height 1-58, weight 76 kg. I am a hypertensive patient with experience - since I was 50 years old! But everything went smoothly. I took cristepin, then Enap. Everything was stable 135/70. Sometimes there were high numbers of 150-160 to 70-80. But in the last couple of years it has become more common to climb 160-170 to 80! Saw Valz - it helped for half a year, then the numbers started getting high! I changed it to Nebilet, but to no avail! For 3 weeks now, my blood pressure has been off the chain! Constantly rises to 180-200 at 60-70. The top one is very high! There are no headaches (very rare), but the head is heavy! I notice that sometimes I am pulled to the side. The doctor prescribed Niperten in the morning (sometimes for heart problems), and Physiotens in the evening. If it rises during the day, indapamide or Fosicard. And if it rises at 22:00, before bedtime, then physiotens. But from tablet to tablet, the pressure rises to 200. I don’t know what the reason is. Sometimes even pills are useless. What should I do?
Lyudmila
Good afternoon I am 62 years old. Height 173. Weight 78 kg. I don’t even know where to start... I drink Magnelis B6 9 pcs., I drank 2 packs and another pack of Magnerot 50 pcs. Now I started Magne-B6 French, 50 tablets, I’ve already drank half of it. Eat fish fat, pharmaceutical lecithin, I drink Dibicor on an empty stomach, I have been eating according to the Malakhova system for 2 years, I have lost 24 kg. Almost all illnesses are gone, but the pressure does not go away. There is also slight angina and ischemia. I have been drinking lisinoton and nebilet every day for I don’t remember how many years. I took other pills before. I used to have metabolic syndrome, but it's been gone for a year now. Now according to the tests: ultrasound of the liver diagnosed hepatomegaly, diffuse changes in the liver, kidneys and pancreas, chronic cholecystitis. A duplex scan of the brain showed atherosclerosis of the bracheocephalic arteries. An ultrasound of the thyroid gland found one nodule, but before there were three. I took tests for hormones, they are normal. I haven’t been to the endocrinologist yet, but I’m planning to go. ALT 20.9, AST 28.2, but the norm is up to 31. No protein was detected in the urine, the analysis is good. The clinical picture and blood biochemistry are normal. However, almost the third week of treatment using your method has ended and there is no result. I try to cut out carbohydrates, but it doesn’t work at all. I just take it with a low glycemic index. I eat four times a day. In the morning, 200 g of raw beet and carrot salad, celery stalks with 1 tbsp. l. flaxseed oil and 2 eggs. For lunch, 120 g of breast or a breast cutlet with beef and 250 g of salad before meals. An afternoon snack of 10 almonds and 200 grams of fruit with a low glycemic index - an apple or pear. Sometimes I add salad. Dinner - salad and salmon or other fish. All three salads with flaxseed oil. In the morning I steam 2 tsp. flax seed. I don’t eat salt; instead I take dry pharmaceutical kelp. This is what nutrition is like. I drink 1.5-2 liters of water a day. Help me cope with hypertension. Thank you!
1. admin Post author
  > almost the third week ends
  > treatment according to your method
  > and no result
  
  You do not indicate what your blood pressure levels were and are.
  
  Eating fruits, beets and carrots, which are prohibited on a low-carb diet, causes a spike in your blood insulin levels. It constricts blood vessels and retains fluid in the body. Perhaps the pressure is increased because of this. I advise you to study the book “The New Revolutionary Atkins Diet” and stick to the diet.
  
  Your blood vessels are also significantly affected by atherosclerosis. In such a situation, reducing the pressure to 120/80 may be completely impossible. If you achieve 140/90, that will be good.
  
  > I used to have metabolic syndrome,
  >but it's been a year since he's been gone
  
  How did you know this? Did the fortune teller whisper or based on test results?
  
  >beginning Magne-B6 French
  
  You will go broke on it :). Order supplements from the USA as I recommend to save 4-6 times.
  
  > I just take it with a low glycemic index.
  
  The glycemic index is nonsense, quackery. Just don't eat any fruits or prohibited vegetables. Suitable sources of fiber include green vegetables and flax seeds. Fruits do you more harm than good.
  1. Lyudmila
    Good evening! Thanks for the answer. You didn't reassure me. But I will still continue to take magnesium, taurine, omega-3, lecithin, vitamins and try to find out the cause of hypertension. Why did I write about metabolic syndrome like this? I understand what it is:
    1. Excess visceral fat (just determined by waist circumference)
    2. High blood pressure (more than 135/90 at rest)
    3. High cholesterol and/or triglycerides with low HDL (low “good” cholesterol)
    4. Increased blood glucose levels - well, I won’t even explain here.
    
    It is believed that any 2 conditions in addition to 1 (that is, in addition to obesity) = metabolic syndrome. So, two years ago my weight was 102 kg, now it’s 78 and everything is fine with my waist, cholesterol has long been normal. I haven’t eaten sweets for two years, except fruits with a low glycemic index. I also excluded flour, potatoes, sugar, vinegar, trans fats, canned food, processed foods, gastronomy, pickled vegetables, caffeine, alcohol, etc. My pancreas is calm, my sugar is normal, I eat three times a day, insulin is released into the blood three times, there are no problems with the gastrointestinal tract. Of the entire list, only blood pressure increases. Therefore, I concluded that metabolic syndrome no longer exists. Sclerosis, yes, noticeable. But magnesium, lecithin and a healthy diet will cleanse the blood vessels, I hope, it just takes time... I took increased doses of magnesium, moving to 350 mg per day. I really want to prescribe Natural Calm magnesium citrate, but I haven’t been able to yet because I’m not good with computers. last week I tried to remove fruits, cereals, bread, all carbohydrates. The body is on strike, a craving for sweets appears, I’ll try to buy and drink chromium picolinate. I'm reading the Atkins diet.
    As for my blood pressure, it does not rise above 140/90, but this is rare, I take pills daily. Previously there was hypotension with a pressure of 90/60, and now there is a crisis and vomiting with readings of 120/80. Just before I found out your site and started drinking magnesium, I was taken away from work in an ambulance and given an injection of magnesium. There were no more crises and I noticed that Capotena began to drink less in addition to lisinoton and nebilet. This is already making me happy. I measure the pressure automatically on my wrist nissei, my norm is 100-110/70.
  2. Inna
    Hello. I am 55 years old, height 159 cm, weight 58 kg. For a year and a half I took lisinopril in the morning, then and in the evening. I felt bad: my head hurt, there was a buzzing in my head, there was pressure on my ears. The doctor prescribed perindopril and indapamide instead. They almost drove me crazy within a week: headache, buzzing, ears and tingling throughout my body. The doctor already prescribed losartan in the morning, but it still gives me a tingling sensation and my heart hurts. I've been drinking for two days. According to your system, I also drink omega-3 and magnesium-B6 for two days. I haven't bought taurine yet. The tests are as follows: cholesterol 8.3 and uric acid 383, urine is normal, I’ll test for hormones. Tell me what I have and what else should I do? One doctor says that it is from the vessels of the head, another - from the cervical vertebra, which is pinching, and the third does not know. Charging according to N.G. Mesnik I do. Thank you.
    Denis
    Hello! Mother is 77 years old, 160 cm, 65 kg. Hypertension has been bothering her for about 20 years - from the moment when, on suspicion of cancer, the thyroid gland was almost completely removed. As it turned out later, it was in vain - on the ultrasound they saw only large nodes and they hurried. Now my mother suffers from hypertension. The pressure sometimes reached 240/110, the working pressure was 150/90. Of the medications, only clonidine and sometimes captopril help reliably combat crises. In autumn and winter, blood pressure reaches 200/90 almost every day. I have to take clonidine two or three times a week.
    According to the results of analyzes and studies:
    Cardiologist: stage 3 hypertension, risk 4
    Endocrinologist: diabetes Type 2
    Orthopedist: spinal osteochondrosis, arthrosis.
    Daily medication intake:
    Glibomet, Coformin, L-thyroxine, Bisoprolol(?), Fosinopril, Arifon retard, Nifedipine, Noliprel.
    + captopril, less often clonidine.
    On the doctor’s recommendation, I took a course of injections of papaverine with dibazole (20 times) + IV magnesium (10 times).
    Now, after 4 months since the beginning of autumn, my blood pressure has become a little better, maybe due to medications or somehow “due to the weather.”
    The question is: how to get rid of at least some of these medications, replacing them with exercises or procedures?
    We live at a resort. There are also radon/hydrogen sulfide baths nearby and physiotherapy.
    We cannot find a doctor capable of an integrated approach from both cardiology and endocrinology... And perhaps from orthopedics?..
    Thank you!
  3. Dubrovskaya
    Hello. I am 30 years old. Height 166 cm, weight 70 kg. Diseases - osteochondrosis, small hernia, heart failure of the 1st degree of the mitral valve, bilateral chronic pyelonephritis, there are small stones in the kidneys, arrhythmia, tachycardia. I sweat a lot, lack of coordination. Lately my blood pressure has been rising, for about a month and a half, mostly 180/110. During attacks, cortisol is elevated. Is there a suspicion of an adrenal tumor?
  4. Irina
    Hello! I am 42 years old, height 175 cm, weight 82 kg. I have a problem that has been bothering me for 4 years. Sudden rises in blood pressure, with trembling, fear, dizziness and tachycardia. Sometimes chest pain. Before lifting, I feel increased sensitivity in my hands and the back of my head, as if high temperature. The pressure rises to 150-160/90-100. Now it rises mainly in the evening, maybe at night. If I can’t fall asleep or wake up abruptly, such an attack begins. There is a fear of falling on the street or even dying. I consulted a cardiologist (ultrasound of the heart, ECG, Holter monitoring) - everything was within normal limits. Endocrinologist - thyroid hormones, ultrasound of the adrenal glands - normal. Therapist - general analysis blood, biochemistry, sugar - normal. Ultrasound of the abdominal cavity and kidneys - no abnormalities. I even consulted a neurologist - without any deviations. The psychotherapist made a diagnosis anxiety disorder with attacks panic attack. I took Amitriptyline + alprazolam according to the regimen for 6 months - attacks of high blood pressure with tremors were less frequent, but did not stop. Other medications periodically prescribed were Phenibut, Glycine, Lorafen, Afobazole, Grandaxin and other tablets. For hypertension and palpitations - Anaprilil, metoprolol, bisoprolol. During the attack itself, I take Capoten under the tongue or Metoprolol. I'm already tired. I would like to find a drug that will prevent blood pressure from rising. Give advice if possible.
  5. Vladimir
    Hello. Is it possible to start the Atkins diet and take dietary supplements if there is an increased level of uric acid in the blood?
  6. Natalia
    Good afternoon My son is 19 years old, height 185 cm, weight 85 kg. Two years ago, during a medical examination at the military registration and enlistment office, it turned out that he had high blood pressure. We underwent an examination, including ABPM, which showed an average blood pressure of 145/80. They rented everything necessary tests, did an ultrasound of the kidneys, adrenal glands, and thyroid gland. We underwent MRI from the vessels of the brain to the kidneys. In general, everything that was prescribed and I read myself. All examinations did not reveal any obvious violations, at least nothing that could affect the pressure. A diagnosis of essential hypertension was made. During these two years, we took a whole bunch of medications. They prescribed one thing, then another. There is no result. The son said that he didn’t want to “poison” his body anymore and stopped taking the pills. As a result of stopping the pills, or because of the duration of the disease, his average blood pressure is now 150/80. There are jumps in upper pressure up to 170. He doesn’t particularly complain about his condition. He says he feels good. Although outwardly I can easily notice his pressure surges. The collar area and face are red. At such moments I measure his blood pressure - as a rule, the upper level is 160-170. Please advise what to do? The only thing he didn’t do was take hormone tests (I plan to send him in the next few days). Our city is small, there are no doctors. The guy is young, maybe he can do without lifelong drug therapy. P.S. The son leads a healthy lifestyle, studies at a military university, there is nutrition, physical education, and sports training. In general, there are no complaints on this side. Thanks in advance for your answer.
  7. Natalia
    Thanks a lot for the article. I am 53 years old, height 167 cm, weight 75 kg. I have hypertension, I think, due to hypothyroidism (TSH is normal) and depression. I have been taking antidepressants for 9 months. Blood pressure is not always elevated. Now mostly in the morning it’s 110-120/60-70, and in the evening it can be 150-170/80-90, severe headaches, a state of restlessness and anxiety. I take 1/4 tablet of bisoprolol and lozap. I took tests several times during the year while in the hospital (3 times) - all indicators were normal, except for leukocytes. Ultrasound of the thyroid gland showed the presence of two nodes (in 2006 there were 7) and hypofunction.
  8. Inna
    Good afternoon
    I am 37 years old, height 180 cm, weight 105 kg. At the same time, it’s difficult to call me very fat - even in my youth, playing sports and having practically no fat, I weighed no less than 80 kg. “Broad bone” - apparently, about me)) Wedding ring Size 20...
    In 2006, a large nodule was discovered in the thyroid gland, I was pregnant. After completion of the hepatitis B, she again turned to the endocrinologist - the node had grown significantly and it was recommended to remove it. In 2008, the entire lobe and isthmus were removed, suspecting an adenoma. Histology results revealed carcinoma. We registered him at the oncology clinic and prescribed levothyroxine in a lethal dose so that TSH was minimal. Of course, I couldn’t live with hypothyroidism for long, so I switched to 100 mg, then to 75. Basically, I felt fine. But last year I started having panic attacks, palpitations, and brain fog. The pressure reached 180/140. The heart is normal, hormones are as usual, bad cholesterol is normal, sugar is high, but also within normal limits. There is a small cyst of 1 cm on the kidney. But in the rest of the thyroid gland there are 3 nodes, one 1.5 cm and cysts. Cardiologists prescribed many medications - I took Enap, metoprolol, carvedilol, and now Concor. The pressure is within 140/100, and the lower one is never less than 90, even if the upper one is 120. The endocrinologist does not see the causes of hypertension in the thyroid gland. I’ve been taking Omega 3 + Coenzyme Q10 + Magnesium from iHerb for 3 months, but there are no special results. Without pills, the pressure rises again. Tell me where else to look for reasons?
  9. Oksana
    Good afternoon Thank you for the article. I am 37 years old, no children yet. Height 169 cm, weight 55 kg. A month ago I had a hypertensive crisis and my blood pressure rose to 140/90. I am hypotensive and my normal blood pressure is 100/60. They called an ambulance twice to relieve the pressure. The next day I went to the hospital. They examined the internal organs, heart, blood vessels, thyroid gland - everything is fine. A diagnosis of neurocirculatory dystonia was made. For a month after discharge I have been taking Adaptol, Vinoxin, Corvasan, Magne B6, Berlipril. A month later, the day before my period there was a sharp jump, I lowered the berlipril, after my period the same thing happened every other day - I had to call an ambulance. The next two days after lunch or in the late afternoon, my blood pressure increased - I took Anaprilin and Berlipril. This morning everything is fine. Tell me, what hormones could this be related to? Thank you.
  10. Lyudmila
    I am 60 years old, height 168 cm, weight 86 kg. A year ago, autoimmune thyroiditis was diagnosed - I take L-thyroxine. Also, bronchial asthma, which is now stabilized, only occasionally requires the use of Berotek. Also urolithiasis, problems with joints, and little things - glaucoma with normal eye pressure, prediabetes. During pregnancy I had high blood sugar, but now it is at the limit - sometimes up to 6.0. My main concerns are swelling in my ankles, joint pain, and the inability to adjust my weight with nutrition. I noticed the increase in pressure by accident myself. Head is spinning. I measured my blood pressure - 160/90. In the fall, I visited the doctors for an examination. There were no heart problems. And the pressure was 110/70. It has been low all my life. I'm out of town now, getting into the city in the near future is problematic. I am a paramedic by training, I started treatment myself - Egilok and Triampur. I’ve been drinking for 3 days, but my blood pressure remains 160/90 in the morning and evening. Please advise which medications are best for me?
  11. Irina
    Hello. Thank you for the information posted on the site, and I really hope the site is still active.
    I am 52 years old, height 169 cm, weight 77 kg. Since childhood, periodic headaches with right side, the pressure was measured at school - it was normal. From about 35 years old, blood pressure levels are consistently elevated - 145/90, by 45 years old - 155-165/95. Headaches are predominantly on the right side, occurring 3-4 times a month. Also weather dependence, heaviness in the occipital part of the head, with a transition to the temporal regions. I didn’t take any pills, except for a very moderate intake of potassium-sparing diuretics (no more than 1-2 times a month), as swelling of the face began to appear in the morning, which could go away on its own during the day. Over the past two years, blood pressure levels have worsened significantly - 170/105. Sometimes goes numb right hand, if you change your body position suddenly, there is a lack of coordination, there is a feeling that I might fall. It appears rarely, for example, in the bathroom when I get up. Swelling of the legs began to appear in the evening and sometimes in the morning. The therapist prescribed Lorist tablets with a diuretic. I drank continuously for about 6 months, but the result was zero. I decided not to poison myself anymore. I went for a full examination. MRI and Doppler showed that the circle of Willis is open, there is significant hypoplasia vertebral artery on the right, the left is compensatory expanded. A course of Cerebrolysin was prescribed - almost to no avail. They pierced the magnesia. The upper pressure temporarily (for no more than a week) dropped to 135, and the lower pressure did not move at all from 105-107. A diagnosis of vertebrobasilar insufficiency was made. The doctor advised me to carry captopril with me and take it when my upper blood pressure is above 170. About two months after the course of treatment, my blood pressure reaches 197/110. Heaviness in the back of the head, it can be difficult to find the right word. For the last three days I have been going to a chiropractor, I don’t take pills on purpose, for the purity of the experiment. He put my vertebrae in place, all the departments. They also inject vitamin B12 into the neck area, massage the cervical-collar area, cupping on the back with punctures, and acupuncture. I feel better, the pressure has dropped to 155, the lower one remains 105. This worries me. Realizing that the relief will be temporary, I ask for advice - what tests should I undergo and which doctor should I contact with my problem?
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The diagnosis of endocrine arterial hypertension is given to men and women who have problems with blood pressure. A violation may be a consequence of the development of a serious disease that is related to a lack or excess of hormones. Therefore, with a regular increase in blood pressure to 140 to 90 mm Hg. Art. and above, you must immediately consult a doctor.

Endocrine hypertension is often observed in people who have the following conditions:

Bad heredity;
Acute form of hypertension;
Lack of pronounced effect after taking medications with antihypertensive effects.

All these factors can sooner or later lead to the development of this pathological process. The occurrence of symptoms of the disease is also accompanied by the following reasons:

Disorders of the thyroid gland. They may manifest as hypothyroidism, hyperthyroidism, or hyperparathyroidism;
Pheochromocytoma. This is the name for a tumor-like formation of the adrenal medulla, which leads to the release of a number of hormones into the blood;
Kohn's syndrome. It is detected when the patient has a neoplasm of the adrenal cortex, which provokes increased production of the hormone aldosterone;
Itsenko-Cushing syndrome. This diagnosis means severe damage to the adrenal cortex or pituitary gland, which leads to increased secretion of certain hormones.

Problems with the thyroid gland negatively affect the condition of many body systems. Endocrine organs are needed to produce important hormones that carry the information required by cells throughout the body. Thanks to them, the consistency of various processes is maintained. Blood pressure is no exception. In order for the thyroid gland to work correctly, a person needs to avoid factors that cause disruption in its functioning.

Malfunctions of the endocrine system lead to many complications, and hypertension is one of them.

Symptoms

Arterial hypertension, which affects the development of endocrine genesis, has symptoms that are similar to the main signs of primary hypertension. However, in the first case, manifestations of the underlying disease will be noticeable.

It must be remembered that the course of this pathological condition may be asymptomatic. Therefore, it is unlikely that it will be possible to determine the disease without special diagnostics. But sometimes with this diagnosis, patients experience the following signs of illness:

Tightness in the temple area;
Muscle weakness;
Headache;
Dizziness;
Facial redness;
Noise in ears;
Pain in the heart area;
Blurred vision;
Nausea.

These conditions may be accompanied by other signs of malaise that are inherent to the specific disease that provoked endocrine hypertension.

With endocrine hypertension, signs of high blood pressure and the underlying disease appear simultaneously

General principles of diagnosis and treatment

If this disease is suspected, markers of endocrine arterial hypertension must be studied. Diagnosis of a pathological process consists of a number of research activities:

Clinical blood test;
Blood chemistry;
MRI of the pituitary gland and adrenal glands;
CT scan of the pituitary gland and adrenal glands;
Blood test for carbohydrate metabolism;
Urine analysis for the content of hormones and their breakdown products.

At the discretion of the doctor, other diagnostic procedures may be performed to help assess the current condition of internal organs that could be affected by endocrine arterial hypertension.

Drug treatment

Endocrine hypertension, which has a detrimental effect on the condition of the arteries and internal organs, requires drug treatment. This type of hypertension is suppressed by different groups medications. When selecting them, some nuances are taken into account:

Age of the patient;
General health;
Diseases that have affected the increase in blood pressure;
Complications;
Treatment prognosis.

To improve the patient’s condition and normalize high blood pressure, the doctor will recommend that he take medications from the following groups:

ACE inhibitors;
Beta blockers;
Alpha blockers;
Diuretics;
Muscle relaxants;
Angiotensin receptor blockers.

These drugs can remove excess fluid from the human body, while increasing the lumen of blood vessels. The result of this treatment is a decrease in blood pressure and dilation of the arteries.

The selection of drug therapy should be carried out on an individual basis.

Surgery

Certain pathological changes that appear against the background of high blood pressure cannot be eliminated with the help of medications. In such situations, only surgical intervention can help the patient. Surgeries are recommended for patients who have tumors that do not allow internal organs to function normally. For example, those diagnosed with Itsenko-Cushing's disease cannot do without it.

After surgery, the patient spends some time in the intensive care unit. The doctor should monitor the patient’s condition for several days. If within 6-7 days no new disorders of the cardiovascular system are identified, he will go home.

Acromegaly

Acromegaly is a disease caused by a tumor in the pituitary gland. The medullary appendage produces growth hormone, which further increases sodium levels in the blood. Due to the tumor, excess fluid begins to accumulate in the body, which has a direct effect on increasing blood pressure by increasing blood volume.

Acromegaly is also caused by cancer processes that develop in the lungs or pancreas. A person who suffers from of this disease, can be recognized by the following external characteristics:

Large tongue, nose and brow ridges;
Large jaw, feet and hands;
Thick skin.

The appearance of a patient with acromegaly does not change immediately. The changes can be clearly seen in photographs from different years in which it is depicted. If, with such symptoms, a person’s blood pressure systematically increases, then the assumptions about this diagnosis are almost always correct.

Changes in appearance are especially noticeable when comparing photos from different years

The disease is diagnosed using hormone levels, CT and MRI. During diagnostic procedures, X-ray contrast agents are usually used.

In most cases, acromegaly requires surgical treatment. The tumor body is removed transnasally, that is, through the nasal cavity. Radiation therapy is prescribed only when surgery is not possible. Conservative treatment with such a diagnosis does not bring positive changes.

Cushing's syndrome

Cushing's syndrome is found in certain pathologies caused by excessive production of glucocorticosteroids. This change leads to the development of tumors in the adrenal glands and pituitary gland. Blood pressure with such deviations increases due to stimulation of the nervous system. Cushing's syndrome is recognized by its characteristic symptoms:

Rosy cheeks;
Visual impairment;
Fat deposits on the neck, face and abdomen;
Mental problems;
Acne;
Striae on the abdomen;
Increased hair growth on the body and face (in women);
Hemorrhages;
Menstrual irregularities;
Diabetes;
Muscle weakness.

All these signs of illness are a good reason to visit a specialist. Diagnosis of this condition is very complicated, since the classic symptoms of the pathology are extremely rare. The results of ultrasound, MRI and CT help the doctor make a correct diagnosis. A blood test is also required.

Endocrine hypertension can be caused by this disorder if Cushing's syndrome is not treated. Medicines in this case are useless. They only help with the development of hypertension. The tumor must be removed using radical methods. This requires surgery or radiation therapy.

Itsenko-Cushing's disease has pronounced manifestations

Pheochromocytoma

The medulla, which is present in the adrenal glands, produces adrenaline and norepinephrine. They affect the strength of heart contractions and heart rate. If pheochromocytoma is found in the adrenal glands, then a neoplasm develops in their tissues, which secretes these hormones randomly. That is why, with such a tumor and high blood pressure, people often experience crises. They appear when produced hormones are released into the blood. The pathological condition is recognized by the following signs:

Cardiopalmus;
Excessive sweating;
Feeling of fear.

Additionally, patients with this disorder complain of the following signs of malaise:

Panic attacks;
Headache;
Pale skin;
Nausea;
Tremor of the limbs;
Decreased blood pressure when changing body position;
Pain in the abdomen and behind the sternum;
Reducing body weight.

During diagnosis, a sample of blood and urine is necessarily examined for the content of metabolites, norepinephrine and adrenaline. Also required visual inspection problem area using CT and ultrasound.

Alpha blockers are often used in the treatment of this pathological condition in order to prevent constant compression of blood vessels with blood, which significantly increases in volume. Additionally, the possibility of developing hypertension is monitored.

The basis of the drug course for pheochromocytoma is beta-blockers. At the discretion of the specialist, the patient is referred for surgical intervention, because only this method can get rid of the tumor.

After surgery, ¼ of all patients continue to have high blood pressure. Then it is associated with primary hypertension or nephropathy, which could occur along with pheochromocytoma.

A benign adrenal tumor can cause excess hormone production

Hyperthyroidism

Hyperthyroidism is an overactive thyroid gland. Most often it occurs due to an overdose of thyroid hormones, Graves' disease and its consequences. Pathology is recognized by a number of characteristic symptoms:

Frequent heartbeat;
Insomnia;
High activity;
Fast fatiguability;
Severe shortness of breath;
Tremor of hands and feet;
Weight loss;
Chest pain;
Frequent urination at night;
Diarrhea;
Sudden change of mood.

If the disease is asymptomatic, it is very difficult to recognize it.

Treatment of hyperthyroidism involves adjusting the functioning of the thyroid gland and eliminating symptoms of abnormality. After excess fluid is removed from the body, the patient is prescribed beta-blockers. Diuretics may be required.

To prevent complications of the painful condition, it is necessary to undergo complete treatment of the thyroid gland. Surgery or exposure of the problem area to radioactive iodine may be required.

Symptoms of hyperthyroidism may not always appear

Hypothyroidism

Hypothyroidism develops due to insufficient internal secretion of thyroid hormones. This condition may cause the development of endocrine hypertension after some time. Hypertension is diagnosed in 1/5 of patients with this disorder.

Hypothyroidism slows down the processes that allow the body to function normally. The disease manifests itself in the form of the following symptoms:

Problems with weight gain;
Menstrual irregularities;
Sleep disorder;
Muscle weakness;
Chilliness;
Slow thinking;
Slow speech.

The disease is diagnosed by the concentration of thyroid hormones, as well as the content of lipids in the blood. Ultrasound helps to evaluate the external data of the organ whose work has been disrupted.

Thyroid hormone replacement therapy helps normalize blood pressure levels. If this technique does not give a positive result, then the patient is prescribed calcium antagonists and diuretics. Angiotensin receptor antagonists may also be needed.

Thyrotoxicosis

Thyrotoxicosis is provoked by an increased amount of hormones produced by the thyroid gland. They provide Negative influence on the performance of the heart and blood vessels. As a result, a person has complaints about the following conditions:

Cardiopalmus;
Hot temper;
Loss of body weight;
Poor sleep;
Heavy sweating;
Fever;
Hand tremors.

During the diagnosis of this disease, it is customary to use hormonal techniques. If the doctor’s suspicions about thyrotoxicosis are confirmed, then the patient is prescribed thyreostatic therapy. In some cases, surgery or radioisotope therapy is recommended.

When the thyroid gland normalizes, blood pressure levels will also return to normal.

Primary hyperaldosteronism

High blood pressure with problems with the endocrine gland can be triggered by increased production of aldosterone in the adrenal glands. As a result, there is an accumulation of excess fluid in the tissues and an increase in the volume of blood that fills the vessels. Blood pressure values that exceed the norm are stable for this diagnosis. Standard antihypertensive drugs do not always help lower blood pressure.

With the development of primary hyperaldosteronism, the following conditions occur:

Weak muscle tone;
Involuntary muscle contractions;
Massive urination.

During diagnostic procedures, a blood sample must be given for analysis. It is examined for the presence of aldosterone, potassium, sodium and renin.

During the treatment of the disease, it is customary to use spironolactone. You also need to take medications with antihypertensive effects, including diuretics.

The neoplasm that occurs during the development of pathology must be removed surgically. This is the only way to get rid of the tumor body. Finishing radical treatment restoration of all body functions that were impaired by the disease is guaranteed.

Hyperparathyroidism

The diagnosis of hyperparathyroidism refers to disease of the parathyroid glands. This condition reveals itself with the following signs:

Weakening of muscle tone;
Lethargy;
Malfunction of the gastrointestinal tract;
Problems with bowel movements.

Sometimes patients with hyperparathyroidism have only one characteristic symptom- high blood pressure. Doctors have not yet been able to understand the mechanism of the increase in blood pressure. It is only known that the parathyroid glands produce a hormone that causes a narrowing of the lumen in the blood vessels and promotes the death of cells that affect the functioning of the kidneys.

The most significant diagnostic measures for such a deviation are laboratory methods. Test results will indicate an increase in calcium levels and a decrease in phosphate levels.

For this diagnosis it is recommended surgical therapy. Removing a tumor or gland that is severely affected is a chance for recovery. After surgery, blood pressure is completely normalized in most cases. If endocrine hypertension is moderate, it is suppressed with medications.

Hypertension, which is accompanied by endocrine diseases, usually manifests itself as severe symptoms. High blood pressure, which is combined with a deficiency or excess of a certain hormone, is a good reason to suspect that the patient is developing this particular disease. Several highly specialized specialists take part in the diagnosis of endocrine hypertension, since pathological process has a detrimental effect on the condition and functioning of various internal organs.

Endocrine arterial hypertension accounts for 1–5% of all diagnosed cases of hypertension. Etiologically to secondary hypertension(in relation to endocrine disorders) includes primary hyperaldosteronism, other mineralocorticoid hypertension, Cushing's syndrome, pheochromocytoma, hyperparathyroidism, acromegaly, hyperthyroidism, hypothyroidism and some other less common endocrine disorders. The first 3 mentioned causative factors of hypertension are resistant diseases. Identifying and eliminating secondary causes is the basis for effective treatment.

Causes of disease development

The most common causes of endocrine hypertension include syndromes caused by overproduction of mineralocorticoids - primary hyperaldosteronism (Conn's syndrome), diseases of tumors of the chromaffin tissues of the sympathetic nervous system (pheochromocytoma, paraganglioma).

More rare is endocrine arterial hypertension in some congenital steroid enzymopathies (congenital adrenal hyperplasia with blockade of 17-α-hydroxylase and 11-β-hydroxylase in the adrenal glands).

Hypertension, mostly mild, often occurs as a result of secondary symptom in a number of other endocrinopathies, therefore, does not apply to the main symptoms of the disease. Such diseases of endocrinological etiology include:

hypercortisolism (ACTH-dependent and ACTH-independent Cushing's syndrome);
thyrotoxicosis;
hypothyroidism;
hyperparathyroidism;
acromegaly;
renin-secreting tumor (Wilms tumor, usually diagnosed in childhood).

Important! Endocrine hypertension in women may be a consequence of taking hormonal contraceptives.

Symptoms of the disease

Hypertension secondary to endocrine disorders is not necessarily manifested by objective symptoms and is often diagnosed incidentally. A nonspecific symptom is headache and a number of heterogeneous manifestations.

Endocrine hypertension is suspected in the following cases:

treatment resistance;
manifestation of the disease at a young age;
sudden deterioration of condition;
sudden onset of severe form;
typical clinical picture and laboratory signs of secondary hypertensive disease.

Basic diagnostic and therapeutic measures

Diagnosis of endocrine hypertension is based on a thorough history and objective examination. The disease is diagnosed by the per exclusion method, by excluding other secondary causes, especially renovascular and renoparenchymal etiology.

The actual inspection is based on specific laboratory samples subject to collection conditions. In case of positive results laboratory research screening examination is carried out.

Treatment depends on the diagnosis and the level of increase in blood pressure with endocrine hypertension:

for hyperfunctional adrenal adenoma with overproduction of mineralocorticoids and pheochromocytoma, unilateral adrenalectomy is performed;
for idiopathic hyperaldosteronism, pharmacological therapy with aldosterone antagonists is prescribed;
for congenital adrenal hyperplasia, suppressive treatment with glucocorticoids is recommended.

With others endocrine diseases, where hypertension is not a dominant disease, treatment depends on the treatment of this endocrine disorder:

for Cushing's disease and acromegaly - transsphenoidal surgery of the pituitary adenoma;
for ACTH-independent hypercortisolism - unilateral adrenalectomy of the adrenal adenoma;
for hyperthyroidism or hypothyroidism, the main condition is the treatment of thyroid dysfunction;
for hyperfunctional parathyroid adenoma, primary hyperparathyroidism - parathyroidectomy.

However, the main condition for the success of the diagnostic algorithm and the effectiveness of treatment is the identification of the potential cause of endocrine hypertension.

Pituitary adenoma with overproduction of growth hormone and the development of acromegaly (or with gigantism arising in childhood as a result of the action of growth hormone before the closure of the epiphyseal plates) is about 40% causal factors arterial hypertension of endocrine origin, a feature of which, as a rule, is renin deficiency. Long-term excess growth hormone causes a number of changes in both the heart and kidneys, leading to the development of hypertension.

Thyrotoxicosis

Thyrotoxicosis is a condition caused by excessive concentrations of thyroid hormones in the blood. In thyrotoxicosis, hormones affect the cardiovascular system, leading to an acceleration of heart rate and pulse, a significant increase in cardiac output, and narrowing of the lumen blood vessels. All this causes the development of stable hypertension. High blood pressure is accompanied by nervousness, irritability, insomnia, weight loss, and sweating.

The incidence of pheochromocytoma is 0.3–0.5% of total number all hypertensive patients, therefore, we are talking about a relatively rare secondary cause of endocrine arterial hypertension. Pheochromocytoma is a tumor of the chromosomal adrenal gland that produces excessive amounts of catecholamines. As a rule, pheochromocytoma is found in a typical adrenal location and is unilateral; in approximately 10% of cases it can be bilateral. Rarely occurs extraadrenally, as a tumor of the sympathetic nervous system (paraganglioma) with localization in the para-aortic ganglia in the abdominal cavity and mediastinum, but also in other places (for example, in the pelvic region around the bladder, etc.). It is often malignant.

The main characteristic of Cushing's syndrome is excessive endogenous production of cortisol. This serious illness associated with high morbidity and mortality. Cushing's disease (ACTH-dependent hypercortisolism) represents about 60–70% of patients with endogenous hypercortisolism. In approximately 5% of cases, paraneoplastic secretion of ACTH (adrenocorticotropic hormone) is detected.

In Cushing's disease, corticotropic cells of the pituitary adenoma produce an increased amount of ACTH, the stimulating effect of which is the hyperplastic expansion of both adrenal glands.

Primary ACTH-independent hypercotism (approximately 20% of patients) is characterized by autonomous overproduction of glucocorticoids by an adrenal adenoma or carcinoma. The secretion of ACTH in this case is suppressed, i.e. we are talking about endocrine hypertension with a deficiency of hormonal production of ACTH.

Primary hyperaldosteronism

Most common reasons Hypertensive endocrine syndromes include overproduction of mineralocorticoids - primary hyperaldosteronism in adrenal adenoma (Conn's syndrome) or bilateral adrenal hyperplasia.

In approximately 50% of cases, laboratory tests show hypokalemia, which can be partially modified by a salt-free diet or the use of potassium-sparing diuretics (Spironolactone, Eplerenone). Renin levels are initially suppressed and aldosterone levels are increased.

Primary hyperaldosteronism occurs in approximately 0.5–1% of all cases of hypertension. The disease is characterized by autonomous hypersecretion of aldosterone - renin activity is inhibited in adrenal adenoma (about 50% of cases). Rarely, the disease causes adrenal cancer, clinically manifested by overproduction of steroids - in addition to mineralocorticoids, glucocorticoids and adrenal androgens.

Hyperthyroidism

Thyroid hormones have a significant positive chronotropic and inotropic effect. When hyperthyroidism is diagnosed, the number of adrenergic receptors increases and their sensitivity to catecholamines increases. In the acute phase of hyperthyroidism, tachycardia is present, cardiac output increases, and hypertension appears, predominantly systolic, with a high pressure amplitude.

Hypothyroidism

A decrease in thyroid function leads to an increase in diastolic blood pressure, therefore, to a decrease in the systolic-diastolic interval. The pathophysiology of cardiovascular disorders is associated with accelerated development of atherosclerosis due to endothelial dysfunction, an increase in the total amount of LDL cholesterol. The disease then develops hemodynamically - symptoms include increased diastolic blood pressure, bradycardia, decreased cardiac output during exercise, increased peripheral vascular resistance by more than 50% (according to ECHO), decreased heart rate.

Important! In general, hypertension in thyroid dysfunction is usually not very severe; what is more important is the worsening of pre-existing hypertension when hypothyroidism occurs. If the dose of thyroid hormone (levothyroxine) is not adjusted, this leads to a decrease in the effectiveness of some classical antihypertensive drugs.

Endocrine ophthalmopathy

We are talking about a complication of thyroid dysfunction. Endocrine ophthalmopathy is a chronic eye disease primarily associated with an autoimmune reaction against the thyroid gland. The disease is characterized by inflammation that affects all structures of the orbit - the external eye muscles, orbital connective and adipose tissue, lacrimal glands, and orbital septum. The result is an increase in volume eyeball, which leads to disruption of the venous outflow from the orbit, a change in the elastic properties of the orbital muscles.

Treatment requires an integrated approach. Prednisolone therapy is often recommended for endocrine ophthalmopathy.

Hyperparathyroidism is a generalized disorder of calcium, phosphate, and bone metabolism as a result of a prolonged increase in parathyroid hormone (PTH).

The disease is more often diagnosed in women (5:1), hyperparathyroidism may be part of multiple endocrine neoplasia. The cause in 85% of cases is adenoma, multiple adenoma, carcinoma, primary hyperplasia.

Typical clinical manifestations include:

nephrolithiasis;
nephrocalcinosis;
bone changes;
cardiovascular diseases (hypertension, left ventricular hypertrophy, mitral and aortic valve calcification);
stomach ulcers;
pancreatitis;
chondrocalcinosis.

Prevention of arterial hypertension

Prevention of high blood pressure consists, first of all, in observing healthy image life:

don't overexert yourself;
if you are overweight, lose weight;
ensure yourself sufficient quantity and quality of sleep;
rest – both passively and actively;
don't overeat;
spend more time in nature;
think optimistically;
do not smoke, do not drink alcohol;
create a varied diet.

Features of therapy

At the onset of the disease, it is advisable to create the right diet that will complement pharmacological treatment. This is the basis for successful therapy.

limiting salt intake (less than 6 g/day);
weight loss;
smoking restrictions;
limiting alcohol consumption (up to 30 g for men, up to 20 g for women);
limiting the intake of certain medications (Ibuprofen, contraception);
increasing sodium intake;
timely treatment of hyperlipidemia.

Drug treatment includes therapy for the underlying disease. Pharmacological therapy for hypertension is recommended when systolic pressure is above 180, diastolic pressure is above 110. Drug intake begins gradually - with low doses, monotherapy or a double combination of drugs from the following therapeutic groups:

diuretics;
β-blockers;
ACE inhibitors;
calcium channel inhibitors;
angiotensin II receptor blockers.

Treatment and prevention can be supported by folk remedies that reduce the influence of risk factors and improve the condition of blood vessels. Use herbs:

hibiscus;
mistletoe;
hop;
ginseng;
Melissa.

Conclusion

Undiagnosed endocrine hypertension leads to the development of very serious complications and organ damage to varying degrees. Early diagnosis of endocrine hypertension and its causal treatment is the best way to prevent complications. Timely, targeted therapy can lead to a complete cure of the disease. The main condition for success is determining the exact cause of the disease during diagnosis.