Arterial hypertension is a persistent increase in pressure in the arteries above 140/90 mmHg. Most often (90-95% of all cases), the causes of the disease cannot be identified, then hypertension is called essential. In a situation where high blood pressure is associated with any pathological condition, it is considered secondary (symptomatic). Symptomatic hypertension is divided into four main groups: renal, hemodynamic, central and endocrine.

In the structure of morbidity, endocrine arterial hypertension occupies 0.1-0.3%. Given the widespread prevalence of hypertension, almost every doctor encounters endocrine arterial hypertension many times in his practice. Unfortunately, the pathology often remains unrecognized and patients receive ineffective treatment for years, which provokes complications in vision, kidneys, heart, and cerebral vessels. In this article we will discuss the main points of symptoms, diagnosis and treatment of arterial hypertension associated with pathology of the endocrine glands.

When is a detailed examination necessary?

Secondary arterial hypertension is rarely diagnosed (about 5% of cases in Russia). However, it can be assumed that in a number of secondary cases the nature of the increase in pressure is simply not detected. In which patient can this situation be suspected? Here are the main groups of patients who need detailed examination:

Those patients in whom maximum doses of antihypertensive drugs according to standard regimens do not lead to stable normalization of blood pressure;
- young patients (up to 45 years old) with severe hypertension (180/100 mmHg and above);
- patients with hypertension whose relatives suffered a stroke at a young age.

Some of these patients have primary hypertension, but this can only be confirmed after a detailed examination. The plan for such diagnostics must include a visit to an endocrinologist. This doctor will evaluate the clinical picture and possibly prescribe hormonal tests.

What endocrine pathology leads to hypertension?

The endocrine glands produce special signaling compounds - hormones. These substances are actively involved in maintaining the constancy of the internal environment of the body. One of the direct or indirect functions of some hormones is to maintain adequate blood pressure. First of all, we are talking about adrenal hormones - glucocorticosteroids (cortisol), mineralocorticoids (aldosterone), catecholamines (adrenaline, norepinephrine). Thyroid hormones from the thyroid gland and growth hormone from the pituitary gland also play a role.

The reason for the increase in pressure in endocrine pathology may be, firstly, the retention of sodium and water in the body. Secondly, hypertension is provoked by the activation of hormones of the sympathetic nervous system. The high tone of this part of the autonomic nervous system leads to increased heart rate, increased force of contraction of the heart muscle, and narrowing of the diameter of blood vessels. So, pathology of the adrenal glands, thyroid gland, and pituitary gland may be the basis of arterial hypertension. Let's take a closer look at each disease.

Acromegaly

Acromegaly is a severe chronic disease that is most often caused by a tumor of the pituitary gland that produces growth hormone. This substance, among other things, affects sodium metabolism in the body, causing an increase in its concentration in the blood. As a result, excess fluid is retained and the volume of circulating blood increases. Such unfavorable changes lead to a persistent increase in blood pressure. Patients with acromegaly have a very characteristic appearance. Growth hormone promotes thickening of the skin and soft tissues, brow ridges, thickening of the fingers, an increase in the size of the feet, and also enlargement of the lips, nose, and tongue. Changes in appearance occur gradually. They should always be confirmed by comparing photographs from different years. If a patient with a typical clinical picture also has arterial hypertension, then the diagnosis of acromegaly becomes more likely.

For an accurate diagnosis, it is necessary to determine the concentration of growth hormone in the blood on an empty stomach and after taking 75 grams of glucose. Another important test is IRF-1 of venous blood. To visualize a pituitary tumor, magnetic resonance or computed tomography with the introduction of a contrast agent is best suited.

Once the diagnosis of acromegaly is confirmed, surgical treatment is most often performed. Basically, transnasal removal of the pituitary tumor is performed. Radiation therapy is performed if surgery is not possible. Treatment with medications alone (somatostatin analogues) is rarely used. This therapy plays a supporting role in the periods before and after radical interventions.

Thyrotoxicosis

Thyrotoxicosis is a condition caused by excessive concentrations of thyroid hormones in the blood. Most often, thyrotoxicosis is provoked by diffuse toxic goiter, toxic adenoma, and subacute thyroiditis. Thyroid hormones affect the cardiovascular system. Under their influence, the heart rate sharply increases, cardiac output increases, and the lumen of blood vessels narrows. All this leads to the development of persistent arterial hypertension. Such hypertension will always be accompanied by nervousness, irritability, insomnia, weight loss, sweating, “heat” in the body, trembling in the fingers.

To confirm the diagnosis of thyrotoxicosis, hormonal tests are prescribed: thyroid-stimulating hormone (TSH), thyroxine (free T4), triiodothyronine (free T3).

If the diagnosis is confirmed, treatment begins with conservative therapy with thyreostatics. Next, surgery or radioisotope treatment may be performed.

Pheochromocytoma

The adrenal medulla normally produces the hormones of “fear and aggression” – adrenaline and norepinephrine. Under their influence, the heart rate increases, the force of contraction of the heart muscle, and the lumen of blood vessels narrows. If a tumor occurs in the adrenal glands or, less often, outside them, producing these hormones uncontrollably, then we are talking about the disease pheochromocytoma. The main feature of hypertension in this endocrine pathology is the presence of crises. In 70% of cases there is no persistent increase in pressure. Only episodes of sharp increases in blood pressure numbers are observed. The cause of such crises is the release of catecholamines into the blood by the tumor. In the classic case, a crisis is accompanied by sweating, rapid heartbeat and a feeling of fear.

To confirm the diagnosis, the patient is prescribed a further examination in the form of an analysis of nonmetanephrine and metanephrine in urine or blood. The adrenal glands are also imaged using ultrasound or computed tomography.

The only effective treatment method is surgery to remove the tumor.

Cushing's disease and syndrome

Cushing's disease causes a tumor in the pituitary gland, and the syndrome causes a tumor in the adrenal gland. The consequence of these diseases is excessive secretion of glucocorticosteroids (cortisol). As a result, the patient not only activates the sympathetic part of the autonomic nervous system and develops arterial hypertension. Typical are mental disorders up to acute psychosis, cataracts, obesity in the abdomen, torso, neck, face, acne, bright blush on the cheeks, hirsutism, stretch marks on the skin of the abdomen, muscle weakness, bruises, bone fractures with minimal trauma, menstrual irregularities in women, diabetes mellitus.

To clarify the diagnosis, the concentration of cortisol in the blood is determined in the morning and at 21:00, then large and small tests with dexamethasone can be performed. To detect a tumor, magnetic resonance imaging of the pituitary gland and ultrasound or computed tomography of the adrenal glands are performed.

Treatment is preferably surgical, removing the tumor in the adrenal gland or pituitary gland. Radiation therapy for Cushing's disease has also been developed. Conservative measures are not always effective. Therefore, medications play a supporting role in the treatment of Cushing's disease and syndrome.

Primary hyperaldosteronism

Increased secretion of aldosterone in the adrenal glands can cause arterial hypertension. The cause of hypertension in this case is fluid retention in the body, an increase in the volume of circulating blood. High blood pressure is constant. The condition is practically not corrected by conventional antihypertensive drugs according to standard regimens. This disease is accompanied by muscle weakness, a tendency to cramps, and frequent excessive urination.

To confirm the diagnosis, the content of potassium, sodium, renin, and aldosterone in the blood plasma is analyzed. Imaging of the adrenal glands should also be performed.

Primary aldosteronism is treated with spironolactone (veroshpiron). Doses of the drug sometimes reach up to 400 mg per day. If the cause of the disease is a tumor, surgical intervention is required.

Endocrine arterial hypertension has a clear clinical picture. In addition to high blood pressure, there are always other signs of excess of one or another hormone. The issues of diagnosis and treatment of such pathology are dealt with jointly by an endocrinologist, cardiologist, and surgeon. Treatment of the underlying disease leads to complete normalization of blood pressure numbers.

Endocrinologist I.G. Tsvetkova

In today's article we will discuss problems that relate to endocrine causes of hypertension, i.e. blood pressure rises due to excessive production of some hormone.

Article outline:

1. First, we'll list the hormones that can cause problems, and you'll learn what role they play in the body when everything is normal.
2. Then we’ll talk about specific diseases that are included in the list of endocrine causes of hypertension
3. And most importantly, we will provide detailed information about the methods of their treatment.

I have made every effort to explain complex medical issues in simple terms. I hope this was more or less possible. The information on anatomy and physiology in the article is presented in a very simplified manner, not detailed enough for professionals, but just right for patients.

Pheochromocytoma, primary aldosteronism, Cushing's syndrome, thyroid problems and other endocrine diseases cause hypertension in approximately 1% of patients. These are tens of thousands of Russian-speaking patients who can be completely cured or at least alleviate their hypertension if smart doctors take care of them. If you are diagnosed with hypertension due to endocrine causes, then you will definitely not be able to cure it without a doctor. Moreover, it is extremely important to find a good endocrinologist, and not to be treated by the first one you come across. You will also find the general information about treatment methods that we provide here useful.

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 with 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.

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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 the endocrine causes of hypertension:

1. 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.
2. Primary hyperaldosteronism is a tumor in one or both adrenal glands that causes too much aldosterone to be produced.
3. 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.
4. Acromegaly is an excess of growth hormone in the body due to a tumor in the pituitary gland.
5. 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.
6. 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 blood 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 procedure 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 of evidence-based medicine. All information about treatment methods, which is published in medical journals and then in books, is collected “from the world, piece by piece.” 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 common 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 blood sugar 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 a tumor cannot be detected using computed tomography or magnetic resonance imaging, 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 also 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 it is impossible to remove the tumor surgically, 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.

2 weeks after surgery, it is recommended to take a urine test for catecholamines. 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 at an earlier stage than the drugs 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.

We 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)). The normal value of 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 loading is when the patient eats 6-9 g of table salt per 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 an ultrasound does not show anything, the presence of adenoma or adrenal hyperplasia cannot be completely ruled out. 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 levels of potassium in the blood in many of them provokes the development of diabetes.

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 are helpful for bilateral adrenal hyperplasia. If a patient experiences side effects or intolerance to spironolacter, then eplerenone should be considered as it 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:

1. First, corticotropin-releasing hormone is produced in the hypothalamus.
2. It acts on the pituitary gland to produce adrenocorticotropic hormone.
3. 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

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 in color, 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 - menstrual irregularities, 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, a one-time negative test result does not prove the absence of the disease, because the level of this hormone physiologically fluctuates within a wide range. 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. The real method of treatment, which 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 Itsenko-Cushing syndrome is controlled with spironolactone, potassium-sparing diuretics, ACE inhibitors, and selective beta blockers. They try to avoid medications that negatively affect metabolism and reduce the level of electrolytes in the blood. Drug therapy for hypertension in this case 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 a 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 it, the rate of 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 surgically removing the pituitary tumor. 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 on the posterior surface of the 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 bone tissue being replaced by connective tissue in the bones, and calcium stones forming in the urinary tract. 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 levels of parathyroid hormone in the blood are 10-70 pg/ml, and the upper limit increases with age. 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.

The main symptoms of an overactive thyroid gland are:

• 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.

The main symptoms of thyroid hormone deficiency are:

• 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. Often there are 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 traditional methods of treating hypertension do not help. 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 + type 1 or type 2 diabetes, then read this article.

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.

Moderate changes in the myocardium: classification and treatment of pathology

Minor deviations from the norm in the structure of the heart can be detected in every second person. They are a consequence of various pathological processes, especially of an inflammatory nature. In a child, a similar problem often occurs during puberty, and in older people - due to age-related changes in the cardiovascular system. They are detected mainly by chance during a routine examination. There is no point in knowingly worrying about the presence of moderate changes in the myocardium without knowing what they are. They usually do not affect the body in any way and do not appear, but the person will have to be fully examined to determine the causative factor and change their lifestyle.

Moderate changes in the myocardium: what is it?

Pathological abnormalities in the structure of the heart predominantly occur in its lower part (in the left ventricle). If they are not particularly pronounced, are not a consequence of cardiac pathology and do not progress, then often there is no clinical picture. Such changes do not always appear on an ECG (electrocardiogram). They can be identified mainly through a more detailed examination.

More pronounced diffuse changes are manifested by characteristic cardiac symptoms. You can find a list of them below:

• pain in the chest area (angina pectoris), provoked by cardiac ischemia;
• a feeling of shortness of breath and the appearance of edema is characteristic of cardiosclerosis;
• dizziness and signs of asthenia (weakness) occur with anemia.

Patients often develop symptoms of chronic heart failure after experiencing a myocardial infarction. In more rare cases, the cause is hidden in thyroid dysfunction. It begins to produce significantly more than the required amount of hormones, which leads to the following symptoms:

• trembling (tremor) of the limbs;
• weight loss;
• bulging (displacement forward) of the eyes, characteristic of exophthalmos.

The symptoms that arise gradually progress. The patient’s quality of life will decrease until shortness of breath appears after any physical activity, which causes a significant decrease in working capacity. If moderate changes in the left ventricular myocardium appear against the background of heart failure, then over time the person may lose the ability to independently perform everyday activities. To prevent such complications, it is necessary to be fully examined to identify the cause of the pathological abnormalities in the structure of the heart. Treatment will be aimed at eliminating it and alleviating the general condition.

Types of pathological changes

Changes in the structure of the heart muscle are divided into several types depending on the factor that influenced their development.

The genesis (reason for development) and localization of the listed types of deviations are different. Based on size, they are divided into diffuse and focal changes in the myocardium. The first type is diagnosed most often. It is characterized by damage to all parts of the heart. Focal deviations are single areas. In both cases, the changed areas are gradually replaced by connective tissue that does not allow electrical impulses to pass through. It will be impossible to reverse the process at this stage.

Causes of deviations in the structure of the myocardium

Each case has its own reasons for the occurrence of deviations in the structure of the myocardium. They have a detrimental effect on the heart and blood vessels. Inflammatory changes appear in a patient due to myocarditis. The disease can be infectious in nature and aseptic, that is, caused without the help of microorganisms. Diffusely located lesions develop due to the influence of such factors:

• Rheumatism affecting connective tissues. The cause of the development of pathology is the entry into the body of a streptococcal infection. It occurs after tonsillitis, tonsillitis, scarlet fever and other similar diseases.
• Typhus caused by the bacteria Rickettsia. It is characterized by damage to the nervous and cardiovascular systems.
• Viral infections, which are characterized by complications on the heart muscle. Measles, rubella and influenza are particularly common.
• Autoimmune disorders caused by lupus erythematosus and rheumatoid arthritis, causing complications in the heart muscle.

Cicatricial abnormalities in the structure of the myocardium manifest themselves mainly for the following reasons:

• Long-term cardiac ischemia leads to increased fibroblast activity. They provoke the proliferation of connective tissue.
• A heart attack appears as a scar. If its extensive form has been experienced, then necrosis affects the volumetric area of ​​the myocardium.
• Surgeries on the heart muscle leave behind a trace in the form of a patch of connective tissue at the site of the intervention.

Dystrophy of cardiac muscle tissue manifests itself mainly due to a failure of metabolic processes in cardiomyocytes of a non-inflammatory nature. The changes gradually worsen against the background of the development of other pathologies.

Heart cells lack vital elements to function normally, causing them to become exhausted and arrhythmias to occur. In medicine, myocardial dystrophy is also called cardiodystrophy. The most current list of reasons for its occurrence is as follows:

• Constant disruptions in the functioning of the liver and kidneys lead to the development of failure of these organs. Toxic substances begin to accumulate in the blood, which disrupt metabolic processes throughout the body.
• Diseases of the endocrine organs (pancreas, thyroid, adrenal glands) provoke excessive production of hormones. They affect the entire body, especially the cardiovascular system.

• Anemia occurs due to an acute deficiency of hemoglobin in the blood. Lack of this iron-containing protein often causes myocardial dystrophy.
• Various irritating factors (stress, overwork, overeating or dieting) gradually provoke depletion of the heart muscle.
• In childhood, the problem arises due to a combination of psycho-emotional overload and insufficient physical activity. In a child, these factors provoke the development of vegetative-vascular dystonia, which disrupts the normal regulation of the heart due to disruptions in the autonomic nervous system.
• Diseases caused by infections (tuberculosis, influenza, malaria) can deplete the body and have a detrimental effect on all its systems.
• Fever and its inherent dehydration overload the heart and blood vessels and provoke dystrophy due to a lack of nutrients.
• Acute intoxications caused by alcohol, medications and chemicals, or chronic intoxications caused by poor environment or work, lead to depletion of the body.

The most common and common cause of heart dystrophy is a lack of nutrients in the body due to an incorrect diet. Sometimes it is provoked by the following diseases:

• atherosclerosis;
• ischemia;
• hypertension;
• arrhythmia;
• myocardial hypertrophy.

Metabolic abnormalities are caused by disruptions at the cellular level. They manifest themselves as impaired exchange of potassium and sodium in cardiomyocytes, as a result of which the heart does not receive the required energy for full contraction and relaxation. If the changes that occur are not serious and occur due to overwork, obesity, stress and hormonal surges (during pregnancy, during puberty), then we are talking about a nonspecific lesion. They are also provoked by disruptions in the metabolism of cardiomyocytes. Severe metabolic disorders in heart cells occur due to the influence of the following factors:

• hypertension;
• cardiomyopathy;
• acute rheumatic fever;
• cardiosclerosis;
• angina pectoris.

It is considered a completely natural phenomenon if the left ventricle of the heart is slightly changed in children or the elderly. In the first case, the problem lies in changes in the body associated with active growth and an imperfect metabolic process. In older patients, deviations in the structure of the myocardium are acceptable due to aging and wear of all tissues.

Diagnostic and treatment methods

The cardiologist prepares treatment only on the basis of the examination results. If the patient does not have a dangerous heart pathology, then the doctor may advise taking vitamin complexes, especially in autumn and winter, monitoring blood pressure levels and adjusting lifestyle. If there is a suspicion of the secondary nature of changes in the myocardium, that is, development under the influence of other diseases, the following diagnostic methods will be prescribed:

• Donating blood to determine the amount of hemoglobin, checking the level of white blood cells and the erythrocyte sedimentation rate.
• Study of the composition of urine to assess the condition of the kidneys.
• Carrying out a biochemical blood test to determine the level of protein, sugar and cholesterol.
• Conducting 24-hour ECG monitoring with and without exercise to assess the condition of the heart.
• Performing an ultrasound examination of internal organs to check for abnormalities in their structure.
• Study of the heart muscle using an echocardiograph to visualize its parts and determine the cause of myocardial changes.
• Use of electrocardiography (ECG) to detect any abnormalities in the heart's rhythm, as well as in its conductivity and structure.

Having received all the necessary data, the doctor will assess the patient’s condition. If the cause is not only in the heart, then he will advise you to consult with other specialists (endocrinologist, gastroenterologist, hematologist) to develop a comprehensive treatment. An important advantage of a timely course of therapy is the high chance of eliminating pathological changes. In fact, in 90% of cases, myocardial cells are able to recover completely.

If even modern diagnostic methods could not help identify the cause of the problem, then treatment is aimed at achieving the following goals:

• stop the clinical picture of heart failure;
• protect cardiomyocytes and restore their functions;
• normalize metabolic processes in the heart.

The following groups of drugs are commonly used in the treatment of heart failure:

• Cardiac glycosides (Strofanthin, Digitoxin) increase vascular tone, eliminate arrhythmias, reduce the duration of the contraction phase of the heart muscle and improve its nutrition.

• Antiarrhythmic drugs (Amiodarone, Dofetilide) block beta and alpha adrenergic receptors, improve myocardial nutrition and have a coronary dilation effect.
• Diuretics (Lasix, Britomar) reduce venous return to the heart and remove excess moisture from the body, lowering blood pressure.

To stimulate metabolic processes, doctors prescribe the following drugs based on beneficial substances:

• "Cocarboxylase" (coenzyme);
• “Doppelgerts Active”, “Asparkam” (magnesium, potassium);
• “B-Complex”, “Neurobion” (B vitamins);
• "Preductal", "Mexidol" (antioxidants);
• "Riboxin" (metabolic agent).

The following drugs may be required as an addition to the main treatment regimen:

• hypotensive;
• sedatives;
• hormonal (for endocrine disruptions);
• antiallergic;
• antibacterial.

Folk remedies are often included in the treatment regimen for myocardial changes, as they saturate the body with necessary substances and calm the nervous system. The most relevant decoctions of the following herbs:

• hawthorn;
• Melissa;
• motherwort;
• peppermint;
• cranberry;
• peony;
• rose hip.

Maintaining a healthy lifestyle

Comprehensive treatment of any pathology consists not only of taking medications, but also of a properly selected diet. In the presence of moderate changes in the myocardium, it is recommended to adhere to the following rules:

• It is not recommended to overeat or starve;
• the daily amount of salt consumed should not exceed 5 g;
• It is imperative to add vegetables and fruits to your diet;
• the daily menu should contain only low-fat varieties of fish and meat;
• You need to eat 4-5 times a day, and take your last meal 3-4 hours before bedtime;
• It is advisable to completely avoid fatty foods;
• It is recommended to cook by steaming or boiling.

The rules of a healthy lifestyle, which are given below, will help normalize metabolic processes in cardiomyocytes:

• sleep at least 6-8 hours a day;
• give up bad habits;
• try to avoid stressful situations;
• exercise at a moderate pace without overload.

Forecast

Moderate changes in the structure of the heart muscle are not pathology. They are a consequence of the influence of other diseases, so if the cause is eliminated in a timely manner, the process can be reversed without harm to health. The prognosis will improve if you follow all the doctor’s recommendations and do not allow the condition to worsen, since cardiomyocytes will need time to fully recover. In mild cases, it can be cured without drug therapy.

A less optimistic prognosis when moderate changes are combined with signs of heart failure. It is possible to completely reverse the process if the muscle tissue of the myocardium has not yet been replaced by connective tissue that does not transmit electrical signals. Doctors usually prescribe medications that improve metabolic processes and give recommendations for correcting nutrition and rest.

Serious diffuse changes cause the development of dangerous forms of heart failure and cardiosclerosis. It is impossible to completely eliminate them. Treatment consists of attempts to stop the pathological process and improve the patient’s quality of life.

Moderate changes in the myocardium are among the most common pathological abnormalities in the structure of the heart muscle. In most cases, they lead to nothing and do not manifest themselves. The problem is usually discovered during a routine examination. As a means of treatment, the doctor prescribes drugs that improve metabolic processes in cardiomyocytes and stabilize the functioning of the heart. If the case is advanced, then it is not possible to completely reverse the changes and the patient will have to take medications for life.

Endocrine arterial hypertension develops as a result of disruption of the production of certain hormones. These diseases account for 1% to 9% of all cases of hypertension. Half of them are caused by dysfunction of the adrenal glands (adrenales), a hormonal organ that plays a key role in regulating blood pressure.

The adrenal glands produce special substances - aldosterone, cortisol, adrenaline, norepinephrine. Treatment of hypertension caused by diseases of the adrenal glands is fundamentally different from other forms of this disease. About 9% of patients can be cured by surgery.

Adrenal glands and blood pressure

The name of this organ indicates its anatomical location above the kidneys; the adrenal gland has a semilunar shape, weighing up to 20 g. It consists of two functional layers - the cortex and the medulla. The cortex secretes corticosteroids (aldosterone, cortisol and androgens). The medulla produces norepinephrine and adrenaline.

Each of these hormones affects blood pressure levels. Aldosterone regulates the absorption of water and sodium in the kidneys, adrenaline increases vascular tone and stimulates the heart, cortisol affects the heart muscle, leading to water and salt retention in the body.

Causes of adrenal hypertension

Arterial hypertension in adrenal endocrinopathies is usually divided into:

• Congenital adrenal hyperplasia (CAH);
• Primary hyperaldosteronism (PHA);
• Cushing's syndrome and disease;
• Impaired deoxycorticosterone production;
• Pheochromocytoma.

Since only the adrenal glands produce aldosterone, they are part of the renin-angiotensin-aldosterone system, which regulates blood pressure levels.

Aldosterone is responsible for the reabsorption of water and sodium in the kidneys, its production is regulated by renin. But in 0.43% of cases, the adrenal glands go out of control and, with normal renin levels, produce large amounts of aldosterone. Fluid retention occurs and the circulating blood volume (CBV) increases, which increases the pressure in the vessels.

PGA

A pathology that develops when there is an excess of aldosterone in the body and decreased production of renin. Accompanied by endocrine hypertension and hypokalemia.

Causes of primary hyperaldosteronism

1. A benign tumor is an adenoma that produces aldosterone (Conn's syndrome);
2. Adrenocortical carcinoma;
3. Primary adrenal hyperplasia and idiopathic.

Hypertension is practically not corrected by conventional antihypertensive drugs. The longer aldosteronism exists, the greater the likelihood of irreversible changes in blood vessels and the development of fibrosis in the heart muscle.

Timely removal of the tumor (for Conn's syndrome) by resection of the adrenal gland normalizes blood pressure in 69% of patients. Hyperplasia is treated conservatively.

Clinical manifestations

Symptoms of primary hyperaldosteronism are a reaction to low levels of potassium in the blood (below 3.6 mmol/l). Patients are concerned about muscle weakness, cramps that worsen at night, muscle pain, thirst, dry mouth, excessive urination (predominant at night).

Characterized by the absence of edema, a moderate increase in systolic and diastolic pressure, and retinopathy. The listed complaints are typical for different causes of this disease (adenoma and hyperplasia). When the pressure rises, a headache appears and the heart worries. Electrocardiograms record rhythm changes and extrasystole.

If the tumor is malignant - carcinoma, in addition to these symptoms, abdominal pain and fever may occur. Malignant adrenocortical carcinomas have an unfavorable course. After removal of the carcinoma, life is prolonged by several months.

Laboratory diagnostics

The diagnosis is confirmed by aldosterone levels exceeding the norm in both biological fluids, low renin levels, and hypokalemia with normal sodium production.

Instrumental examination methods

It is recommended to determine the cause of hyperaldosteronism (tumor or hyperplasia) using scans of the adrenal glands, MRI, computed tomography (diagnostic accuracy 95%). In Conn's syndrome, images of the adrenal glands reveal a small formation, not exceeding 2-3 cm in diameter. Malignant tumors are large and have uneven contours.

Treatment

If Conn's syndrome is confirmed, patients are recommended to undergo endoscopic surgery to remove the tumor. Hormone replacement therapy is not required in the postoperative period. If the patient refuses surgery or there are contraindications for it, the aldosterone antagonist drug Veroshpiron is prescribed.

It is also recommended for non-tumor forms of the disease - adrenal hyperplasia, at a dose of 250-300 mg per day for a long period under the control of potassium levels and ECG. If hyperkalemia is observed, it is recommended to reduce the daily dose of the drug. Veroshpiron normalizes blood pressure, protects the heart muscle from fibrosis, and increases potassium levels.

Secondary hyperaldosteronism

The listed symptoms of the disease are characteristic of another pathology - secondary hyperaldosteronism, which develops as a consequence of the following diseases:

• Narrowing of the renal arteries;
• Essential arterial hypertension;
• Malignant hypertension;
• Abuse of diuretics and laxatives.

Secondary hyperaldosteronism is characterized by decreased sodium levels, increased renin activity in the blood, and decreased aldosterone production after salt load.

Hypersecretion of II-deoxycorticosterone

One of the causes of endocrine adrenal hypertension is the perverted production of 11-deoxycorticosterone. This substance is a precursor to the hormone cortisol. When enzymes malfunction, there is a failure in converting it into cortisol.

A large amount of accumulated 11-deoxycorticosterone leads to sodium retention, increased urinary potassium excretion, increased circulating blood volume and increased blood pressure. This pathology is a hypertensive form of CAH (associated with gene mutation).

When examining patients, an increase in levels of adrenal androgens in the blood serum and an increase in 17-ketosteroids in the urine are revealed. Treatment is carried out with the help of glucocorticoid hormones - hydrocortisone, prednisolone, dexamethasone.

Pheochromocytoma

An endocrine tumor that produces norepinephrine and adrenaline. In 91% of cases it is located in the adrenal medulla, 10% in another location. Timely diagnosis of the tumor is important due to the presence of serious complications. Occurs in - 0.5% -1% of all patients with hypertension.

Symptoms

The manifestation of the disease depends on the level of hormones produced. Characteristic symptoms of pheochromocytoma are:

• Frequent hypertensive crises (1-7 times a week);
• Heart dysfunction;
• Stomach ache;
• Dyspnea;
• Low-grade fever;
• Weight loss;
• Increased excitability, trembling of fingers;
• Poor circulation of the extremities (cold to the touch, with a bluish tint);
• Intense headache, which is accompanied by nausea, vomiting;
• Constipation;
• Increased sweating, feeling of lack of air and palpitations during crises;
• Ineffectiveness of standard treatment for hypertension.

It is customary to distinguish three stages of this adrenal hypertension - initial, compensated and decompensated. At the initial stage of the disease, crises are rare, they are short-lived, systolic pressure is 200 mmHg.

The compensated stage is characterized by constant hypertension, weekly crises, during which the level of glucose in the blood and urine increases.

The decompensated form has its own differences - daily prolonged crises with an increase in blood pressure up to 300 mmHg. persistent hyperglycemia, visual complications.

Complications

Against the background of a constant increase in vascular tone (provoked by pheochromocytoma), during crises myocardial infarction, stroke, acute pulmonary edema, shock, hemorrhage into the adrenal gland with subsequent tumor necrosis and death can occur.

Diagnostics

Based on the above complaints, pheochromocytoma can be suspected, especially if they occur in young people. Laboratory confirmation of the diagnosis is an increase in metanephrine, normetanephrine, adrenaline, norepinephrine, and dopamine in the patient’s daily urine. Before taking the test, you need to follow the preparation rules - exclude some foods and medications.

Computed tomography, MRI, scintigraphy with labeled isotopes make it possible to determine the exact location of pheochromocytoma. The information content of the methods reaches 95%-97%.

Treatment

The only effective treatment for this disease is surgical removal of the tumor.

It should be carried out in specialized clinics that have experience in such interventions and postoperative management of patients; in 95% of cases, after removal of the formation, complete recovery occurs.

About 10% of pheochromocytomas become malignant. This process can be supported by the large size of the formation (6 cm or more) and the high content of dopamine in daily urine. Metastases of this tumor can be in the liver, lymph nodes, lungs, and bones. After treatment, the five-year survival rate is 45% of all cases.

Hypercortisolism

This condition includes Itsenko-Cushing's disease, a severe disorder of neuroendocrine regulation, leading to bilateral enlargement of the adrenal cortex. Overproduction of corticosteroids (cortisol) by the adrenal glands is the cause of endocrine hypertension.

Cortisol ensures human adaptation to stress factors; its production by the adrenal glands is stimulated by another hormonal organ - the pituitary gland through adrenocorticotropic hormone (ACTH).

The production of this hormone increases against the background of a microadenoma (benign tumor) in the pituitary gland. ACTH constantly forces the adrenal cortex to work, as a result of which it hypertrophies.

Hypercortism may be a consequence of Itsenko-Cushing syndrome, which develops as a result of long-term use of glucocorticoid hormones or the occurrence of a tumor in the adrenal cortex.

Manifestations of the disease

Arterial hypertension in this pathology is moderate, but its prolonged existence leads to vascular disorders.

• Disproportionate obesity;
• Muscular atrophy of the limbs;
• Moon-shaped face;
• Purple stretch marks on the body;
• Osteoporosis;
• Mental disorders;
• Thirst;
• Increased blood glucose levels;
• Heart failure;
• Excessive hair growth.

Hypercortisolism is supported by increased levels of cortisol and ACTH in the blood, 17-OX and free cortisol in the urine per day, and a high dexamethasone test.

Computed tomography and MRI of the adrenal glands and brain can see the location and determine the size of the tumor in the pituitary gland and adrenal glands or detect thickening of the adrenal cortex.

Treatment

Endocrine hypertension with hypercortisolism can be treated with conventional therapy, but without tumor removal, the severity of the patient’s condition increases. When a clear localization of pituitary microadenoma is determined, a neurosurgical operation is performed in a specialized hospital. Recovery occurs in 80% of cases, but relapse may occur.

Replacement therapy is carried out for a short time. If it is not possible to determine the tumor, proton therapy is recommended for the pituitary gland and simultaneous removal of one adrenal gland. Neoplasms (adrenales) are surgically removed and short-term replacement therapy is carried out.

The main drug treatment for Cushing's disease is the prescription of drugs that suppress the production of ACTH and blockers of corticosteroid production. Against this background, it is additionally recommended:

1. Vitamins, potassium preparations;
2. Antihypertensives – ACE inhibitors;
3. Spironolactone;
4. Osteoporosis is treated.

In severe cases of the disease, both adrenal glands are removed, followed by lifelong replacement therapy with glucomineralocorticoids. All patients require long-term observation by an endocrinologist, therapist, or neurologist.

Endocrine arterial hypertension accounts for 1–5% of all diagnosed cases of hypertension. Etiologically, 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 secondary symptom in a number of other endocrinopathies, and therefore is not one of 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 can 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 laboratory test results, a 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.

For other endocrine diseases where hypertension is not the dominant disease, treatment depends on the therapy for the endocrine disorder:

• for Cushing's disease and acromegaly - transsphenoidal surgery of the pituitary adenoma;
• for ACTH-independent hypercortisolism - unilateral adrenalectomy of the adrenal adenoma;
• in case of 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 that arose in childhood as a result of exposure to growth hormone before the closure of the epiphyseal plates) is about 40% of the causative factors of 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 the heart rate and pulse, a significant increase in cardiac output, and a narrowing of the lumen of blood vessels. All this causes the development of stable hypertension. High blood pressure is accompanied by nervousness, irritability, insomnia, weight loss, and sweating.

The frequency of pheochromocytoma is 0.3–0.5% of the total number of 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. It is a serious disease 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

The most common causes of hypertension 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 the volume of the eyeball, which leads to disruption of the venous outflow from the orbit and 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 maintaining a healthy lifestyle:

• 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 varying degrees of organ damage. 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.

Arterial hypertension is an increase in blood pressure: systolic - more than 139 mmHg, and diastolic - more than 89 mmHg. The increase in pressure can be isolated (only systolic or only diastolic), but more often it is combined. Up to 15% of all arterial hypertension is secondary, that is, caused by existing diseases of internal organs, of which a significant proportion is endocrine symptomatic hypertension.

It is customary to divide arterial hypertension into 4 degrees of severity. The level of blood pressure, its persistence and the severity of damage to target organs (eyes, heart, kidneys, brain, blood vessels) are taken into account:

• The transient form is characterized by unstable arterial hypertension. The pressure rises to 160/100 mmHg. Art. There is no development of target organ dysfunctions. The clinical picture is poorly expressed.
• Labile arterial hypertension is manifested by a persistent increase in pressure, up to 180-110 mm Hg. Art. A return to the acceptable norm without the use of drugs with a hypotensive effect actually does not occur. The symptoms are quite pronounced. Proliferation of the left ventricle and stenosis of retinal vessels are observed. A blood test can detect a decrease in creatine concentration.
• A stable type of hypertension is characterized by an increase in pressure above 180/100 mmHg. Art. on an ongoing basis. The indicators can be reduced only with the help of medications with antihypertensive properties. They will have to be taken for a long time. Pathological changes are observed in all target organs. The patient develops coronary heart disease and hypertensive encephalopathy. The likelihood of myocardial infarction and ischemic stroke increases significantly. The eyes may exhibit retinal hemorrhages and papilledema.
• Malignant hypertension poses the greatest danger to the patient's life. The blood pressure level becomes significantly higher than 180/110 mm Hg. Art. There is a significant increase in the lower (diastolic) indicator. Crises often occur, which are characterized by a rapid increase in blood pressure. They are treated with intravenous medications. Pathological changes in target organs are irreversible and significantly worsen the prognosis for recovery and restoration of working capacity.

Difference between forms of the disease

To effectively combat secondary (symptomatic) hypertension, it is necessary to learn to distinguish it from the primary (essential) form. Their treatment methods are completely different. The reason for the increase in pressure of the symptomatic version of the disease is the development of an endocrinological disease or impaired renal function. Taking antihypertensive drugs will only temporarily alleviate the condition. To completely eliminate the problem, it is necessary to treat the underlying pathological process.

Secondary hypertension differs from primary hypertension in the following ways:

• an attack of arterial hypertension manifests itself sharply;
• blood pressure is elevated quite steadily;
• occurs regardless of gender and age;
• medications help only temporarily;
• the lower pressure reading is significantly higher than normal;
• secondary hypertension is accompanied by panic attacks.

Secondary arterial hypertension in endocrine diseases

Typically, endocrine symptomatic arterial hypertension develops due to a pathological process that causes disruption of hormonal regulation of all organs and systems, especially the cardiovascular system. In endocrine diseases, primary importance is given to the pressor effects of different types of hormones.

Endocrine causes of hypertension consist in the development of pathological processes in the following organs:

• pituitary;
• adrenal glands;
• thyroid gland;
• parathyroid glands.

The reason for the increase in blood pressure against the background of the development of malfunctions in the functioning of the endocrine glands lies in the retention of moisture in the body and the excessive synthesis of hormones that enhance the influence of the sympathetic nervous system. These factors contribute to the narrowing of blood vessels and increased heart rate, which leads to the manifestation of secondary hypertension.

The clinical picture of dysfunction of the endocrine glands is represented by a variety of specific symptoms of a malfunction in hormonal balance. However, in some cases, arterial hypertension is the only manifestation of the disease.

Pathology of the pituitary gland

The pituitary gland is the central gland of the endocrine system. Hormones produced by the pituitary gland regulate metabolic processes throughout the body; their excess or deficiency secondarily causes changes in the functioning of other endocrine glands and target organs. Among the diseases of the pituitary gland that cause the development of symptomatic arterial hypertension are acromegaly and Itsenko-Cushing's disease.

Acromegaly. This disease is typical for people in the age group from 30 to 50 years, mainly women; more often caused by a pituitary adenoma, causing hyperproduction of somatotropic hormone (GH). Growth hormone is a regulator of the processes of growth and development of the body, and therefore its excessive amount leads to metabolic disorders and the development of hyperplastic processes throughout the body.

Patients suffering from acromegaly attract attention by disproportionately tall stature, elongated limbs, rough facial features with a massive lower jaw, prominent brow ridges, and swelling of the soft tissues. Patients are also concerned about sweating, seborrhea, common osteoarthritis with pain in the joints, headaches, mood swings, decreased motivation, and muscle weakness. The causes of hypertension in acromegaly lie in sodium and water retention due to hormonal imbalance. Diagnosis of the disease is based on an X-ray examination of the skull and determination of the concentration of somatotropic hormone in the blood.

Itsenko-Cushing's disease. The disease is caused by a tumor or hyperplastic process in the adenohypophysis, producing an increased amount of adrenocorticotropic hormone (ACTH), which has a potentiating effect on the secretion of pressor hormones by the adrenal cortex.

Hormonal disorders are so pronounced that they are reflected in the specific appearance of the patient:

• moon-shaped face, blush on the cheeks, obesity of the upper half of the body;
• formation of skin atrophic changes (striae), hyperpigmented spots;
• excessive hair growth (hypertrichosis);
• disorders of the sexual sphere: in women – disruption of the menstrual cycle and reproductive function; in men – decreased libido;
• mental disorders: decreased or increased mood, insomnia, nervousness, asthenia, sometimes psychosis;
• osteoporosis: brittle bones, frequent fractures, back pain.

Arterial hypertension has a persistent malignant nature, reaching high numbers - 200/150 mmHg or more. Diagnostically significant is an increase in the concentration of 17-corticosteroids and 17-hydroxycorticosteroids in the urine and cortisol in the blood.

Pathology of the adrenal glands

Hypertension caused by diseases of the adrenal glands accounts for at least half of all endocrine hypertension, since the hormones they produce - catecholamines and corticosteroids - are directly involved in the regulation of blood pressure. Among the diseases of the adrenal glands that cause secondary hypertension are the following:

Pheochromocytoma. This is a tumor formed from the adrenal medulla (less often from chromaffin cells located outside the adrenal glands), producing catecholamines (adrenaline and norepinephrine) - hormones that are of paramount importance in the regulation of blood pressure, increasing the tone of the vascular wall, causing vasoconstriction, and an increase in cardiac output. This type of tumor rarely causes hypertension, in less than 0.2 percent of clinical cases.

Increased pressure in pheochromocytoma often has a crisis course, in some cases - against the background of permanently increased pressure. Crises with pheochromocytoma are caused by a sharp release of large amounts of hormones into the blood and occur with intense headaches and tachycardia. As a rule, they are provoked by a stressful situation, heavy food intake and are accompanied by a feeling of palpitations, increased sweating, changes in complexion (redness or paleness), hand tremors, fear of death, psychomotor agitation, abdominal and lower back pain. Arterial hypertension in this disease often cannot be corrected with medications.

Diagnosis of the disease is based on determining elevated levels of catecholamines and their metabolic products in the urine, as well as ultrasound examination or CT scan of the adrenal glands.

Conn's syndrome (primary hyperaldosteronism). This disease is detected in 0.4% of patients with high blood pressure. The cause of the syndrome is a benign or malignant tumor, as well as hyperplastic processes in the adrenal cortex, which causes a significant increase in the amount of aldosterone in the blood. Hypersecretion of aldosterone causes disturbances in the water-salt balance - increased excretion of potassium in the urine, retention of sodium and water in the body, leading to an increase in circulating blood volume, increased cardiac output, which is the main pathogenetic link in the development of hypertension.

Blood pressure in primary hyperaldosteronism does not increase sharply, but gradually, but can reach high, uncontrollable numbers. Diastolic blood pressure increases to a greater extent, and pulse pressure decreases. In the clinical picture, in addition to hypertension, there are manifestations of hypokalemia: convulsions, general weakness, paresthesia, as well as an increase in the amount of urine excreted, thirst.

Significant in the diagnostic search is a decrease in potassium in the blood below 15 mg% during repeated studies, an increase in the level of aldosterone in the urine.

Itsenko-Cushing syndrome. The etiology of this disease is a tumor process or hyperplasia of the adrenal cortex, causing increased production of cortisol. Symptoms, including features of arterial hypertension, are similar to the clinical picture of Itsenko-Cushing's disease.

Pathology of the thyroid gland

This organ of the endocrine system produces the hormones thyroxine and triiodothyronine, which affect the growth of cellular structures and metabolism in general. An increase in blood pressure occurs both with increased thyroid function and with its decrease, but in both cases it has its own characteristics.

Hypothyroidism. A condition caused by insufficient production of thyroid hormones, the main causes of which are autoimmune damage, insufficient intake of iodine in the body, as well as partial or total removal of the thyroid gland due to injury or other pathological processes.

With hypothyroidism, there is an increase primarily in diastolic pressure, including at night, which is caused by a decrease in cardiac output, a decrease in heart rate, an increase in vascular resistance, and retention of water and sodium ions in the tissues. The clinical picture also reveals increased body weight, swelling, dry skin, hair loss, shortness of breath, drowsiness, decreased mood, attention, memory, interruptions in heart function, constipation, decreased libido.

With this disease, blood tests reveal a decrease in the concentration of thyroxine, triiodothyronine, and an increase in TSH.

Thyrotoxicosis. The main pathogenetic moment in the development of hypertension in this case is the formation and circulation in the blood of a large amount of thyroid hormones, causing an increase in cardiac output and an increase in heart rate. A feature of thyrotoxicosis is an almost isolated increase in systolic blood pressure with unchanged or decreased diastolic pressure.

Mental disorders are noteworthy: emotional instability, tearfulness, irritability, resentment, insomnia. Sexual dysfunction and other symptoms of metabolic disorders occur: sweating, weight loss, hair loss, exophthalmos, arrhythmias, palpitations, hand tremors, diarrhea.

Diagnosis is based on determining elevated levels of thyroid hormones in the blood.

Pathology of the parathyroid glands

The parathyroid glands produce parathyroid hormone, which is the central hormone that regulates the balance of phosphorus and calcium in the body. Pathological processes in the parathyroid glands (tumor, hyperplasia) lead to disruption of phosphorus-calcium metabolism. A disease that changes blood pressure levels upward is hyperparathyroidism.

The pathogenesis of hypertension in hyperparathyroidism is based on an increase in the concentration of calcium ions in the blood, causing vasoconstriction and increasing the elasticity of the vascular wall. Symptoms of hyperparathyroidism: thirst, polyuria, lethargy, absent-mindedness, general weakness, tooth loss, decreased intestinal motility, constipation, spinal pain, pathological fractures, deformities of the musculoskeletal system, convulsions.

Other reasons

Hypothalamic syndrome of puberty. The cause of this disease has not yet been precisely established. Its development can be influenced by disorders suffered in the perinatal period, as well as birth trauma, intoxication, etc. This condition manifests itself in adolescence with hormonal disruptions, such as increased secretion of ACTH and adrenal hormones. Patients usually complain of headaches, hunger, and thirst. They develop secondary sexual characteristics early and have mental disorders. Arterial hypertension can be either transient or persistent.

Features of treatment

Symptomatic arterial hypertension is only a sign of an underlying disease. For successful treatment it is necessary to identify the cause and eliminate it. For some pathologies, this means removal of the tumor, for others, hormone replacement therapy. However, it is not always possible to carry out etiotropic therapy, and therefore blood pressure is corrected with antihypertensive drugs: ACE inhibitors, calcium and aldosterone antagonists, diuretics, beta-blockers. In this case, the choice of drug is determined by its effectiveness in influencing the central link in the pathogenesis of the development of hypertension in a specific endocrine disease.

Consequently, endocrine symptomatic hypertension is a complex of pathologies that directly affect the increase in blood pressure. Standards of treatment for primary hypertension in this case will be ineffective - first you need to influence the human endocrine system. Only by adjusting the hormonal levels can progress in therapy be achieved.