Can low sodium cause headaches: Can your sodium level be too low?

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Can your sodium level be too low?

Symptoms of a low sodium level include nausea, vomiting, headache, confusion, feeling weak or tired, restlessness, muscle weakness, spasms or cramps and seizures or passing out.

Most Americans eat much more sodium than their bodies require. Too much sodium can worsen high blood pressure and heart failure. For these reasons, many Americans are advised to reduce the amount of sodium they eat. Because there is so much sodium in most foods, it is very difficult to eat too little.

But can sodium in the blood be low even if the amount of sodium in the body is too high? It can.

Low blood sodium is called “hyponatremia.” Although an underlying health condition usually causes low blood sodium levels, there are still signs that indicate if your levels are low.

What causes low blood sodium levels?

A low blood sodium level is a problem for many people.

“It usually happens with other ongoing problems,” said Dr. Kelley Anderson, a Marshfield Clinic cardiologist. “Low blood sodium rarely occurs in healthy people.”

The blood’s sodium reflects how diluted the blood is, not how much sodium is in the body.

One of the common causes of low blood sodium is heart failure. “Heart failure” means the heart is unable to supply your body with the blood flow it needs. The body tries to maintain blood flow by releasing certain hormones. Vasopressin is one of those hormones.

“When vasopressin increases, your kidneys retain pure water,” Dr. Anderson said. “That dilutes your blood, resulting in low sodium levels.”

Other causes include some mental disorders or cirrhosis of liver.

Symptoms of low blood sodium

The signs and symptoms of hyponatremia are common for a lot of other conditions. Some symptoms include nausea, vomiting, headache, confusion, feeling weak or tired, restlessness, muscle weakness, spasms or cramps and seizures or passing out.

“It can be tricky because a vast majority of people who have these symptoms may not have low sodium,” Dr. Anderson said. “Just because they have these symptoms, it doesn’t mean they have to run and get their sodium checked. So always check with your doctor first.”

A normal blood sodium level is around 140 mEq/L (milliequivalents per Liter). If it’s less than 135, it is considered low. When the level is below 130 or lower, more problems can occur.

How to treat low blood sodium levels

Blood levels of electrolytes are usually done to find out if sodium levels are low. Patients with conditions that cause hyponatremia usually have their blood checked regularly.

Dr. Anderson says most people don’t need to monitor their own sodium levels.

“In a healthy person, the body automatically maintains normal blood sodium.” Dr. Anderson said. “On the other hand, the body does not always do a good job of maintaining normal total body sodium. So people should remember sodium in your blood does not always reflect sodium in the body.”

The treatment of hyponatremia depends on how low the blood sodium is, the individual’s medical problems and their medications and dietary habits.

If you are experiencing symptoms that can be associated with low blood sodium, contact your provider.

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Hyponatremia – Symptoms and causes

Overview

Hyponatremia occurs when the concentration of sodium in your blood is abnormally low. Sodium is an electrolyte, and it helps regulate the amount of water that’s in and around your cells.

In hyponatremia, one or more factors — ranging from an underlying medical condition to drinking too much water — cause the sodium in your body to become diluted. When this happens, your body’s water levels rise, and your cells begin to swell. This swelling can cause many health problems, from mild to life-threatening.

Hyponatremia treatment is aimed at resolving the underlying condition. Depending on the cause of hyponatremia, you may simply need to cut back on how much you drink. In other cases of hyponatremia, you may need intravenous electrolyte solutions and medications.

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Symptoms

Hyponatremia signs and symptoms may include:

Nausea and vomiting
Headache
Confusion
Loss of energy, drowsiness and fatigue
Restlessness and irritability
Muscle weakness, spasms or cramps
Seizures
Coma

When to see a doctor

Seek emergency care for anyone who develops severe signs and symptoms of hyponatremia, such as nausea and vomiting, confusion, seizures, or lost consciousness.

Call your doctor if you know you are at risk of hyponatremia and are experiencing nausea, headaches, cramping or weakness. Depending on the extent and duration of these signs and symptoms, your doctor may recommend seeking immediate medical care.

Causes

Sodium plays a key role in your body. It helps maintain normal blood pressure, supports the work of your nerves and muscles, and regulates your body’s fluid balance.

A normal blood sodium level is between 135 and 145 milliequivalents per liter (mEq/L). Hyponatremia occurs when the sodium in your blood falls below 135 mEq/L.

Many possible conditions and lifestyle factors can lead to hyponatremia, including:

Certain medications. Some medications, such as some water pills (diuretics), antidepressants and pain medications, can interfere with the normal hormonal and kidney processes that keep sodium concentrations within the healthy normal range.
Heart, kidney and liver problems. Congestive heart failure and certain diseases affecting the kidneys or liver can cause fluids to accumulate in your body, which dilutes the sodium in your body, lowering the overall level.
Syndrome of inappropriate anti-diuretic hormone (SIADH). In this condition, high levels of the anti-diuretic hormone (ADH) are produced, causing your body to retain water instead of excreting it normally in your urine.
Chronic, severe vomiting or diarrhea and other causes of dehydration. This causes your body to lose electrolytes, such as sodium, and also increases ADH levels.
Drinking too much water. Drinking excessive amounts of water can cause low sodium by overwhelming the kidneys’ ability to excrete water. Because you lose sodium through sweat, drinking too much water during endurance activities, such as marathons and triathlons, can also dilute the sodium content of your blood.
Hormonal changes. Adrenal gland insufficiency (Addison’s disease) affects your adrenal glands’ ability to produce hormones that help maintain your body’s balance of sodium, potassium and water. Low levels of thyroid hormone also can cause a low blood-sodium level.
The recreational drug Ecstasy. This amphetamine increases the risk of severe and even fatal cases of hyponatremia.

Risk factors

The following factors may increase your risk of hyponatremia:

Age. Older adults may have more contributing factors for hyponatremia, including age-related changes, taking certain medications and a greater likelihood of developing a chronic disease that alters the body’s sodium balance.
Certain drugs. Medications that increase your risk of hyponatremia include thiazide diuretics as well as some antidepressants and pain medications. In addition, the recreational drug Ecstasy has been linked to fatal cases of hyponatremia.
Conditions that decrease your body’s water excretion. Medical conditions that may increase your risk of hyponatremia include kidney disease, syndrome of inappropriate anti-diuretic hormone (SIADH) and heart failure, among others.
Intensive physical activities. People who drink too much water while taking part in marathons, ultramarathons, triathlons and other long-distance, high-intensity activities are at an increased risk of hyponatremia.

Complications

In chronic hyponatremia, sodium levels drop gradually over 48 hours or longer — and symptoms and complications are typically more moderate.

In acute hyponatremia, sodium levels drop rapidly — resulting in potentially dangerous effects, such as rapid brain swelling, which can result in a coma and death.

Premenopausal women appear to be at the greatest risk of hyponatremia-related brain damage. This may be related to the effect of women’s sex hormones on the body’s ability to balance sodium levels.

Prevention

The following measures may help you prevent hyponatremia:

Treat associated conditions. Getting treatment for conditions that contribute to hyponatremia, such as adrenal gland insufficiency, can help prevent low blood sodium.
Educate yourself. If you have a medical condition that increases your risk of hyponatremia or you take diuretic medications, be aware of the signs and symptoms of low blood sodium. Always talk with your doctor about the risks of a new medication.
Take precautions during high-intensity activities. Athletes should drink only as much fluid as they lose due to sweating during a race. Thirst is generally a good guide to how much water or other fluids you need.
Consider drinking sports beverages during demanding activities. Ask your doctor about replacing water with sports beverages that contain electrolytes when participating in endurance events such as marathons, triathlons and other demanding activities.
Drink water in moderation. Drinking water is vital for your health, so make sure you drink enough fluids. But don’t overdo it. Thirst and the color of your urine are usually the best indications of how much water you need. If you’re not thirsty and your urine is pale yellow, you are likely getting enough water.

Low sodium levels (hyponatremia): Symptoms and causes

Hyponatremia occurs when sodium levels in the blood are too low. Symptoms include lethargy, confusion, and fatigue. It can result from underlying conditions, such as kidney failure, or other factors, such as drinking too much water or taking certain medications.

Sodium is an electrolyte that plays an essential role in regulating the levels of water and other substances in the body. The definition of a low sodium level is below 135 milliequivalents per liter (mEq/L).

As the condition worsens, people may experience symptoms, such as:

vomiting
muscle twitches
seizures

Severe hyponatremia occurs when levels drop below 125 mEq/L. Health issues arising from extremely low sodium levels may be fatal.

Hyponatremia is the most common electrolyte disorder that doctors encounter. Research suggests that approximately 1.7 percent of people in the United States have the condition. It is more prevalent among people with cancer.

Mild hyponatremia may not cause symptoms. When symptoms occur they include:

If the condition worsens, it can cause severe symptoms, particularly in older adults. Severe symptoms may include:

vomiting
muscle weakness, spasms, and twitching
seizures
coma

Hyponatremia can result in death in extreme cases.

Other medical conditions and factors that can cause sodium levels to fall include:

diarrhea or vomiting
heart failure
kidney disease
liver disease
medication use
syndrome of inappropriate ADH secretion (SIADH)

People with SIADH produce excessive levels of the anti-diuretic hormone (ADH), which can lower sodium levels

Other causes include:

Drinking too much water.
Drug use. Taking the recreational drug ecstasy increases the risk of severe hyponatremia in some cases. Hyponatremia from ecstasy use can be fatal, especially in females.
Hormone disorders. These include Addison’s disease, which reduces the body’s production of the hormones cortisol and aldosterone and hypothyroidism, which is characterized by low levels of thyroid hormone.

Certain factors increase the risk of developing hyponatremia, including:

age
having specific conditions, such as SIADH or kidney, heart, or liver disease
taking certain diuretics, antidepressants, or pain medications
taking ecstasy
drinking excessive amounts of water
intense exercise, which may cause people to drink lots of water quickly

People who are at risk of hyponatremia or develop symptoms should see their doctor right away as they may need urgent medical treatment.

People with symptoms including vomiting, seizures, or loss of consciousness require immediate attention. They should call an ambulance or go to the nearest emergency department.

To diagnose low sodium levels, a doctor will take a medical history, perform a physical examination, and order a blood test.

If the blood test shows low sodium levels, the doctor will typically need to perform additional tests to determine the cause.

Treatment for hyponatremia involves:

Restoring blood sodium levels

Those who have mild to moderate hyponatremia resulting from lifestyle factors or medication may be able to increase sodium to normal levels by:

drinking less fluids (often less than 1 quart per day)
adjusting medication dose or switching medications

Individuals with severe symptoms often require hospitalization and an intravenous (IV) sodium treatment to get their sodium levels back to normal. They may also require drugs to treat seizures or other hyponatremia symptoms.

Treating the underlying cause

Where the underlying cause of hyponatremia is a medical condition or hormonal disorder, people will usually need further treatment.

For example, people with liver, kidney, or heart problems may receive medications or surgery. Kidney problems often require dialysis, and people with liver or heart conditions may need a transplant.

People with a thyroid disorder can typically manage their symptoms and prevent hyponatremia and other complications with medications and lifestyle changes.

SIADH usually requires ongoing treatment to prevent hyponatremia. Individuals with the condition may need to restrict fluid intake, take salt tablets, or use medications.

Share on PinterestSports drinks containing electrolytes can help prevent low blood sodium levels after intense exercise.

To avoid low blood sodium levels:

avoid drinking excessive amounts of water
consume sports drinks during intense exercise
do not take ecstasy
seek treatment for medical conditions
discuss medication use with a doctor
seek medical care if vomiting or diarrhea persist

The outlook for people with low sodium levels depends on the severity of the condition and the underlying cause.

Acute hyponatremia, which develops quickly, is more severe than chronic cases, which have a longer onset time. In severe cases, hyponatremia can be fatal.

To improve their outlook, people should be aware of the symptoms of hyponatremia and seek prompt medical attention if they experience any of them. Those at risk of low sodium levels should be especially vigilant.

Low sodium levels (hyponatremia): Symptoms and causes

As the condition worsens, people may experience symptoms, such as:

vomiting
muscle twitches
seizures

Severe hyponatremia occurs when levels drop below 125 mEq/L. Health issues arising from extremely low sodium levels may be fatal.

Mild hyponatremia may not cause symptoms. When symptoms occur they include:

If the condition worsens, it can cause severe symptoms, particularly in older adults. Severe symptoms may include:

vomiting
muscle weakness, spasms, and twitching
seizures
coma

Hyponatremia can result in death in extreme cases.

Other medical conditions and factors that can cause sodium levels to fall include:

diarrhea or vomiting
heart failure
kidney disease
liver disease
medication use
syndrome of inappropriate ADH secretion (SIADH)

People with SIADH produce excessive levels of the anti-diuretic hormone (ADH), which can lower sodium levels

Other causes include:

Drinking too much water.
Drug use. Taking the recreational drug ecstasy increases the risk of severe hyponatremia in some cases. Hyponatremia from ecstasy use can be fatal, especially in females.
Hormone disorders. These include Addison’s disease, which reduces the body’s production of the hormones cortisol and aldosterone and hypothyroidism, which is characterized by low levels of thyroid hormone.

Certain factors increase the risk of developing hyponatremia, including:

age
having specific conditions, such as SIADH or kidney, heart, or liver disease
taking certain diuretics, antidepressants, or pain medications
taking ecstasy
drinking excessive amounts of water
intense exercise, which may cause people to drink lots of water quickly

People who are at risk of hyponatremia or develop symptoms should see their doctor right away as they may need urgent medical treatment.

People with symptoms including vomiting, seizures, or loss of consciousness require immediate attention. They should call an ambulance or go to the nearest emergency department.

To diagnose low sodium levels, a doctor will take a medical history, perform a physical examination, and order a blood test.

If the blood test shows low sodium levels, the doctor will typically need to perform additional tests to determine the cause.

Treatment for hyponatremia involves:

Restoring blood sodium levels

Those who have mild to moderate hyponatremia resulting from lifestyle factors or medication may be able to increase sodium to normal levels by:

drinking less fluids (often less than 1 quart per day)
adjusting medication dose or switching medications

Treating the underlying cause

Where the underlying cause of hyponatremia is a medical condition or hormonal disorder, people will usually need further treatment.

For example, people with liver, kidney, or heart problems may receive medications or surgery. Kidney problems often require dialysis, and people with liver or heart conditions may need a transplant.

People with a thyroid disorder can typically manage their symptoms and prevent hyponatremia and other complications with medications and lifestyle changes.

SIADH usually requires ongoing treatment to prevent hyponatremia. Individuals with the condition may need to restrict fluid intake, take salt tablets, or use medications.

Share on PinterestSports drinks containing electrolytes can help prevent low blood sodium levels after intense exercise.

To avoid low blood sodium levels:

avoid drinking excessive amounts of water
consume sports drinks during intense exercise
do not take ecstasy
seek treatment for medical conditions
discuss medication use with a doctor
seek medical care if vomiting or diarrhea persist

The outlook for people with low sodium levels depends on the severity of the condition and the underlying cause.

Acute hyponatremia, which develops quickly, is more severe than chronic cases, which have a longer onset time. In severe cases, hyponatremia can be fatal.

Low sodium levels (hyponatremia): Symptoms and causes

As the condition worsens, people may experience symptoms, such as:

vomiting
muscle twitches
seizures

Severe hyponatremia occurs when levels drop below 125 mEq/L. Health issues arising from extremely low sodium levels may be fatal.

Mild hyponatremia may not cause symptoms. When symptoms occur they include:

If the condition worsens, it can cause severe symptoms, particularly in older adults. Severe symptoms may include:

vomiting
muscle weakness, spasms, and twitching
seizures
coma

Hyponatremia can result in death in extreme cases.

Other medical conditions and factors that can cause sodium levels to fall include:

diarrhea or vomiting
heart failure
kidney disease
liver disease
medication use
syndrome of inappropriate ADH secretion (SIADH)

People with SIADH produce excessive levels of the anti-diuretic hormone (ADH), which can lower sodium levels

Other causes include:

Drinking too much water.
Drug use. Taking the recreational drug ecstasy increases the risk of severe hyponatremia in some cases. Hyponatremia from ecstasy use can be fatal, especially in females.
Hormone disorders. These include Addison’s disease, which reduces the body’s production of the hormones cortisol and aldosterone and hypothyroidism, which is characterized by low levels of thyroid hormone.

Certain factors increase the risk of developing hyponatremia, including:

age
having specific conditions, such as SIADH or kidney, heart, or liver disease
taking certain diuretics, antidepressants, or pain medications
taking ecstasy
drinking excessive amounts of water
intense exercise, which may cause people to drink lots of water quickly

People who are at risk of hyponatremia or develop symptoms should see their doctor right away as they may need urgent medical treatment.

People with symptoms including vomiting, seizures, or loss of consciousness require immediate attention. They should call an ambulance or go to the nearest emergency department.

To diagnose low sodium levels, a doctor will take a medical history, perform a physical examination, and order a blood test.

If the blood test shows low sodium levels, the doctor will typically need to perform additional tests to determine the cause.

Treatment for hyponatremia involves:

Restoring blood sodium levels

Those who have mild to moderate hyponatremia resulting from lifestyle factors or medication may be able to increase sodium to normal levels by:

drinking less fluids (often less than 1 quart per day)
adjusting medication dose or switching medications

Treating the underlying cause

Where the underlying cause of hyponatremia is a medical condition or hormonal disorder, people will usually need further treatment.

For example, people with liver, kidney, or heart problems may receive medications or surgery. Kidney problems often require dialysis, and people with liver or heart conditions may need a transplant.

People with a thyroid disorder can typically manage their symptoms and prevent hyponatremia and other complications with medications and lifestyle changes.

SIADH usually requires ongoing treatment to prevent hyponatremia. Individuals with the condition may need to restrict fluid intake, take salt tablets, or use medications.

Share on PinterestSports drinks containing electrolytes can help prevent low blood sodium levels after intense exercise.

To avoid low blood sodium levels:

avoid drinking excessive amounts of water
consume sports drinks during intense exercise
do not take ecstasy
seek treatment for medical conditions
discuss medication use with a doctor
seek medical care if vomiting or diarrhea persist

The outlook for people with low sodium levels depends on the severity of the condition and the underlying cause.

Acute hyponatremia, which develops quickly, is more severe than chronic cases, which have a longer onset time. In severe cases, hyponatremia can be fatal.

Low sodium levels (hyponatremia): Symptoms and causes

As the condition worsens, people may experience symptoms, such as:

vomiting
muscle twitches
seizures

Severe hyponatremia occurs when levels drop below 125 mEq/L. Health issues arising from extremely low sodium levels may be fatal.

Mild hyponatremia may not cause symptoms. When symptoms occur they include:

If the condition worsens, it can cause severe symptoms, particularly in older adults. Severe symptoms may include:

vomiting
muscle weakness, spasms, and twitching
seizures
coma

Hyponatremia can result in death in extreme cases.

Other medical conditions and factors that can cause sodium levels to fall include:

diarrhea or vomiting
heart failure
kidney disease
liver disease
medication use
syndrome of inappropriate ADH secretion (SIADH)

People with SIADH produce excessive levels of the anti-diuretic hormone (ADH), which can lower sodium levels

Other causes include:

Drinking too much water.
Drug use. Taking the recreational drug ecstasy increases the risk of severe hyponatremia in some cases. Hyponatremia from ecstasy use can be fatal, especially in females.
Hormone disorders. These include Addison’s disease, which reduces the body’s production of the hormones cortisol and aldosterone and hypothyroidism, which is characterized by low levels of thyroid hormone.

Certain factors increase the risk of developing hyponatremia, including:

age
having specific conditions, such as SIADH or kidney, heart, or liver disease
taking certain diuretics, antidepressants, or pain medications
taking ecstasy
drinking excessive amounts of water
intense exercise, which may cause people to drink lots of water quickly

People who are at risk of hyponatremia or develop symptoms should see their doctor right away as they may need urgent medical treatment.

People with symptoms including vomiting, seizures, or loss of consciousness require immediate attention. They should call an ambulance or go to the nearest emergency department.

To diagnose low sodium levels, a doctor will take a medical history, perform a physical examination, and order a blood test.

If the blood test shows low sodium levels, the doctor will typically need to perform additional tests to determine the cause.

Treatment for hyponatremia involves:

Restoring blood sodium levels

Those who have mild to moderate hyponatremia resulting from lifestyle factors or medication may be able to increase sodium to normal levels by:

drinking less fluids (often less than 1 quart per day)
adjusting medication dose or switching medications

Treating the underlying cause

Where the underlying cause of hyponatremia is a medical condition or hormonal disorder, people will usually need further treatment.

For example, people with liver, kidney, or heart problems may receive medications or surgery. Kidney problems often require dialysis, and people with liver or heart conditions may need a transplant.

People with a thyroid disorder can typically manage their symptoms and prevent hyponatremia and other complications with medications and lifestyle changes.

SIADH usually requires ongoing treatment to prevent hyponatremia. Individuals with the condition may need to restrict fluid intake, take salt tablets, or use medications.

Share on PinterestSports drinks containing electrolytes can help prevent low blood sodium levels after intense exercise.

To avoid low blood sodium levels:

avoid drinking excessive amounts of water
consume sports drinks during intense exercise
do not take ecstasy
seek treatment for medical conditions
discuss medication use with a doctor
seek medical care if vomiting or diarrhea persist

The outlook for people with low sodium levels depends on the severity of the condition and the underlying cause.

Acute hyponatremia, which develops quickly, is more severe than chronic cases, which have a longer onset time. In severe cases, hyponatremia can be fatal.

Results From the Trial of Nonpharmacologic Interventions in the Elderly

Am J Public Health. 2016 July; 106(7): 1270–1275.

Liwei Chen, MD, PhD,Zhenzhen Zhang, PhD, Wen Chen, MD, Paul K. Whelton, MD, and Lawrence J. Appel, MD

Liwei Chen is with the Department of Public Health Sciences, Clemson University, Clemson, SC. Zhenzhen Zhang is with the School of Public Health, Oregon Health & Science University, Portland. Wen Chen is with the Department of Pathology, VA Medical Center, Washington, DC. Paul K. Whelton is with the Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA. Lawrence J. Appel is with the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, MD.

Corresponding author.Correspondence should be sent to Liwei Chen, Assistant Professor, Department of Public Health Sciences, Clemson University, 511 Edwards Hall, Clemson, SC 29631 (e-mail: ude.nosmelc@ciewil). Reprints can be ordered at http://www.ajph.org by clicking the “Reprints” link.CONTRIBUTORS

L. Chen wrote the first draft of the article. L. Chen, Z. Zhang, and W. Chen conducted the statistical analyses. P. K. Whelton and L. J. Appel acquired the data. All authors conceptualized and designed the study, interpreted the results, and revised the article.

Peer Reviewed

Accepted February 15, 2016.

Abstract

Objectives. To determine the effect of sodium (Na) reduction on occurrence of headaches.

Methods. In the Trial of Nonpharmacologic Interventions in the Elderly, 975 men and woman (aged 60–80 years) with hypertension were randomized to a Na-reduction intervention or control group and were followed for up to 36 months. The study was conducted between 1992 and 1995 at 4 clinical centers (Johns Hopkins University, Wake Forest University School of Medicine, Robert Wood Johnson Medical School, and the University of Tennessee).

Results. Mean difference in Na excretion between the Na-reduction intervention and control group was significant at each follow-up visit (P < .001) with an average difference of 38.8 millimoles per 24 hours. The occurrence of headaches was significantly lower in the Na-reduction intervention group (10.5%) compared with control (14.3%) with a hazard ratio of 0.59 (95% confidence interval = 0.40, 0.88; P = .009). The risk of headaches was significantly associated with average level of Na excretion during follow-up, independent of most recent blood pressure. The relationship appeared to be nonlinear with a spline relationship and a knot at 150 millimoles per 24 hours.

Conclusions. Reduced sodium intake, currently recommended for blood pressure control, may also reduce the occurrence of headaches in older persons with hypertension.

Headache is a common health problem in adults, resulting in approximately 18 million physician visits in the United States each year.1 Globally, the estimated lifetime prevalence of headaches in adults is 66%.2 The most common types of headaches are nonvascular and are commonly termed “tension headaches.”1 Tension headaches have been attributed to muscle spasm in the head, neck, and shoulders in response to stress, fatigue or environmental factors like noise or bright lights.3 However, the pathophysiology of tension headaches is uncertain.

Headaches have been associated with elevated blood pressure (BP), including sustained severe hypertension, malignant hypertension, and paroxysmal hypertension.4 In the Hypertension Optimal Treatment trial, in which participants were randomized to 1 of 3 diastolic BP goals, headaches were reduced in all treatment groups, independent of BP goal and type of antihypertensive drug.5

High sodium intake is associated with elevated BP, and clinical trials have demonstrated that sodium-reduction (NaD) lowers BP in individuals with or without hypertension.6–13 A high intake of sodium potentially leads to headaches through a direct effect on BP or indirectly through a BP-independent mechanism. However, few studies have investigated the relationship of sodium intake to the occurrence of headaches. In preliminary observations from the Trial of Nonpharmacologic Interventions in the Elderly (TONE), we reported that individuals who were assigned to the NaD intervention had a lower incidence of headaches.13 A more recent analysis using data collected from the Dietary Approaches to Stop Hypertension (DASH)-sodium trial reported that NaD was associated with a lower risk of headaches,14 replicating the earlier observation from the TONE study. We aimed to expand on the original observation from TONE by examining the relationship between sodium intake and headaches, with a particular focus on assessing dose–response relationship.

METHODS

TONE was a multicenter, randomized controlled trial designed to test the efficacy of nonpharmacologic interventions as a means to control hypertension in the elderly. A detailed description of the design and methods of this trial has been published elsewhere.15 Eligible individuals were aged 60 to 80 years, were community dwelling, and had hypertension controlled on single antihypertensive medication. Major exclusion criteria included history of a heart attack or stroke within the preceding 6 months, current angina pectoris, congestive heart failure, insulin-dependent diabetes mellitus, serious mental or physical illness, unexplained or involuntary weight loss of 4.5 kilograms or greater during the previous year, hypercreatinemia (> 2.0 mg/dL), hyperkalemia (> 5.5 mmol/L), and anemia (hemoglobin level < 11 g/dL).

We randomly assigned overweight persons (body mass index [BMI; defined as weight in kilograms divided by the square of height in meters] > 27.3 kg/m² in men, > 27.8 kg/m² in women) to 1 of 4 groups in a 2 × 2 factorial design (usual care, weight loss alone, reduced sodium alone, or combined weight loss and reduced sodium). We assigned nonoverweight persons to usual care or reduced sodium intake. The NaD goal for the reduced sodium groups, both NaD alone and NaD combined with weight loss, was to achieve and maintain a 24-hour dietary sodium intake of 80 millimoles (1800 mg) or less. Three months after the start of intervention, we employed a standardized protocol to gradually taper and withdraw antihypertensive medication in participants whose BP remained less than 150/90 millimeters of mercury.

The primary trial outcome was a composite endpoint that included recurrence of high BP, resumption of antihypertensive medication, or a clinical cardiovascular event. During follow-up, we restarted antihypertensive medication if (1) systolic BP was 190 millimeter of mercury or more or diastolic BP was 110 millimeters of mercury or more at a single visit (average of 3 BP measurements), (2) mean systolic BP was 170 millimeters of mercury or more or diastolic BP was 100 millimeters of mercury or more over 2 consecutive visits (average of 6 BP measurements), or (3) mean systolic BP was 150 millimeters of mercury or more or diastolic BP rose to 90 millimeters of mercury or more at 3 consecutive visits (average of 9 BP measurements).

We enrolled participants between August 30, 1992, and June 27, 1994. We collected TONE data at 2 screening visits to establish study eligibility, a randomization visit, drug withdrawal visits (90 days after the start of intervention), and 11 subsequent quarterly follow-up visits (beginning 6 months after randomization). Closeout visits occurred between July and December 1995. The median follow-up in TONE was 29 months (range = 1–36 months). We conducted the study at 4 clinical centers (Johns Hopkins University, Wake Forest University School of Medicine, Robert Wood Johnson Medical School, and the University of Tennessee).13 Staff members, who were blinded to the participant’s randomized treatment assignment, obtained outcome information.

Variables

We estimated dietary sodium intake by measurement of carefully collected 24-hour urinary sodium excretion. We analyzed urinary sodium levels by flame photometry.13 In TONE we ascertained headaches by participant self-report of an adverse event at any follow-up visit. At each follow-up visit, participants completed a brief self-reported medical history and adverse events questionnaire. A study nurse evaluated any participant who reported an intercurrent health-related concern. If a participant reported a medical problem that was potentially serious (e.g., angina) or a symptom that was severe (e.g., headache or chest pain) the nurse completed an adverse event form. A physician then reviewed and coded the adverse event by type (e.g., stroke, myocardial infarction, headache). We also collected and coded the date of the event. Both the nurse and physician were unaware on the participant’s treatment assignment.

Trained observers who were masked to intervention assignment measured BP. At each visit, we obtained 3 BP measurements while participants rested in the seated position. We collected detailed demographic and socioeconomic information including age, gender, race, physical activity, smoking habits, and alcohol intake at baseline.15 We also collected interval medical information, medication use, and body weight measurement at each visit.

Statistical Analyses

We expressed descriptive data for identification of baseline characteristics as well as urinary sodium excretion at each visit as means (SD) for continuous variables and counts (%) for categorical variables. We used the Student t test and χ² test to compare continuous variables and discrete variables, respectively. For all the analyses, the primary outcome was headache, which we identified by means of adverse event reports.

First, we compared incidence of headaches between those in the NaD intervention group (i.e., the NaD alone plus combined weight loss and NaD interventions) and their counterparts in the control group (i.e., usual care plus weight loss alone interventions). We used Kaplan-Meier plots to explore temporal patterns for cumulative incidence of headaches and Cox proportional hazard regressions to estimate the hazard ratio (HR) and 95% confidence interval (CI) for comparison of first occurrence of a headache between the 2 groups. Because this comparison was on the basis of randomized assignments, we only adjusted for variables that were significantly different between the NaD intervention and control groups (i.e., time-varying drug withdraw status and BPs). Although we conducted the main analyses between the NaD and control groups, we also performed a sensitivity analysis to compare headaches among the 4 original group assignments of the factorial design (i.e., usual care, weight loss alone, NaD alone, and combined weight loss and NaD interventions).

Second, we examined whether there were a dose–response relationship and threshold effect between sodium intake and the occurrence of headaches. The exposure was 24-hour urinary sodium excretion, measured as the average level during follow-up. We used Cox proportional hazard regressions to investigate the frequency of new onset headaches, assessed as an adverse event (incident headaches postrandomization). In these models, we combined participants from all intervention groups and we included potential confounders such as age, gender, race, physical activity, smoking, alcohol intake, headaches at baseline, average weight loss during follow-up, and drug withdraw status (time-varying variable) in the adjusted analyses. To explore whether the relationship of headaches with sodium intake was independent of BP, we additionally adjusted for the most recent BP. We performed all statistical analyses using SAS version 9.4 (SAS Institute, Cary, NC). We considered a P value of less than .05 (2 sides) statistically significant.

RESULTS

displays the baseline characteristics of all TONE study participants by assignment to the NaD intervention or control. Of the 975 individuals, 52% were men, 76% were White, and the mean (SD) age was 65.8 (4.6) years. Mean (SD) 24-hour urinary sodium excretion at baseline was 148.5 (54) millimoles per 24 hours. Overall, there was no statistically significant difference in baseline characteristics by group (NaD vs control).

TABLE 1—

Baseline Characteristics of Participants by Randomly Assigned Group: Trial of Nonpharmacologic Interventions in the Elderly, United States, 1992–1995

Characteristic	Control (n = 488), Mean (SD) or %	Sodium Reduction (n = 487), Mean (SD) or %	All^a (n = 975), Mean (SD) or %
Age, y	65.8 (4.5)	65.8 (4.7)	65.8 (4.6)
Male	51.8	52.6	52.2
White	74.8	77.2	76.0
SBP, mmHg	128.1 (9.3)	128.4 (9.4)	128.2 (9.3)
DBP, mmHg	71.3 (7.4)	71.4 (7.2)	71.4 (7.3)
Urine sodium, mmol/24 h	148.6 (54.9)	148.4 (53.4)	148.5 (54.2)
Weight, lb	180.0 (26.3)	180.7 (28.4)	180.3 (27.4)
BMI, kg/m²	28.9 (3.5)	28.9 (3.6)	28.9 (3.5)
Alcohol user	34.8	35.5	35.2
Currently smokes	4.9	5.7	5.3

Participant attendance rates were 90%, 86%, and 86% at the 9-, 18-, and 30-month follow-up visits. BP measurements were available for 100% of the visits. We collected 24-hour urine samples in 867 (88.9%), 804 (82.5%), and 421 (82.1%) participants at the 9-, 18-, and 30-month visits, respectively.

Urinary Sodium Excretion and Headache Occurrence

Baseline urinary sodium excretion did not differ between the NaD and control groups (Table A, available as a supplement to the online version of this article at http://www.ajph.org). We observed significantly greater reductions in urinary sodium from baseline in the NaD group compared with the control group at the 9-, 18-, and 30-month follow-up visits. The mean changes in urinary sodium excretion in the NaD group were −40.9, −43.2, and −45.3 millimoles per 24 hours at the 9-, 18-, and 30-month follow-up visits, respectively. Corresponding mean changes in the control group were 0.4, −3.1, and −4.5 millimoles per 24 hours, respectively. During follow-up, the mean between-group difference in average urinary sodium excretion was 38.8 millimoles per 24 hours.

During follow-up, 126 participants reported headache as an adverse event, and 13 (10.3%) reported headache twice as an adverse event. We used the first reported headache as our study outcome. displays the cumulative incidence of headaches during follow-up by randomized assignment. In the control group, 14.3% reported headaches during follow-up. By contrast, only 10.5% reported headaches in the NaD group (log-rank test, P = .012).

Cumulative Incidence of Headaches by Intervention Group (Reduced Sodium vs Control): Trial of Nonpharmacologic Interventions in the Elderly, United States, 1992–1995

Note. We used the log-rank test to compare the group difference (P = .012).

The HR for headaches in the NaD group compared with control was 0.56 (95% CI = 0.38, 0.83; P = .01) after adjustment for clinical center, time-varying drug withdrawal status, and average weight loss during follow-up (model 2). After further adjustment for most recent systolic and diastolic BP before the occurrence of headaches (model 3), the HR was essentially unchanged (HR = 0.59; 95% CI = 0.40, 0.88; P = .02). In the sensitivity analysis, the HR for headaches (model 3) was 0.83 (95% CI = 0.49, 1.40; P = .48) in the weight loos alone intervention, 0.61 (95% CI = 0.39, 0.95; P = .03) in the NaD alone intervention, and 0.47 (95% CI = 0.25, 0.92; P = .03) in the combined weight loos and NaD intervention compared with the control group.

Observational Analyses and Dose–Response Relationship

summarizes results from the Cox proportion hazard models using average urinary sodium excretion during follow-up as the primary exposure. We identified a statistically significant direct association of headaches with average urinary sodium excretion. After adjustment for clinical center, age, smoking, race, gender, alcohol use, physical activity, average weight loss during follow-up, and drug withdrawal status (model 2), a 10 millimoles per 24 hour higher level of urinary sodium excretion was associated with a hazard of headaches that was 7.0% higher (95% CI = 4%, 11%, P ≤ .001). The association between urinary sodium excretion and risk of headaches persisted after further adjustment for most recent systolic BP and diastolic BP in model 3. Because headaches were more common in women (17.0%) than in men (8.8%), we further stratified our analyses by gender. The magnitude of the associations was similar in both gender; the HR of headaches associated with a 10 millimoles per 24 hours higher level of urinary sodium excretion was 1.09 (95% CI = 1.03, 1.15) for men and 1.07 (95% CI = 1.02, 1.12) for women.

TABLE 2—

HR (95% CI) of Headaches by Level of Urinary Sodium Excretion During Follow-Up: Trial of Nonpharmacologic Interventions in the Elderly, United States, 1992–1995

		Average Urinary Sodium as Categorical Variable^b
Model	Average Urinary Sodium Excretion as a Continuous Variable,^a HR (95% CI)	120–150 mmol/24 h, HR (95% CI)	> 150 mmol/24 h, HR (95% CI)
Model 1^c	1.04 (1.00, 1.07)	1.01 (0.62, 1.66)	1.65 (1.11, 2.46)
Model 2^d	1.07 (1.04, 1.11)	1.15 (0.67, 1.95)	2.27 (1.45, 3.55)
Model 3^e	1.07 (1.04, 1.11)	1.26 (0.74, 2.16)	2.32 (1.48, 3.65)

In exploratory analyses, the relationship between headaches and absolute urinary sodium level appeared to be nonlinear, with a threshold between 120 to 150 millimoles per 24 hours. We noted the greatest evidence for an association between urinary sodium excretion and occurrence of headaches above this threshold. For this reason, we categorized the participants into 3 groups on the basis of their average urinary sodium excretion during follow-up: (1) less than 120 millimoles per 24 hours (below the threshold, lower sodium intake), (2) 120–150 millimoles per 24 hours (close to threshold, moderate sodium intake), and (3) more than 150 millimoles per 24 hours (above threshold, higher sodium intake). Compared with the category of lower sodium intake, individuals with moderate sodium intake did not exhibit a significantly higher risk of headaches (HR = 1.26; 95% CI = 0.74, 2.16; P = .39). However, individuals in the higher sodium intake category had a significantly higher risk of headaches than did those in the lower sodium intake category (HR = 2.32; 95% CI = 1.48, 3.65; P ≤ .001).

During spline interpolation, we identified knots at 120 millimoles per 24 hours and 150 millimoles per 24 hours. Above the 150 millimoles per 24 hours knot, an increase of 10 millimoles per 24 hours in urinary sodium excretion was associated with an increase of 9.7% in the hazard of headaches (95% CI = 3.4%, 16.9%; P = .002) after adjusting for age, smoking, race, gender, alcohol use, physical activity, average weight loss during follow-up, and drug withdrawal status. This positive association remained significant with further adjustment for most recent BPs in model 3 (HR = 1.09; 95% CI = 1.02, 1.18; P = .004). The risk of headaches increased dramatically and significantly as the urinary sodium excretion level was above the 150 millimoles per 24 hours (Figure A, available as a supplement to the online version of this article at http://www.ajph.org).

DISCUSSION

In this analysis of 975 persons, aged 60 to 80 years who participated in the TONE trial, we found that NaD was associated with a lower risk of headaches over the course of 36 months of follow-up. Specifically, individuals who were randomly assigned to a NaD intervention had a lower cumulative incidence of headaches than did their counterparts in the control group. In an observational analysis, urinary sodium excretion, measured as an average level during follow-up, was associated with occurrence of incident headaches, independent of other risk factors, baseline headaches, use of BP lowering medications, and most recent level of BP. We observed an apparent threshold effect, with the risk of headaches increasing progressively above a urinary sodium excretion of 150 millimoles per 24 hours. Above the sodium excretion threshold of 150 millimoles per 24 hours, risk of incident headaches was higher by 7.8% for every 10 millimoles average increase in 24-hour urinary sodium; below this threshold, there was no significant relationship.

Although numerous studies have assessed the effects of a reduced sodium intake on BP6,7,11–13 and several studies have assessed the relationship between headaches and BP,4,5,16,17 the relationship between sodium intake and the occurrence of headaches has received scant attention. The most relevant study is the DASH-Sodium trial, a randomized, controlled feeding study that tested the effects of 3 levels of sodium intake (50, 100, and 150 mmol/24 hr) in 2 different diets (the DASH diet and a typical American diet). In a recent secondary analysis of this trial, a reduced sodium intake was associated with significantly lower risk of headache (odds ratio[OR] = 0.69; P = .05, among those consuming a typical American diet, and OR = 0.69; P = .04, among those consuming the DASH diet) in adults with prehypertension and stage 1 hypertension.14

By contrast to TONE, study participants in the DASH-Sodium trial tended to be younger, with a mean (SD) age of 48 years.10 Also, the 2 trial designs and duration of follow-up were different (a cross-over trial with approximately 30 days of follow-up for each period of intervention in the DASH-Sodium trial and a parallel arm trial with a median follow-up of 29 months in the TONE trial), the extent of NaD was almost twofold greater in the DASH-Sodium trial than in the TONE trial, and the methods used to ascertain headaches were different in the 2 studies (symptom check list in the DASH-Sodium trial and adverse event reporting in the TONE trial). Overall, the findings from our analysis and the corresponding DASH-Sodium report provide consistent evidence regarding the apparent effect of sodium intake on the occurrence of headaches. Because of the use of adverse events reporting as the method of ascertainment for headaches in the TONE trial, it seems likely that the results from this trial may have highlighted the relationship between NaD and more severe headaches.

The mechanisms underlying an association between sodium intake and headaches are uncertain. Sodium intake may be related to headaches through a direct effect on BP or indirectly through other BP-independent mechanisms. Excessive intake of sodium is a well-established risk factor for high BP, and NaD can lower BP in hypertensive and nonhypertensive individuals.6–13 Elevated BP has been associated with headaches independent of weight status and antihypertensive drug therapy.4,5 Therefore, it is possible that a high intake of sodium may lead to headaches through a direct effect on BP. However, controlling for recent BP in the Cox regression models did not attenuate the association between sodium and headaches in our analyses, suggesting that the effect of sodium on headaches might be independent of BP.

One proposed BP-independent mechanism relates to changes in vascular smooth muscle tone. Sodium intake is an important determinant of smooth muscle cell reactivity, which is in part mediated by changes in extracellular volume and perhaps by changes in intracellular calcium. A high sodium intake increases the reactivity of arterioles and the BP response to stress or sympathetic simulation.18 In a study of patients with asthma, a moderate reduction in sodium intake led to an improvement in asthma symptoms, potentially related to changes in bronchial smooth muscle tone.19 Such findings suggest that nonvascular headaches might be part of a continuum with vascular headaches at 1 extreme.20 Still, we cannot totally rule out an effect of BP in our study because we measured BP at prespecified follow-up visits, not at the time of the headaches.

Strengths and Limitations

Our study has several strengths. First, the sample size of TONE trial was relatively large (n = 975), and the duration of follow-up was relatively long (up to 3 years). Second, we collected information on potential adverse events at each study visit; a study clinician who was blinded to the participant’s treatment allocation verified these. Third, we estimated sodium intake by means of carefully collected 24-hour urine samples, with averaging of several samples for the observational analyses: twice before randomization and once at the 9-month, 18-month, and 30-month follow-up visits. Of the available methods, mean 24-hour urinary excretion of sodium collected from multiple occasions provides the most accurate estimate of dietary sodium intake for observational analyses.21 Study limitations include a lack of specific information regarding participant headaches severity and duration and prior history of headaches.

Nevertheless, headaches reported as an adverse event in TONE were associated with baseline headache experience,22 and we adjusted for baseline headaches in our observational analyses. Again, because we did not measured BP at the time of the event, inferences about the relationship between BP and headaches are uncertain. However, there were no differences when we compared BP measured at the study visit closest to the adverse event and the average BP during the follow-ups for study participants. The average time between most recent BP measurement and occurrence of adverse event headache was 12.3 days for those who had adverse event headache, which is relative short. Although the assortment of headaches in this study is probably not subject to reporting bias or directly related to the intervention assignments, we were unable to rule out the possibility that the observed improvement in occurrence of headaches in the NaD group could be a surrogate of improving general well-being.

Conclusions

Our findings suggest that reducing sodium intake lowers the risk of headaches in older persons with hypertension. Our findings are consistent with results from the DASH-Sodium trial, which enrolled a middle-aged study population and used a different approach to ascertainment. Whether a reduced sodium intake lowers the risk of headaches in other populations (e.g., persons with migraine headaches) is unknown. From a policy perspective, these data provide an additional rationale in support of recommendations by the American Heart Association, US federal government, Institute of Medicine, World Health Organization, and others to reduce dietary sodium intake.23

ACKNOWLEDGMENTS

The Trial of Nonpharmacologic Interventions in the Elderly (TONE) trial was supported by the National Institutes of Health (grants R01 AG-09799, R01 H-48642, R01 AG-09771, R01 AG-09773, P60 AG-10484, and K08 HLO2642).

We thank the TONE participants and staff for their contributions to the study.

HUMAN PARTICIPANT PROTECTION

The institutional review boards at Johns Hopkins University, Wake Forest University School of Medicine, Robert Wood Johnson Medical School, and the University of Tennessee approved the trial protocol. Oversight of the trial was also provided by an external data and safety monitoring board appointed by staff at the National Institute on Aging and the National Heart, Long, and Blood Institute. All potential study participants provided written informed consent. Clinical Trial Registration: clinicaltrials.gov identifier {“type”:”clinical-trial”,”attrs”:{“text”:”NCT00000535″,”term_id”:”NCT00000535″}}NCT00000535.

REFERENCES

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Sodium level in dialysate for chronic hemodialysis

What is the problem?

The kidneys control the body’s salt and water balance by regulating urine production. When the kidneys stop working, urination stops or becomes insufficient, and the water-salt balance is maintained with dialysis. Physicians managing hemodialysis patients should select the appropriate amount of sodium for use in dialysis fluids used to cleanse the patient’s blood.If the sodium level in these fluids is too high, it can cause the patient to feel thirsty after treatment, excessive water intake and fluid overload by the time the next treatment is started, which can lead to heart damage. On the other hand, if the sodium level in dialysis fluids is too low, the patient may experience seizures and a drop in blood pressure, which causes discomfort and can also damage the heart. The “correct” dialysis fluid sodium level is unknown.

What have we done?

We pooled all studies of people treated with hemodialysis that compared results between people who received low sodium in dialysis fluid and people who received higher sodium.

What have we found?

We found 12 studies comparing low dialysis fluid sodium levels with neutral or high sodium levels. Many studies were conducted before 2000, research technologies and patients are not always relevant today.Most of them were short-term, lasting only a few weeks. Our main findings in these studies were that low sodium levels in dialysis fluid improved blood pressure and decreased salt and water inflow between dialysis sessions, which is probably good, but increases the number of cramps and episodes of low blood pressure experienced by patients. during dialysis, which is definitely bad. The studies did not provide us with enough information about the participating patients to know which patients might benefit from low sodium dialysis and which patients might benefit.Studies have not provided accurate information on the effect of low sodium dialysis fluids on heart structure and function, or on patient quality of life and survival.

Conclusions

We are uncertain whether low dialysis fluid sodium improves the general health and well-being of people on hemodialysis, as a combination of likely good and bad effects occurs, and the available studies have not been designed (or well designed) for examining the effect of the intervention on the heart or on the general health and well-being of patients.Larger, more recent and specific research is needed to assess the medium and long-term effects of low sodium levels in dialysis fluid and to better inform clinical practice.

Hypertension

The diagnosis of “hypertension” is made in cases where, according to blood pressure measurements taken on two different days, the value of systolic pressure on that and on the other day is equal to or exceeds 140 mm Hg. Art. and / or the diastolic pressure on both days is equal to or greater than 90 mm Hg.Art.

What are the risk factors for hypertension?

Controllable risk factors include unhealthy diets (excessive salt intake, high levels of saturated fat and wastes in the diet, inadequate intake of fruits and vegetables), insufficient physical activity, tobacco and alcohol use, and overweight and obesity.

Uncontrollable risk factors include the presence of hypertension in immediate family members, age over 65, and comorbid conditions such as diabetes or kidney disease.

What are the typical symptoms of hypertension?

Hypertension is called the “silent killer”. Most patients with hypertension are not even aware of the problem, since hypertension often does not give alarming signals and is asymptomatic. That is why it is so important to regularly measure your blood pressure.

When symptoms occur, they may include headaches in the early morning hours, nosebleeds, irregular heart rhythms, blurred vision, and ringing in the ears.Severe hypertension can cause weakness, nausea, vomiting, confusion, internal tension, chest pain, and muscle tremors.

The only way to detect hypertension is to have your blood pressure measured by a healthcare professional. Blood pressure measurement is quick and painless. Blood pressure can also be measured independently using automatic devices, but a medical professional should be used to assess risk and associated disorders.

What are the complications of uncontrolled hypertension?

Among other complications, hypertension can seriously damage the heart. Excessive pressure can cause the walls of the arteries to lose their elasticity and reduce the flow of blood and oxygen to the heart muscle. This high blood pressure and decreased blood flow can cause:

chest pain, also called angina pectoris;
A heart attack that occurs when the blood supply to the heart is blocked, as a result of which the cells of the heart muscle die from oxygen starvation.The longer blood flow is blocked, the more serious the damage to the heart;
heart failure, in which the pumping function of the heart muscle cannot fully provide other essential organs with blood and oxygen;
cardiac arrhythmia, which can lead to sudden death.

Hypertension can also cause stroke, ruptured or blocked arteries that supply blood and oxygen to the brain.

In addition, hypertension can cause renal failure caused by kidney damage.

Why is hypertension a problem in low- and middle-income countries?

The prevalence of hypertension varies across WHO regions and countries in different income categories. Hypertension is most prevalent in the WHO African Region (27%) and least in the Region of the Americas (18%).

Analysis of current trends shows that the number of adults with hypertension has increased from 594 million in 1975 to 1.13 billion in 2015.and mainly at the expense of low- and middle-income countries. This risk is mainly due to increased risk factors for hypertension among these populations.

How can the burden of hypertension be reduced?

Reducing high blood pressure prevents heart attacks, strokes and kidney damage and other health problems.

Prevention

Reducing salt intake (to less than 5 g per day)
Increasing the proportion of fruits and vegetables in the diet
Regular physical activity
Quitting tobacco use
Reducing alcohol consumption
Restricting food consumption high in saturated fat
Eliminate or reduce trans fats from food

Control hypertension

Reduce and manage stress conditions
Routine blood pressure checks
Treating high blood pressure
Treating other diseases

How is WHO responding to the problem of hypertension?

In 2016To help governments prevent and treat cardiovascular disease, WHO and the US Centers for Disease Control and Prevention have launched the Global Hearts initiative.

The HEARTS technical package, part of five Global Hearts technical packages, aims to improve the prevention and management of cardiovascular diseases, including the detection and management of hypertension. The five modules of the HEARTS technical package (health counseling, evidence-based treatment protocols, access to essential drugs and technologies, team delivery and monitoring systems) provide a strategic approach to cardiovascular health promotion across a wide range of countries the world.

Implementation of the HEARTS technical package started in 15 countries (Barbados, Bhutan, Colombia, Chile, China, Cuba, Ethiopia, India, Iran, Morocco, Nepal, Philippines, Tajikistan, Thailand and Vietnam). First advances have already been made in this area with the massive introduction of protocols in case management, increased access to medicines and technologies, and improved quality of outcome assessment.

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Memorial Sloan Kettering Cancer Center

This document, provided by Lexicomp ^®, contains all the information you need to know about the drug, including the indications, route of administration, side effects and when you should contact your healthcare provider.

Trade names: USA

CeleXA

Trade names: Canada

ACCEL-Citalopram [DSC]; ACT Citalopram; AG-Citalopram; APO-Citalopram; Auro-Citalopram; BIO-Citalopram; CCP-Citalopram; CeleXA; Citalopram-10; Citalopram-20; Citalopram-40; CTP 30; DOM-Citalopram; ECL-Citalopram [DSC]; JAMP-Citalopram; Mar-Citalopram; MINT-Citalopram; MYLAN-Citalopram [DSC]; NAT-Citalopram; NRA-Citalopram; NU-Citalopram [DSC]; PMS-Citalopram; Priva-Citalopram; RAN-Citalo; RIVA-Citalopram; SANDOZ Citalopram; SEPTA-Citalopram; TEVA-Citalopram; VAN-Citalopram [DSC]

Warning

For all patients taking this drug:

Drugs like this have increased the likelihood of suicidal thoughts or actions in children and young people.This risk may be higher in people who have attempted suicide or have had suicidal thoughts in the past. All people taking this drug must be closely monitored. Call your doctor right away if you have signs such as depressed mood (depression), nervousness, anxiety, grumpiness, or anxiety attacks, or if other mood or behavior changes occur or worsen. Call your doctor immediately if you have suicidal thoughts or attempted suicides.

Children:

This medicine is not approved for use in children. However, your doctor may decide that the benefits of using this drug outweigh the risks associated with it. If your child has received this drug, ask the doctor about the benefits and risks. Talk to your doctor if you have any questions about how your child is using this drug.

What is this drug used for?

The drug is used to treat depression.
This medicinal product can be used for other indications. Consult your doctor.

What should I tell my doctor BEFORE taking this drug?

If you are allergic to citalopram or any of the other ingredients of this medicine.
If you are allergic to this drug, any of its ingredients, other drugs, foods or substances. Tell your doctor about your allergy and how it manifested itself.
If you are taking any of the following drugs: linezolid or methylene blue.
If you are taking one of the following drugs: Escitalopram or pimozide.
If you are taking any medications that can cause certain types of heart rhythm disturbances (prolonged QT interval). There are many medications that can cause these problems. If you are unsure, check with your doctor or pharmacist.
If you have taken a drug for depression or Parkinson’s disease in the past 14 days.These include isocarboxazid, phenelzine, tranylcypromine, selegiline, or rasagiline. An episode of very high blood pressure may occur.
If you have any of the following health problems: prolonged ECG QTc interval or other heart rhythm disturbances, bradycardia, or low levels of potassium or magnesium.
If you have heart failure (weakened heart).
If you have recently had a myocardial infarction.

This list of drugs and diseases that may be adversely associated with this drug is not exhaustive.

Tell your doctor and pharmacist about all medicines you take (both prescription and over-the-counter, natural products and vitamins) and your health problems. You need to make sure that this drug is safe for your medical conditions and in combination with other drugs you are already taking. Do not start or stop taking any medication or change the dosage without your doctor’s approval.

What do I need to know or do while taking this drug?

For all patients taking this drug:

Tell all healthcare providers that you are taking this drug. These are doctors, nurses, pharmacists and dentists.
Avoid driving vehicles or other activities that require increased attention until you see how this drug affects you.
Do not stop taking this drug suddenly without talking to your doctor.This can increase the risk of side effects. If necessary, this drug should be stopped gradually as directed by your doctor.
A dangerous heart rhythm disorder (prolonged QT interval on the ECG) has happened with this drug. There have been rare cases of sudden death in people taking this drug. Consult your doctor.
Avoid drinking alcohol while taking this drug.
Consult your doctor before using marijuana, other forms of cannabis, prescription or over-the-counter drugs that may slow you down.
If you are depressed after starting this drug, your sleep and appetite may improve quickly. Other symptoms of depressed mood may take up to 4 weeks to improve.
This drug may increase the risk of bleeding. Sometimes bleeding can be life-threatening. Consult your doctor.
The risk of eye problems may be increased in some patients with this drug. Your doctor may order you to see an ophthalmologist to see if you are at increased risk of developing these eye problems.Call your doctor right away if you have eye pain, change in vision, swelling, or redness around the eye.
This drug may lower sodium levels. Very low sodium levels can be life-threatening, leading to seizures, fainting, difficulty breathing, or death.
If you are 65 years of age or older, use this drug with caution. You may have more side effects.
Tell your doctor if you are pregnant, planning to become pregnant, or breastfeeding.The benefits and risks for you and your child will need to be discussed.
Taking this drug during the third trimester of pregnancy may cause some health problems in the newborn. Consult your doctor.

Children:

Use with caution in children. Consult your doctor.
In some cases, the drug may affect the growth rate in children and adolescents. They may need to check their growth rate regularly.Consult your doctor.

What side effects should I report to my doctor immediately?

WARNING. In rare cases, some people with this drug can cause serious and sometimes deadly side effects. Call your healthcare professional or get medical attention right away if you have any of the following signs or symptoms, which may be associated with serious side effects:

Signs of an allergic reaction, such as rash, hives, itching, reddened and swollen skin with blisters or scaling, possibly associated with fever, wheezing or wheezing, tightness in the chest or throat, difficulty breathing, swallowing or speaking, unusual hoarseness, swelling in the mouth, face, lips, tongue, or throat.
Signs of low sodium levels such as headache, trouble concentrating, memory impairment, confusion, weakness, seizures, and balance problems.
Signs of bleeding such as vomiting or coughing up blood; vomiting of the type of coffee grounds; blood in the urine; black, red, or tarry stools; bleeding from the gums; non-cyclic vaginal bleeding; bruising that occurs or increases for no reason; bleeding that you cannot stop.
Pain or pressure in the chest.
Rapid, slow heartbeat, or irregular heartbeat.
Shortness of breath.
Dizziness or fainting.
Convulsions.
Unexplained weight fluctuations.
Sexual problems such as decreased sex drive or ejaculation problems.
Penile erection that lasts more than 4 hours.
Menstrual irregularities.
A serious and sometimes fatal complication called serotonin syndrome may occur.This risk may increase with the concomitant use of certain other drugs. Call your doctor right away if you develop agitation, imbalance, confusion, hallucinations, fever, tachycardia or irregular heartbeat, flushing, muscle twitching or stiffness, seizures, tremors or tremors, excessive sweating, severe diarrhea, nausea or vomiting , very severe headache.

What are some other side effects of this drug?

Any medicine can have side effects.However, many people have little or no side effects. Call your doctor or get medical help if these or any other side effects bother you or do not go away:

Nausea.
Sleepiness.
Dry mouth.
Lack of hunger.
Feeling tired or weak.
Diarrhea.
Constipation.
Sleep disorders.
Shivering.
Excessive sweating.
Yawning.
Signs of a cold.

This list of possible side effects is not exhaustive. If you have any questions about side effects, please contact your doctor. Talk to your doctor about side effects.

You can report side effects to the National Health Office.

You can report side effects to the FDA at 1-800-332-1088. You can also report side effects at https: // www.fda.gov/medwatch.

What is the best way to take this drug?

Use this drug as directed by your healthcare practitioner. Read all the information provided to you. Follow all instructions strictly.

All forms of issue:

Take this medication with or without food.
Continue taking this drug as directed by your doctor or other healthcare professional, even if you feel well.

Oral solution:

Doses of liquid preparation should be measured with caution. Use the dispenser that comes with the medicine. If a dispenser is not included in the package, ask your pharmacist for a dosing product for this drug.

What should I do if a dose of a drug is missed?

Take the missed dose as soon as you can.
If it’s time to take your next dose, do not take the missed dose and then return to your normal dose schedule.
Do not take 2 doses at the same time or an additional dose.

How do I store and / or discard this drug?

Store at room temperature.
Store in a dry place. Do not store in the bathroom.
Store all medicines in a safe place. Keep all medicines out of the reach of children and pets.
Dispose of unused or expired drugs.Do not empty into toilet or drain unless directed to do so. If you have any questions about the disposal of your medicinal products, consult your pharmacist. Your area may have drug recycling programs.

General information on medicinal products

If your health does not improve or even worsens, see your doctor.
You should not give your medicine to anyone and take other people’s medicines.
Some medicines may come with other patient information sheets. If you have questions about this drug, talk with your doctor, nurse, pharmacist, or other healthcare professional.
A separate patient instruction sheet is attached to the product. Please read this information carefully. Reread it every time you replenish your supply. If you have questions about this drug, talk with your doctor, pharmacist, or other healthcare professional.
If you think an overdose has occurred, call a Poison Control Center immediately or seek medical attention. Be prepared to tell or show which drug you took, how much and when it happened.

Use of information by consumer and limitation of liability

This information should not be used to make decisions about taking this or any other drug. Only the attending physician has the necessary knowledge and experience to make decisions about which drugs are appropriate for a particular patient.This information does not guarantee that the drug is safe, effective, or approved for the treatment of any disease or specific patient. Here are only brief general information about this drug. It does NOT contain all available information on the possible use of the drug with instructions for use, warnings, precautions, information about interactions, side effects and risks that may be associated with this drug. This information should not be construed as a treatment guide and does not replace information provided to you by your healthcare professional.Check with your doctor for complete information on the possible risks and benefits of taking this drug.

Copyright

History of salt | Healthy food manufacturer “Palitra of Tastes”

Salt History

Salt has been a constant companion of mankind since ancient times. It is reliably known that salt was present in the diet of the inhabitants of ancient Egypt, and it is also mentioned in the Chinese pharmaceutical treatise “Pen-Tsao-Kan-Mu”, which is about 4700 years old.According to archaeological data in India, already in the IV-III millennia BC, the inhabitants of the Indus Valley mined salt, the geographer Strabo writes about the salt mines in the Punjab mountains. Salt became an indispensable product that was on the table of the aristocracy and ordinary people, spreading geographically across Europe, Asia and Africa. Paradoxically, the inhabitants of pre-Columbian America did not know salt – they widely used red pepper in their cooking. In some historical periods, salt was very expensive – so much so that it acted as a monetary equivalent.The salt tax (invented by the rulers of ancient China and later spread in other states) has been a stable source of replenishment of the state treasury for centuries, but if extortions became an unnecessarily heavy burden, then the thirst for salt led to riots that went down in history as salt.

In France, during the reign of the Valois dynasty, the authorities went even further, obliging each subject, starting from the age of 8, to purchase at least 7 kilograms of salt annually at state prices.Simple arithmetic shows that eating this amount of salt was not easy, even considering the use of salt to prepare food for future use.

Salt production

Table salt, table salt, rock salt, table salt and even sodium chloride – all these are different names from childhood for the product we are accustomed to. Salt of marine origin usually contains impurities of various mineral salts, which can give the final product different color shades.Salt is divided into four grades, depending on the purity: extra, premium, first and second grade. Mankind knows several methods of salt extraction, however, on an industrial scale, it is mainly mine (or quarry) extraction of rock salt, as well as a method of evaporation of salt from brines, are used. The product obtained by evaporation is characterized by a high sodium chloride content, a low content of foreign impurities, and a fine-crystalline structure. Salt gets to our table, going through the processes of grinding and cleaning from impurities contained in it.

Effect of salt on human health

The World Health Organization recommends no more than 2000 mg of sodium per day, which corresponds to 5 grams or one teaspoon of salt in the diet of an adult. Salt is a food that loves moderation. Excessive consumption by people prone to hypertension can cause an increase in blood pressure, which can ultimately lead to the development of cardiovascular disease. Also, excessive saturation of the body with sodium promotes the leaching of calcium from the body, which can contribute to the development of osteoporosis in the long term.

Paradoxically, like many other foods, with all the “side effects”, salt is a necessary product for the body. The sodium in salt has an important effect on the regulation of body fluids. If a person does not consume enough salt, it can lead to dehydration. Indirect symptoms indicating a lack of sodium (acting as an electrolyte) may include headaches, weakness, and apathy. In addition, when there is a shortage of sodium in the body, the level of so-called “bad cholesterol” low density increases.Low sodium levels also increase the risk of death from heart failure. In addition, in people with type 2 diabetes, refusing salt can be fatal.

Iodized salt

Edible iodized salt is a type of edible table salt, the composition of which is enriched with iodide or potassium iodate. Manufacturers give preference to iodate as an element more resistant to temperature and humidity. Salt enriched with potassium iodate has a significantly longer shelf life.Salt, in the preparation of which iodide is used, needs additional stabilization with sodium thiosulfate.

The use of iodized salt contributes to the effective prevention of diseases caused by chronic iodine deficiency. At risk are at least 2 billion people living in areas experiencing persistent iodine deficiency. Switzerland became a pioneer in the spread of iodized salt – the population of a rich and prosperous alpine country suffered from a chronic lack of iodine.

In our country, the first scientific studies of the problem of iodine deficiency began at the end of the 20s of the last century, the founder of the direction was the outstanding surgeon-endocrinologist, specialist in the prevention of endemic goiter Oleg Vladimirovich Nikolaev. Dr. Nikolaev and his colleagues from Kabardino-Balkaria launched a program in 1933 that required the supply of iodized salt to the population of the region. For seven years of work, it was possible to reduce the prevalence of endemic goiter among the population of Kabardino-Balkaria from 69% to 0.9% !!! When consumed regularly, iodized salt helps to replenish the iodine deficiency in the body.The following symptoms can prevent a lack of iodine in the body: hair loss, stratification of nails, swelling of the face, dry skin, drowsiness, tearfulness, depressed mood. Lack of iodine can lead to more serious diseases – for example, an enlarged thyroid gland (endemic goiter). If people have lived for generations in a territory poor in such an important microelement as iodine, in the future such a shortage can lead to the development of childhood dementia. On the canvases of the Renaissance masters, a considerable number of people with signs of congenital dementia are depicted.Modern scientists believe that feeble-minded people from old paintings were mostly victims of iodine deficiency.

Legislative support for salt iodization

More than 113 countries of the world have adopted various laws aimed at the prevention of iodine deficiency using iodized salt. In these countries, iodized salt is actively produced by the food industry, enterprises prepare food with iodized salt, it is sold in stores, and the product is widely available to the population.

Some states have gone even further, making the production and sale of iodized salt mandatory at the legislative level. Among the CIS countries, mention should be made of Kazakhstan, where non-alternative salt iodization has been enshrined in the relevant law since 2002. Over the past years, the authorities of Kazakhstan have made significant progress in preventing iodine deficiency among the population.

In Russia, the situation with iodine depletion is depressing: the Endocrinological Research Center of the Ministry of Health provides data according to which, due to iodine deficiency in our country, more than 1.5 million adults and 650 thousand children annually need specialized endocrinological care.The deficit is largely due to the fact that no more than 30% of Russians consume iodized salt on an ongoing basis.

In 2019, at the initiative of the Ministry of Health of the Russian Federation, a draft law was developed, according to which Russia plans to switch to universal iodization of table salt and its use in products for the prevention of iodine deficiency diseases, Rossiyskaya Gazeta reports.

If the bill is supported, Russia will be able to solve the problem of iodine deficiency and the diseases caused by it.At the moment, their own health is in the hands of conscientious citizens, iodized salt is presented in large quantities in stores, and people who care about their health can choose the iodized product, and not ordinary table salt.

The Palitra company offers an innovative product food salt Valetek. The Valetek salt with a low sodium content contains useful trace elements – potassium, magnesium and iodine.

Potassium is responsible for maintaining the heart, nervous and muscular systems, removing excess fluid from the body.Magnesium – maintains vascular tone, contributes to the normal functioning of cells. Iodine – ensures the correct functioning of the thyroid gland, has a positive effect on the full mental development of children. Palette experts are convinced that salt should not only be tasty, but also healthy.

Salt for health!

Predmenstrual’nyy sindrom | Prilepskaya | Gynecology

Premenstrual syndrome (PMS) is a complex pathological symptom complex that occurs 2-10 days before the onset of menstruation and manifests itself in neuropsychic, vegetative-vascular and metabolic-endocrine disorders.PMS symptoms disappear in the first days or immediately after the end. In total, there are about 150 PMS symptoms that occur in different combinations, but the most characteristic are the following: increased fatigue, engorgement and tenderness of the mammary glands, bloating, nausea, sometimes vomiting, sleep disturbance and coordination, swelling of the limbs of varying severity, back pain and pelvic area, weight gain, itchy skin, pain in the heart, tachycardia. With PMS, headache, dizziness, constipation, and thirst can also occur.Often, patients complain of a change in taste, increased appetite, fever, chills, memory impairment, vision; there may be a craving for alcohol or sweets, etc. Irritability, tearfulness, depression, aggressiveness, indecision, forgetfulness, hypochondriacal thoughts, suspiciousness, increased exactingness towards others, isolation, unmotivated fear of “expected unhappiness”, a feeling of loneliness are often noted. bad mood or its rapid change, etc. The basis of the diagnosis of PMS is the cyclical nature of the appearance of pathological symptoms.Establishing a diagnosis is helped by keeping a diary during one menstrual cycle – a questionnaire in which all pathological symptoms are noted daily. The frequency of PMS varies widely and ranges from 25 to 90%. In 5-10% of women, PMS symptoms are pronounced. PMS affects women of childbearing age. This syndrome is observed during the ovulatory cycle, more often in women of mental labor living in cities (Yu.A. Komarova, 1987). Theories developed to explain the onset of PMS For many years, various researchers from different countries have made numerous attempts to clarify the etiological aspects and pathogenetic mechanisms of PMS.There are numerous theories that have been developed to explain the onset of PMS. However, none of them explains all the symptoms that can occur. The hormonal theory is the most prevalent. It is based on a violation of the ratio of estrogens and gestagens in favor of the former. Estrogens cause sodium and fluid retention in the intercellular space and lead to the development of edema (J.A. Johnson, 1970), which causes complaints of pasty extremities, engorgement and tenderness of the mammary glands, flatulence, headache.In addition, under the influence of estrogens, the secretion of angiotensinogen by the liver, a protein that is a precursor of angiotensin II, increases. High levels of agiotensin II increase the production of aldosterone (W.S. Peart, 1978), which in turn leads to fluid retention and edema. Estrogens stimulate the adrenal glomerular region, which also increases aldosterone secretion. Estrogens can accumulate in the limbic system and lead to the development of neuropsychiatric symptoms in PMS.The theory of water intoxication is based on a violation of water-salt metabolism. Water is the most abundant chemical compound in the world. The total water content in the human body is 55%. The body’s water is either extracellular or intracellular. Extracellular water is part of the blood, interstitial and transcellular fluid. Blood plasma consists of water (intravascular water about 90%), organic (9%) and inorganic (1%) substances. About 6% of all plasma substances are proteins.Circulating plasma water averages about 4% of body weight or 2–2.5 liters. The intercellular (interstitial) fluid averages 18% of the body weight, i.e. approximately 12 liters. Transcellular fluid (about 1.5% of body weight) is located in various spaces of the body: cerebrospinal fluid, synovial fluid (joints, tendons, etc.), gastric and intestinal juices, fluid of the capsule cavity of the glomerulus and kidney tubules (primary urine), fluid serous cavities (pleural, pericardium, abdominal, etc.)), moisture of the eye chambers. The water exchange regulation system has a complex structure (see figure). The function of the water exchange regulation system is closely related to the systems for the control of salt metabolism and osmotic pressure. The system of regulation of water exchange in the body includes the central, afferent and efferent links. The central link is the thirst center (water-regulating). Its neurons are found mainly in the anterior hypothalamus. This center is associated with areas of the cerebral cortex involved in the formation of feelings of thirst or water comfort.The afferent link of the system includes sensory nerve endings and nerve fibers from various organs and tissues of the body (oral mucosa, vascular bed, stomach, intestines and other tissues), distant receptors (mainly visual and auditory). Impulse from receptors of various types (chemo-, osmo-, baro-, thermoreceptors, possibly some others) goes to the neurons of the hypothalamus. The most important in this case are: an increase in the osmolarity of blood plasma, hypohydration of cells and an increase in the level of angiotensin II.Regular stimuli from the lust center neurons (nerve, humoral) are addressed to effector structures, which include the kidneys, sweat glands, intestines, and lungs. These organs to a greater extent (kidneys) or to a lesser extent (for example, lungs) ensure the elimination of deviations in the water content, as well as salt in the body. The antidiuretic hormone (ADH), the renin-angiotensin-aldosterone system, atrial natriuretic factor (atriopeptin), catecholamines, prostaglandins (PG) and mineralocorticoids (P.F. Litvitsky, 2002). In PMS, the effectiveness of this system is insufficient, as a result of which hyperhidria and edema develop. With PMS, hyperosmolar hyperhydration most often develops, characterized by increased osmolarity of the extracellular fluid, exceeding that in the cells. This is due to changes in the renin-angiotensin-aldosterone system that occur during PMS. The resulting hyperaldosteronism leads to excessive reabsorption of sodium and water in the kidneys and causes an increase in the volume and osmolarity of the extracellular fluid.The latter leads to hypohydration of cells (as a result of the release of fluid from them into the extracellular space along the gradient of osmotic pressure). Thus, with PMS, mixed dyshidria develops: extracellular overhydration and intracellular hypohydration. According to most authors, fluid retention in the body is one of the manifestations of an imbalance in the neuroendocrine system. Fluid retention in the 2nd phase of the menstrual cycle is also observed in the norm, and with premenstrual syndrome it is more pronounced.In the literature, there are many reports of premenstrual fluid retention in a woman’s body. The nature of the symptoms is determined by the interest of the tissues where edema develops (brain – headache, nausea, vomiting; intestines – bloating; joints – pain in the joints, in the spine, eyes – blurred vision, etc.). Discomfort, nausea, pain, and bloating are also common manifestations of local angioedema. The mammary gland increases by 100 ml during the menstrual cycle, starting from the moment of ovulation and reaching a maximum by the first day of menstruation.Before menstruation, there is an increase in blood flow, an increase in fluid content in the connective tissue, the development of interlobular edema, and expansion of the interlobular ducts. In addition, extracellular hyperhydration and intracellular hypohydration lead to hypervolemia, increased circulating blood volume (BCC), increased cardiac output, increased arterial and central venous pressure, cerebral edema, increased intracranial and intraocular pressure, cell hypoxia, headache, drowsiness, irritability, aggression, depression, insomnia, eating disorders, decreased libido and other neuropsychiatric disorders.In addition, severe thirst, which develops in connection with hyperosmolarity of blood plasma and hypohydration of cells, leading to additional water intake, aggravates the severity of the patient’s condition and can lead in severe cases to hyperosmolar syndrome (due to excess sodium and / or glucose). Supporters of hyperadrenocortical activity and an increase in aldosterone believe that in the 1st phase of the cycle, under the influence of estrogens, an increase in the level of renin and angiotensin II in the blood plasma occurs, which leads to an increased production and release of aldosterone.In the 2nd phase of the cycle, progesterone, unlike estrogens, does not increase the concentration of renin, but it can induce an increase in its activity, as a result of which the secretion of aldosterone and its release is further increased. Thus, with PMS, sodium is reabsorbed in the renal tubules, with the loss of potassium, calcium and the accumulation of fluid in the tissues (primary aldosteronism), and progesterone is an antagonist of aldosterone and, if it is insufficient, secondary hyperaldosteronism may develop.Supporters of this theory believe that it is hyperaldosteronism that can explain the mechanism for the development of many PMS symptoms. Hyperaldosteronism develops as a result of overproduction of aldosterone by the adrenal cortex. Hyperaldosteronism is characterized by the presence of edema, hypokalemia, hypernatremia, renovascular arterial hypertension, disorders of neuromuscular excitability, nephropathy, and visual disturbances. Arterial hypertension develops as a result of an increase in sodium in the blood plasma (hyperosmia), which causes a chain of the following phenomena: activation of osmoreceptors and stimulation of ADH in the posterior lobe of the pituitary gland, an increase in fluid reabsorption in the distal renal tubules, proportional to hyperosmia, an increase in BCC in a narrowed vascular bed, an increase in cardiac output ejection and increase in blood pressure.The mechanism of reduced vision is a violation of the blood supply to the retina. Impaired renal function is expressed in hypostenuria (due to low sodium content in the urine) and oliguria (due to increased sodium reabsorption), with severe symptoms, polyuria and nocturia may develop. As a result of hypernatremia, the sodium content in myocytes and nerve cells increases. Hypernatremia, hypokalemia, alkalosis leads to degenerative changes in cells and paresthesias, muscle weakness, convulsions.The development of PMS can also be associated with the presence of vitamin deficiency in the 2nd phase of the cycle. For example, vitamin B in the treatment of PMS has been used since 1940 by D.P. Rose (1978), after reviewing the rather controversial literature regarding the interaction of vitamin B6 and sex steroids, concluded that an excess of estrogen can lead to a lack of vitamin B6, both as a result of a violation of its redistribution in tissues, and as a result of stimulation of liver enzymes. which bind vitamin B6. Estrogen-induced deficiency of pyrodoxal phosphate (vitamin B6) leads to a decrease in the synthesis of serotonin from tryptophan, which is the cause of depression in both women using combined estrogen-progestogen contraceptives (COCs) and women with PMS.In addition, there are reports that a lack of pyridoxal phosphate can cause a decrease in the dopaminergic function of the hypothalamus and an increase in the level of prolactin in the blood. Treatment with vitamin B6 promotes increased dopamine secretion, decreased prolactin, and decreased or disappeared PMS symptoms. However, until now, the effectiveness of vitamin therapy is only an assumption, and the hypothesis about the role of vitamins in hormonal metabolism has yet to be proven. It is possible that with PMS there is a cyclic vitamin deficiency.According to doctors from the United States, premenstrual syndrome, which is expressed in a rapid change in mood, tension, dizziness, headaches and other symptoms, can be caused by a lack of magnesium and calcium in the body. It is possible that PMS is the first manifestation of calcium deficiency. Deficiency of unsaturated fatty acids in food, as well as deficiency of vitamins B6, A, magnesium, ascorbic acid and zinc, apparently plays an important role in the pathogenesis of PMS, since these factors cause deficiency of prostaglandin E1.Violation of the synthesis of prostaglandins in a woman’s organs (brain, mammary glands, gastrointestinal tract, kidneys, reproductive system) can contribute to the appearance of symptoms such as depression, irritability, nervousness, mastalgia, pain and bloating, fever, etc. a role in the pathogenesis of PMS is attributed to an increase in prolactin in the 2nd phase of the cycle. This increase may play a role in mental disorders and contributes to fluid retention in the body.It has been proven that estradiol affects the activity of neurons and the concentration of neurotransmitters in the brain. Even G.E. Abraham (1980) and E. Geller (1982) believed that it is estrogens that influence mood. They affect the activity of monoamine oxidase (MAO). This enzyme is involved in the oxidation of biogenic amines such as norepinephrine, epinephrine, serotonin, and dopamine. Epinephrine causes nausea, increased serotonin levels – nervous tension, insomnia, palpitations, impaired attention. Dopamine disrupts the balance of these 3 amines, causing mental disturbances.It is believed that there is an optimal level of serotonin and its change in the direction of increase or decrease leads to aggression or depression. The absorbed fluid is partially controlled by the renin-angiotensin system. When this system is activated, serotonin levels rise. In turn, he controls the renin-angiotensin system through feedback. There is also an allergic theory that PMS is the result of hypersensitivity to endogenous progesterone. In the literature, there is a report of a 23-year-old woman complaining of ulceration in the mouth and vulva during the premenstrual period; the author interpreted this as an allergic reaction to endogenous progesterone.An autoimmune progesterone-dependent dermatitis that occurs during the premenstrual period has also been described. The theory of psychosomatic disorders leading to the onset of PMS has a large number of supporters. At the same time, it is believed that somatic factors play a primary role, and mental ones follow biochemical changes resulting from changes in hormonal status. The large number of psychosomatic symptoms in PMS creates the need for further development of this hypothesis. S.L. Israel (1938) believed that cyclical changes in behavior in women with PMS are based on subconsciously expressed psychogenic causes. He suggested that the cause of neuroendocrine dysfunction is unresolved conflicts and hidden differences in marriage. Proponents of the psychosomatic theory report the effectiveness of psychotherapy, antidepressants and sedatives in the treatment of PMS. Some authors note the hereditary factor of the disease. Thus, there are a huge number of different theories explaining the development of premenstrual syndrome.However, none of these theories can be considered completely correct. Most likely, the etiology of PMS is multifactorial. Insufficiently studied pathogenesis and a variety of clinical manifestations of PMS have led to a variety of therapeutic agents in the treatment of this pathology, since clinicians recommend one or another type of therapy, based on their own interpretation of the pathogenesis of PMS. Treatment Pathogenetic therapy should combine measures aimed at the most pronounced manifestations of disorders in the hypothalamus.A rational treatment regimen includes: psychotherapy, balanced nutrition, exercise therapy, the use of tranquilizers, antidepressants, vitamins A, B, C and sex hormones. Physiotherapy is quite effective. Exercise relieves stress and increases the release of endorphins. Running, climbing stairs, bicycling, walking, or aerobics is great. In connection with absolute or relative hyperestrogenism, therapy with gestagens (norkolut, dyufaston, etc.) is indicated. Hormone therapy is not prescribed immediately, but after examination according to tests of functional diagnostics and is prescribed depending on the revealed changes.COCs are also used in the treatment of PMS. You can also use agonists of releasing hormones, whose action is based on an antiestrogenic effect (danazol, danoval, danol, etc., 200-400 mg per day). However, many patients do not tolerate adrenergic side effects and menopausal symptoms well. Due to the frequent increase in the level of serotonin and histamine, antihistamines are prescribed (tavegil, diazolin, suprastin, teralen, etc. at night) every day for 2 days before the deterioration of the condition, including the 1st day of menstruation.In order to improve blood supply and energy processes of the brain, the use of nootropil, aminolone is shown from the 1st day of the cycle for 2-3 weeks 2-3 cycles. With an increase in the level of prolactin, the drug of choice is bromocriptine (parlodel) in the 2nd phase of the cycle 2 days before the deterioration of the condition, within 8-10 days. Water exchange regulation scheme. (ANS – autonomic nervous system, PNS – atrial natriuretic factor, receptors – sensitive nerve endings, ADH – antidiuretic hormone, ACTH – adrenocorticotropic hormone) Given the increase in aldosterone levels in patients with edematous PMS, an aldosterone antagonist – verosh can be recommended as diuretics , the diuretic effect of which is moderately pronounced and manifests itself on the 2-5th day of treatment.Prescribe veroshpiron 4 days before the onset of PMS symptoms, 25 mg 2 times a day before the onset of menstruation. Other diuretics can also be used, such as: diacarb, which inhibits the enzyme carbonic anhydrase in the proximal convoluted tubule of the nephron, reduces the reabsorption of sodium and water, thereby reducing the concentration of sodium in the blood and its osmolarity, increases urinary excretion of sodium ions, has a diuretic effect … Considering that carbonic anhydrase is found in almost all organs and tissues, diacarb, inhibiting it, has a decongestant effect on the brain, reducing intracranial pressure, on the organs of vision, reducing intraocular pressure and improving vision.Diacarb normalizes water and electrolyte balance in PMS, relieves PMS symptoms such as headaches, pain in the lower abdomen and lumbar region, reduces tenderness and engorgement of the mammary glands, increases urine volume and relieves premenstrual epileptic readiness. It is prescribed at 250-500 mg in the 2nd phase of the cycle. Given that diacarb removes potassium from the body against the background of its use, it is necessary to follow a diet with limited salt intake and replenish the lack of potassium (potassium orotate).The maximum diuretic effect is achieved when the drug is taken every other day. Diuretic drugs are indicated for women with edema syndrome. Prescribe also drugs that reduce the synthesis of prostaglandins: naprosin 240 mg 2 times a day 2-3 days before the onset of menstruation, diclofenac ketoprofen (ketonal), piroxicam, rapten rapid 1 tablet 3 times a day. Inhibitors, prostaglandin synthetases, are considered the drugs of choice for women in the treatment of PMS with pain. Prostaglandin synthetase inhibitors lower the level of prostaglandins in the blood and relieve many of the symptoms of PMS.Antiprostaglandin drugs are rapidly absorbed and act within 2-6 hours, have an analgesic effect. Most of them need to be taken 1-4 times a day during the 2nd phase of the cycle. The course of treatment usually lasts 3 menstrual cycles. The effect of non-steroidal anti-inflammatory drugs, as a rule, persists for 2-4 months after their withdrawal, then the symptoms return, but are less intense. In our practice, we widely use Rapten Rapid in patients with PMS.Rapten Rapid is the potassium salt of Diclofenac. Diclofenac potassium is a derivative of phenylacetic acid, belongs to non-steroidal anti-inflammatory drugs and has been used since 1983. Rapten Rapid has a pronounced anti-inflammatory, analgesic and antipyretic effect. After the introduction of diclofenac, only the active substance, diclofenac, enters the bloodstream, potassium cations remain in the gastrointestinal tract and are excreted in the feces. Rapten Rapid is rapidly absorbed and takes effect within 30 minutes.This drug is excreted from the body mainly in the urine in free and conjugated form; 30–35% of the administered dose is excreted in the bile. The main mechanism of action of rapten rapid is the inhibitory effect on cyclooxygenase, which promotes the conversion of arachidonic acid to prostaglandin. In addition, by reducing the release of inflammatory mediators from granulocytes, basophilic cells and mast cells, this drug inhibits the inflammation process, lowers the sensitivity of blood vessels to bradykinin and histamine, inhibits prothrombin synthesis and platelet aggregation.With emotional lability from the 10th day of the menstrual cycle, psychotropic drugs can be prescribed: neuroleptics (sonopax) and tranquilizers (seduxen, rudotel). Also effective are antidepressants (serotonin reuptake inhibitors) – sertraline, zoloft, Prozac, etc., which are prescribed daily for 3-6 menstrual cycles in a continuous mode. Vitamin therapy is used to treat PMS. Vitamins A and E are used every other day – 15 injections of vitamin E and 15 injections of vitamin A. Prescription of the drug “Magne B6” may be effective, especially when anxiety and depressive conditions increase in the 2nd phase of the cycle.Herbal medicine can be successfully used in the treatment of PMS. As it turned out, the “Abraham tree” (Agnucaston) acts on the dopamine receptors of the hypothalamus. In the hypothalamic-pituitary system, these receptors are located on lactotrophic cells. The activation of these receptors by dopamine leads to a decrease in the release of prolactin. A decrease in prolactin content causes regression of pathological processes in the mammary glands and relieves cyclical pain syndrome. PMS treatment is carried out after the diagnosis is established in cycles: 3-6 months reception, 3-6 months break.In the first cycle, vitamin therapy, diet therapy, etc. are prescribed. In the 2nd and 3rd cycles, diuretics, drugs acting on the central nervous system, hormones, and prolactin inhibitors are prescribed. Treatment, as well as psychotherapeutic effects, as a rule, gives a positive result. If PMS symptoms recur after a few months, treatment can be repeated. Thus, premenstrual syndrome is a fairly common disease, the etiology and pathogenesis of which are not well understood. Because of this, there is no single drug that is effective for all symptoms at the same time.One thing is certain: the difference between the state before and after treatment is the difference between a woman whose symptoms of the disease do not allow her to lead a normal life, and a woman who has a short-term onset of symptoms that do not require treatment with medication.

Kira E.F., Beskrovny S.V., Skryabin O.N. Progestogel in the treatment of premenstrual syndrome. Journal of Obstetrics and Women’s Diseases.2000; 3: 59–61,
Komarova Yu.I. Dis .. Cand. honey. nauk, 1986.
Mayorov M.V. Premenstrual syndrome: riddles of pathogenesis, problems of therapy. Pharmacist, 2001; 13.
Smetnik V.P., Tumilovich L.G. Non-operative gynecology St. Petersburg: SOTIS, 1995; 129–38.
Frank, R. T .: The hormonal causes of premenstrual tension. Arch. Neurol. Psychiatry 26: 1053, 1931.
Robert L.Reid, S.S.C. Yen., American. J. Obstet. Gynecol. 1981; 139: 85.
WPA Depression Bulletin, Sex Hormones and Mood Disorders in Women, 2002.
Ann F. Walker et all. Magnesium Supplementation Alleviates Premenstrual Symptoms of Fluid Retention. Journal of women, s health., 1998; 7 (9): 1157–65.
Taylor R.W. Clin. Endokr. 1981; 14: 1-9.
Andersch B, Hahn L. Progesterone treatment of premenstrual tension: A double blind study.J Psychosom Res 29: 489, 1985.
Dalton K: The Premenstrual Syndrome and Progesterone Therapy. Chicago, Year Book Medical Publishers, 1977.
Dalton K: Similarity of symptomatology of premenstrual syndrome and of toxaemia of pregnancy and their response to progesterone. Br Med J 2: 1071, 1964.
Dalton, K .: The influence of menstruation on health and disease, Proc. R. Soc. Med. 57:18, 1964.
Dalton, K.: Menstruation and crime, Br. Med.J. 2: 1752, 1961.
Dalton, K .: Effect of menstruation on schoolgirls weekly work, Br. Med.J. 1: 326, 1960.
Parker, A. S .: The premenstrual tension syndrome, Med. Clin. North Am. 44: 339, 1960.

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Influence on the ability to drive and use mechanisms

The drug may cause drowsiness, dizziness, especially at the beginning of treatment.It is unacceptable to drive or operate machinery if it affects you negatively.

Important information about the ingredients of Amitriptyline tablets

If you have been informed that you have an intolerance to some sugars, consult your doctor before taking this medicine.

How to take Amitriptyline

Amitriptyline should be taken exactly as directed by your doctor. If you have any doubts, you should consult with your healthcare professional or pharmacist.

Not all dosing regimens are possible with different dosage forms and doses of the drug.

The appropriate form of release and the dose of the drug should be chosen for the starting 3 and subsequent increasing doses.

Depression

Adults :

The recommended starting dose is 25 mg twice daily. Depending on the clinical effect, the dose can be increased up to 150 mg / day, divided into two doses.

Elderly patients (over 65 years old) and patients with cardiovascular diseases

The recommended starting dose is 10-25 mg per day. Depending on the clinical effect, the dose can be increased to 100 mg / day, divided into two doses. If you are taking between 100 mg and 150 mg of the drug, you may need to consult your doctor more often.

Use in children and adolescents

Amitriptyline is not recommended for use in children and adolescents for the treatment of depression.For more information see section 2.

Neuropathic pain, chronic headaches Tension type and prevention of migraine

Your healthcare provider will select the correct dose for your symptoms and your body’s response to treatment.

Adults :

The recommended starting dose is 10-25 mg in the evening.

The recommended daily dose is 25-75 mg.

Depending on the clinical effect, the dose may be gradually increased. If you are taking more than 100mg / day, you may need to consult your doctor more often. Take the drug once a day or divide the dose into two doses, your doctor will tell you.

Elderly patients (over 65 years old) and patients with cardiovascular diseases

The recommended starting dose is 10-25 mg in the evening.

Depending on the clinical effect of the drug, the dose may be gradually increased.

If you are taking more than 75mg / day, you may need to consult your doctor more often.

Use in children and adolescents

Amitriptyline is not recommended for children and adolescents for the treatment of neuropathic pain, chronic tension-type headache and for the prevention of migraine.For more information, see the section What you need to know before using Amitriptyline.

Bedwetting

Use in children and adolescents

Recommended dose for children:

Children under 6 years of age: See section “Do not take Amitriptyline tablets”
Children 6 to 10 years of age: 10-20 mg daily. In this age group, the appropriate release forms are used.
Children 11 years and older: 25-50 mg.

The dose should be increased gradually.

The drug should be taken 1 or an hour and a half before bedtime.

Before starting treatment, your healthcare provider should perform an ECG to check for signs of an irregular heartbeat.

Your doctor will re-evaluate the condition of the body after 3 months of treatment and, if necessary, perform a second ECG.

Do not stop taking this medicine without consulting your doctor.

Special patient groups

Patients with liver disease or known as “slow metabolizers” are usually given lower doses.

Your healthcare professional may have blood samples to measure amitriptyline levels (see the Things to Know Before You Use Amitriptyline).

How and when to take Amitriptyline

The drug should be taken during or after meals.

The tablets should be swallowed whole with water. Do not chew tablets.

Treatment period

Do not change the dose of the drug or stop taking the drug without consulting a doctor.

Depression

As with other drugs used to treat depression, this too may take several weeks before you feel any improvement in your condition.

In the treatment of depression, the duration of treatment is individual and is usually at least 6 months. The duration of treatment is determined by your attending physician.

Continue taking Amitriptyline for as long as prescribed by your doctor. The disease can persist for a long time. If you stop treatment too early, your symptoms may recur.

Neuropathic pain, chronic headaches Tension type and prevention of migraine

It may take several weeks for your condition to improve.

Consult your doctor about the duration of treatment and continue taking the drug until the doctor stops it.

Bedwetting

Your attending physician will determine the need to continue treatment after 3 months of taking the drug.

If you took more Amitriptyline than recommended

If you have taken more amitriptyline than prescribed by your doctor, you should immediately contact your doctor or the nearest hospital emergency room, even if you do not have any discomfort or symptoms of poisoning.Bring the package of the medicine with you if you go to the doctor or hospital.

Overdose symptoms include:

pupil dilation
fast or irregular heartbeat
Difficulty urinating
dry mouth or tongue
intestinal obstruction
seizures
fever
Anxiety
confusion
hallucinations
involuntary movements
lowering of blood pressure, weak pulse, pallor
difficulty breathing
cyanosis of the skin
decrease in heart rate
sleepiness
loss of consciousness
coma
Various heart diseases such as heart block, heart failure, hypotension, cardiogenic shock, metabolic acidosis, hypokalemia.

If you forget to take Amitriptyline

Take the next dose at the usual time. Do not take a double dose of the drug to compensate for the missed dose.

If you stop taking Amitriptyline

Your healthcare professional will decide when and how to stop treatment to avoid any unwanted symptoms that may occur if the drug is suddenly discontinued (for example, headache, feeling unwell, insomnia, and irritability).

If you have any further questions on the use of this medicine, ask your doctor or pharmacist.

City Clinical Hospital. F.I. Inozemtseva

The adrenal glands are a paired organ, on the right and left they are located above the kidneys,
lie in the retroperitoneal tissue. The right adrenal gland is triangular in shape, located
above the upper pole of the right kidney, directly adjacent to the inferior vena cava.
The left adrenal gland has a lunate shape, located partially above the upper
pole of the left kidney, in contact with the pancreas, spleen,
the cardiac part of the stomach.The adrenal glands are supplied with a large amount
arteries. Venous blood flows through the central adrenal vein (on the right it flows directly into the lower
vena cava, on the left – into the left renal vein).

Hormones
adrenal glands

In the adrenal medulla
generated:

Adrenaline – important
hormone in the fight against stress. Activation of this hormone and its production
increases both with positive emotions and stress, trauma. Under
the influence of adrenaline can enlarge and dilate the pupils, breathing
becomes more frequent, blood pressure rises, hot flush is felt
forces.Increases resistance to pain
sensations.
Norepinephrine – hormone
stress, which is considered the precursor to adrenaline. Renders less
effect on the body, is involved in the regulation of blood pressure, which
allows you to stimulate the work of the heart muscle

Adrenal cortex
produces hormones of the corticosteroid class, which are divided into three layers:
glomerular, bundle, reticular zone. Hormones
glomerular zone produce:

Aldosterone – hormone
responsible for the exchange of potassium and sodium ions in human blood.Participates in water-salt metabolism,
helps to increase blood circulation, increases blood pressure
Corticosterone –
inactive hormone, participates in the water-salt balance
Deoxycorticosterone
– a hormone that increases resistance in the human body, gives strength to the muscles
and the skeleton, also regulates the water-salt balance

Hormones of the adrenal bundle zone:

Cortisol is a hormone
preserving the body’s energy resources, participates in carbohydrate metabolism.Cortisol levels often fluctuate, so in the morning it is much higher than
in the evening
Corticosterone – (see.
above) is also produced by the bundle zone

Hormones of the reticular zone:

Androgens – sex
hormones that affect sexual characteristics: libido, increase in muscle
mass and strength, body fat, lipids and cholesterol levels in the blood

Based on
of the above – adrenal hormones perform an important function in the body
a person, their excess or deficiency can lead to disruption throughout the body.

Diseases of the adrenal glands can be divided into pathology forms – tumors, cysts and functions – aldosteroma, corticosteroma, pheochromocytoma, androsteroma, estroma. To help diagnose diseases of the adrenal glands or to identify violations in their functionality, you can use a series of examinations that the doctor prescribes after the collected history. To make a diagnosis, the doctor determines the hormones of the adrenal glands, which makes it possible to identify an excess or deficiency of the latter. In adrenal tumors, the main screening diagnostic method is ultrasound, but a more accurate picture is given by CT or MRI of the abdominal and retroperitoneal organs.The results of the examination allow us to draw up a complete picture of the disease, determine the cause, identify certain disorders in the work of the adrenal glands and other organs and, accordingly, prescribe treatment, which can be carried out both by a conservative method and by surgery

Adrenal diseases:

Itsenko’s syndrome- Cushing’s is a pathological symptom complex resulting from an increased release of the hormone cortisol from the adrenal cortex by the tumor.The production of cortisol and corticosterone is regulated by the pituitary gland by the production of adrenocorticotropic hormone. The activity of the pituitary gland is controlled by the hormones of the hypothalamus – statins and liberins. This multi-stage regulation is necessary to ensure the coherence of body functions and metabolic processes, a violation of one of the links can cause hypersecretion of adrenal cortex hormones, which will lead to the development of Itsenko-Cushing’s syndrome. Unlike Itsenko-Cushing’s disease, the syndrome is manifested by a primary increase in hyperfunction of the adrenal cortex, while in Insenko-Cushing’s disease, ACTH-producing pituitary adenoma is the basis.In 20% of cases, the cause of Itsenko-Cushing’s syndrome is a tumor of their adrenal cortex. The most characteristic symptom of the syndrome is obesity according to the cushingoid type (fatty deposits on the face, neck, chest, abdomen, back with relatively thin limbs), the face becomes reddish-purple, muscle atrophy, and a decrease in muscle tone and strength are observed. Diagnostics: determination of the excretion of cortisol in daily urine, determination of cortisol in the blood, determination of ACTH in the blood, conduct a small dexamethasone test (normally taking dexamethasone reduces the level of cortisol, with Itsenko-Kushching syndrome, there is no decrease), CT or MRI of the abdominal organs is performed.If there is a neoplasm in the adrenal gland, surgical treatment is performed. Symptomatic treatment for Itsenko-Cushing’s syndrome includes the use of antihypertensive, diuretic, hypoglycemic drugs, cardiac glycosides. With Itsenko-Cushing’s disease, surgical treatment of pituitary adenoma is performed.

Conn’s syndrome (primary hyperaldosteronism, aldosteroma) is a symptom complex due to the greater production of aldosterone by the adrenal cortex. The cause is most often a tumor of the adrenal gland, less often – hyperplasia of the glomerular zone of the cortex.In patients, the amount of potassium decreases and the concentration of sodium in the blood increases, because of this, blood pressure rises.

The syndrome was first described by a scientist from America by Horse in 1955, which is why it got its name.

Symptoms:
weakness, fatigue, tachycardia, convulsions, headache, thirst, paresthesia
limbs, increased blood pressure.

Connes Syndrome
accompanied by signs of damage to the heart and blood vessels, kidneys, muscle tissue.Arterial hypertension is malignant and resistant to hypotensive
therapy.

Diagnostics:
a study of blood electrolytes (high sodium, low potassium in the blood),
increase in the level of aldosterone in plasma, calculation of daily urine output, determination
the level of renin in the blood, the ratio of the activity of plasma aldosterone and renin,
determination of the level of aldosterone in daily urine, CT or MRI of the abdominal organs
– determination of neoplasms in the adrenal glands.

Medical
measures are aimed at correcting high blood pressure,
metabolic disorders, as well as to prevent possible complications,
due to high blood pressure and a decrease in potassium in the blood.Conservative therapy is not radically capable of improving the condition of patients,
complete recovery occurs only after surgical removal of the tumor.

Pheochromocytoma is a hormonally active tumor that actively secretes adrenaline and norepinephrine. Pheochromocytoma leads to the release of adrenaline or norepinephrine into the bloodstream, which leads to the development of specific disorders in patients – a persistent crisis increase in blood pressure (sometimes more than 200/100 mm Hg), not amenable to antihypertensive therapy, palpitations.Most often, pheochromocytoma is a tumor of the adrenal gland. Diagnostics is based on radiation and hormonal research methods. Radiation diagnostics: CT or MRI of the abdominal and retroperitoneal organs. Hormones: determination of the level of chromogranin A, ACTH, aldosterone, renin, blood cortisol, determination of metanephrines, normetanephrines in daily urine. The presence of formation in the adrenal gland, an increase in the level of metanephrines and normetanephrines in daily urine allows suspecting a pheochromocytoma.The main method of treatment for pheochromocytoma is adrenalectomy with a tumor. Special attention is paid to the preparation for the operation – the tasks of the preoperative preparation of patients with pheochromocytoma are to normalize the blood pressure level, eliminate its dangerous fluctuations during the day, and slow down the heart rate. Doxazosin (Cardura) is used as the main drug used to prepare for surgery. The drug is prescribed at least 2 weeks before the planned operation. The method of access for surgical treatment depends on the size of the tumor, its location, hormonal activity

Estroma is a tumor of the adrenal cortex that produces a large number of female sex hormones – estrogens.As a rule, these tumors are malignant. Estromas are very rare, clinically they are manifested in males by impotence, bilateral gynecomastia, fenimization of the physique, and sometimes testicular hypotrophy. In most patients, along with feminization, there are signs of hypersecretion of gluco- and mineralocorticoids. Therefore, the diagnosis consists in examining specific hormones in the blood, performing CT or MRI of the abdominal organs. Surgical treatment – removal of the adrenal tumor.

Androsteroma is a hormonally active tumor of the adrenal gland that produces male sex hormones in large quantities.The picture of the disease in women is characterized by a disorder of the menstrual cycle (amenorrhea or oligomenorrhea), hypertrophy of the clitoris, hair growth of the face and body, masculinization of the figure, coarsening of the voice, and sometimes male-pattern baldness. In some patients, hypertension and disorders of carbohydrate metabolism in the form of hyperglycemia and a moderate increase in sugar in the urine may be observed. In men, androsteromas are extremely rare and do not show any external signs, therefore, they are diagnosed at a late stage of the disease.Diagnostics consists in performing CT scan of the abdominal organs or MRI of the abdominal organs, the content of a high titer of androgens and their metabolites in daily urine. Treatment – removal of the adrenal gland tumor

Hormonally inactive adrenal tumor – adrenal gland formation, most often of a benign nature, not producing high amounts of hormones. These adrenal tumors can be of various sizes. Patients with hormonally inactive formations in the adrenal gland less than 3 cm are shown observation, study of hormones in dynamics.When tumors are more than 3 cm in size, or when the tumor grows more than 1 cm per year, surgical treatment is indicated. Diagnostics includes hormonal and biochemical blood and urine tests, CT or MRI of the abdominal organs.

Surgical treatment of diseases of the adrenal glands:

Currently, operations on the adrenal glands can be
made by traditional “open” access, or using
high-tech methods (endoscopic operations). Standard Access
for adrenalectomy, lumbotomy or
laparotomy – enough
traumatic and time consuming interventions.Such
accesses as transphrenic, subphrenic, transthoracic. Endocrine Surgery Center widely uses
endoscopic techniques in adrenal surgery, which can be both laparoscopic,
and extraperitoneal access.

Can low sodium cause headaches: Can your sodium level be too low?

Can your sodium level be too low?

What causes low blood sodium levels?

Symptoms of low blood sodium

How to treat low blood sodium levels

About The Team

Heart Care Team

Hyponatremia – Symptoms and causes

Overview

Products & Services

Symptoms

When to see a doctor

Causes

Risk factors

Complications

Prevention

Low sodium levels (hyponatremia): Symptoms and causes

Restoring blood sodium levels

Treating the underlying cause

Low sodium levels (hyponatremia): Symptoms and causes

Restoring blood sodium levels

Treating the underlying cause

Low sodium levels (hyponatremia): Symptoms and causes

Restoring blood sodium levels

Treating the underlying cause

Low sodium levels (hyponatremia): Symptoms and causes

Restoring blood sodium levels

Treating the underlying cause

Results From the Trial of Nonpharmacologic Interventions in the Elderly

Abstract

METHODS

Variables

Statistical Analyses

RESULTS

TABLE 1—

Urinary Sodium Excretion and Headache Occurrence

Observational Analyses and Dose–Response Relationship

TABLE 2—

DISCUSSION

Strengths and Limitations

Conclusions

ACKNOWLEDGMENTS

HUMAN PARTICIPANT PROTECTION

REFERENCES

Sodium level in dialysate for chronic hemodialysis

Hypertension

What are the risk factors for hypertension?

What are the typical symptoms of hypertension?

What are the complications of uncontrolled hypertension?

Why is hypertension a problem in low- and middle-income countries?

How can the burden of hypertension be reduced?

Prevention

Control hypertension

How is WHO responding to the problem of hypertension?

Memorial Sloan Kettering Cancer Center

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City Clinical Hospital. F.I. Inozemtseva

Hormones adrenal glands

Adrenal diseases:

Surgical treatment of diseases of the adrenal glands:

Hormones
adrenal glands