Hypercalcemia. Symptoms, causes, diagnosis and treatment. Hypercalciuria - what is it, causes, symptoms, treatment Use if thrombosis hypercalcemia is present

Everyone knows that calcium is necessary for the body for the strength of bones, teeth, and normal muscle function, and its deficiency leads to serious consequences. But an excess of this trace element in the blood is harmful to the body, a person begins to feel bad, internal organs suffer from an imbalance.

Hypercalcemia can occur not only due to excessive calcium intake, but also due to various disorders in the functioning of internal organs. Most often, the pathology is associated with another serious disease, so hypercalcemia requires mandatory treatment under the supervision of an experienced specialist. Otherwise, the condition provokes serious complications.

Prevention

It is impossible to prevent hereditary diseases that provoke hypercalcemia. Since at the moment there are no research methods that would reveal pathology even in the womb. But, if there are people with a gene mutation in the family, then the probability of transmitting the pathology to the child is high.

It is quite possible to prevent hypercalcemia associated with malnutrition, gastrointestinal problems, immobilization, and even tumors by observing the following recommendations.

It is necessary to lead a healthy and active lifestyle, eat right, do exercises, do not drink alcohol and drugs. A healthy lifestyle is the prevention of many diseases, so you can reduce the risk of tumors in the body, prevent disorders in the digestive tract.
If there were relatives in the family who suffered from malignant diseases, a person needs to be attentive to his health and undergo regular examinations. The sooner the pathology is detected, the less negative consequences will occur.
If the patient is immobilized for a long time due to injury, it is necessary to start rehabilitation with active actions as soon as possible. As soon as the doctor gives the go-ahead for physiotherapy exercises, the patient should not be lazy, exercise therapy should be taken responsibly, this will help prevent a number of diseases, including muscle atrophy, hypercalcemia due to bone destruction, vein or arterial thrombosis in the immobilized area.
It is impossible to take vitamin D and calcium without indications and give these drugs to a child. If it seems to the patient that he needs to take vitamins, you must first visit a doctor and take tests, and only then, if the specialist prescribes, start taking them.
It is very important to monitor your diet, everything should be in moderation. Do not abuse products with calcium, drink too much milk, especially with stomach problems.

Definitely, it is simply impossible to predict everything in the world, so it is recommended to simply lead a healthy lifestyle and visit specialists on time, not to take medication without a doctor's prescription. Proper attitude to your health will help to avoid many problems.

About the disease (video)

Hypercalcemia is a medical term used to refer to a person's condition in which the level of free calcium in the blood is elevated. There are a lot of reasons for such a pathological condition, there are even characteristic symptoms for hypercalcemia.

Classification

In medicine, it is customary to distinguish three degrees of hypercalcemia:

light- indications of the level of free calcium in the blood will not exceed 2 mmol / l, and total calcium - 3 mmol / l;
medium severity- total calcium is within 3 - 3.5 mmol / l, free - 2 - 2.5 mmol / l;
heavy- the level of free calcium is 2.5 mmol / l and above, the total - 3.5 mmol / l and above.

Why does hypercalcemia syndrome occur?

Most often, namely in 9 out of 10 cases of diagnosing the pathology in question, the causes of the development of hypercalcemia syndrome are either an oncological process in the body, or pathologies of the parathyroid glands. These pathologies lead to the "resorption" of bone tissue (bone resorption), which is accompanied by the release of calcium ions into the blood. Hypercalcemia syndrome may be present in the following cancers:

kidney tumors;
neoplasms in the lungs;
blood diseases (multiple myeloma,);
prostate cancer;
colon cancer.

Doctors identify several other factors that can be considered the cause of the development of the condition in question:

hypervitaminosis D;
Paget's disease;
familial hypocalciuric hypercalcemia;
prolonged immobilization;
thyrotoxicosis;
Jansen's metaphyseal chondrodysplasia;
increased absorption of calcium in the small intestine with a simultaneous decrease in its excretion by urine;
congenital lactase deficiency;
long-term use of lithium preparations;
acute or chronic adrenal insufficiency;
long-term use of theophylline and thiazide diuretics.

Causes of hypercalcemia

The level of calcium in the blood is a constant value in our body. High levels have a negative effect on the tubules of the kidneys, which leads to a decrease in the ability of these organs to concentrate urine. The result is the release of a large amount of urine, and the consequence of this whole complex of problems is a large increase in the level of calcium in the blood.

Moderate hypercalcemia provokes an increase in the contractility of the heart muscle, and an increased amount of calcium in the blood reduces contractility. Excess calcium leads to the development of arrhythmia, a confident increase in blood pressure. The most serious consequence of high calcium levels in the blood is sudden cardiac death, or cardiac arrest. Fortunately, this condition is extremely rare.

A high level of calcium in the blood also negatively affects the functioning of the central nervous system. At the beginning of the pathological process, a person will feel only increased fatigue, weakness, unmotivated irritability, slight lethargy and unobtrusive. But as the hypercalcemia syndrome progresses, these symptoms become more pronounced, which can lead to disorientation of the patient in time / space and coma.

Note: one must be able to distinguish the pathology in question from pseudohypercalcemia. This "false" state is characterized by an increase in the level of albumin in the blood, which causes an increase in the level of total calcium. Often, such a violation occurs with the progression of multiple myeloma, or against the background. It is easy to distinguish between these two conditions: with real hypercalcemia, the level of free calcium in the blood will be significantly increased, but in the second case it remains within the normal range.

Symptoms of hypercalcemia syndrome

If the disease in question is mild, then there will be no pronounced clinical manifestations. If the increase in the level of calcium in the blood proceeds to a moderate or severe degree, then the patient will notice the following symptoms:

general weakness;
light;
lethargy;
hallucinations;
disorientation in space and environment;
impaired consciousness (up to coma).

With a high level of calcium in the blood, clear symptoms from the cardiovascular system will also be determined:

confident;
sudden cardiac arrest.

With a pathological lesion of the organs of the urinary system, an increase in the volume of urine excreted will be noted, and with a neglected pathology, on the contrary, a decrease in volume.

Symptoms of damage to the digestive system in hypercalcemia syndrome:

stool disorders (predominantly present);
loss of appetite, up to a complete refusal of food;
pain in the epigastric region, girdle character, occurring immediately after eating.

In the case of a prolonged course of hypercalcemia, the patient may experience calcification of the structures of the kidneys, calcium will be deposited in the cells of blood vessels, skin, lungs, heart and stomach.

Note:most often, patients come to the doctor with complaints of pain in the joints and bones. It is in this case that specialists conduct examinations and detect hypercalcemia.

The most dangerous condition develops during a hypercalicemic crisis. It is characterized by nausea and persistent/uncontrolled vomiting, severe pain in the abdomen, convulsions, and a sudden increase in body temperature. The consciousness of the patient in this case will be confused, which ends in stupor and coma. Unfortunately, in most cases, it is impossible to save a patient with the rapid development of a hypercalcemic crisis.

Diagnostic measures

Diagnosis is not only to specifically identify the disease in question - it is important to find out the cause that led to such a violation. A doctor can suspect hypercalcemia syndrome based on the patient's complaints and comparing them with the presence of a history of cancer. But even these data do not allow making a diagnosis, the patient must undergo a full examination. As a rule, experts recommend taking blood tests to determine the level of total calcium (the study is carried out twice) and to determine the level of free calcium.

In order for the results of the examination to be as reliable as possible, the patient must follow certain rules:

Do not drink alcoholic beverages the day before the scheduled examination.
30 hours before the scheduled examination, avoid heavy physical exertion.
Three days before the test, foods high in calcium are excluded from the diet, as this can “lubricate” the results.
For 8 hours, the patient must completely refuse to eat.

If blood tests for the level of total and free calcium revealed that the indicators are too high, then the doctor will have to find out the true cause of such a pathology. For this, the patient will be assigned an additional examination:

urine analysis to determine the amount of calcium excreted with it;
blood test for the presence of indicators of bone metabolism;
urine analysis to detect or confirm the absence of Bens-Jones protein in it;
a blood test for the level of PTH and PTH-like peptides;
with an emphasis on renal tests.

If the hypercalcemia syndrome is associated with oncological pathology, then the patient will have a low level of phosphate in the blood, an increased level of PTH-like peptides, but in the urine a normal or slightly higher level of calcium in the urine will be detected.

If the syndrome in question is associated with multiple myeloma, then Bence-Jones protein will be detected in the urine, and a high level of ESR and a normal level of phosphates will be detected in the blood.

When carrying out diagnostic measures, instrumental methods can also be used:

kidneys;
bone radiography;
densitometry (allows you to diagnose osteoporosis).

Treatment of hypercalcemia

Severe hypercalcemia requires immediate qualified medical care.

Urgent care

If the doctor "sees" a severe degree of the condition under consideration, then the patient is placed in a hospital and a number of intensive care measures are carried out:

Note:the result of the introduction of furosemide may be a decrease in the level of potassium and magnesium in the blood, so the doctor must constantly monitor the content of these trace elements.

with or renal failure, infusion therapy is categorically contraindicated, therefore, patients are prescribed peritoneal dialysis or hemodialysis;
intravenous administration of bisphosphonates - drugs that reduce the level of calcium in the blood;
administration of calcitonin by intramuscular, intravenous or subcutaneous route.

Treatment of mild to moderate hypercalcemia

When the serious condition of the patient is stopped, therapeutic measures do not stop - they continue, but in a different volume. The patient is assigned:

pamidronic acid intravenously drip 1 time in a month and a half for 2-5 years;
calcitonin - daily, by subcutaneous or intramuscular injection;
glucocorticosteroids - for example, prednisolone;
mitomycin is an antitumor drug that is prescribed only if hypercalcemia is present against the background of an oncological disease;
gallium nitrate - administered intravenously, helps to reduce the rate of release of calcium from the bones.

If the patient has been diagnosed with asymptomatic or mild hypercalcemia, then infusion therapy is not carried out, but bisphosphonates are prescribed orally.

Hypercalcemia syndrome is a condition that poses a certain danger to human health and even life. Doctors do not give any specific predictions to such patients - it all depends on what underlying disease is taking place. In some cases, to normalize the level of calcium in the blood, it is enough to stop the medication, in many cases the condition in question requires lifelong medication to correct the level of calcium in the blood.

Hypercalcemia is a total plasma calcium concentration of more than 10.4 mg/dL (> 2.60 mmol/L) or a plasma ionized calcium level of more than 5.2 mg/dL (> 1.30 mmol/L). The main causes include hyperparathyroidism, vitamin D toxicity, and cancer. Clinical manifestations include polyuria, constipation, muscle weakness, impaired consciousness, coma. Diagnosis is based on determining the level of ionized calcium in plasma and the level of parathyroid hormone. Treatment of hypercalcemia is aimed at increasing calcium excretion and reducing bone resorption and includes the use of saline, sodium diuresis and drugs such as pamidronate.

ICD-10 code

E83.5 Disorders of calcium metabolism

Causes of hypercalcemia

Hypercalcemia usually develops as a result of excessive bone resorption.

Primary hyperparathyroidism is a generalized disorder resulting from excessive secretion of parathyroid hormone (PTH) by one or more parathyroid glands. Probably the most common cause of hypercalcemia. The frequency increases with age and is higher in postmenopausal women. It is also observed with a high frequency in 3 or more decades after irradiation of the neck area. There are familial and sporadic forms. Familial forms with parathyroid adenomas are observed in patients with other endocrine tumors. Primary hyperparathyroidism causes hypophosphatemia and increased bone resorption.

Although asymptomatic hypercalcemia is common, nephrolithiasis is also common, especially when hypercalciuria develops due to prolonged hypercalcemia. In patients with primary hyperparathyroidism, histological examination reveals a parathyroid adenoma in 90% of cases, although it is sometimes difficult to differentiate an adenoma from a normal gland. About 7% of cases are associated with hyperplasia of 2 or more glands. Parathyroid cancer is determined in 3% of cases.

The main causes of hypercalcemia

Increased bone resorption

Cancer with bone metastases: especially carcinoma, leukemia, lymphoma, multiple myeloma.
Hyperthyroidism.
Humoral hypercalcemia in malignant neoplasms: i.e. cancer hypercalcemia in the absence of bone metastases.
Immobilization: especially in young, growing patients, with orthopedic fixation, with Paget's disease; also in elderly patients with osteoporosis, paraplegia and quadriplegia.
Excess parathyroid hormone: primary hyperparathyroidism, parathyroid carcinoma, familial hypocalciuric hypercalcemia, secondary hyperparathyroidism.
Vitamin D toxicity, A.

Excess FA absorption and/or calcium intake

Milk-alkaline syndrome.
Sarcoidosis and other granulomatous diseases.
Vitamin D toxicity.

Elevated plasma protein concentration

Unclear mechanism.
Osteomalacia induced by aluminum.
Hypercalcemia in children.
Intoxication with lithium, theophylline.
Myxedema, Addison's disease, Cushing's disease after surgery.
Malignant neuroleptic syndrome
Treatment with thiazide diuretics.
Artifact
Contact of blood with contaminated dishes.
Prolonged venous stasis during blood sampling

The syndrome of familial hypocalciuric hypercalcemia (FHH) is autosomal dominant. In most cases, an inactivating mutation of the gene encoding the calcium-sensitive receptor occurs, resulting in the need for high plasma calcium levels to inhibit PTH secretion. The secretion of PTH stimulates the excretion of phosphates. There is persistent hypercalcemia (usually asymptomatic), often from an early age; normal or slightly elevated PTH levels; hypocalciuria; hypermagnesemia. Renal function is normal, nephrolithiasis is not typical. However, severe pancreatitis sometimes develops. This syndrome, associated with parathyroid hyperplasia, is not cured by subtotal parathyroidectomy.

Secondary hyperparathyroidism occurs when prolonged hypercalcemia caused by conditions such as kidney failure or intestinal malabsorption syndrome stimulates increased secretion of PTH. There is hypercalcemia or less commonly normocalcemia. Calcium sensitivity of the parathyroid glands may be reduced due to glandular hyperplasia and an increase in set point (i.e., the amount of calcium needed to decrease PTH secretion).

Tertiary hyperparathyroidism refers to conditions where the secretion of PTH becomes autonomous. Usually seen in patients with long-term secondary hyperparathyroidism, such as those with end-stage kidney disease lasting several years.

Cancer is a common cause of hypercalcemia. Although there are several mechanisms, the increase in plasma calcium levels mainly occurs as a result of bone resorption. Humoral cancerous hypercalcemia (i.e., hypercalcemia without or with minimal bone metastases) occurs more often with squamous cell adenoma, renal cell adenoma, breast, prostate, and ovarian cancer. Previously, many cases of humoral cancerous hypercalcemia have been associated with ectopic PTH production. However, some of these tumors secrete a PTH-related peptide that binds to PTH receptors in bone and kidney and mimics many of the hormone's effects, including bone resorption. Hematologic malignancies, most commonly myeloma, but also some lymphomas and lymphosarcomas, cause hypercalcemia by releasing a group of cytokines that stimulate bone resorption by osteoclasts, resulting in foci of osteolytic damage and/or diffuse osteopenia. Hypercalcemia may result from local release of osteoclast-activating cytokines or prostaglandins and/or direct bone reabsorption by metastatic tumor cells.

High levels of endogenous calcitriol are also a likely cause. Although plasma concentrations are usually low in patients with solid tumors, elevated levels are sometimes observed in patients with lymphomas. Exogenous vitamin D at pharmacological doses causes increased bone resorption as well as increased intestinal absorption of calcium, leading to hypercalcemia and hypercalciuria.

Granulomatous diseases such as sarcoidosis, tuberculosis, leprosy, berylliosis, histoplasmosis, coccidioidomycosis lead to hypercalcemia and hypercalciuria. In sarcoidosis, hypercalcemia and hypercalciuria develop as a result of unregulated conversion of the inactive form of vitamin D to the active form, probably due to the expression of the enzyme 1-hydroxylase in the mononuclear cells of sarcoid granulomas. Similarly, in patients with tuberculosis and silicosis, elevated levels of capcitriol were noted. There must also be other mechanisms for the development of hypercalcemia, since patients with hypercalcemia and leprosy have a decrease in calcitriol levels.

Immobilization, especially prolonged bed rest in patients with risk factors, may lead to hypercalcemia due to accelerated bone resorption. Hypercalcemia develops within days or weeks of starting bed rest. Patients with Paget's disease are most at risk of hypercalcemia during bed rest.

Idiopathic neonatal hypercalcemia (Williams syndrome) is an extremely rare sporadic disorder with dysmorphic facial features, cardiovascular abnormalities, renal vascular hypertension, and hypercalcemia. Metabolism of PTH and vitamin D is normal, but the response of calcitonin to calcium administration may be abnormal.

In milk-alkali syndrome, excessive intake of calcium and alkali occurs, usually when self-medicating with calcium carbonate antacids for dyspepsia or to prevent osteoporosis. Hypercalcemia, metabolic alkalosis and renal failure develop. The availability of effective drugs for the treatment of peptic ulcer disease and osteoporosis has significantly reduced the incidence of this syndrome.

Symptoms of hypercalcemia

In mild hypercalcemia, many patients are asymptomatic. The condition is often detected during routine laboratory testing. Clinical manifestations of hypercalcemia include constipation, anorexia, nausea and vomiting, abdominal pain, and intestinal obstruction. Violation of the concentration function of the kidneys leads to polyuria, nocturia and polydipsia. An increase in plasma calcium levels of more than 12 mg / dl (more than 3.0 mmol / l) causes emotional lability, impaired consciousness, delirium, psychosis, stupor and coma. Neuromuscular symptoms of hypercalcemia include skeletal muscle weakness. Hypercalciuria with nephrolithiasis is quite common. Less commonly, prolonged or severe hypercalcemia causes reversible acute renal failure or irreversible kidney damage due to nephrocalcinosis (deposition of calcium salts in the kidney parenchyma). Patients with hyperparathyroidism may develop peptic ulcers and pancreatitis, but the causes are not related to hypercalcemia.

Severe hypercalcemia causes a shortening of the QT interval on the ECG, the development of arrhythmias, especially in patients taking digoxin. Hypercalcemia greater than 18 mg/dL (greater than 4.5 mmol/L) can cause shock, kidney failure, and death.

Diagnosis of hypercalcemia

Hypercalcemia - diagnosis is based on the determination of the level of total plasma calcium more than 10.4 mg / dl (more than 2.6 mmol / l) or the level of ionized plasma calcium more than 5.2 mg / dl (more than 1.3 mmol / l). Hypercalcemia may be masked by low serum proteins; if protein and albumin levels are abnormal, or if elevated ionized calcium levels are suspected (eg, if symptoms of hypercalcemia are present), plasma ionized calcium levels should be measured.

The cause is evident from the history and clinical findings in more than 95% of patients. Careful history taking is necessary, especially assessment of previous plasma calcium concentrations; physical examination; chest x-ray; laboratory studies, including the determination of electrolytes, blood urea nitrogen, creatinine, ionized calcium phosphate, alkaline phosphatase and serum protein immunoelectrophoresis. In patients without an obvious cause of hypercalcemia, intact PTH and urinary calcium should be determined.

Asymptomatic hypercalcemia existing for several years or present in several family members increases the possibility of CHH. Primary hyperparathyroidism usually appears later in life, but may exist for several years before symptoms appear. If there is no obvious cause, plasma calcium levels less than 11 mg/dl (less than 2.75 mmol/l) are indicative of hyperparathyroidism or other non-malignant causes, while levels greater than 13 mg/dl (more than 3.25 mmol/l ) suggest cancer.

The chest x-ray is particularly useful as it detects most granulomatous diseases such as tuberculosis, sarcoidosis, silicosis, as well as primary lung cancer, lysis, and lesions of the bones of the shoulder, ribs, and thoracic spine.

X-ray examination can also reveal the effect of secondary hyperparathyroidism on the bone, more often in patients on long-term dialysis. In generalized fibrous osteodystrophy (often due to primary hyperparathyroidism), increased osteoclast activity causes bone loss with fibrous degeneration and the formation of cystic and fibrous nodes. Since the characteristic bone lesions are seen only in progressive disease, the use of x-rays is not recommended in asymptomatic patients. X-ray examination usually shows bone cysts, a heterogeneous appearance of the skull, subperiosteal bone resorption in the phalanges and distal ends of the clavicles.

Determining the cause of hypercalcemia is often based on laboratory tests.

In hyperparathyroidism, plasma calcium levels are rarely greater than 12 mg/dl (greater than 3.0 mmol/l), but plasma ionized calcium levels are almost always elevated. Low plasma phosphate levels suggest hyperparathyroidism, especially when combined with increased phosphate excretion. When hyperparathyroidism leads to changes in bone structure, plasma alkaline phosphatase levels are often elevated. An elevated level of intact PTH, especially an inadequate rise (i.e., in the absence of hypocalcemia), is diagnostic. In the absence of a family history of endocrine neoplasia, neck radiation, or other apparent cause, primary hyperparathyroidism is suspected. Chronic kidney disease suggests the presence of secondary hyperparathyroidism, but primary hyperparathyroidism may also exist. In patients with chronic kidney disease, high plasma calcium levels and normal phosphate levels suggest primary hyperparathyroidism, while elevated phosphate levels suggest secondary hyperparathyroidism.

The need to localize the parathyroid tissue before surgery on the parathyroid glands is controversial. CT scans with or without biopsy, MRI, ultrasound, digital angiography, thallium 201 and technetium99 scans have been used for this purpose and have been highly accurate, but have not improved the usually high rate of success of parathyroidectomies performed by experienced surgeons. Technetium 99 sestamibi can be used to determine solitary adenomas, which has greater sensitivity and specificity.

In residual or recurrent hyperparathyroidism after gland surgery, imaging is required, which can reveal abnormally functioning parathyroid glands in atypical locations of the neck and mediastinum. Technetium 99 sestamibi is the most sensitive imaging modality. Several imaging studies (MRI, CT, ultrasound in addition to technetium-99 sestamibi) are sometimes necessary before a second parathyroidectomy.

Plasma calcium concentrations greater than 12 mg/dL (greater than 3 mmol/L) suggest tumors or other causes, but not hyperparathyroidism. In humoral cancerous hypercalcemia, PTH levels are usually low or undetectable; phosphate levels are often low; metabolic alkalosis, hypochloremia and hypoalbuminemia are observed. Suppression of PTH differentiates this condition from primary hyperparathyroidism. Humoral hypercalcemia carcinoma can be diagnosed by detecting PTH-related peptide in plasma.

Anemia, azotemia, and hypercalcemia suggest myeloma. The diagnosis of myeloma is confirmed by bone marrow examination or by the presence of monoclonal gammopathy.

If Paget's disease is suspected, it is necessary to begin research with x-rays.

GHH, diuretic therapy, renal failure, lactose-alkali syndrome can cause hypercalcemia without hypercalciuria. CHS is differentiated from primary hyperparathyroidism by early onset, frequent hypermagnesemia, and the presence of hypercalcemia without hypercalciuria in many family members. Fractional calcium excretion (the ratio of calcium clearance to creatinine clearance) is low (less than 1%) in CHS; in primary hyperparathyroidism is almost always increased (1-4%). Intact PTH may be elevated or within normal limits, probably reflecting changes in the re-regulation of parathyroid function.

Milk-alkaline syndrome is defined by a history of increased intake of calcium antacids, as well as by a combination of hypercalcemia, metabolic alkalosis, and sometimes azotemia with hypocalciuria. The diagnosis is confirmed if calcium levels quickly return to normal when calcium and alkali are discontinued, but renal failure may persist in the presence of nephrocalcinosis. Circulating PTH is usually low.

In hypercalcemia caused by sarcoidosis and other granulomatous diseases, as well as lymphomas, plasma levels of calcitriol may be elevated. Vitamin D toxicity is also characterized by an increase in calcitriol levels. In other endocrine causes of hypercalcemia, such as thyrotoxicosis and Addison's disease, typical laboratory findings for these disorders support the diagnosis.

Treatment of hypercalcemia

There are 4 main strategies for reducing plasma calcium concentration: decreasing intestinal absorption of calcium, increasing urinary calcium excretion, decreasing bone resorption, and removing excess calcium by dialysis. The treatment used depends on the cause and degree of hypercalcemia.

Mild hypercalcemia - treatment [plasma calcium level less than 11.5 mg/dl (less than 2.88 mmol/l)], in which the symptoms are mild, is determined after diagnosis. The root cause is corrected. If symptoms are significant, treatment should be aimed at lowering plasma calcium levels. Oral phosphate may be used. When taken with food, calcium binds to prevent absorption. The initial dose is 250 mg of elemental P04 (as sodium or potassium salt) 4 times a day. The dose may be increased to 500 mg 4 times a day if necessary. Another treatment is to increase urinary calcium excretion by giving isotonic saline with a loop diuretic. In the absence of significant heart failure, 1-2 liters of saline is administered over 2-4 hours, since hypovolemia is usually observed in patients with hypercalcemia. To maintain a diuresis of 250 ml/h, intravenous administration of 20-40 mg of furosemide is performed every 2-4 hours. To avoid hypokalemia and hypomagnesemia, these electrolytes are monitored every 4 hours during treatment, and if necessary, intravenous replacement. Plasma calcium begins to decline after 2-4 hours and reaches normal levels within 24 hours.

Moderate hypercalcemia - treatment [plasma calcium levels greater than 11.5 mg/dl (greater than 2.88 mmol/l) and less than 18 mg/dl (less than 4.51 mmol/l)] may be treated with isotonic saline and a loop diuretic, as described above, or depending on the cause, drugs that reduce bone resorption (calcitonin, bisphosphonates, plicamycin or gallium nitrate), glucocorticoids, or chloroquine.

Calcitonin is normally released in response to hypercalcemia by C-cells of the thyroid gland, reduces plasma calcium levels by inhibiting osteoclast activity. A safe dose is 4-8 IU/kg subcutaneously every 12 hours. Efficacy in the treatment of cancer-associated hypercalcemia is limited by the short duration of action, the development of tachyphylaxis, and the lack of response in more than 40% of patients. But the combination of calcitonin and prednisolone can control plasma calcium levels for several months in patients with cancer. If calcitonin stops working, it can be stopped for 2 days (prednisolone continues) and then resumed.

Bisphosphonates inhibit osteoclasts. They are usually the drugs of choice for cancer-associated hypercalcemia. For the treatment of Paget's disease and cancer-associated hypercalcemia, etidronate 7.5 mg per 1 kg is used intravenously once a day for 3-5 days. It can also be used at 20 mg per 1 kg orally once a day. Pamidronate is used for cancer-associated hypercalcemia once at a dose of 30-90 mg intravenously with a repeat after 7 days. Reduces plasma calcium levels for 2 weeks. Zoledronate can be used at a dose of 4-8 mg intravenously and reduces plasma calcium levels for more than 40 days on average. Oral bisphosphonates (alendronate or residronate) may be used to maintain normal calcium levels.

Plikamycin 25 mcg/kg IV once daily in 50 ml 5% dextrose over 4 to 6 hours is effective in patients with cancer-induced hypercalcemia but is less commonly used because other drugs are safer. Gallium nitrate is also effective in these conditions, but is rarely used due to renal toxicity and limited clinical experience. The addition of glucocorticoids (eg, prednisone 20–40 mg orally once daily) effectively controls hypercalcemia by reducing calcitriol production and intestinal absorption of calcium in patients with vitamin D toxicity, neonatal idiopathic hypercalcemia, and sarcoidosis. Some patients with myeloma, lymphoma, leukemia, or metastatic cancer need 40-60 mg of prednisone once a day. However, more than 50% of these patients do not respond to glucocorticoids, and the response (if present) takes several days; this usually necessitates other treatment.

Chloroquine PO 500 mg orally once daily inhibits calcitriol synthesis and reduces plasma calcium levels in patients with sarcoidosis. Routine ophthalmic examination (eg, retinal examination within 6–12 months) is mandatory to detect retinal lesions in a dose-dependent manner.

Severe hypercalcemia - Treatment [plasma calcium greater than 18 mg/dl (greater than 4.5 mmol/l) or severe symptoms] is the need for hemodialysis with low calcium dialysates in addition to the described treatment. Hemodialysis is the safest and most reliable short-term treatment for patients with renal insufficiency.

Intravenous phosphate should only be used when life-threatening hypercalcemia and other methods have failed and hemodialysis is not possible. No more than 1 g intravenously within 24 hours should be administered; usually one or two doses over two days lower plasma calcium levels by 10-15 days. Soft tissue calcification and acute renal failure may develop. Intravenous sodium sulfate is more dangerous and less effective and should not be used.

Treatment of hyperparathyroidism in patients with renal insufficiency is combined with phosphate restriction and the use of PO binders to prevent hyperphosphatemia and metastatic calcification. In renal insufficiency, aluminum-containing substances should be avoided to prevent accumulation in the bone and severe osteomalacia. Despite the use of phosphate binders, dietary phosphate restriction is necessary. The administration of vitamin D in renal failure is dangerous and requires frequent monitoring of calcium and phosphate levels. Treatment should be limited to patients with symptomatic osteomalacia (not associated with aluminum), secondary hyperparathyroidism, or postoperative hypocalcemia. Although calcitriol is often given with oral calcium to suppress secondary hyperparathyroidism, results vary in patients with end-stage kidney disease. Parenteral calcitriol is better at preventing secondary hyperparathyroidism in such patients, as high plasma levels directly suppress PTH release.

Elevated serum calcium often complicates vitamin D therapy in dialysis patients. Simple osteomalacia may respond to ingestion of 0.25-0.5 mcg per day of calcitriol, and correction of postoperative hypercalcemia may require long-term administration of 2 mcg of calcitriol per day and more than 2 g of elemental calcium per day. The calcimimetic cinacalcet represents a new class of drugs that lower PTH levels in dialysis patients without increasing serum calcium. Aluminum-induced osteomalacia is commonly seen in dialysis patients who have taken large amounts of aluminum-containing phosphate binders. In these patients, aluminum removal with deferoxamine is required before improvements in bone damage associated with calcitriol can begin.

Symptomatic or progressive hyperparathyroidism is treated surgically. The adenomatous glands are removed. The remaining parathyroid tissue is also usually removed, as it is difficult to identify the parathyroid glands during subsequent surgical examination. To prevent the development of hypoparathyroidism, a small area of the normal parathyroid gland is reimplanted into the abdomen of the sternocleidomastoid muscle or subcutaneously on the forearm. Sometimes tissue cryopreservation is used for subsequent transplantation in case of hypoparathyroidism.

The indication for surgery in patients with mild primary hyperparathyroidism is controversial. The Summary Report of a 2002 National Institutes of Health Symposium on Asymptomatic Primary Hyperparathyroidism lists the following indications for surgery: Plasma calcium is 1 mg/dL (0.25 mmol/L) above normal; calciuria more than 400 mg/day (10 mmol/day); creatinine clearance is 30% below the age norm; peak bone density at the femur, lumbar spine, or radius 2.5 standard deviations below control; age less than 50 years; possibility of deterioration in the future.

If surgery is not performed, the patient should remain active (avoid immobilization), eat a diet low in calcium, drink plenty of fluids to reduce the chance of nephrolithiasis, and avoid drugs that increase plasma calcium levels, such as thiazide diuretics. Plasma calcium levels and renal function should be assessed every 6 months, bone density every 12 months.

Although patients with asymptomatic primary hyperparathyroidism without an indication for surgery may be treated conservatively, concerns remain about subclinical bone disease, hypertension, and life expectancy. Although CHS develops due to the presence of histologically abnormal parathyroid tissue, the response to subtotal parathyroidectomy is unsatisfactory. Since severe clinical manifestations are rare, intermittent drug therapy is usually sufficient.

In mild hyperparathyroidism, plasma calcium levels fall to normal levels 24 to 48 hours after surgery; calcium levels need to be monitored. In patients with severe generalized fibrous osteodystrophy, prolonged symptomatic hypocalcemia may occur after surgery if 10–20 g of elemental calcium has not been administered a few days before surgery. Even with preoperative Ca administration, there may be a need for higher doses of Ca and vitamin D, while bone calcium (hypercalcemia) is in excess.

Pressure spikes? The pressure is normal from the first application and forever! Bring your blood pressure back to normal with Hypertostop in minutes without harm to your health!

The basis of health is the balance of all metabolic processes. If a part of the system fails, continuous disturbances begin, leading to a general failure, dysfunction. One such pathological disorder is hypercalcemia.

What is hypercalcemia, why is it dangerous for humans? The Latin term for the disorder translates as "abnormally elevated calcium" and this is the most complete description of the disease.

Normally, the body regulates the content of all minerals involved in metabolic processes, including calcium. However, in some diseases, metabolism is disturbed, an increase in calcium in the blood plasma is recorded. Hypercalcemia is a pathological condition in which the level of total calcium exceeds the norm of 2.5 mmol / l. In adults, such a metabolic disorder, most often, signals other serious pathologies in the body; in young children, it can be caused by an overdose of drugs.

The main disorders that can provoke an increase in calcium in the blood and plasma:

increased absorption of calcium by the intestinal mucosa;
functional disorders of calcium filtration by the kidneys;
enhanced immobilization of calcium from bone tissues.

An increase in calcium in the patient's blood or plasma does not always indicate pathology, it can also be due to dietary habits, the intake of nutritional supplements and vitamins.

With stable hypercalcemia, the work of the kidneys is disrupted, due to the inhibition of the function of glomerular filtration, fibrosis develops, the formation of crystals, various forms of pyelonephritis.

Degrees

Shocking statistics! Hypertension is the most common disease of the cardiovascular system. It has been established that 20-30% of the adult population suffers from it. In order not to lead to complications and operations, people who have learned bitter experience to reduce pressure at home use ...

There are several degrees of severity of the hypercalcemic condition:

in a mild degree, the disease is characterized by an increase in calcium in the blood or plasma of not more than 3 mmol / l;
in moderate severity, the norms exceed 3.0 mmol / l;
in severe degree - the level of calcium exceeds 3.5 mmol / l.

A mild degree is almost always corrected by eliminating the causes that caused the condition. Most often, these are drugs, vitamin supplements, dietary supplements, or a diet rich in calcium.

Metabolism disorders in children

Hypercalcemia in children is much less common than in adults and is accompanied by increased excretion of calcium from bone tissue, and the kidneys and gastrointestinal tract almost do not take part in the process.

The mild form is accompanied by a violation of the sucking reflex, vomiting, weight loss, polyuria, constipation, and muscle hypotension. With prolonged and persistent hypercalcemia, symptoms of damage to the central nervous system, gastrointestinal tract, kidneys, heart and other organs develop.

The causes of the development of the disease in a child can be:

hyperparathyroidism in the mother, which leads to transient transmission to the newborn;
physiological prematurity;
lack of phosphorus or excess of vitamin D;
hyperthyroidism;
hereditary mutation of calcium receptors, the state of hypocalciuric hypercalcemia;
tumor processes, for example, parathyroid adenoma;
congenital pathologies, for example, Williams syndrome with characteristic external signs;
post-procedural complications in the form of subcutaneous scleromas or necrosis.

In most children, hypercalcemia is diagnosed incidentally, most often it is an asymptomatic transient course, which resolves on its own by the age of one. The hypercalcemic state caused by drugs is corrected by diet - in this case, rare complications in the form of kidney failure and the formation of calcium conglomerates are possible.

Congenital pathologies, tumor processes, some other forms of hypercalcemia in children can be corrected by surgical interventions or long-term therapy of the condition, such forms are incurable.

Manifestations of the disease

Symptoms of hypercalcemia - what is it, and what manifestations should I pay attention to? Signs that indicate an increase in calcium in the blood depend entirely on the severity of the condition. In weak and chronic forms, they are expressed quite blurry, may be accompanied by such manifestations:

disorders of the digestive system, constipation, nausea, vomiting, abdominal pain, complete or partial loss of appetite;
frequent urination (polyuria).

With moderate hypercalcemia, patients most often complain of pain in the bones and joints.

In acute forms, the symptoms intensify:

an increase in blood pressure develops, which can be replaced by a sharp decrease in dehydration, asystole, changes in ECG parameters, collapse;
weakness, drowsiness, lethargy, stupor, possible depression, psychosis, coma;
anorexia, accompanied by weight loss;
the filtration rate of the renal glomeruli decreases, polyuria, nephrocalcinosis, and acidosis develop. In the urine of the patient at this moment, erythrocytes and a moderate amount of protein can be detected;
the musculature reacts with spasm, myopathy.

With hypercalcemia caused by tumor processes, acute pyelonephritis develops as a consequence of the ability of some tumor cells to enhance calcium absorption into the gastrointestinal mucosa, as well as remove it from bones and tissues.

In a condition caused by acute hypercalcemia with pronounced symptoms, a crisis may develop, accompanied by confusion, uncontrolled vomiting, abrupt entry into a coma, which, as a rule, ends in death.

The reasons

The causes of hypercalcemia can be the following diseases and conditions:

various manifestations of primary hyperparathyroidism - after kidney transplantation, familial, sporadic;
other variants of hyperparathyroidism - familial hypercalciuria, tertiary hyperparathyroidism with functional renal failure;
malignant processes: myelomas, leukemias, lymphomas, sarcoidosis, granulomas;
acute infectious diseases: tuberculosis, leprosy, coccidiosis and others;
diseases of the endocrine system: pathology of the adrenal glands, thyrotoxicosis and others;
condition after resuscitation procedures;
increased excretion of calcium from bone tissue, a state of immobilization;
neonatal idiopathic calcemia, Williams syndrome;
drug provocation: thiazide diuretics, vitamins A, D, lithium, estrogen, androgens, Burnett's syndrome or milk-alkaline syndrome, which develops while taking antacids and dairy products (or with high calcium content);
AIDS.

The mechanism of development of the disorder has not yet been thoroughly studied, so it is difficult to say with certainty what it is - hypercalcemia. Recent studies have shown that the most common cause of severe and moderate manifestations are thyroid diseases, malignant processes and the use of thiazide diuretics. In addition, mild metabolic disorders of this nature are often found in menopausal women.

Diagnostics

Difficulties in making a diagnosis lie in the fact that it is important for the doctor and for the patient not to establish hypercalcemia, but to find out and eliminate the cause of its occurrence.

Since there can be many reasons for the condition, the initial examination begins with preparation for the analysis of total and free calcium in the blood:

the patient is recommended a diet with the complete exclusion of foods and drugs that may affect the result of the analysis;
you need to donate blood on an empty stomach, a light low-fat dinner is allowed;
it is unacceptable to drink alcohol the day before and conduct physiotherapy procedures.

If the norms exceed the permissible, additional studies are prescribed:

kidney tests;
blood test for parathyroid hormone-like peptide (PTH-peptide) and parathyroid hormone (PTH);
urinalysis for Bence-Jones protein;
urine test for calcium;
blood test for signs of bone metabolism;
general clinical detailed blood test;
blood test for phosphorus levels.

As additional research methods, based on the results of the tests, ultrasound of the kidneys, determination of the level of vitamin D in the blood, a blood test for PSA and other tumor markers, a blood test for cortisol, alkaline phosphatase, blood serum albumins, HIV infection, X-ray examination of bone tissue, lungs, immunoelectrophoresis, bone marrow puncture, abdominal sonography.

How to help with metabolic disorders?

Treatment of hypercalcemia is performed depending on the severity of the patient's condition. In some cases, emergency and urgent measures are prescribed to remove the elevated calcium level; for chronic and congenital pathologies, long-term therapeutic treatment with a diet is provided.

In general, the treatment of hypercalcemia is more about eliminating the causes of the imbalance than restoring the level of calcium in the blood. And each reason requires its own approach.

Ambulance for emergencies

A severe degree of hypercalcemia involves moving the patient to a hospital or intensive care unit, where he will be given saline and diuretics (furosemide). If a patient has cardiovascular or renal insufficiency, instead of a dropper with saline, dialysis is prescribed, an injection of calcitonin or bisphosphonates is performed.

Removal of acute symptoms is carried out under the supervision of a doctor and control of the level of calcium and other trace elements in the blood.

Therapeutic appointments

After the main acute symptoms of hypercalcemia are removed, therapeutic treatment is prescribed. With asymptomatic and mild form, there is no need to prescribe droppers, only bisphosphonates.

In a state of moderate severity, pamidronic acid droppers, intramuscular glucocorticoids, calcitonin, and gallium nitrate are prescribed to suppress the immobilization process. Treatment is canceled gradually, after the complete disappearance of signs of hypercalcemia.

Surgery

For 2 years now, a miracle drug for the treatment of hypertension and high blood pressure has been on the European market. In terms of efficiency, it is several times superior to analogues - it gives not only a quick effect after the start of use, but also restores the natural functions of the body. It does not have any side effects. And now he appeared in Russia ...

Surgical treatment of hypercalcemia is indicated for patients with parathyroid adenoma and neonatal hyperparathyroidism. After the operation, various complications are possible:

hypocalcemia, with the development of "hungry" bones (pronounced osteoporosis), with complete removal of the glands;
hypercalcemia - with incomplete removal of the glands, it may persist, in which case repeated surgical intervention is required;
the operation may cause paresis of the vocal cords, temporary or permanent;
when a parathyroid adenoma is removed, a relapse of hyperparathyroidism is possible, which will provoke hypercalcemia.

If the operation went without complications, the level of calcium in the blood is restored within a few days. The resulting complications require repeated surgical interventions or lifelong prescription of vitamin D preparations and the use of calcium preparations for some time (with complete removal of the parathyroid glands).

Condition prevention

Prevention of hypercalcemia is possible if it is caused by the use of medicines, dietary supplements, vitamins, homeopathic and folk remedies. This mild drug-induced hypercalcemia is corrected by discontinuation of the offending drug and a diet low in calcium.

It is more difficult to adjust the diet with severe and complicated degrees of hypercalcemia, since the condition is most often caused by severe pathologies of organs and tissues. In this case, the therapist will help - it is he who treats the disease. Without consulting a specialist, you should not prescribe calcium or vitamin preparations at all, especially for children. The dosage is selected based on the individual characteristics of the organism, and perhaps the one that you have prescribed for yourself will cause an inadequate reaction and hypercalcemia.

How to quickly restore immunity?

Have you noticed that you have gained a lot of weight lately? The skin became somehow dull, the hair and nails were brittle, there were problems with digestion.

All these symptoms are caused by a weakened immune system. Familiar symptoms, right? All this can talk about problems with the immune system. How to quickly get rid of these problems ...

Hypercalcemia is the most common life-threatening metabolic disorder in malignant neoplasms. Most often, hypercalcemia is complicated by multiple myeloma and metastatic breast cancer (up to 40% of patients), however, it can also develop in patients with lymphogranulomatosis, lymphomas, leukemia, etc. Despite the fact that many diseases can lead to hypercalcemia, most often its development is due to hyperfunction of the parathyroid glands or various malignant tumors.

Other causes account for less than 10% of cases hypercalcemia. A normal parathyroid hormone level excludes hyperparathyroidism with a high degree of probability.

Hypercalcemia due to malignant tumor, most often has an acute onset and severe clinical symptoms requiring hospitalization and emergency care. On the contrary, asymptomatic chronic hypercalcemia is more often due to hyperfunction of the parathyroid glands.

In malignant neoplasms, two main mechanisms are responsible for development. In one of them (humoral), tumor cells release biologically active substances into the systemic circulation, causing increased osteolysis both in the areas of bone metastases and beyond. The development of humorally conditioned hypercalcemia can also be observed in the absence of bone metastases. Most often, a parathyroid-like substance (protein) and the active form of vitamin D3 are responsible for the development of this type of hypercalcemia in cancer patients.

With osteolytic type hypercalcemia destruction of bone tissue occurs only in the area of metastatic lesion. In this case, bone resorption is due to paracrine (local) stimulation of osteoclasts by various cytokines released by tumor cells. A combination of both mechanisms is also possible.

Parathyroid-like substance(a protein partially homologous to normal parathyroid hormone, but different from it in immunological definition) is responsible for the development of hypercalcemia in many solid tumors, but in oncohematological practice it is of clinical importance only in patients with T-cell lymphoma/leukemia. In lymphogranulomatosis, non-Hodgkin's lymphomas, multiple myeloma, the development of humorally caused hypercalcemia is more often associated with excessive formation of the active form of vitamin D3 (1.25 OH2-vitamin D3) under the influence of specific enzymes contained in tumor cells.

Identification of cytokines responsible for the osteolytic type hypercalcemia, is difficult due to the impossibility of their determination in the systemic circulation. It is believed that IL-1, IL-6, tumor necrosis factor, PgE, etc. are involved in the development of osteolytic hypercalcemia in various malignant neoplasms. However, it is most likely that in most cases the development of hypercalcemia in patients with malignant tumors is due to a complex of biologically active substances . In addition, it must be remembered that the presence of a malignant tumor in a patient does not exclude the presence of other causes of hypercalcemia (chronic renal failure, an overdose of vitamins D and A, hyperthyroidism, etc.).

Clinical manifestations hypercalcemia are diverse and affect many organs and systems, and are also able to "mask" as other diseases. The development of hypercalcemia may be accompanied by the following symptoms: thirst, weight loss, polyuria, dehydration, muscle weakness, lethargy, convulsions, psychosis, nausea, vomiting, constipation, intestinal obstruction, renal failure, bradycardia and ventricular arrhythmias. The severity of manifestations varies widely depending on the severity of hypercalcemia, the rate of increase in calcium levels and the general condition of the patient. In patients with acutely developing hypercalcemia, the most common initial symptoms are nausea, vomiting, thirst, and polyuria.

With absence qualified assistance stupor or coma develops, which can be taken (given thirst, history of polyuria, etc.) for manifestations of diabetes mellitus. In this situation, the correct diagnosis and the initiation of specific therapy are vital, since the dehydration that develops due to vomiting and polyuria can significantly aggravate the course of hypercalcemia, closing the "vicious" circle.

Serum total calcium level(routinely determined in most laboratories) usually adequately reflects the severity of hypercalcemia.
However, only 40% serum calcium is present in a physiologically active ionized form, while 50% is associated with blood proteins (mainly albumin) and up to 10% forms complexes with anions (bicarbonate, phosphate, citrate, etc.). The biological (and pathological) effects of an increase in calcium levels depend precisely on the size of the ionized fraction. The proportion of ionized calcium increases with hypoalbuminemia and, accordingly, decreases with hyperproteinemia (for example, with multiple myeloma). When changes affect only the level of albumin, the following formula can be used to more accurately characterize the severity of hypercalcemia:

corrected calcium (mmol/l) = total calcium (mol/l) + 0.8 x.

If the patient has a severe hyperproteinemia, direct determination of ionized calcium in the laboratory is necessary.

Of course, the best treatment hypercalcemia caused by tumor growth is the treatment of the underlying disease, however, this complication is most often observed in patients with advanced tumors resistant to anticancer therapy. In this regard, and also given that hypercalcemia poses an immediate threat to the life of the patient, the main method of emergency therapy is symptomatic measures aimed at reducing the level of calcium in the blood (by increasing calcium excretion in the urine and reducing bone resorption).

Attempts reduce the intake of calcium in the body(calcium-reduced diet) are ineffective for tumor-induced hypercalcemia.
Reception should be suspended drugs that reduce calcium excretion (thiazide diuretics), reduce renal blood flow (nonsteroidal anti-inflammatory drugs, H2 blockers), and, of course, drugs that directly cause hypercalcemia (calcium drugs, vitamin D, retinoids).

The key moment in emergency treatment of patients with hypercalcemia is hydration, which, in addition to increasing calcium excretion, avoids the effects of dehydration due to vomiting and polyuria. At the same time, even massive hydration (4 liters per day or more) does not allow stopping hypercalcemia in most patients with malignant neoplasms. During such treatment, temporary normalization of calcium levels is observed only in a third of patients. The previously widely used method of creating "forced diuresis" using furosemide, according to studies, unfortunately does not increase the effectiveness of hydration therapy.

Furthermore, furosemide potentially able to increase the phenomena of hypovolemia and calcium reabsorption in the kidneys. Hydration, however, remains a necessary initial component of therapy in patients with hypercalcemia, as it is necessary to correct hypovolemia (which is the most life-threatening) and allows you to maintain adequate kidney function, preventing the crystallization of calcium salts in the tubules.

The first line of therapy aimed at reducing bone resorption, currently recognized bisphosphonates (synthetic analogs of pyrophosphate, resistant to pyrophosphatase). These drugs, by binding to bone matrix molecules (crystalline hydroxyapatites), suppress the metabolic activity of osteoclasts, which leads to a decrease in bone resorption and, accordingly, a decrease in the extraction of calcium from it. The advantages of bisphosphonates, which determine their widespread use, are high efficiency (hypercalcemia stops in 80-100% of patients) with low toxicity (20% of patients may develop fever, flu-like syndrome, or moderately severe local reactions at the injection site). The effect of bisphosphonates develops quite quickly (within a few days) and persists for a long time.

Currently, the following drugs are available for use, which have shown their clinical efficacy: aredia (pamidronate), bondronate (ibandronate), zometa (zolendronate). Calcitonin (miacalcic) also has the ability to reduce calcium levels by increasing its renal excretion and reducing bone resorption. This drug is the fastest acting (onset of action after 2-4 hours). The main disadvantage of calcitonin is the short duration of action. The peak of the therapeutic effect falls on 24-48 hours of treatment, followed by a rapid decrease in the effect. Corticosteroids are also able to inhibit bone resorption by osteoclasts, however, due to their less activity and more side effects, they are used only in patients with tumors that are sensitive to this type of therapy. Plikamycin (mitramycin) and gallium nitrate, used in foreign practice for resistance to bisphosphonate therapy, are not available in Russia.

When choosing the tactics of managing a patient with hypercalcemia it is necessary to assess the severity of the patient's condition and the level of calcium in the blood. The level of total calcium more than 3 mmol / l and / or the presence of symptoms of hypercalcemia (especially dehydration, CNS disorders) is an absolute indication for hospitalization. In the event of hypercalcemia, the patient should immediately begin hydration. The rate of rehydration depends on the severity of water deficiency and the presence of concomitant cardiovascular and renal diseases in the patient. With severe dehydration and the absence of concomitant pathology, the administration of saline at a rate of 300-400 ml / h for 3-4 hours can be considered optimal. Slower hydration is necessary in the presence of cardiac pathology, especially congestive heart failure.

Strict control over diuresis(corrected for baseline dehydration), electrolyte levels (potassium, magnesium, sodium, chloride) and creatinine are essential for this therapy. The use of furosemide is permissible only in case of fluid retention after adequate rehydration. Immediately after adequate diuresis is established (usually 2-3 hours after the start of hydration, hourly diuresis becomes equal to the volume of fluid injected), it is necessary to start the administration of bisphosphonates at the recommended dose (aredia 90 mg, bondronate 2-6 mg or zometa 4 mg ). Due to the risk of developing nephrotoxicity, it is necessary to strictly observe the recommended rate of administration (duration of infusion: aredia and bondronate - at least 2 hours, zometa at least 15 minutes). For critically ill patients and/or with calcium levels greater than 3.8 mmol/l, it is recommended to use a combination of bisphosphonate with calcitonin (8 IU every 6 hours, intramuscularly for 2-3 days), which allows to achieve a faster effect.