Hypercalcemia in malignant tumors. Hypercalcemia in malignant neoplasms Treatment of severe stage of the disease

Hypercalcemia is a medical term used to describe a human condition in which the level of free calcium in the blood is elevated. There are many reasons for this pathological condition; there are even characteristic symptoms for hypercalcemia.

Classification

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

  • light– readings of the level of free calcium in the blood will not exceed 2 mmol/l, and total calcium – 3 mmol/l;
  • average severity– total calcium is in the range of 3 – 3.5 mmol/l, free calcium – 2 – 2.5 mmol/l;
  • heavy– free calcium level is 2.5 mmol/l and higher, total calcium level is 3.5 mmol/l and higher.

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. The mentioned 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 cancer diseases:

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

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

  • hypervitaminosis D;
  • Paget's disease;
  • familial hypocalciuric hypercalcemia;
  • prolonged immobility;
  • thyrotoxicosis;
  • Jansen's metaphyseal chondrodysplasia;
  • increased absorption of calcium in the small intestine with a simultaneous decrease in its excretion in the urine;
  • congenital lactase deficiency;
  • long-term use of lithium drugs;
  • 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 kidney tubules, 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 contractility of the heart muscle, and an increased amount of calcium in the blood reduces contractility. Excess calcium leads to the development of arrhythmia and a steady increase in blood pressure. The most serious consequence of elevated blood calcium is sudden cardiac death, or cardiac arrest. This condition, fortunately, is extremely rare.

High levels of calcium in the blood also negatively affect the functioning of the central nervous system. At the beginning of the pathological process, a person will only feel increased fatigue, weakness, unmotivated irritability, slight inhibition and unobtrusiveness. 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: you need to 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 disorder occurs with the progression of multiple myeloma, or against the background. It is easy to distinguish these two conditions: with real hypercalcemia, the level of free calcium in the blood will be significantly increased, but in the second case it will remain within normal limits.

Symptoms of hypercalcemia syndrome

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

  • general weakness;
  • light;
  • lethargy;
  • hallucinations;
  • disturbance of orientation in space and environment;
  • disturbance of consciousness (up to coma).

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

  • confident;
  • sudden cardiac arrest.

With pathological damage to the organs of the urinary system, there will be an increase in the volume of urine excreted, and with advanced pathology, on the contrary, a decrease in volume.

Symptoms of damage to the digestive system in hypercalcemia syndrome:

  • bowel disorders (mainly present);
  • loss of appetite, up to complete refusal of food;
  • pain in the epigastric region, girdling in nature, occurring immediately after eating.

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

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

The most dangerous condition develops during hypercalcemic crisis. It is characterized by nausea and constant/uncontrollable vomiting, severe pain in the abdominal area, convulsions, and a sudden increase in body temperature. The patient’s consciousness 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 about specifically identifying the disease in question - it is important to find out the cause that led to such a disorder. A doctor can suspect hypercalcemia syndrome based on the patient’s complaints and comparing them with the presence of a history of cancer. But 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 examination results to be as reliable as possible, the patient must follow certain rules:

  1. The day before the scheduled test, do not drink alcoholic beverages.
  2. Avoid heavy physical activity 30 hours before your scheduled examination.
  3. Foods high in calcium are excluded from your diet three days before the test, as this can blur the results.
  4. The patient must completely stop eating within 8 hours.

If blood tests for the level of total and free calcium reveal that the levels are too high, then the doctor will have to find out the true cause of this pathology. It is for this purpose that the patient will be prescribed additional examination:

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

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

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

  • kidney;
  • X-ray of bones;
  • 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 in question, then the patient is placed in a hospital and a number of intensive care measures are carried out:

Note:the result of the administration 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 microelements.

  • In case of renal failure, infusion therapy is strictly contraindicated, so patients are prescribed peritoneal dialysis or hemodialysis;
  • intravenous administration of bisphosphonates - drugs that reduce calcium levels in the blood;
  • administration of calcitonin intramuscularly, intravenously or subcutaneously.

Treatment of mild to moderate hypercalcemia

When the patient’s serious condition is relieved, therapeutic measures do not stop - they continue, but to a different extent. The patient is prescribed:

  • pamidronic acid intravenous drip once every one and a half months 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 cancer;
  • gallium nitrate – administered intravenously, helps reduce the rate of calcium release from 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 such patients any specific forecasts - it all depends on what underlying disease is occurring. In some cases, to normalize the level of calcium in the blood, it is enough to stop taking medications; in many cases, the condition in question requires lifelong medication to correct the level of calcium in the blood.

Hypercalcemia develops relatively frequently in cancer patients. It is more often associated with bone metastases, and is less common in the absence of any bone damage by a tumor. According to a number of authors, out of 433 cancer patients with hypercalpyemia, bone metastases were identified in 86% of patients. In more than half of the cases, development occurs with metastases of breast cancer, less often with lung and kidney cancer. Approximately 15% of patients are diagnosed with hemoblastosis. In these patients, hypercalcemia usually occurs with diffuse tumor involvement of the bones, although sometimes there are no signs of bone involvement at all.

In approximately 10% of cases, hypercalcemia develops in the absence of radiological or scintigraphic signs of bone damage. In such cases, the pathogenesis of hypercalcemia is associated with the tumor's production of humoral mediators that activate osteoclasts, the main of which is parathyroid hormone-related protein. Many other cytokines have been identified with possible bone-resorptive activity. Prostaglandins are potent stimulators of bone resorption and may also play a role in hypercalcemia in cancer. It is also possible that the tumor is associated with primary hyperparathyroidism or other causes of hypercalcemia (for example, vitamin D intoxication or sarcoidosis).

Clinical manifestations and diagnosis

Hypercalcemia in cancer patients is often accompanied by severe disturbances in well-being. Due to a decrease in the concentrating ability of the kidneys, polyuria and nocturia occur early. Patients often complain of anorexia, nausea, constipation, muscle weakness and fatigue. As hypercalcemia progresses, severe dehydration, azotemia, stupor, and coma occur. In addition to hypercalcemia, biochemical blood tests indicate hypokalemia, increased levels of blood urea nitrogen and creatinine. Patients with hypercalcemia often develop hypochloremic metabolic alkalosis (while metabolic acidosis is more common in primary hyperparathyroidism). Serum phosphorus concentrations vary. The content of parathyroid hormone can also be normal, increased or decreased. The best method for identifying bone lesions is a scan, which can reveal lesions in the bones that are not visible on x-rays.

Treatment

The goals of treatment for hypercalcemia are to reduce serum calcium concentrations and treat the underlying disease. For moderate hypercalcemia (albumin-corrected serum calcium concentration 12-13 mg/dL) or asymptomatic cases, complete hydration and treatment of the tumor itself may be sufficient ( surgery,chemotherapyor radiation therapy). In contrast, severe, life-threatening hypercalcemia requires emergency treatment, including stimulation of renal calcium excretion in patients with normal renal function and administration of drugs that reduce bone resorption.
To treat hypercalcemia, drugs with varying duration of action and effectiveness are used, so complete treatment of severe hypercalcemia requires an integrated approach.

  • . Rehydration with 0.9% sodium chloride solution.
  • . Use of bisphosphonates (pamidronic or zoledronic acid).
  • . Forced saline diuresis (0.9% sodium chloride solution and furosemide).

Rehydration and restoration of blood volume is the most important stage in the treatment of hypercalcemia. Rehydration is carried out using a 0.9% sodium chloride solution (often 4-6 liters must be administered during the first day). Rehydration without additional measures can only slightly reduce the concentration of calcium in the blood serum (up to 10%). However, rehydration stimulates the kidneys, making it easier to excrete calcium in the urine.

Salt diuresis. After restoration of blood volume, diuresis can be stimulated. Sodium competitively inhibits calcium resorption in the tubules, so intravenous administration of 0.9% sodium chloride solution significantly increases calcium clearance. Since correction of hypercalcemia requires the administration of large volumes of 0.9% sodium chloride solution, central venous pressure must be constantly monitored during treatment. Intravenous drip administration of 0.9% sodium chloride solution 250-500 ml/h with intravenous administration of 20-80 mg furosemide every 2-4 hours leads to a significant increase in the excretion of calcium ions in the urine and a slight decrease in the concentration of calcium in the blood serum in most patients. This method requires strict monitoring of the heart and lungs to prevent fluid overload. In addition, to maintain electrolyte balance, constant monitoring of blood biochemical parameters and compensation for losses of sodium, potassium, magnesium and water ions is necessary. In some cases, a decrease in the level of calcium in the blood serum can be achieved by intravenous drip administration of 0.9% sodium chloride solution 125-150 ml/h in combination with intravenous administration of furosemide at a dose of 40-80 mg 1-2 times a day.

Bisphosphonates are potent inhibitors of normal and pathological bone resorption by osteoclasts. They bind calcium phosphate and inhibit the growth and dissolution of phosphate crystals. In addition, drugs in this group can directly inhibit the resorptive activity of osteoclasts.

Pamidronic and zoledronic acids— bone resorption inhibitors and highly effective drugs for the treatment of hypercalcemia in cancer. For several years, pamidronic acid has been the drug of choice for the treatment of hypercalcemia in cancer patients. Zoledronic acid is more convenient to use (shorter course of treatment) and just as effective.
For moderate hypercalcemia (serum calcium concentration 12-13.5 mg/dL), 60-90 mg of pamidronic acid is recommended to be administered intravenously once over 4 hours per day. The maximum recommended dose of zoledronic acid is 4 mg. The drug is administered once intravenously, the infusion duration is at least 15 minutes. If ineffective, administration can be repeated after 3-4 days.

Side effects. Pamidronic and zoledronic acids are generally well tolerated and no serious side effects have been reported. In rare cases, after administration of the drug, a slight (1°C) rise in temperature is noted. It is believed that short-term fever is associated with the release of cytokines from osteoclasts. Approximately 20% of patients experience pain, redness, swelling and hardness at the injection site. Hypocalcemia, hypophosphatemia, or hypomagnesemia is observed in 15% of patients. In patients with impaired renal excretion, both drugs should be used cautiously. During dental procedures and oral diseases, necrosis of the mandible may be an adverse side effect of bisphosphonates.

Glucocorticoids. The mechanism by which glucocorticoids reduce calcium concentrations is multiple and complex. Intravenous administration of large doses of hydrocortisone (or its analogues) - 250-500 mg every 8 hours can be effective in the treatment of hypercalcemia associated with lymphoproliferative diseases (such as HXJ1 and multiple myeloma) and breast cancer with bone metastases. However, it may take several days for glucocorticoids to reduce serum calcium concentrations. Maintenance therapy begins with prednisolone 10-30 mg/day orally.

Phosphate Food Additives. Phosphates are taken as an adjunct to the primary treatment for hypercalcemia in cancer. Ingestion of phosphates impedes the absorption of calcium ions in the intestine and stimulates the deposition of insoluble calcium salts in bones and tissues. Taking 1.5-3 g of elemental phosphorus can slightly reduce calcium levels and also reduce calcium excretion in the urine. The dose of phosphates taken orally is usually limited by diarrhea. Phosphate supplementation is contraindicated in patients with renal failure or hyperphosphatemia due to the risk of soft tissue calcification. To prevent metastatic calcification, it is necessary to control the concentration of calcium and phosphorus, as well as the solubility of calcium in the presence of phosphorus ions.

Other drugs

Mithramycin is not currently used or recommended for hypercalcemia. Calcitonin is rarely used due to the need for repeated doses and the rapid development of drug resistance. However, it acts quickly and can be prescribed for hypercalcemia in patients with heart failure. Calcitonin is prescribed at a dose of 4 IU/kg subcutaneously or intramuscularly every 12 hours. The dose can be increased to 8 IU/kg if no effect is observed within 24-48 hours.

HYPERCALCIEMIA IN MALIGNANT TUMORS honey.
Malignant tumors are the most common cause of hypercalcemia. Frequency: 5-10% of patients with malignant
tumors.

Risk factors

Dehydration
Immobilization.
Malignant tumors with bone metastases
(for example, multiple myeloma, lymphoma) can lead to hypercalcemia resulting from increased bone resorption, less often due to the local action of humoral substances (for example, osteoclast activating factor) secreted by the metastatic tumor. The content of cAMP in the urine is reduced, which reflects the suppression of PTH synthesis by the resulting hypercalcemia. Tumors without bone metastases (eg, hypernephroma, pancreatic cancer, squamous cell carcinoma of the lung, cervix and esophagus, head and neck tumors) cause hypercalcemia, in 80% of cases secreting PTH-related peptide (PTH-P), a humoral factor that acts like PTH and PTH binding to PTH receptors, but not detectable by radioimmunoassay PTH. PTH-P may cause biochemical effects similar to PTH, including hypophosphatemia and increased urinary cAMP. Detection of increased
the level of PTH-P and normal or low PTH levels allows us to differentiate hypercalcemia in a malignant disease from primary hyperparathyroidism.

Clinical picture

determined by hypercalcemia and tumor process
Diagnostics is aimed at identifying the location of the tumor (ultrasound, CG or MRI)
Treatment is etiotropic (tumor removal), pathogenetic and symptomatic
Forced diuresis (1-2 l of 0.9% NaCl solution IV in combination with furosemide 80-100 mg IV every 2-12 hours during the day). If necessary, pre-conduct rehydration therapy. To replenish fluid loss and prevent hypokalemia, a solution containing 0.9% NaCl and 5% glucose in a 4:1 ratio with the addition of KS1 (20 mEq/l) is administered intravenously.
If it is necessary to further reduce calcium levels, use calcitonin (4-8 IU/kg i.c. or i.m. every 8-12 hours), etidronate, etidronate disodium 7.5 mg/kg i.v. daily for 3-7 days or pamidronate (60-90 mg IV once), plicamycin 25 mcg/kg in 50 ml of 5% glucose solution IV drip for 3-6 hours.
Glucocorticoids (for example, prednisolone 40-60 mg/day) do not reduce calcium concentrations in solid tumors.
Hemodialysis is indicated for concomitant renal failure.

Course and prognosis

Hypercalcemia in patients with malignant tumors, as a rule, portends an imminent death. The average life expectancy after diagnosis of tumor hypercalcemia usually does not exceed 30 days.
see also
Reduction. PTH-P - PTH peptide

ICD

E83.5 Calcium metabolism disorder

Note

True ectopic PTH production is observed
extremely rare.

Directory of diseases. 2012 .

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Hypercalcemia is the most common life-threatening metabolic disorder in malignant neoplasms. Most often, hypercalcemia is complicated by myeloma and metastatic breast cancer (up to 40% of patients), but 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 caused by hyperfunction of the parathyroid glands or various malignant tumors.

Other causes account for less than 10% of cases hypercalcemia. A normal level of parathyroid hormone 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 often caused by 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 areas of metastatic bone damage and beyond. The development of humorally caused hypercalcemia can be observed in the absence of metastatic bone lesions. Most often, 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 lesions. In this case, bone resorption is caused by paracrine (local) stimulation of osteoclasts by various cytokines secreted 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 when immunologically determined) is responsible for the development of hypercalcemia in many solid tumors, but in oncohematological practice it is of clinical significance only in patients with T-cell lymphoma/leukemia. In lymphogranulomatosis, non-Hodgkin's lymphomas, multiple myeloma, the development of humoral hypercalcemia is 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 caused by 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, overdose of vitamins D and A, hyperthyroidism, etc.).

Clinical manifestations hypercalcemia are diverse and affect many organs and systems, and are also able to “masquerade” 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 acute 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, a history of polyuria, etc.) for manifestations of diabetes mellitus. In this situation, making the correct diagnosis and starting specific therapy are vital, since dehydration developing as a result of vomiting and polyuria can significantly aggravate the course of hypercalcemia, closing a “vicious” circle.

Serum total calcium level(routinely determined in most laboratories) usually adequately reflects the severity of hypercalcemia.
However, only 40% whey 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 increasing calcium levels depend specifically 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 albumin levels, 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 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, but this complication is most often observed in patients with advanced tumors resistant to antitumor therapy. In this regard, and also taking into account that hypercalcemia poses an immediate threat to the patient’s life, the main method of emergency treatment is symptomatic measures aimed at reducing calcium levels in the blood (by increasing calcium excretion in the urine and reducing bone resorption).


Attempts reduce calcium intake in the body(a diet with reduced calcium content) for hypercalcemia caused by a tumor are ineffective.
Reception must 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 supplements, vitamin D, retinoids).

The key point in emergency treatment of patients with hypercalcemia is hydration, which, in addition to increasing calcium excretion, avoids the consequences of dehydration caused by vomiting and polyuria. At the same time, even massive hydration (4 liters per day or more) does not stop hypercalcemia in most patients with malignant neoplasms. With this treatment, temporary normalization of calcium levels is observed in only a third of patients. The previously widely used technique of creating “forced diuresis” using furosemide, according to research, unfortunately, does not increase the effectiveness of hydration therapy.

Moreover, furosemide has the potential to increase hypovolemia and calcium reabsorption in the kidneys. Hydration, however, remains a necessary initial component of therapy for patients with hypercalcemia, as it is necessary to correct hypovolemia (which represents the greatest danger to life) and allows maintaining adequate renal function by preventing the crystallization of calcium salts in the tubules.

The first line of therapy aimed at reducing bone resorption, bisphosphonates (synthetic analogues of pyrophosphate, resistant to pyrophosphatase) are currently recognized. These drugs, by binding to molecules of the bone matrix (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 is relieved in 80-100% of patients) with low toxicity (20% of patients may develop fever, flu-like syndrome or moderate local reactions in the area of ​​administration). The effect of bisphosphonates develops quite quickly (within a few days) and persists for a long time.

The following drugs are currently available for use and have shown their effectiveness: clinical effectiveness: Aredia (pamidronate), Bondronate (ibandronate), Zometa (zoledronate). Calcitonin (miacalcic) also has the ability to reduce calcium levels by increasing its renal excretion and reducing bone resorption. This drug is the most fast-acting (onset of action in 2-4 hours). The main disadvantage of calcitonin is its short duration of action. The peak of therapeutic effect occurs at 24-48 hours of treatment, followed by a rapid decrease in effect. Corticosteroids can also inhibit bone resorption by osteoclasts, but due to their lower activity and more side effects, they are used only in patients with tumors sensitive to this type of therapy. Plicamycin (mithramycin) and gallium nitrate, used in foreign practice for resistance to bisphosphonate therapy, are not available in Russia.

When choosing tactics for 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. A total calcium level of more than 3 mmol/l and/or the presence of symptoms of hypercalcemia (especially dehydration, central nervous system disorders) is an absolute indication for hospitalization. In case of hypercalcemia, the patient should be started on hydration immediately. The rate of rehydration depends on the severity of water deficiency and the presence of concomitant cardiovascular and renal diseases in the patient. In case of severe dehydration and the absence of concomitant pathology, the introduction 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(adjusted for initial dehydration), the level of electrolytes (potassium, magnesium, sodium, chlorine) and creatinine is necessary when carrying out such therapy. Furosemide should only be used in cases of fluid retention after adequate rehydration. Immediately after adequate diuresis has been established (usually 2-3 hours after the start of hydration, hourly diuresis becomes equal to the volume of fluid administered), it is necessary to begin 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 adhere to the recommended rate of administration (duration of infusion: Aredia and Bondronate - at least 2 hours, Zometa at least 15 minutes). For patients who are critically ill and/or with calcium levels greater than 3.8 mmol/l, it is recommended to use a combination of a bisphosphonate with calcitonin (8 IU every 6 hours, intramuscularly for 2-3 days), which allows for a faster effect.

In severely ill patients, malignant tumors are the most common cause of hypercalcemia. It is usually caused by increased bone resorption.

  1. Metastases, -a; m. A secondary focus of the disease that appears due to the transfer of tumor cells or microorganisms through the blood or lymph from the primary focus. From Greek metastasis - movement.

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  2. Ectopic production of PTH is rare. Humoral paraneoplastic hypercalcemia is caused by the production of PTH-like peptides by various types of tumors (squamous cell carcinoma of various locations, kidney cancer, tumors of the parotid salivary glands). PTH-like peptides stimulate bone resorption and, by binding to PTH receptors in the kidneys, increase tubular reabsorption. PTH-like peptides are not detected by PTH tests.
    Metabolites, -oe; pl. Intermediate products of metabolism in human cells, many of which have a regulatory effect on biochemical. and physiol. processes in the body.

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    Prostaglandins are a family of short-lived compounds synthesized in cells from 20-carbon polyenoic acids (usually from arachidonic acid) with the participation of prostaglandin synthetase; Depending on the structure of the ring, prostaglandins are divided into 9 classes, representatives of which have specific activity in different types of cells. First isolated from prostate secretion.

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    Tumors that rarely or never develop hypercalcemia despite a high incidence of bone metastases.

V. Colon cancer.

Diagnostics

1. Manifestations of hypercalcemia depend both on the serum level of free calcium and on the rate of its increase. If calcium levels rise quickly, stupor and coma occur; and. A life-threatening condition caused by dysfunction of the brain stem; characterized by a complete loss of human consciousness, disappearance of muscle reflexes, impaired blood circulation, breathing and metabolism; deep K. is accompanied by the absence of even primitive responses (for example, to pain) and refers to terminal conditions

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1) Polyuria, nocturia, polydipsia.

2) Loss of appetite.

4) Weakness,

Late symptoms

1) Apathy, irritability, Depression - a state of pathologically low mood with a negative, pessimistic assessment of one’s present, past and future.

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2) Severe muscle weakness.

5) Visual impairment.

V. Treatment with thiazide diuretics.

d. Overdose of vitamin D or A.

d. Burnett's syndrome.

e. Familial benign hypercalcemia (familial hypocalciuric hypercalcemia).

and. Other reasons:

1) immobility with increased bone metabolism (for example, with Paget's disease, multiple myeloma);

2) tuberculosis, Sarcoidosis, -a; m. A disease of unknown origin, accompanied by the formation of specific. granulomas in the lungs, lymphatic. nodes, on the skin.

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6) acute renal failure in the recovery phase of diuresis;

7) severe liver diseases;

8) theophylline poisoning.

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