Many cellular activities, such as enzyme activity, neuronal transmission, cardiac function, and coagulation, calcium is an essential cation in the human body. A minor portion of the body’s calcium is also present in cells and extracellular fluids, but the majority is contained in the bones as calcium phosphate.
The active form of calcium, free or ionized calcium, makes about 45% of the serum calcium content, while 10% is bound to anions. The remaining 10% is attached to proteins. While alkalosis can have the opposite result, systemic acidosis can decrease calcium’s affinity for albumin and raise serum levels.
The greatest levels of serum calcium are seen in newborns and babies; these levels drop during childhood and adolescence, and by the time an individual is 17 years old, they have stabilized. With normal blood calcium levels ranging from 8.8 mg/dL to 10.8 mg/dL, hypercalcemia is defined as a serum calcium concentration with two standard deviations over the mean values. Ninety percent of all instances of hypercalcemia are caused by primary hyperparathyroidism and cancer.
Epidemiology
The prevalence of hypercalcemia in the general population is estimated to be between 1% and 2%. In most cases (90%), hypercalcemia is caused by primary hyperparathyroidism or malignancy.
The prevalence of primary hyperparathyroidism in the general population ranges from 0.2% to 0.8%, increasing with age. Additionally, hypercalcemia is associated with 2% of all cancers, with a prevalence of 0.4% to 1.3% in the pediatric age group.
Anatomy
Pathophysiology
Calcium levels in the body are regulated through a complex interplay of hormones, receptors, and vitamins. The primary contributors involved in this regulation include the plasma membrane calcium receptor, parathyroid hormone (PTH) and its receptor, calcitonin and its receptor, and the actions of vitamin D on various organs such as the kidneys, bones, and intestines. PTH is significant in calcium regulation as it directly stimulates calcium resorption from bones and indirectly increases calcium absorption from the gut through stimulating the production of vitamin D3.
Primary hyperparathyroidism is a condition where there is an abnormal secretion of PTH from the parathyroid gland. This can be caused by a solitary adenoma or diffuse hyperplasia of the gland and results in an abnormal set point in the relationship between calcium and PTH levels. On the other hand, familial hypocalciuric hypercalcemia is an inherited condition caused by a mutation in the calcium-sensing receptor gene.
Ectopic vitamin D production can also result in elevated calcium levels and can be caused by granulomatous lesions. In rare cases, transient neonatal hypercalcemia can also occur in infants born to mothers with hypoparathyroidism. Hypercalcemia resulting from primary hyperparathyroidism is usually mild and can remain asymptomatic for years. However, hypercalcemia associated with malignancy is characterized by rapidly increasing calcium levels.
Etiology
An excessive amount of parathyroid hormone is the major cause of hypercalcemia. Hyperplasia or adenoma of the gland, familial hypocalcciuric hypercalcemia, and multiple endocrine neoplasia syndromes are among the PTH-mediated causes (type1 2A). An inactivating mutation in the calcium-sensing receptor gene causes the autosomal dominant disorder known as familial hypocalcciuric hypercalcemia.
The second essential etiology to take into account is a malignancy, even though it is more frequent in adults than in juvenile patients. Higher calcium levels can be linked to rhabdomyosarcoma, leukemia, lymphomas, and renal carcinomas through the action of PTH-related peptides. In addition to being consequent to excessive milk consumption, hypervitaminosis D can also be caused by granulomatous diseases, including sarcoidosis, TB, or fungal infections.
Hypercalcemia can have endocrine causes, including thyrotoxicosis (caused by thyroid hormone stimulating osteoclast function), hypoadrenalism, and pheochromocytomas. Acute or chronic renal failure, the milk-alkali syndrome, lithium, thiazide diuretics, subcutaneous fat necrosis, Williams syndrome, hypophosphatasia, Murk Jansen syndrome, hypervitaminosis A, acute or chronic renal failure, and extended immobilization are some other unrelated reasons.
Short stature, subvalvular aortic stenosis, elfin facies, and developmental delay are the hallmarks of Williams-Beuren syndrome. Extremely small stature (short-limbed dwarfism), protruding eyes, wide-open fontanelles, high-arched palate, and micrognathia are characteristics of Murk-Jansen syndrome.
Genetics
Prognostic Factors
When a benign condition causes hypercalcemia, the prognosis is favorable; however, the prognosis is poor when the etiology is malignancy. Patients with hypercalcemia linked to cancer frequently experience symptoms and require recurrent hospital stays.
Most patients pass away within a few months when hypercalcemia is driven by ectopic synthesis of PTH-related protein. The osteolytic metastatic lesions bring on fractures, nerve compression, and paralysis.
Clinical History
Clinical History
The primary signs in both acute and chronic conditions involve gastrointestinal, renal, and neuromuscular function. Nausea, anorexia, vomiting, polydipsia, polyuria, dehydration, confusion, depression, and weakness are frequent symptoms of acute hypercalcemia, which can develop into a stupor and coma.
Chronic hypercalcemia patients may have a history of constipation, dyspepsia (usually not related to a real ulcer), pancreatitis, and nephrolithiasis but few other signs or symptoms.
Hypercalcemia symptoms are often present when blood calcium levels are higher than 12 mg/dl. Regardless of origin, the general signs and symptoms can be summed up as groans, bones, stones, moans, thrones, and mental overtones.
Groans: Pain, vomiting, and nausea are gastrointestinal symptoms. Pancreatitis and peptic ulcer disease can result from hypercalcemia.
Bones: Complications associated with bones, such as bone discomfort. Osteomalacia, osteoporosis, , arthritis, and pathological fractures can all be caused by hypercalcemia.
Stones: Presence of renal stones in the patient which induces pain.
Moans: Indicates drowsiness and ill feeling.
Thrones: Polydipsia, polyuria, and constipation are recognized as thrones.
Mental overtones: Lethargy, confusion, depression, and memory loss are psychic overtones.
Physical Examination
Physical Examination
Initial symptoms include increased thirst, polydipsia, and polyuria; however, nephrolithiasis and nephrocalcinosis develop in chronic instances. Impaired focus and changed mental state ranging from bewilderment to irritation are examples of neurologic characteristics.
Extreme hypercalcemia prevents cardiac and neuromuscular depolarization, which results in arrhythmias and weak muscles. Hypercalcemia may also shorten the QT interval on EKG due to an accelerated rate of cardiac repolarization. Arrhythmias such as bradycardia and first-degree atrioventricular block are possible, as is digitalis sensitivity. As a result, acute hypercalcemia can be a life-threatening medical emergency.
Encephalopathy can occur at values over 14 mg/dL, and levels over 15 mg/dL constitute a medical emergency. A sign of pancreatitis should be severe, immediate abdominal discomfort. Osseous alterations, characterized radiographically by subperiosteal and endosteal bone resorption, can cause bone discomfort, aberrant gait patterns, and fractures. Hypercalcemia can result in poor weight growth and failure to thrive in newborns and young children.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Hypermagnesemia
Hyperphosphatemia
Hyperparathyroidism
Williams Syndrome
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Even in asymptomatic people, treatment for hypercalcemia is necessary if the patient has symptoms or if their calcium level is above 15 mg/dL. Treatment of hypercalcemia aims to decrease bone resorption, decrease GI absorption, and promote extracellular fluid clearance. The goal of immediate therapy is to replenish any fluid deficit and induce diuresis (urine output of 200 to 300 mL/h), which is achieved by infusing 0.9% saline at twice the maintenance rate while promoting calcium excretion in the urine.
Hydration can increase urine calcium excretion by enhancing glomerular calcium filtration and lowering sodium and calcium tubular reabsorption. Although this therapy is always essential, it should be administered cautiously in individuals with impaired cardiovascular or renal function. The preferred therapy method for individuals with heart failure or renal insufficiency is hemodialysis, which rapidly lowers serum calcium levels.
Although loop diuretics may increase renal excretion, paradoxical hypercalcemia might develop owing to bone resorption. Hence, they should be taken cautiously. Dialysis is also reserved for severely hypercalcemic patients who have failed previous treatments. Peritoneal dialysis and hemodialysis are both successful treatments.
Cinacalcet, a calcimimetic, can be used for the treatment of hypercalcemia induced by severe primary HPT (especially if caused by a parathyroid carcinoma). Although subcutaneous administration of calcitonin is an alternative, the effects are often moderate and short-lived. Mithramycin is frequently given to individuals with hypercalcemia linked to cancer because it can inhibit osteoclast activity. However, the medication causes serious kidney, liver, and bone marrow damage.
Glucocorticoids like hydrocortisone may be used, especially if the underlying condition is known to respond to this medication. Patients with hypercalcemia caused by hematologic malignancies such as lymphoma or myeloma and those with vitamin D intoxication or granulomatous disease, where 1,25(OH)2D synthesis and action may be impeded, may benefit.
Steroids can treat hypercalcemia from high vitamin D since they block one alpha-hydroxylase activity. Hypervitaminosis D has also been treated with ketoconazole, an antifungal drug that inhibits 1-alpha-hydroxylase activity. Encourage movement as tolerated and get enough water to avoid hypercalcemia or immobility.
Many cellular activities, such as enzyme activity, neuronal transmission, cardiac function, and coagulation, calcium is an essential cation in the human body. A minor portion of the body’s calcium is also present in cells and extracellular fluids, but the majority is contained in the bones as calcium phosphate.
The active form of calcium, free or ionized calcium, makes about 45% of the serum calcium content, while 10% is bound to anions. The remaining 10% is attached to proteins. While alkalosis can have the opposite result, systemic acidosis can decrease calcium’s affinity for albumin and raise serum levels.
The greatest levels of serum calcium are seen in newborns and babies; these levels drop during childhood and adolescence, and by the time an individual is 17 years old, they have stabilized. With normal blood calcium levels ranging from 8.8 mg/dL to 10.8 mg/dL, hypercalcemia is defined as a serum calcium concentration with two standard deviations over the mean values. Ninety percent of all instances of hypercalcemia are caused by primary hyperparathyroidism and cancer.
The prevalence of hypercalcemia in the general population is estimated to be between 1% and 2%. In most cases (90%), hypercalcemia is caused by primary hyperparathyroidism or malignancy.
The prevalence of primary hyperparathyroidism in the general population ranges from 0.2% to 0.8%, increasing with age. Additionally, hypercalcemia is associated with 2% of all cancers, with a prevalence of 0.4% to 1.3% in the pediatric age group.
Calcium levels in the body are regulated through a complex interplay of hormones, receptors, and vitamins. The primary contributors involved in this regulation include the plasma membrane calcium receptor, parathyroid hormone (PTH) and its receptor, calcitonin and its receptor, and the actions of vitamin D on various organs such as the kidneys, bones, and intestines. PTH is significant in calcium regulation as it directly stimulates calcium resorption from bones and indirectly increases calcium absorption from the gut through stimulating the production of vitamin D3.
Primary hyperparathyroidism is a condition where there is an abnormal secretion of PTH from the parathyroid gland. This can be caused by a solitary adenoma or diffuse hyperplasia of the gland and results in an abnormal set point in the relationship between calcium and PTH levels. On the other hand, familial hypocalciuric hypercalcemia is an inherited condition caused by a mutation in the calcium-sensing receptor gene.
Ectopic vitamin D production can also result in elevated calcium levels and can be caused by granulomatous lesions. In rare cases, transient neonatal hypercalcemia can also occur in infants born to mothers with hypoparathyroidism. Hypercalcemia resulting from primary hyperparathyroidism is usually mild and can remain asymptomatic for years. However, hypercalcemia associated with malignancy is characterized by rapidly increasing calcium levels.
An excessive amount of parathyroid hormone is the major cause of hypercalcemia. Hyperplasia or adenoma of the gland, familial hypocalcciuric hypercalcemia, and multiple endocrine neoplasia syndromes are among the PTH-mediated causes (type1 2A). An inactivating mutation in the calcium-sensing receptor gene causes the autosomal dominant disorder known as familial hypocalcciuric hypercalcemia.
The second essential etiology to take into account is a malignancy, even though it is more frequent in adults than in juvenile patients. Higher calcium levels can be linked to rhabdomyosarcoma, leukemia, lymphomas, and renal carcinomas through the action of PTH-related peptides. In addition to being consequent to excessive milk consumption, hypervitaminosis D can also be caused by granulomatous diseases, including sarcoidosis, TB, or fungal infections.
Hypercalcemia can have endocrine causes, including thyrotoxicosis (caused by thyroid hormone stimulating osteoclast function), hypoadrenalism, and pheochromocytomas. Acute or chronic renal failure, the milk-alkali syndrome, lithium, thiazide diuretics, subcutaneous fat necrosis, Williams syndrome, hypophosphatasia, Murk Jansen syndrome, hypervitaminosis A, acute or chronic renal failure, and extended immobilization are some other unrelated reasons.
Short stature, subvalvular aortic stenosis, elfin facies, and developmental delay are the hallmarks of Williams-Beuren syndrome. Extremely small stature (short-limbed dwarfism), protruding eyes, wide-open fontanelles, high-arched palate, and micrognathia are characteristics of Murk-Jansen syndrome.
When a benign condition causes hypercalcemia, the prognosis is favorable; however, the prognosis is poor when the etiology is malignancy. Patients with hypercalcemia linked to cancer frequently experience symptoms and require recurrent hospital stays.
Most patients pass away within a few months when hypercalcemia is driven by ectopic synthesis of PTH-related protein. The osteolytic metastatic lesions bring on fractures, nerve compression, and paralysis.
Clinical History
The primary signs in both acute and chronic conditions involve gastrointestinal, renal, and neuromuscular function. Nausea, anorexia, vomiting, polydipsia, polyuria, dehydration, confusion, depression, and weakness are frequent symptoms of acute hypercalcemia, which can develop into a stupor and coma.
Chronic hypercalcemia patients may have a history of constipation, dyspepsia (usually not related to a real ulcer), pancreatitis, and nephrolithiasis but few other signs or symptoms.
Hypercalcemia symptoms are often present when blood calcium levels are higher than 12 mg/dl. Regardless of origin, the general signs and symptoms can be summed up as groans, bones, stones, moans, thrones, and mental overtones.
Groans: Pain, vomiting, and nausea are gastrointestinal symptoms. Pancreatitis and peptic ulcer disease can result from hypercalcemia.
Bones: Complications associated with bones, such as bone discomfort. Osteomalacia, osteoporosis, , arthritis, and pathological fractures can all be caused by hypercalcemia.
Stones: Presence of renal stones in the patient which induces pain.
Moans: Indicates drowsiness and ill feeling.
Thrones: Polydipsia, polyuria, and constipation are recognized as thrones.
Mental overtones: Lethargy, confusion, depression, and memory loss are psychic overtones.
Physical Examination
Initial symptoms include increased thirst, polydipsia, and polyuria; however, nephrolithiasis and nephrocalcinosis develop in chronic instances. Impaired focus and changed mental state ranging from bewilderment to irritation are examples of neurologic characteristics.
Extreme hypercalcemia prevents cardiac and neuromuscular depolarization, which results in arrhythmias and weak muscles. Hypercalcemia may also shorten the QT interval on EKG due to an accelerated rate of cardiac repolarization. Arrhythmias such as bradycardia and first-degree atrioventricular block are possible, as is digitalis sensitivity. As a result, acute hypercalcemia can be a life-threatening medical emergency.
Encephalopathy can occur at values over 14 mg/dL, and levels over 15 mg/dL constitute a medical emergency. A sign of pancreatitis should be severe, immediate abdominal discomfort. Osseous alterations, characterized radiographically by subperiosteal and endosteal bone resorption, can cause bone discomfort, aberrant gait patterns, and fractures. Hypercalcemia can result in poor weight growth and failure to thrive in newborns and young children.
Differential Diagnoses
Hypermagnesemia
Hyperphosphatemia
Hyperparathyroidism
Williams Syndrome
Even in asymptomatic people, treatment for hypercalcemia is necessary if the patient has symptoms or if their calcium level is above 15 mg/dL. Treatment of hypercalcemia aims to decrease bone resorption, decrease GI absorption, and promote extracellular fluid clearance. The goal of immediate therapy is to replenish any fluid deficit and induce diuresis (urine output of 200 to 300 mL/h), which is achieved by infusing 0.9% saline at twice the maintenance rate while promoting calcium excretion in the urine.
Hydration can increase urine calcium excretion by enhancing glomerular calcium filtration and lowering sodium and calcium tubular reabsorption. Although this therapy is always essential, it should be administered cautiously in individuals with impaired cardiovascular or renal function. The preferred therapy method for individuals with heart failure or renal insufficiency is hemodialysis, which rapidly lowers serum calcium levels.
Although loop diuretics may increase renal excretion, paradoxical hypercalcemia might develop owing to bone resorption. Hence, they should be taken cautiously. Dialysis is also reserved for severely hypercalcemic patients who have failed previous treatments. Peritoneal dialysis and hemodialysis are both successful treatments.
Cinacalcet, a calcimimetic, can be used for the treatment of hypercalcemia induced by severe primary HPT (especially if caused by a parathyroid carcinoma). Although subcutaneous administration of calcitonin is an alternative, the effects are often moderate and short-lived. Mithramycin is frequently given to individuals with hypercalcemia linked to cancer because it can inhibit osteoclast activity. However, the medication causes serious kidney, liver, and bone marrow damage.
Glucocorticoids like hydrocortisone may be used, especially if the underlying condition is known to respond to this medication. Patients with hypercalcemia caused by hematologic malignancies such as lymphoma or myeloma and those with vitamin D intoxication or granulomatous disease, where 1,25(OH)2D synthesis and action may be impeded, may benefit.
Steroids can treat hypercalcemia from high vitamin D since they block one alpha-hydroxylase activity. Hypervitaminosis D has also been treated with ketoconazole, an antifungal drug that inhibits 1-alpha-hydroxylase activity. Encourage movement as tolerated and get enough water to avoid hypercalcemia or immobility.
Many cellular activities, such as enzyme activity, neuronal transmission, cardiac function, and coagulation, calcium is an essential cation in the human body. A minor portion of the body’s calcium is also present in cells and extracellular fluids, but the majority is contained in the bones as calcium phosphate.
The active form of calcium, free or ionized calcium, makes about 45% of the serum calcium content, while 10% is bound to anions. The remaining 10% is attached to proteins. While alkalosis can have the opposite result, systemic acidosis can decrease calcium’s affinity for albumin and raise serum levels.
The greatest levels of serum calcium are seen in newborns and babies; these levels drop during childhood and adolescence, and by the time an individual is 17 years old, they have stabilized. With normal blood calcium levels ranging from 8.8 mg/dL to 10.8 mg/dL, hypercalcemia is defined as a serum calcium concentration with two standard deviations over the mean values. Ninety percent of all instances of hypercalcemia are caused by primary hyperparathyroidism and cancer.
The prevalence of hypercalcemia in the general population is estimated to be between 1% and 2%. In most cases (90%), hypercalcemia is caused by primary hyperparathyroidism or malignancy.
The prevalence of primary hyperparathyroidism in the general population ranges from 0.2% to 0.8%, increasing with age. Additionally, hypercalcemia is associated with 2% of all cancers, with a prevalence of 0.4% to 1.3% in the pediatric age group.
Calcium levels in the body are regulated through a complex interplay of hormones, receptors, and vitamins. The primary contributors involved in this regulation include the plasma membrane calcium receptor, parathyroid hormone (PTH) and its receptor, calcitonin and its receptor, and the actions of vitamin D on various organs such as the kidneys, bones, and intestines. PTH is significant in calcium regulation as it directly stimulates calcium resorption from bones and indirectly increases calcium absorption from the gut through stimulating the production of vitamin D3.
Primary hyperparathyroidism is a condition where there is an abnormal secretion of PTH from the parathyroid gland. This can be caused by a solitary adenoma or diffuse hyperplasia of the gland and results in an abnormal set point in the relationship between calcium and PTH levels. On the other hand, familial hypocalciuric hypercalcemia is an inherited condition caused by a mutation in the calcium-sensing receptor gene.
Ectopic vitamin D production can also result in elevated calcium levels and can be caused by granulomatous lesions. In rare cases, transient neonatal hypercalcemia can also occur in infants born to mothers with hypoparathyroidism. Hypercalcemia resulting from primary hyperparathyroidism is usually mild and can remain asymptomatic for years. However, hypercalcemia associated with malignancy is characterized by rapidly increasing calcium levels.
An excessive amount of parathyroid hormone is the major cause of hypercalcemia. Hyperplasia or adenoma of the gland, familial hypocalcciuric hypercalcemia, and multiple endocrine neoplasia syndromes are among the PTH-mediated causes (type1 2A). An inactivating mutation in the calcium-sensing receptor gene causes the autosomal dominant disorder known as familial hypocalcciuric hypercalcemia.
The second essential etiology to take into account is a malignancy, even though it is more frequent in adults than in juvenile patients. Higher calcium levels can be linked to rhabdomyosarcoma, leukemia, lymphomas, and renal carcinomas through the action of PTH-related peptides. In addition to being consequent to excessive milk consumption, hypervitaminosis D can also be caused by granulomatous diseases, including sarcoidosis, TB, or fungal infections.
Hypercalcemia can have endocrine causes, including thyrotoxicosis (caused by thyroid hormone stimulating osteoclast function), hypoadrenalism, and pheochromocytomas. Acute or chronic renal failure, the milk-alkali syndrome, lithium, thiazide diuretics, subcutaneous fat necrosis, Williams syndrome, hypophosphatasia, Murk Jansen syndrome, hypervitaminosis A, acute or chronic renal failure, and extended immobilization are some other unrelated reasons.
Short stature, subvalvular aortic stenosis, elfin facies, and developmental delay are the hallmarks of Williams-Beuren syndrome. Extremely small stature (short-limbed dwarfism), protruding eyes, wide-open fontanelles, high-arched palate, and micrognathia are characteristics of Murk-Jansen syndrome.
When a benign condition causes hypercalcemia, the prognosis is favorable; however, the prognosis is poor when the etiology is malignancy. Patients with hypercalcemia linked to cancer frequently experience symptoms and require recurrent hospital stays.
Most patients pass away within a few months when hypercalcemia is driven by ectopic synthesis of PTH-related protein. The osteolytic metastatic lesions bring on fractures, nerve compression, and paralysis.
Clinical History
The primary signs in both acute and chronic conditions involve gastrointestinal, renal, and neuromuscular function. Nausea, anorexia, vomiting, polydipsia, polyuria, dehydration, confusion, depression, and weakness are frequent symptoms of acute hypercalcemia, which can develop into a stupor and coma.
Chronic hypercalcemia patients may have a history of constipation, dyspepsia (usually not related to a real ulcer), pancreatitis, and nephrolithiasis but few other signs or symptoms.
Hypercalcemia symptoms are often present when blood calcium levels are higher than 12 mg/dl. Regardless of origin, the general signs and symptoms can be summed up as groans, bones, stones, moans, thrones, and mental overtones.
Groans: Pain, vomiting, and nausea are gastrointestinal symptoms. Pancreatitis and peptic ulcer disease can result from hypercalcemia.
Bones: Complications associated with bones, such as bone discomfort. Osteomalacia, osteoporosis, , arthritis, and pathological fractures can all be caused by hypercalcemia.
Stones: Presence of renal stones in the patient which induces pain.
Moans: Indicates drowsiness and ill feeling.
Thrones: Polydipsia, polyuria, and constipation are recognized as thrones.
Mental overtones: Lethargy, confusion, depression, and memory loss are psychic overtones.
Physical Examination
Initial symptoms include increased thirst, polydipsia, and polyuria; however, nephrolithiasis and nephrocalcinosis develop in chronic instances. Impaired focus and changed mental state ranging from bewilderment to irritation are examples of neurologic characteristics.
Extreme hypercalcemia prevents cardiac and neuromuscular depolarization, which results in arrhythmias and weak muscles. Hypercalcemia may also shorten the QT interval on EKG due to an accelerated rate of cardiac repolarization. Arrhythmias such as bradycardia and first-degree atrioventricular block are possible, as is digitalis sensitivity. As a result, acute hypercalcemia can be a life-threatening medical emergency.
Encephalopathy can occur at values over 14 mg/dL, and levels over 15 mg/dL constitute a medical emergency. A sign of pancreatitis should be severe, immediate abdominal discomfort. Osseous alterations, characterized radiographically by subperiosteal and endosteal bone resorption, can cause bone discomfort, aberrant gait patterns, and fractures. Hypercalcemia can result in poor weight growth and failure to thrive in newborns and young children.
Differential Diagnoses
Hypermagnesemia
Hyperphosphatemia
Hyperparathyroidism
Williams Syndrome
Even in asymptomatic people, treatment for hypercalcemia is necessary if the patient has symptoms or if their calcium level is above 15 mg/dL. Treatment of hypercalcemia aims to decrease bone resorption, decrease GI absorption, and promote extracellular fluid clearance. The goal of immediate therapy is to replenish any fluid deficit and induce diuresis (urine output of 200 to 300 mL/h), which is achieved by infusing 0.9% saline at twice the maintenance rate while promoting calcium excretion in the urine.
Hydration can increase urine calcium excretion by enhancing glomerular calcium filtration and lowering sodium and calcium tubular reabsorption. Although this therapy is always essential, it should be administered cautiously in individuals with impaired cardiovascular or renal function. The preferred therapy method for individuals with heart failure or renal insufficiency is hemodialysis, which rapidly lowers serum calcium levels.
Although loop diuretics may increase renal excretion, paradoxical hypercalcemia might develop owing to bone resorption. Hence, they should be taken cautiously. Dialysis is also reserved for severely hypercalcemic patients who have failed previous treatments. Peritoneal dialysis and hemodialysis are both successful treatments.
Cinacalcet, a calcimimetic, can be used for the treatment of hypercalcemia induced by severe primary HPT (especially if caused by a parathyroid carcinoma). Although subcutaneous administration of calcitonin is an alternative, the effects are often moderate and short-lived. Mithramycin is frequently given to individuals with hypercalcemia linked to cancer because it can inhibit osteoclast activity. However, the medication causes serious kidney, liver, and bone marrow damage.
Glucocorticoids like hydrocortisone may be used, especially if the underlying condition is known to respond to this medication. Patients with hypercalcemia caused by hematologic malignancies such as lymphoma or myeloma and those with vitamin D intoxication or granulomatous disease, where 1,25(OH)2D synthesis and action may be impeded, may benefit.
Steroids can treat hypercalcemia from high vitamin D since they block one alpha-hydroxylase activity. Hypervitaminosis D has also been treated with ketoconazole, an antifungal drug that inhibits 1-alpha-hydroxylase activity. Encourage movement as tolerated and get enough water to avoid hypercalcemia or immobility.
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