Phosphate is a crucial element for various cellular functions in the body. It plays a critical role in the replication of DNA and RNA as essential components of nucleic acids. Additionally, it serves as an energy source for molecular functions by contributing to the production of ATP.
Furthermore, phosphate adds or removes phosphate groups to or from proteins, acting as an on/off switch to regulate molecular activity. Given its vital role in numerous cellular functions, disturbances in serum phosphate levels can significantly affect the body. Hypophosphatemia occurs when the adult serum phosphate level falls below 2.5 mg/dL.
A normal serum phosphate level in infants is significantly higher, approximately 7 mg/dL. Hypophosphatemia is a common laboratory abnormality often detected incidentally during routine blood tests. Low phosphate levels can lead to various symptoms, including muscle weakness, bone pain, and confusion.
Epidemiology
In most cases, patients with hypophosphatemia do not show any symptoms. However, the condition is prevalent among certain groups of people, such as those with alcoholism, diabetic ketoacidosis, or sepsis, with a frequency of up to 80%. The morbidity, or the diseased state, associated with hypophosphatemia varies greatly and depends on its underlying cause and severity.
For instance, individuals with severe hypophosphatemia may experience muscle weakness, respiratory failure, and cardiac dysfunction. On the other hand, those with milder forms of hypophosphatemia may experience symptoms such as bone pain, loss of appetite, and difficulty concentrating.
Anatomy
Pathophysiology
Hypophosphatemia can occur due to inadequate phosphate intake over a prolonged period, malabsorption in the intestines, or phosphate binding by certain medications. Most diets contain enough phosphate to meet the body’s needs, and renal adaptations can compensate for short-term deficiencies.
Intestinal malabsorption can be caused by various factors, including chronic diarrhea, which increases phosphate losses through the intestines. Certain medications, such as aluminum and magnesium antacids, can bind with phosphate, resulting in a net loss of phosphate from the body. This reaction creates non-absorbable aluminum or magnesium-bound phosphate salts.
The primary mechanism for increased phosphate excretion occurs in the renal system, where the proximal and distal tubules reabsorb up to 70% and 15% of filtered phosphate, respectively. The regulation of phosphate resorption depends on serum phosphate concentration, whereby mild phosphate depletion triggers increased reabsorption via sodium-phosphate cotransporters in the proximal tubule and increased formation of these transporters.
Conversely, parathyroid hormone inhibits the activity of sodium-phosphate cotransporters, thereby increasing phosphate excretion. In addition, several factors, such as fibroblast growth factor 23, fibroblast growth factor 7, extracellular matrix phosphoglycoprotein, and secreted frizzled-related protein-4, decrease phosphate reabsorption by sodium-phosphate cotransporters. Therefore, an increase in parathyroid hormone levels may lead to hypophosphatemia.
Etiology
Hypophosphatemia is typically caused by one of three factors insufficient intake of phosphate, excessive excretion of phosphate, or a shift of phosphate from the extracellular space into the intracellular space. Insufficient phosphate intake can occur due to inadequate dietary intake or malabsorption of phosphate in the gastrointestinal tract.
In some cases, patients with chronic alcoholism or anorexia nervosa may not consume enough phosphate in their diet to maintain normal levels in the blood. Excessive phosphate excretion can result from conditions such as renal tubular disorders, hyperparathyroidism, and certain medications such as diuretics. When the kidneys excrete too much phosphate, it can lead to hypophosphatemia.
The third cause of hypophosphatemia is the shift of phosphate from the extracellular space into the intracellular space. This can occur in various situations, including refeeding syndrome, diabetic ketoacidosis, and respiratory alkalosis. In these conditions, the body’s cells rapidly take up phosphate from the blood, decreasing phosphate concentration in the extracellular space.
Genetics
Prognostic Factors
Clinical History
Clinical History
When the body experiences prolonged hypophosphatemia, the result can be a variety of negative impacts on different systems in the body. One of the most significant effects is decreased bone mineralization, leading to osteoporosis, osteopenia, osteomalacia, and rickets. The central nervous system can also be affected, leading to metabolic encephalopathy due to ATP depletion.
Symptoms can include irritability, altered mental state, numbness, paresthesias, seizures, or even coma. The heart can also be impacted, with possible systolic heart failure and increased risk of arrhythmias due to less stable myocytes. Hypophosphatemia can also affect pulmonary function, leading to hypoventilation, particularly concerning ventilator-dependent patients.
Those with gastrointestinal issues may also experience dysphagia or ileus due to ATP deficiency. Additionally, generalized muscle weakness and rhabdomyolysis may occur, leading to renal injury and increased creatinine phosphokinases, particularly in acute or chronic hypophosphatemia cases, such as in individuals with alcohol use disorder.
While rare, hypophosphatemia can also impact the hematology systems, such as increased erythrocyte rigidity, predisposing individuals to hemolysis, reduced phagocytosis, and granulocyte chemotaxis by white blood cells, as well as thrombocytopenia.
Physical Examination
Physical Examination
Although most patients with mild hypophosphatemia do not experience symptoms, those with severe hypophosphatemia may present with various clinical manifestations. One of the most common symptoms of hypophosphatemia is generalized weakness, which can range from mild to moderate in severity.
In addition, patients with severe hypophosphatemia may experience altered mental status and focal neurologic findings such as numbness or reflexive weakness. Cardiac manifestations of hypophosphatemia may include heart failure, as phosphate is critical in maintaining normal cardiac function. Muscle pain and muscle weakness may also be present in severe cases of hypophosphatemia.
Take 1 to 2 tablets orally every 4 hours
One packet dissolved in 75 ml of water Low urinary phosphate
Take 1 to 2 tablets orally every 6 hours Dosage Modifications
Renal impairment: Be cautious while using it in patients with long-term kidney disease or impaired kidney function
4 years: Safety and efficacy not determined
≥4 years: take 1 tablet orally every 6 hours
1 packet orally every 6 hours dissolved in 75 ml of water Low urinary phosphate
<4 years: safety and efficacy not determined
≥4 years: take 1 to 2 tablets orally every 6 hour
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Phosphate is a crucial element for various cellular functions in the body. It plays a critical role in the replication of DNA and RNA as essential components of nucleic acids. Additionally, it serves as an energy source for molecular functions by contributing to the production of ATP.
Furthermore, phosphate adds or removes phosphate groups to or from proteins, acting as an on/off switch to regulate molecular activity. Given its vital role in numerous cellular functions, disturbances in serum phosphate levels can significantly affect the body. Hypophosphatemia occurs when the adult serum phosphate level falls below 2.5 mg/dL.
A normal serum phosphate level in infants is significantly higher, approximately 7 mg/dL. Hypophosphatemia is a common laboratory abnormality often detected incidentally during routine blood tests. Low phosphate levels can lead to various symptoms, including muscle weakness, bone pain, and confusion.
In most cases, patients with hypophosphatemia do not show any symptoms. However, the condition is prevalent among certain groups of people, such as those with alcoholism, diabetic ketoacidosis, or sepsis, with a frequency of up to 80%. The morbidity, or the diseased state, associated with hypophosphatemia varies greatly and depends on its underlying cause and severity.
For instance, individuals with severe hypophosphatemia may experience muscle weakness, respiratory failure, and cardiac dysfunction. On the other hand, those with milder forms of hypophosphatemia may experience symptoms such as bone pain, loss of appetite, and difficulty concentrating.
Hypophosphatemia can occur due to inadequate phosphate intake over a prolonged period, malabsorption in the intestines, or phosphate binding by certain medications. Most diets contain enough phosphate to meet the body’s needs, and renal adaptations can compensate for short-term deficiencies.
Intestinal malabsorption can be caused by various factors, including chronic diarrhea, which increases phosphate losses through the intestines. Certain medications, such as aluminum and magnesium antacids, can bind with phosphate, resulting in a net loss of phosphate from the body. This reaction creates non-absorbable aluminum or magnesium-bound phosphate salts.
The primary mechanism for increased phosphate excretion occurs in the renal system, where the proximal and distal tubules reabsorb up to 70% and 15% of filtered phosphate, respectively. The regulation of phosphate resorption depends on serum phosphate concentration, whereby mild phosphate depletion triggers increased reabsorption via sodium-phosphate cotransporters in the proximal tubule and increased formation of these transporters.
Conversely, parathyroid hormone inhibits the activity of sodium-phosphate cotransporters, thereby increasing phosphate excretion. In addition, several factors, such as fibroblast growth factor 23, fibroblast growth factor 7, extracellular matrix phosphoglycoprotein, and secreted frizzled-related protein-4, decrease phosphate reabsorption by sodium-phosphate cotransporters. Therefore, an increase in parathyroid hormone levels may lead to hypophosphatemia.
Hypophosphatemia is typically caused by one of three factors insufficient intake of phosphate, excessive excretion of phosphate, or a shift of phosphate from the extracellular space into the intracellular space. Insufficient phosphate intake can occur due to inadequate dietary intake or malabsorption of phosphate in the gastrointestinal tract.
In some cases, patients with chronic alcoholism or anorexia nervosa may not consume enough phosphate in their diet to maintain normal levels in the blood. Excessive phosphate excretion can result from conditions such as renal tubular disorders, hyperparathyroidism, and certain medications such as diuretics. When the kidneys excrete too much phosphate, it can lead to hypophosphatemia.
The third cause of hypophosphatemia is the shift of phosphate from the extracellular space into the intracellular space. This can occur in various situations, including refeeding syndrome, diabetic ketoacidosis, and respiratory alkalosis. In these conditions, the body’s cells rapidly take up phosphate from the blood, decreasing phosphate concentration in the extracellular space.
Clinical History
When the body experiences prolonged hypophosphatemia, the result can be a variety of negative impacts on different systems in the body. One of the most significant effects is decreased bone mineralization, leading to osteoporosis, osteopenia, osteomalacia, and rickets. The central nervous system can also be affected, leading to metabolic encephalopathy due to ATP depletion.
Symptoms can include irritability, altered mental state, numbness, paresthesias, seizures, or even coma. The heart can also be impacted, with possible systolic heart failure and increased risk of arrhythmias due to less stable myocytes. Hypophosphatemia can also affect pulmonary function, leading to hypoventilation, particularly concerning ventilator-dependent patients.
Those with gastrointestinal issues may also experience dysphagia or ileus due to ATP deficiency. Additionally, generalized muscle weakness and rhabdomyolysis may occur, leading to renal injury and increased creatinine phosphokinases, particularly in acute or chronic hypophosphatemia cases, such as in individuals with alcohol use disorder.
While rare, hypophosphatemia can also impact the hematology systems, such as increased erythrocyte rigidity, predisposing individuals to hemolysis, reduced phagocytosis, and granulocyte chemotaxis by white blood cells, as well as thrombocytopenia.
Physical Examination
Although most patients with mild hypophosphatemia do not experience symptoms, those with severe hypophosphatemia may present with various clinical manifestations. One of the most common symptoms of hypophosphatemia is generalized weakness, which can range from mild to moderate in severity.
In addition, patients with severe hypophosphatemia may experience altered mental status and focal neurologic findings such as numbness or reflexive weakness. Cardiac manifestations of hypophosphatemia may include heart failure, as phosphate is critical in maintaining normal cardiac function. Muscle pain and muscle weakness may also be present in severe cases of hypophosphatemia.
Take 1 to 2 tablets orally every 4 hours
One packet dissolved in 75 ml of water Low urinary phosphate
Take 1 to 2 tablets orally every 6 hours Dosage Modifications
Renal impairment: Be cautious while using it in patients with long-term kidney disease or impaired kidney function
4 years: Safety and efficacy not determined
≥4 years: take 1 tablet orally every 6 hours
1 packet orally every 6 hours dissolved in 75 ml of water Low urinary phosphate
<4 years: safety and efficacy not determined
≥4 years: take 1 to 2 tablets orally every 6 hour
medtigo
Hypophosphatemia
Updated :
August 24, 2023
Phosphate is a crucial element for various cellular functions in the body. It plays a critical role in the replication of DNA and RNA as essential components of nucleic acids. Additionally, it serves as an energy source for molecular functions by contributing to the production of ATP.
Furthermore, phosphate adds or removes phosphate groups to or from proteins, acting as an on/off switch to regulate molecular activity. Given its vital role in numerous cellular functions, disturbances in serum phosphate levels can significantly affect the body. Hypophosphatemia occurs when the adult serum phosphate level falls below 2.5 mg/dL.
A normal serum phosphate level in infants is significantly higher, approximately 7 mg/dL. Hypophosphatemia is a common laboratory abnormality often detected incidentally during routine blood tests. Low phosphate levels can lead to various symptoms, including muscle weakness, bone pain, and confusion.
In most cases, patients with hypophosphatemia do not show any symptoms. However, the condition is prevalent among certain groups of people, such as those with alcoholism, diabetic ketoacidosis, or sepsis, with a frequency of up to 80%. The morbidity, or the diseased state, associated with hypophosphatemia varies greatly and depends on its underlying cause and severity.
For instance, individuals with severe hypophosphatemia may experience muscle weakness, respiratory failure, and cardiac dysfunction. On the other hand, those with milder forms of hypophosphatemia may experience symptoms such as bone pain, loss of appetite, and difficulty concentrating.
Hypophosphatemia can occur due to inadequate phosphate intake over a prolonged period, malabsorption in the intestines, or phosphate binding by certain medications. Most diets contain enough phosphate to meet the body’s needs, and renal adaptations can compensate for short-term deficiencies.
Intestinal malabsorption can be caused by various factors, including chronic diarrhea, which increases phosphate losses through the intestines. Certain medications, such as aluminum and magnesium antacids, can bind with phosphate, resulting in a net loss of phosphate from the body. This reaction creates non-absorbable aluminum or magnesium-bound phosphate salts.
The primary mechanism for increased phosphate excretion occurs in the renal system, where the proximal and distal tubules reabsorb up to 70% and 15% of filtered phosphate, respectively. The regulation of phosphate resorption depends on serum phosphate concentration, whereby mild phosphate depletion triggers increased reabsorption via sodium-phosphate cotransporters in the proximal tubule and increased formation of these transporters.
Conversely, parathyroid hormone inhibits the activity of sodium-phosphate cotransporters, thereby increasing phosphate excretion. In addition, several factors, such as fibroblast growth factor 23, fibroblast growth factor 7, extracellular matrix phosphoglycoprotein, and secreted frizzled-related protein-4, decrease phosphate reabsorption by sodium-phosphate cotransporters. Therefore, an increase in parathyroid hormone levels may lead to hypophosphatemia.
Hypophosphatemia is typically caused by one of three factors insufficient intake of phosphate, excessive excretion of phosphate, or a shift of phosphate from the extracellular space into the intracellular space. Insufficient phosphate intake can occur due to inadequate dietary intake or malabsorption of phosphate in the gastrointestinal tract.
In some cases, patients with chronic alcoholism or anorexia nervosa may not consume enough phosphate in their diet to maintain normal levels in the blood. Excessive phosphate excretion can result from conditions such as renal tubular disorders, hyperparathyroidism, and certain medications such as diuretics. When the kidneys excrete too much phosphate, it can lead to hypophosphatemia.
The third cause of hypophosphatemia is the shift of phosphate from the extracellular space into the intracellular space. This can occur in various situations, including refeeding syndrome, diabetic ketoacidosis, and respiratory alkalosis. In these conditions, the body’s cells rapidly take up phosphate from the blood, decreasing phosphate concentration in the extracellular space.
Clinical History
When the body experiences prolonged hypophosphatemia, the result can be a variety of negative impacts on different systems in the body. One of the most significant effects is decreased bone mineralization, leading to osteoporosis, osteopenia, osteomalacia, and rickets. The central nervous system can also be affected, leading to metabolic encephalopathy due to ATP depletion.
Symptoms can include irritability, altered mental state, numbness, paresthesias, seizures, or even coma. The heart can also be impacted, with possible systolic heart failure and increased risk of arrhythmias due to less stable myocytes. Hypophosphatemia can also affect pulmonary function, leading to hypoventilation, particularly concerning ventilator-dependent patients.
Those with gastrointestinal issues may also experience dysphagia or ileus due to ATP deficiency. Additionally, generalized muscle weakness and rhabdomyolysis may occur, leading to renal injury and increased creatinine phosphokinases, particularly in acute or chronic hypophosphatemia cases, such as in individuals with alcohol use disorder.
While rare, hypophosphatemia can also impact the hematology systems, such as increased erythrocyte rigidity, predisposing individuals to hemolysis, reduced phagocytosis, and granulocyte chemotaxis by white blood cells, as well as thrombocytopenia.
Physical Examination
Although most patients with mild hypophosphatemia do not experience symptoms, those with severe hypophosphatemia may present with various clinical manifestations. One of the most common symptoms of hypophosphatemia is generalized weakness, which can range from mild to moderate in severity.
In addition, patients with severe hypophosphatemia may experience altered mental status and focal neurologic findings such as numbness or reflexive weakness. Cardiac manifestations of hypophosphatemia may include heart failure, as phosphate is critical in maintaining normal cardiac function. Muscle pain and muscle weakness may also be present in severe cases of hypophosphatemia.
Differential Diagnoses
Delirium
Dilated cardiomyopathy
Hypothyroidism
Insulin overdose
Myopathies
Rhabdomyolysis
Uremic encephalopathy
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