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Phosphorus, Phosphate



Interactions

Phosphorus/Drug Interactions:
  • ACE inhibitorsACE inhibitors: According to secondary sources, ACE inhibitors may decrease blood levels of phosphorus.
  • AlcoholAlcohol: According to secondary sources, alcohol (ethanol) may increase urinary phosphorus. Wine may enhance absorption of phosphorus (as well as calcium and magnesium).
  • AntacidsAntacids: According to secondary sources, antacids containing aluminum, calcium, or magnesium may bind phosphate in the gut and prevent its absorption, potentially leading to hypophosphatemia when used chronically.
  • AnticonvulsantsAnticonvulsants: According to secondary sources, some anticonvulsants (including phenobarbital and carbamazepine) may lower phosphorus levels and increase levels of alkaline phosphatase.
  • AntidiabeticsAntidiabetics: The use of prophylactic phosphate therapy in diabetic ketoacidosis is controversial (21; 22). In general, phosphate replacement is not routinely recommended, based on the lack of clinical benefit in some studies, as well as the potential for adverse effects, such as hypocalcemia and soft tissue calcification. High doses of insulin may lower blood levels of phosphorus in diabetic ketoacidosis patients (23).
  • AntihypertensivesAntihypertensives: In epidemiological research, increased blood phosphorus was associated with decreased blood pressure (7). According to secondary sources, excessive intake of phosphates may cause severe hypotension.
  • Bile acid sequestrantsBile acid sequestrants: According to secondary sources, bile acid sequestrants such as cholestyramine (Questran®) and colestipol (Colestid®) may decrease oral absorption of phosphate. Therefore, oral phosphate supplements should be administered at least one hour before or four hours after these agents.
  • CalcimimeticsCalcimimetics: In a meta-analysis, calcimimetic therapy was shown to decrease blood levels of phosphorus (24).
  • Cardiovascular agentsCardiovascular agents: In humans, increased phosphate levels in the blood were associated with decreases in blood pressure and increased cardiovascular adverse effects and mortality, especially in kidney disease patients on dialysis (10; 11; 12; 13; 15; 16; 7). According to secondary sources, excessive intake of phosphates may cause electrolyte disturbances including hypocalcemia, severe hypotension, or abnormal heart rhythms.
  • CorticosteroidsCorticosteroids: According to secondary sources, corticosteroids may increase urinary phosphorus levels.
  • DiureticsDiuretics: According to secondary sources, a combination of phosphorus supplements and potassium-sparing diuretics may cause hyperkalemia.
  • Electrolyte modulatorsElectrolyte modulators: According to secondary sources, excessive intake of phosphates may cause electrolyte disturbances, including hypocalcemia (low calcium blood levels). According to secondary sources, medications that may affect electrolyte levels should be used cautiously with phosphates. Examples include amiloride (Midamor®); angiotensin-converting enzyme (ACE) inhibitors such as benazepril (Lotensin®), captopril (Capoten®), enalapril (Vasotec®), fosinopril (Monopril®), lisinopril (Zestril®, Prinivil®), quinapril (Accupril®), or ramipril (Altace®); cyclosporine; cardiac glycosides (Digoxin®); heparins; anti-inflammatory drugs; potassium-containing agents; salt substitutes; spironolactone (Aldactone®); and triamterene (Dyrenium®). According to secondary sources, phosphates may increase fecal levels of calcium in some assays, cause a false decrease in some serum and urine test results (by inhibiting emission in some flame methods and by competing with EDTA for calcium), decrease urine magnesium levels, and decrease serum levels of potassium.
  • EstrogensEstrogens: In women, estradiol had phosphaturic properties (25).
  • Gastrointestinal agentsGastrointestinal agents: According to secondary sources, adverse effects of phosphorus may include abdominal pain, gastrointestinal irritation, and diarrhea. Potassium acid phosphate may cause dyspepsia in patients with a history of peptic ulcer disease, and aluminum phosphate may cause constipation, according to secondary sources.
  • Hepatotoxic agentsHepatotoxic agents: According to secondary sources, liver disease may be worsened with excessive phosphorus or phosphate supplementation.
  • Osteoporosis drugsOsteoporosis drugs: Phosphorus is vital to the formation of bones and teeth, and healthy bones and soft tissues require the proper balance of calcium and phosphorus levels to grow and develop. Early research shows that high amounts of phosphorus may have negative effects on bone density (8; 9). An imbalance between phosphate and calcium content in the diet may lead to osteoporosis. According to secondary sources, excessive phosphorus or phosphate supplementation may worsen rickets and osteomalacia.
  • Phosphate bindersPhosphate binders: In a meta-analysis, the use of phosphate binders decreased blood phosphate levels (26; 27).
  • Renal agentsRenal agents: In patients with kidney disease, increased phosphorus levels in the blood have been associated with increased all-cause and cardiovascular mortality (15; 16). Dietary intakes and urinary levels of phosphorus were found to be increased in male renal stone formers vs. healthy controls (4). According to secondary sources, excessive intake of phosphates may cause calcification of kidney tissue or acute kidney failure.

Phosphorus/Herb/Supplement Interactions:
  • ACE inhibitorsACE inhibitors: According to secondary sources, ACE inhibitors may decrease blood levels of phosphorus.
  • AntacidsAntacids: According to secondary sources, antacids containing aluminum, calcium, or magnesium may bind phosphate in the gut and prevent its absorption, potentially leading to hypophosphatemia when used chronically.
  • AnticonvulsantsAnticonvulsants: According to secondary sources, some anticonvulsants (including phenobarbital and carbamazepine) may lower phosphorus levels and increase levels of alkaline phosphatase.
  • Anti-inflammatory agentsAnti-inflammatory agents: According to secondary sources, corticosteroids may increase urinary phosphorus levels.
  • Bile acid sequestrantsBile acid sequestrants: According to secondary sources, bile acid sequestrants such as cholestyramine (Questran®) and colestipol (Colestid®) may decrease oral absorption of phosphate. Therefore, oral phosphate supplements should be administered at least one hour before or four hours after these agents.
  • CalcimimeticsCalcimimetics: In a meta-analysis, calcimimetic therapy was shown to decrease blood levels of phosphorus (24).
  • CalciumCalcium: In women, increased calcium may decrease phosphorus absorption (28). According to secondary sources, calcium may impair phosphates in the body and result in calcium deposits in tissues.
  • Cardiovascular agentsCardiovascular agents: In humans, increased phosphate levels in the blood were associated with decreases in blood pressure and increased cardiovascular adverse effects and mortality, especially in kidney disease patients on dialysis (10; 11; 12; 13; 15; 16; 7). According to secondary sources, excessive intake of phosphates may cause electrolyte disturbances including hypocalcemia, severe hypotension, or abnormal heart rhythms.
  • DiureticsDiuretics: According to secondary sources, a combination of phosphorus supplements and potassium sparing diuretics may cause hyperkalemia (high blood potassium).
  • Electrolyte modulatorsElectrolyte modulators: According to secondary sources, excessive intake of phosphates may cause electrolyte disturbances, including hypocalcemia. According to secondary sources, medications that may affect electrolyte levels should be used cautiously with phosphates. Examples include amiloride (Midamor®); angiotensin-converting enzyme (ACE) inhibitors such as benazepril (Lotensin®), captopril (Capoten®), enalapril (Vasotec®), fosinopril (Monopril®), lisinopril (Zestril®, Prinivil®), quinapril (Accupril®), or ramipril (Altace®); cyclosporine; cardiac glycosides (Digoxin®); heparins; anti-inflammatory drugs; potassium-containing agents; salt substitutes; spironolactone (Aldactone®); and triamterene (Dyrenium®). According to secondary sources, phosphates may increase fecal levels of calcium in some assays, cause a false decrease in some serum and urine test results (by inhibiting emission in some flame methods and by competing with EDTA for calcium), decrease urine magnesium levels, and decrease serum levels of potassium.
  • Gastrointestinal agentsGastrointestinal agents: According to secondary sources, adverse effects from phosphorus may include abdominal pain, gastrointestinal irritation, and diarrhea. Potassium acid phosphate may cause dyspepsia in patients with a history of peptic ulcer disease, and aluminum phosphate may cause constipation, according to secondary sources.
  • HepatotoxinsHepatotoxins: According to secondary sources, liver disease may be worsened with excessive phosphorus or phosphate supplementation.
  • Hormonal herbs and supplementsHormonal herbs and supplements: In women, estradiol had phosphaturic properties (25).
  • HypoglycemicsHypoglycemics: The use of prophylactic phosphate therapy in diabetic ketoacidosis is controversial (21; 22). In general, phosphate replacement is not routinely recommended, based on the lack of clinical benefit in some studies, as well as the potential for adverse effects, such as hypocalcemia and soft tissue calcification. High doses of insulin may lower blood levels of phosphorus in diabetic ketoacidosis patients (23).
  • HypotensivesHypotensives: In epidemiological research, increased blood phosphorus was associated with decreased blood pressure (7). According to secondary sources, excessive intake of phosphates may cause severe hypotension.
  • MagnesiumMagnesium: According to secondary sources, phosphates may decrease urine magnesium levels.
  • NiacinNiacin: In patients with metabolic syndrome dyslipidemia, once-daily, extended-release niacin lowered serum phosphorus concentrations (29).
  • Osteoporosis agentsOsteoporosis agents: Phosphorus is vital to the formation of bones and teeth, and healthy bones and soft tissues require the proper balance of calcium and phosphorus levels to grow and develop. Early research shows that high amounts of phosphorus may have negative effects on bone density (8; 9). An imbalance between phosphate and calcium content in the diet may lead to osteoporosis. According to secondary sources, excessive phosphorus or phosphate supplementation may worsen rickets and osteomalacia.
  • Phosphate bindersPhosphate binders: In a meta-analysis, use of phosphate binders decreased blood phosphate levels (26; 27).
  • PotassiumPotassium: According to secondary sources, potassium supplements taken together with a phosphate may result in high blood levels of potassium (hyperkalemia).
  • Pumpkin seedPumpkin seed: According to secondary sources, pumpkin seed may increase urine phosphates.
  • Renal agentsRenal agents: In patients with kidney disease, increased phosphorus levels in the blood have been associated with increased all-cause and cardiovascular mortality (15; 16). Dietary intakes and urinary levels of phosphorus were found to be increased in male renal stone formers vs. healthy controls (4). According to secondary sources, excessive intake of phosphates may cause calcification of kidney tissue or acute kidney failure.
  • Vitamin DVitamin D: According to secondary sources, excessive doses of calcitriol, the active form of vitamin D (or its analogs), may result in hyperphosphatemia. Vitamin D compounds increased serum phosphorus in patients with chronic kidney disease not requiring dialysis (20).

Phosphorus/Food Interactions:
  • AlcoholAlcohol: According to secondary sources, alcohol (ethanol) may increase urinary phosphorus. Wine may enhance absorption of phosphorus (as well as calcium and magnesium).
  • FructoseFructose: In laboratory and human research, high fructose intake has been associated with decreased serum phosphorus and increased urinary loss of phosphorus (30).
  • High-phosphate beverages, cola drinksHigh-phosphate beverages, cola drinks: In hemodialysis and chronic kidney disease patients, salivary phosphate secretion was increased and was related to consumption of phosphate in beverages (31). Cola drinks contain significant amounts of phosphate; excessive intake may result in hyperphosphatemia and hypocalcemia, according to secondary sources.
  • Pumpkin seedPumpkin seed: According to secondary sources, pumpkin seed may increase urine phosphates.
  • Salt substitutesSalt substitutes: According to secondary sources, salt substitutes high in potassium may lower phosphorus levels.

Phosphorus/Lab Interactions:
  • Acid phosphataseAcid phosphatase: According to secondary sources, phosphates may cause a false decrease in some acid phosphatase serum test results.
  • Alkaline phosphataseAlkaline phosphatase: According to secondary sources, phosphates may cause a false decrease in some alkaline phosphatase serum test results.
  • AmmoniaAmmonia: According to secondary sources, phosphates may cause a false decrease in some plasma ammonia test results by inhibiting formation of indophenol color in Berthelot reaction.
  • Ankle-brachial indexAnkle-brachial index: In community-living older men, higher phosphorus levels were associated with a low ankle-brachial index (a measurement of atherosclerosis and arterial stiffness) (14). In patients with chronic kidney disease, higher phosphorus levels were associated with a high ankle-brachial index (14).
  • Blood pressureBlood pressure: In epidemiological research, increased blood phosphorus was associated with decreased blood pressure (7). According to secondary sources, excessive intake of phosphates may cause severe hypotension.
  • Bone densityBone density: Phosphorus is vital to the formation of bones and teeth, and healthy bones and soft tissues require the proper balance of calcium and phosphorus levels to grow and develop. Early research shows that high amounts of phosphorus may have negative effects on bone density (8; 9). An imbalance between phosphate and calcium content in the diet may lead to osteoporosis. According to secondary sources, excessive phosphorus or phosphate supplementation may worsen rickets and osteomalacia.
  • Electrolyte levelsElectrolyte levels: According to secondary sources, excessive intake of phosphates may cause electrolyte disturbances including hypocalcemia. According to secondary sources, medications that may affect electrolyte levels should be used cautiously with phosphates. Examples include amiloride (Midamor®); angiotensin-converting enzyme (ACE) inhibitors such as benazepril (Lotensin®), captopril (Capoten®), enalapril (Vasotec®), fosinopril (Monopril®), lisinopril (Zestril®, Prinivil®), quinapril (Accupril®), or ramipril (Altace®); cyclosporine; cardiac glycosides (Digoxin®); heparins; anti-inflammatory drugs; potassium-containing agents; salt substitutes; spironolactone (Aldactone®); and triamterene (Dyrenium®). According to secondary sources, phosphates may increase fecal levels of calcium in some assays, cause a false decrease in some serum and urine test results (by inhibiting emission in some flame methods and by competing with EDTA for calcium), decrease urine magnesium levels, and decrease serum levels of potassium.
  • Heart rateHeart rate: According to secondary sources, excessive intake of phosphates may cause abnormal heart rhythms.
  • Parathyroid hormoneParathyroid hormone: According to secondary sources, phosphates may increase plasma levels of parathyroid hormone.

Copyright © 2011 Natural Standard (www.naturalstandard.com)


The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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