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Drug overview for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione):
Generic name: CALCIUM CARBONATE/CHOLECALCIFEROL (VIT D3)/PHYTONADIONE
Drug class: Calcium
Therapeutic class: Electrolyte Balance-Nutritional Products
Calcium salts are used as a source of calcium, an essential nutrient Phytonadione is a fat-soluble naphthoquinone derivative that is identical cation. to naturally occurring vitamin K1.
Vitamin D analogs are used to prevent or treat rickets or osteomalacia and to manage hypocalcemia associated with hypoparathyroidism or pseudohypoparathyroidism. Since calcitriol is more expensive than ergocalciferol, use of the former drug is generally reserved for patients with inadequate metabolism of ergocalciferol. The initial treatment of severe hypocalcemia is immediate IV administration of a calcium salt such as calcium gluconate.
Vitamin D analogs are then used to maintain normocalcemia. Because of its shorter onset of action, calcitriol may be preferable to ergocalciferol in the acute treatment of hypocalcemia. Oral calcitriol also is used in the management of secondary hyperparathyroidism and resultant metabolic bone disease in patients with moderate to severe chronic kidney disease (CKD) who do not yet require maintenance dialysis therapy (predialysis patients) and in the management of hypocalcemia and resultant metabolic bone disease in patients with CKD undergoing dialysis.
IV calcitriol is used in the management of hypocalcemia in patients with chronic renal failure undergoing dialysis. IV or oral doxercalciferol is used for the treatment of secondary hyperparathyroidism in patients with CKD undergoing dialysis. Oral doxercalciferol also is used for the treatment of secondary hyperparathyroidism in patients with stage 3 or 4 CKD who do not yet require maintenance dialysis (predialysis patients).
IV paricalcitol is used in the prevention and treatment of secondary hyperparathyroidism in patients with stage 5 CKD, while oral paricalcitol is used in the prevention and treatment of secondary hyperparathyroidism in patients with stage 3 or 4 CKD as well as in those with stage 5 CKD requiring hemodialysis or peritoneal dialysis. Calcifediol is used in the treatment of secondary hyperparathyroidism in patients with stage 3 or 4 CKD and vitamin D insufficiency. Because of the risk of toxicity, therapy with vitamin D analogs should be closely monitored, and indiscriminate use of these drugs should be avoided.
Calcium salts are used as a source of calcium cation for the treatment or Phytonadione is used in the prophylaxis and/or treatment of coagulation disorders due to faulty formation of factors II, VII, IX, and X caused by prevention of calcium depletion in patients in whom dietary measures are inadequate. Conditions that may be associated with calcium deficiency vitamin K deficiency or interference with vitamin K activity. Phytonadione include hypoparathyroidism, achlorhydria, chronic diarrhea, vitamin D is more effective than, and is preferred to, other vitamin K preparations deficiency, steatorrhea, sprue, pregnancy and lactation, menopause, in the presence of impending or actual hemorrhage.
However, because pancreatitis, renal failure, alkalosis, and hyperphosphatemia. phytonadione may require 3 hours or longer to stop active bleeding, Administration of certain drugs (e.g., some diuretics, anticonvulsants) may administration of clotting factors (e.g., prothrombin complex concentrate (human)), fresh whole blood, or plasma may be necessary for more rapid sometimes result in hypocalcemia which may warrant calcium replacement control of severe bleeding. therapy.
Calcium should be administered in long-term electrolyte replacement regimens and is also recommended for the routine prophylaxis of hypocalcemia during transfusions with citrated blood. Administration of calcium salts should not preclude the use of other measures intended to correct the underlying cause of calcium depletion.
Generic name: CALCIUM CARBONATE/CHOLECALCIFEROL (VIT D3)/PHYTONADIONE
Drug class: Calcium
Therapeutic class: Electrolyte Balance-Nutritional Products
Calcium salts are used as a source of calcium, an essential nutrient Phytonadione is a fat-soluble naphthoquinone derivative that is identical cation. to naturally occurring vitamin K1.
Vitamin D analogs are used to prevent or treat rickets or osteomalacia and to manage hypocalcemia associated with hypoparathyroidism or pseudohypoparathyroidism. Since calcitriol is more expensive than ergocalciferol, use of the former drug is generally reserved for patients with inadequate metabolism of ergocalciferol. The initial treatment of severe hypocalcemia is immediate IV administration of a calcium salt such as calcium gluconate.
Vitamin D analogs are then used to maintain normocalcemia. Because of its shorter onset of action, calcitriol may be preferable to ergocalciferol in the acute treatment of hypocalcemia. Oral calcitriol also is used in the management of secondary hyperparathyroidism and resultant metabolic bone disease in patients with moderate to severe chronic kidney disease (CKD) who do not yet require maintenance dialysis therapy (predialysis patients) and in the management of hypocalcemia and resultant metabolic bone disease in patients with CKD undergoing dialysis.
IV calcitriol is used in the management of hypocalcemia in patients with chronic renal failure undergoing dialysis. IV or oral doxercalciferol is used for the treatment of secondary hyperparathyroidism in patients with CKD undergoing dialysis. Oral doxercalciferol also is used for the treatment of secondary hyperparathyroidism in patients with stage 3 or 4 CKD who do not yet require maintenance dialysis (predialysis patients).
IV paricalcitol is used in the prevention and treatment of secondary hyperparathyroidism in patients with stage 5 CKD, while oral paricalcitol is used in the prevention and treatment of secondary hyperparathyroidism in patients with stage 3 or 4 CKD as well as in those with stage 5 CKD requiring hemodialysis or peritoneal dialysis. Calcifediol is used in the treatment of secondary hyperparathyroidism in patients with stage 3 or 4 CKD and vitamin D insufficiency. Because of the risk of toxicity, therapy with vitamin D analogs should be closely monitored, and indiscriminate use of these drugs should be avoided.
Calcium salts are used as a source of calcium cation for the treatment or Phytonadione is used in the prophylaxis and/or treatment of coagulation disorders due to faulty formation of factors II, VII, IX, and X caused by prevention of calcium depletion in patients in whom dietary measures are inadequate. Conditions that may be associated with calcium deficiency vitamin K deficiency or interference with vitamin K activity. Phytonadione include hypoparathyroidism, achlorhydria, chronic diarrhea, vitamin D is more effective than, and is preferred to, other vitamin K preparations deficiency, steatorrhea, sprue, pregnancy and lactation, menopause, in the presence of impending or actual hemorrhage.
However, because pancreatitis, renal failure, alkalosis, and hyperphosphatemia. phytonadione may require 3 hours or longer to stop active bleeding, Administration of certain drugs (e.g., some diuretics, anticonvulsants) may administration of clotting factors (e.g., prothrombin complex concentrate (human)), fresh whole blood, or plasma may be necessary for more rapid sometimes result in hypocalcemia which may warrant calcium replacement control of severe bleeding. therapy.
Calcium should be administered in long-term electrolyte replacement regimens and is also recommended for the routine prophylaxis of hypocalcemia during transfusions with citrated blood. Administration of calcium salts should not preclude the use of other measures intended to correct the underlying cause of calcium depletion.
DRUG IMAGES
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The following indications for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione) have been approved by the FDA:
Indications:
Hypocalcemia prevention
Hypocalcemia
Osteoporosis
Post-menopausal osteoporosis prevention
Prevention of vitamin D deficiency
Vitamin D deficiency
Professional Synonyms:
Abnormally decreased serum calcium prophylaxis
Abnormally decreased serum calcium
Hypocalcemia prophylaxis
Postmenopausal osteoporosis prophylaxis
Indications:
Hypocalcemia prevention
Hypocalcemia
Osteoporosis
Post-menopausal osteoporosis prevention
Prevention of vitamin D deficiency
Vitamin D deficiency
Professional Synonyms:
Abnormally decreased serum calcium prophylaxis
Abnormally decreased serum calcium
Hypocalcemia prophylaxis
Postmenopausal osteoporosis prophylaxis
The following dosing information is available for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione):
Dose, frequency of administration, and duration of treatment with phytonadione depend on the severity of the prothrombin deficiency and the response of the patient; the lowest effective dose of phytonadione should be used.
Dosage of the oral calcium supplements is usually expressed in grams or mg of elemental calcium and depends on the requirements of the individual patient. Dosage of parenteral calcium replacements is usually expressed as mEq of calcium and depends on individual patient requirements. One mEq of elemental calcium is equivalent to 20 mg.
See Table 1 for the approximate calcium content of the various calcium salts.
Table 1.
Calcium Salt Calcium Content calcium acetate 253 mg (12.7 mEq) per g calcium carbonate 400 mg (20 mEq) per g calcium chloride 270 mg (13.5 mEq) per g calcium citrate 211 mg (10.6 mEq) per g calcium gluceptate 82 mg (4.1 mEq) per g calcium gluconate 90 mg (4.5 mEq) per g calcium glycerophosphate 191 mg (9.6 mEq) per g calcium lactate 130 mg (6.5 mEq) per g calcium phosphate dibasic anhydrous 290 mg (14.5 mEq) per g calcium phosphate dibasic dihydrate 230 mg (11.5 mEq) per g calcium phosphate tribasic 400 mg (20 mEq) per g
Oral calcium supplements usually are administered in 3 or 4 divided doses daily. Optimum calcium absorption may require supplemental vitamin D in individuals with inadequate vitamin D intake, those with impaired renal activation of the vitamin, or those not receiving adequate exposure to sunlight.
If calcium administration is necessary during cardiac arrest, an IV dose of Dietary intake of ergocalciferol and cholecalciferol varies among 0.109-0.218 mEq/kg (repeated as necessary) using calcium chloride has been individual patients, and dietary intake should always be considered when recommended.
Alternatively, adults have been given IV calcium doses of 7-14 calculating the appropriate dosage of vitamin D analogs. During therapy mEq using calcium chloride. However, routine administration of calcium in with vitamin D analogs, dosage depends on the nature and severity of the patients with cardiac arrest is not recommended.
(See Advanced patient's hypocalcemia and must be individualized to maintain serum calcium Cardiovascular Life Support under Uses: Parenteral Preparations.) concentrations of 9-10 mg/dL. In the management of hypoparathyroidism,
pseudohypoparathyroidism, and familial hypophosphatemia, the range between therapeutic and toxic effects is narrow; however, hypercalcemia may occur at any time when therapeutic doses of vitamin D analogs are used, and careful monitoring is imperative. In the management of secondary hyperparathyroidism, dosage of vitamin D analogs should be individualized according to serum or plasma intact parathyroid hormone (iPTH) concentrations and serum calcium and phosphorus concentrations.
During therapy with vitamin D analogs, patients should receive adequate amounts of calcium through management of diet or administration of calcium supplements; however, overdosage of calcium may lead to hypercalcemia. Dosage of vitamin D analogs should be decreased when symptoms improve and before biochemical normality or complete bone healing has occurred because requirements for vitamin D analogs often decrease after bone healing occurs. In patients who become bedridden (especially children), dosage reduction may occasionally be needed to avoid hypercalcemia.
If administration of calcium is indicated for the treatment of hypocalcemia, calcium-channel blocker overdosage, hypermagnesemia, or hyperkalemia during pediatric resuscitation, experts recommend a pediatric IV or IO+ calcium dose of 0.272 mEq/kg using calcium chloride. In critically ill children, calcium chloride may provide a greater increase in ionized calcium than calcium gluconate.
The appropriate dose should be administered by slow IV or IO+ injection.
When calcium acetate is used orally to control hyperphosphatemia in adults with chronic renal failure, the recommended initial dosage is 1.334 g of calcium acetate (338 mg of calcium) with each meal. Dosage may be increased gradually according to serum phosphate concentrations, provided hypercalcemia does not occur.
The manufacturer states that most patients require about 2-2.67 g (about 500-680 mg of calcium) with each meal. However, some experts state that the dosage of calcium provided by calcium-containing phosphate binders should not exceed 1.5
g daily and that the total calcium intake (including dietary calcium) should not exceed 2 g daily. These experts state that dialysis patients who remain hyperphosphatemic despite such therapy should receive a calcium-containing phosphate binder in combination with a non-calcium-, non-aluminum-, non-magnesium-containing phosphate binder. The manufacturer recommends that serum calcium concentrations be monitored twice weekly during initiation of calcium acetate therapy and subsequent dosage adjustment; serum phosphorus concentrations also should be monitored periodically.
If hypercalcemia occurs, dosage should be reduced or the salt should be withheld. If severe hypercalcemia occurs, specific measures (e.g., hemodialysis) for the management of overdosage may be necessary. Patients should be advised of the importance of dosage compliance, adherence to instructions about diet, and avoidance of concomitant use of antacids or other preparations containing clinically important concentrations of calcium.
Patients also should be advised of potential manifestations of hypercalcemia.
For the treatment of hyperkalemia with secondary cardiac toxicity, 2.25-14 mEq of calcium may be administered IV while monitoring the ECG. Doses may be repeated after 1-2 minutes if necessary.
Magnesium intoxication in adults is treated initially with 7 mEq of IV calcium; subsequent doses should be adjusted according to patient response. Alternatively, for the treatment of hypermagnesemia in adults, an IV calcium dose of 6.8-13.6
mEq using 10% calcium chloride (5-10 mL) has been administered, and repeated as necessary.
For the treatment of drug-induced cardiovascular emergencies associated with calcium-channel blocking agent toxicity in pediatric patients, an IV calcium dose of 0.272 mEq/kg using 10% calcium chloride (0.2 mL/kg) has been administered over 5-10 minutes; if a beneficial effect was observed, an IV calcium infusion of 0.27-0.68
mEq/kg per hour using calcium chloride has been administered. Ionized calcium concentrations should be monitored to prevent hypercalcemia.
Calcium is also administered IV during exchange transfusions in neonates in a dosage of 0.45 mEq of calcium after every 100 mL of citrated blood exchanged. In adults receiving transfusions of citrated blood, about 1.35
mEq of calcium should be administered IV concurrently with each 100 mL of citrated blood.
In the calcium infusion test+, calcium is given IV in a dosage of 0.25 mEq/kg per hour for a 3-hour period; serum gastrin concentrations are determined 30 minutes before the infusion, at the start of the infusion, and at 30-minute intervals thereafter for 4 hours. In most patients with Zollinger-Ellison syndrome, preinfusion serum gastrin concentrations increase by more than 50% or by greater than 500 pg/mL during the infusion.
In the diagnosis of medullary thyroid carcinoma+, about 7 mEq of calcium is given IV over 5-10 minutes. In patients with medullary thyroid carcinoma, plasma calcitonin concentrations are elevated above normal basal concentrations.
Dosage of the oral calcium supplements is usually expressed in grams or mg of elemental calcium and depends on the requirements of the individual patient. Dosage of parenteral calcium replacements is usually expressed as mEq of calcium and depends on individual patient requirements. One mEq of elemental calcium is equivalent to 20 mg.
See Table 1 for the approximate calcium content of the various calcium salts.
Table 1.
Calcium Salt Calcium Content calcium acetate 253 mg (12.7 mEq) per g calcium carbonate 400 mg (20 mEq) per g calcium chloride 270 mg (13.5 mEq) per g calcium citrate 211 mg (10.6 mEq) per g calcium gluceptate 82 mg (4.1 mEq) per g calcium gluconate 90 mg (4.5 mEq) per g calcium glycerophosphate 191 mg (9.6 mEq) per g calcium lactate 130 mg (6.5 mEq) per g calcium phosphate dibasic anhydrous 290 mg (14.5 mEq) per g calcium phosphate dibasic dihydrate 230 mg (11.5 mEq) per g calcium phosphate tribasic 400 mg (20 mEq) per g
Oral calcium supplements usually are administered in 3 or 4 divided doses daily. Optimum calcium absorption may require supplemental vitamin D in individuals with inadequate vitamin D intake, those with impaired renal activation of the vitamin, or those not receiving adequate exposure to sunlight.
If calcium administration is necessary during cardiac arrest, an IV dose of Dietary intake of ergocalciferol and cholecalciferol varies among 0.109-0.218 mEq/kg (repeated as necessary) using calcium chloride has been individual patients, and dietary intake should always be considered when recommended.
Alternatively, adults have been given IV calcium doses of 7-14 calculating the appropriate dosage of vitamin D analogs. During therapy mEq using calcium chloride. However, routine administration of calcium in with vitamin D analogs, dosage depends on the nature and severity of the patients with cardiac arrest is not recommended.
(See Advanced patient's hypocalcemia and must be individualized to maintain serum calcium Cardiovascular Life Support under Uses: Parenteral Preparations.) concentrations of 9-10 mg/dL. In the management of hypoparathyroidism,
pseudohypoparathyroidism, and familial hypophosphatemia, the range between therapeutic and toxic effects is narrow; however, hypercalcemia may occur at any time when therapeutic doses of vitamin D analogs are used, and careful monitoring is imperative. In the management of secondary hyperparathyroidism, dosage of vitamin D analogs should be individualized according to serum or plasma intact parathyroid hormone (iPTH) concentrations and serum calcium and phosphorus concentrations.
During therapy with vitamin D analogs, patients should receive adequate amounts of calcium through management of diet or administration of calcium supplements; however, overdosage of calcium may lead to hypercalcemia. Dosage of vitamin D analogs should be decreased when symptoms improve and before biochemical normality or complete bone healing has occurred because requirements for vitamin D analogs often decrease after bone healing occurs. In patients who become bedridden (especially children), dosage reduction may occasionally be needed to avoid hypercalcemia.
If administration of calcium is indicated for the treatment of hypocalcemia, calcium-channel blocker overdosage, hypermagnesemia, or hyperkalemia during pediatric resuscitation, experts recommend a pediatric IV or IO+ calcium dose of 0.272 mEq/kg using calcium chloride. In critically ill children, calcium chloride may provide a greater increase in ionized calcium than calcium gluconate.
The appropriate dose should be administered by slow IV or IO+ injection.
When calcium acetate is used orally to control hyperphosphatemia in adults with chronic renal failure, the recommended initial dosage is 1.334 g of calcium acetate (338 mg of calcium) with each meal. Dosage may be increased gradually according to serum phosphate concentrations, provided hypercalcemia does not occur.
The manufacturer states that most patients require about 2-2.67 g (about 500-680 mg of calcium) with each meal. However, some experts state that the dosage of calcium provided by calcium-containing phosphate binders should not exceed 1.5
g daily and that the total calcium intake (including dietary calcium) should not exceed 2 g daily. These experts state that dialysis patients who remain hyperphosphatemic despite such therapy should receive a calcium-containing phosphate binder in combination with a non-calcium-, non-aluminum-, non-magnesium-containing phosphate binder. The manufacturer recommends that serum calcium concentrations be monitored twice weekly during initiation of calcium acetate therapy and subsequent dosage adjustment; serum phosphorus concentrations also should be monitored periodically.
If hypercalcemia occurs, dosage should be reduced or the salt should be withheld. If severe hypercalcemia occurs, specific measures (e.g., hemodialysis) for the management of overdosage may be necessary. Patients should be advised of the importance of dosage compliance, adherence to instructions about diet, and avoidance of concomitant use of antacids or other preparations containing clinically important concentrations of calcium.
Patients also should be advised of potential manifestations of hypercalcemia.
For the treatment of hyperkalemia with secondary cardiac toxicity, 2.25-14 mEq of calcium may be administered IV while monitoring the ECG. Doses may be repeated after 1-2 minutes if necessary.
Magnesium intoxication in adults is treated initially with 7 mEq of IV calcium; subsequent doses should be adjusted according to patient response. Alternatively, for the treatment of hypermagnesemia in adults, an IV calcium dose of 6.8-13.6
mEq using 10% calcium chloride (5-10 mL) has been administered, and repeated as necessary.
For the treatment of drug-induced cardiovascular emergencies associated with calcium-channel blocking agent toxicity in pediatric patients, an IV calcium dose of 0.272 mEq/kg using 10% calcium chloride (0.2 mL/kg) has been administered over 5-10 minutes; if a beneficial effect was observed, an IV calcium infusion of 0.27-0.68
mEq/kg per hour using calcium chloride has been administered. Ionized calcium concentrations should be monitored to prevent hypercalcemia.
Calcium is also administered IV during exchange transfusions in neonates in a dosage of 0.45 mEq of calcium after every 100 mL of citrated blood exchanged. In adults receiving transfusions of citrated blood, about 1.35
mEq of calcium should be administered IV concurrently with each 100 mL of citrated blood.
In the calcium infusion test+, calcium is given IV in a dosage of 0.25 mEq/kg per hour for a 3-hour period; serum gastrin concentrations are determined 30 minutes before the infusion, at the start of the infusion, and at 30-minute intervals thereafter for 4 hours. In most patients with Zollinger-Ellison syndrome, preinfusion serum gastrin concentrations increase by more than 50% or by greater than 500 pg/mL during the infusion.
In the diagnosis of medullary thyroid carcinoma+, about 7 mEq of calcium is given IV over 5-10 minutes. In patients with medullary thyroid carcinoma, plasma calcitonin concentrations are elevated above normal basal concentrations.
Phytonadione may be administered orally or parenterally (IV, IM, or subcutaneously). The parenteral preparation also has been administered orally+ in neonates. The route of administration of phytonadione depends on the severity of the prothrombin deficiency and the risks associated with administration by each route.
The manufacturers state that because of the possibility of severe adverse reactions (see Cautions: Adverse Effects), IV or IM administration is indicated only when other routes of administration are not feasible and the serious risk is justified. However, the effects of phytonadione have been reported to be delayed and/or unpredictable following subcutaneous injection, and subcutaneous administration may be less effective for reversal of excessive anticoagulation than IV or oral administration. The American College of Chest Physicians (ACCP) and other clinicians recommend IV administration of phytonadione in emergency situations for major bleeding due to vitamin K-antagonist anticoagulants because of its more rapid onset; these clinicians recommend that subcutaneous administration be avoided.
Oral administration of phytonadione usually reduces international normalized ratio (INR) levels in 24-48 hours and generally is recommended over parenteral administration in selected asymptomatic (nonbleeding) patients with hypoprothrombinemia due to vitamin K-antagonist anticoagulants. In patients with decreased bile secretion, bile salts (e.g., ox bile extract 300 mg or dehydrocholic acid 500 mg) should be given with each oral dose of phytonadione to ensure absorption. Parenteral administration is indicated in patients who are unable to retain or absorb the drug from the GI tract.
When phytonadione injection is administered IV, it should be injected at a rate not exceeding 1 mg/minute. The drug may be diluted for infusion with 0.9% sodium chloride, 5% dextrose, or 5% dextrose in 0.9%
sodium chloride injection; other diluents that may contain benzyl alcohol should not be used. (See Cautions: Pediatric Precautions.) The drug should be administered immediately after dilution, and any unused portion of the dilution and the unused contents of the ampul or vial should be discarded. The infusion container must be protected from light at all times.
(See Chemistry and Stability: Stability.) The acetate, carbonate, citrate, gluconate, lactate, and phosphate salts of calcium are administered orally. It has been recommended that most oral calcium supplements be administered 1-1.5 hours after meals or with a demulcent (e.g., milk).
However, calcium carbonate powder (i.e., CAL CARB-HD(R)) should generally be administered with meals, since the manufacturer recommends mixing the powder with food for administration. Calcium salts used to bind dietary phosphate in patients with end-stage renal disease should be administered with meals (e.g., 10-15 minutes before, or during, the meal). Calcium chloride and calcium gluconate may be administered IV.
Calcium chloride also may be administered by intraosseous (IO) injection+ in the setting of pediatric resuscitation; onset of action and systemic concentrations are comparable to those achieved with venous administration. Parenteral calcium salts may be administered in large volume IV infusion fluids. IV calcium injections must be administered slowly at a rate not exceeding 0.7-1.8
mEq/minute, and the injection should be stopped if the patient complains of discomfort. Following IV injection, the patient should remain recumbent for a short time. Close monitoring of serum calcium concentrations is essential during IV administration of calcium.
Calcium chloride should not be injected IM or into subcutaneous or perivascular tissue, since severe necrosis and sloughing may occur. Although other calcium salts may cause mild to severe local reactions, they are generally less irritating than calcium chloride. (See Cautions.) The fixed combination of calcium glycerophosphate and calcium lactate is injected IM.
Although some manufacturers previously stated that calcium gluconate could be injected IM when IV administration was not possible, manufacturers of calcium gluconate currently state that the drug should not be injected IM or into subcutaneous tissue because of the potential for severe local reactions. In children, calcium salts should not be administered through scalp veins. Oral administration of calcium supplements or calcium-rich foods should replace parenteral calcium therapy as soon as possible.
The interaction of calcium and phosphate in parenteral nutrition solutions is a complex phenomenon; various factors have been identified as playing a role in the solubility or precipitation of a given combination. Calcium salts are conditionally compatible with phosphate in parenteral nutrition solutions; incompatibility is dependent on a solubility and concentration phenomenon and is not entirely predictable. Precipitation may occur during compounding or at some time after compounding is completed.
Specialized references should be consulted for specific compatibility information. Vitamin D analogs are usually administered orally; however, calcitriol, doxercalciferol, and paricalcitol may be given by IV injection. Ergocalciferol may be given by IM injection; however, a suitable formulation of the drug for IM injection no longer is commercially available in the US.
The manufacturers state that because of the possibility of severe adverse reactions (see Cautions: Adverse Effects), IV or IM administration is indicated only when other routes of administration are not feasible and the serious risk is justified. However, the effects of phytonadione have been reported to be delayed and/or unpredictable following subcutaneous injection, and subcutaneous administration may be less effective for reversal of excessive anticoagulation than IV or oral administration. The American College of Chest Physicians (ACCP) and other clinicians recommend IV administration of phytonadione in emergency situations for major bleeding due to vitamin K-antagonist anticoagulants because of its more rapid onset; these clinicians recommend that subcutaneous administration be avoided.
Oral administration of phytonadione usually reduces international normalized ratio (INR) levels in 24-48 hours and generally is recommended over parenteral administration in selected asymptomatic (nonbleeding) patients with hypoprothrombinemia due to vitamin K-antagonist anticoagulants. In patients with decreased bile secretion, bile salts (e.g., ox bile extract 300 mg or dehydrocholic acid 500 mg) should be given with each oral dose of phytonadione to ensure absorption. Parenteral administration is indicated in patients who are unable to retain or absorb the drug from the GI tract.
When phytonadione injection is administered IV, it should be injected at a rate not exceeding 1 mg/minute. The drug may be diluted for infusion with 0.9% sodium chloride, 5% dextrose, or 5% dextrose in 0.9%
sodium chloride injection; other diluents that may contain benzyl alcohol should not be used. (See Cautions: Pediatric Precautions.) The drug should be administered immediately after dilution, and any unused portion of the dilution and the unused contents of the ampul or vial should be discarded. The infusion container must be protected from light at all times.
(See Chemistry and Stability: Stability.) The acetate, carbonate, citrate, gluconate, lactate, and phosphate salts of calcium are administered orally. It has been recommended that most oral calcium supplements be administered 1-1.5 hours after meals or with a demulcent (e.g., milk).
However, calcium carbonate powder (i.e., CAL CARB-HD(R)) should generally be administered with meals, since the manufacturer recommends mixing the powder with food for administration. Calcium salts used to bind dietary phosphate in patients with end-stage renal disease should be administered with meals (e.g., 10-15 minutes before, or during, the meal). Calcium chloride and calcium gluconate may be administered IV.
Calcium chloride also may be administered by intraosseous (IO) injection+ in the setting of pediatric resuscitation; onset of action and systemic concentrations are comparable to those achieved with venous administration. Parenteral calcium salts may be administered in large volume IV infusion fluids. IV calcium injections must be administered slowly at a rate not exceeding 0.7-1.8
mEq/minute, and the injection should be stopped if the patient complains of discomfort. Following IV injection, the patient should remain recumbent for a short time. Close monitoring of serum calcium concentrations is essential during IV administration of calcium.
Calcium chloride should not be injected IM or into subcutaneous or perivascular tissue, since severe necrosis and sloughing may occur. Although other calcium salts may cause mild to severe local reactions, they are generally less irritating than calcium chloride. (See Cautions.) The fixed combination of calcium glycerophosphate and calcium lactate is injected IM.
Although some manufacturers previously stated that calcium gluconate could be injected IM when IV administration was not possible, manufacturers of calcium gluconate currently state that the drug should not be injected IM or into subcutaneous tissue because of the potential for severe local reactions. In children, calcium salts should not be administered through scalp veins. Oral administration of calcium supplements or calcium-rich foods should replace parenteral calcium therapy as soon as possible.
The interaction of calcium and phosphate in parenteral nutrition solutions is a complex phenomenon; various factors have been identified as playing a role in the solubility or precipitation of a given combination. Calcium salts are conditionally compatible with phosphate in parenteral nutrition solutions; incompatibility is dependent on a solubility and concentration phenomenon and is not entirely predictable. Precipitation may occur during compounding or at some time after compounding is completed.
Specialized references should be consulted for specific compatibility information. Vitamin D analogs are usually administered orally; however, calcitriol, doxercalciferol, and paricalcitol may be given by IV injection. Ergocalciferol may be given by IM injection; however, a suitable formulation of the drug for IM injection no longer is commercially available in the US.
No dosing information available.
No generic dosing information available.
The following drug interaction information is available for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione):
There are 0 contraindications.
There are 4 severe interactions.
These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.
| Drug Interaction | Drug Names |
|---|---|
| Selected Anticoagulants (Vitamin K antagonists)/Vitamin K SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Anticoagulants interfere with the activation of vitamin K-dependent clotting factors. Vitamin K administration may reverse this effect. CLINICAL EFFECTS: The pharmacological effect of anticoagulants may be reversed resulting in thrombus formation. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients receiving anticoagulants should avoid eating unusual increases in foods high in vitamin K content. The time of highest risk for a coumarin-type drug interaction is when the precipitant drug is initiated or discontinued. Contact the prescriber before initiating, altering the dose or discontinuing either drug. DISCUSSION: Numerous reports have demonstrated that vitamin K interferes with the hypoprothrombinemic effects of anticoagulants. However, reports of clinically important consequences are uncommon. A clearer understanding of the mechanism by which these drugs act has made it possible to use vitamin K to control bleeding side effects of warfarin therapy. One should be aware of the vitamin K content of enteral feeding products being administered to patients on anticoagulant therapy. Prothrombin time should be monitored when these products are given. |
ANISINDIONE, DICUMAROL, JANTOVEN, PHENINDIONE, WARFARIN SODIUM |
| Oral Phosphate Supplements; Urinary pH Modifiers/Aluminum; Calcium; Magnesium SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Medications containing significant amounts of aluminum, calcium, or magnesium may bind to the phosphate and prevent its absorption.(1) CLINICAL EFFECTS: Concurrent use of medications containing significant amounts of aluminum, calcium, or magnesium may result in decreased effectiveness of phosphate supplements and urinary pH modifiers high in phosphate.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients receiving phosphate supplements or urinary pH modifiers high in phosphate should be instructed to avoid medications containing aluminum, calcium, or magnesium.(1) Some phosphate laxative products used as phosphate supplements may contain sufficient quantities of phosphate to interact as well. DISCUSSION: The manufacturer of K-Phos states that products containing aluminum, calcium, or magnesium may bind to the phosphate and prevent its absorption. Therefore, patients receiving phosphate supplements and urinary pH modifiers high in phosphate should be instructed to avoid products containing aluminum, calcium, or magnesium.(1) |
K-PHOS NO.2, K-PHOS ORIGINAL, POTASSIUM PHOSPHATE, SODIUM PHOSPHATE DIBASIC, UROQID-ACID NO.2 |
| Raltegravir (600 mg HD)/Calcium Carbonate SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Calcium carbonate may alter raltegravir absorption by altering gastric pH and binding to raltegravir in the GI tract, preventing its absorption.(1) CLINICAL EFFECTS: Calcium carbonate may reduce levels and clinical effectiveness of raltegravir.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Calcium carbonate is not recommended for patients receiving one daily raltegravir (600 mg HD tablets).(1) DISCUSSION: Simultaneous administration of calcium carbonate (3000 mg) with raltegravir (1200 mg singe dose given as two 600 mg HD tablets) decreased raltegravir maximum concentration (Cmax), area-under-curve (AUC), and minimum concentration (Cmin) by 74%, 72%, and 48%, respectively.(1,2) Administration of calcium carbonate (3000 mg) 12 hours after raltegravir (1200 mg singe dose given as two 600 mg HD tablets) decreased raltegravir Cmax, AUC, and Cmin by 2%, 10%, and 57%, respectively.(1,2) Data from in vitro(3) and in vivo simulations(4) suggest that magnesium's effect on raltegravir may involve chelation as well as changes in pH. Calcium may have a similar effect. |
ISENTRESS HD |
| Erdafitinib/Serum Phosphate Level-Altering Drugs SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Medications that alter serum phosphate may interfere with interpretation of phosphate levels that are needed to determine initial erdafitinib dose.(1) CLINICAL EFFECTS: Serum phosphate levels that are elevated by concomitant medications may result in an inappropriately low dose and decreased effectiveness of erdafitinib. Serum phosphate levels that are decreased by concomitant medications may result in an inappropriately high dose and increased toxicity from erdafitinib. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturer of erdafitinib states that agents that alter serum phosphate levels should be avoided before the initial dose increase period for erdafitinib based on serum phosphate levels (days 14 to 21).(1) DISCUSSION: Concomitant administration of serum phosphate level-altering agents during the initial dose increase period of erdafitinib based on serum phosphate levels (days 14 to 21) may interfere with serum phospate levels and lead to incorrect dosing of erdafitinib.(1) Agents that may alter serum phosphate levels linked to this monograph include: aluminum carbonate, aluminum hydroxide, calcium acetate, calcium carbonate, calcium citrate, cod liver oil, ferric citrate, lanthanum, magnesium carbonate, magnesium hydroxide, potassium phosphate, sevelamer, sodium phosphate, sucroferric oxyhydroxide, tenapanor, and vitamin D.(1) |
BALVERSA |
There are 29 moderate interactions.
The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.
| Drug Interaction | Drug Names |
|---|---|
| Tetracyclines/Divalent & Trivalent Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Di- and trivalent cations may form chelation complexes with tetracyclines, preventing their absorption.(1,2) CLINICAL EFFECTS: Simultaneous administration of di- or trivalent cations may result in decreased levels of and therapeutics effects from tetracyclines. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Administer tetracyclines at least two hours before or after the di- or trivalent cations. When used for the treatment of H. pylori infection, tetracyclines and bismuth should be given simultaneously. The US manufacturer of omadacycline states to fast for at least four hours, administer omadacycline, and then wait four hours before taking di- or trivalent cations.(21) DISCUSSION: Concurrent administration of aluminum hydroxide or divalent cations (such as calcium, magnesium, or zinc) has been shown to significantly decrease the gastrointestinal absorption of tetracycline.(3-5) Concurrent administration of tetracycline and magnesium-aluminum hydroxide gel has been shown to decrease the tetracycline area-under-curve (AUC) by 90%.(6) Magnesium-aluminum silicate has been shown to decrease the AUC of tetracycline by 27%.(7) Demeclocycline(8,9) methacycline,(10) chlortetracycline,(11) and oxytetracycline(10,12) have been shown to interact with aluminum hydroxide and/or dairy products. Doxycycline has been reported to interact with aluminum hydroxide gel.(13) Aluminum magnesium hydroxide has been shown to decrease doxycycline absorption by 84%.(14) Minocycline absorption has been shown to be impaired by aluminum, calcium, and magnesium.(15) Bismuth subsalicylate has been shown to decrease absorption of doxycycline and tetracycline by 37%(16) and 34%,(17) respectively. Since sucralfate is an aluminum salt of a sulfated disaccharide, it may also prevent absorption of tetracyclines. This complex has been used to provide site-specific delivery of tetracycline to gastric ulcers in the treatment of Helicobacter pylori gastric ulcer disease and may be useful in some indications.(18) Quinapril tablets contain a high percentage of magnesium and have been shown to decrease the absorption of tetracycline by 28-37%.(19) Lanthanum is expected to interact with tetracyclines as well.(20) |
AVIDOXY, AVIDOXY DK, BENZODOX 30, BENZODOX 60, BISMUTH-METRONIDAZOLE-TETRACYC, DEMECLOCYCLINE HCL, DORYX, DORYX MPC, DOXYCYCLINE HYCLATE, DOXYCYCLINE IR-DR, DOXYCYCLINE MONOHYDRATE, EMROSI, MINOCYCLINE ER, MINOCYCLINE HCL, MINOCYCLINE HCL ER, MONDOXYNE NL, MORGIDOX, NUZYRA, ORACEA, OXYTETRACYCLINE HCL, PYLERA, SEYSARA, TARGADOX, TETRACYCLINE HCL, XIMINO |
| Penicillamine, Oral/Polyvalent Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Penicillamine chelates with polyvalent cations such as aluminum, calcium, iron, magnesium, and zinc in the GI tract reducing the absorption of the penicillamine. CLINICAL EFFECTS: Reduced (to 30% of fasting) bioavailability of penicillamine with decreased pharmacologic response. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: In order to assure systemic absorption and maximal effectiveness from penicillamine, counsel patient to separate penicillamine by at least 1 hour before or 1 hours after any medications or products containing polyvalent cations such as antacids or mineral supplements. Monitor clinical status for decreased effectiveness and adjust the penicillamine dose if necessary. DISCUSSION: Clinical studies with polyvalent cations have not been conducted. Multivitamins with low doses of cations including iron and zinc may decrease penicillamine absorption so insure patient is aware of the risks. |
CUPRIMINE, D-PENAMINE, DEPEN, PENICILLAMINE, PENICILLAMINE(D-) |
| Slt Cation-Donating Antacids/Polystyrene Sulfonate SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Polystyrene sulfonate may bind the cation from the antacid, resulting in increased intestinal absorption of non-neutralized bicarbonate, which may result in systemic alkalosis and decreased potassium binding by polystyrene sulfonate. Intestinal obstruction has occurred with aluminum hydroxide because of concretion. CLINICAL EFFECTS: Simultaneous oral use may result in metabolic alkalosis and a decrease in the potassium lowering effect of polystyrene sulfonate. Intestinal obstruction has been reported with aluminum hydroxide. PREDISPOSING FACTORS: Patients with renal failure may be at a higher risk of systemic alkalosis. PATIENT MANAGEMENT: Consider the use of alternative agents to cation-donating antacids in patients receiving oral polystyrene sulfonate when possible. If concurrent use is required, separate the dosing by several hours.(1) Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: In a study in 11 patients with decreased renal function, the administration of magnesium hydroxide and sodium polystyrene sulfonate produced moderate to moderately severe metabolic alkalosis.(2) There are case reports documenting this affect as well.(3-7) Intestinal obstruction has been reported with aluminum hydroxide and sodium polystyrene sulfonate.(8) If the polystyrene sulfonate is administered rectally, a clinically significant interaction is not likely to occur. |
KIONEX, SODIUM POLYSTYRENE SULFONATE, SPS |
| Itraconazole; Ketoconazole/Agents Affecting Gastric pH SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Antacids, buffers in didanosine products, H2 antagonists, and proton-pump inhibitors increase the stomach pH. Quinapril tablets may contain a high percentage of magnesium. Since some orally administered azole antifungal agents require an acidic medium for optimal absorption, agents may decrease the absorption of azole antifungal agents. CLINICAL EFFECTS: Simultaneous administration of an antacid, buffered didanosine, a H2 antagonist, or a proton-pump inhibitor may result in decreased therapeutic effects of the azole antifungal. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: If the concurrent administration of these two agents cannot be avoided, consider administering two capsules of glutamic acid hydrochloride 15 minutes before administering the antifungal and separate the administration times of the antifungal and the agent affecting gastric pH by at least two hours. DISCUSSION: Itraconazole, ketoconazole, and posaconazole require an acidic medium for predictable dissolution and absorption decreases as pH increases and proton pump inhibitors are expected to decrease their absorption.(1-4) In a study in 11 healthy subjects, omeprazole (40 mg daily) decreased the maximum concentration (Cmax) and area-under-curve (AUC) of itraconazole (200 mg single dose) by 66% and 64%, respectively.(5) In a study in 15 healthy subjects, omeprazole (40 mg daily) had no effect on the pharmacokinetics of itraconazole solution.(6) In a study in 9 healthy subjects, omeprazole (60 mg) decreased the AUC of ketoconazole (200 mg single dose) by 83.4% compared to control (ketoconazole alone). Administration of Coca-Cola (240 ml) with ketoconazole and omeprazole raised ketoconazole AUC to 65% of control values.(7) Omeprazole has been shown to have no significant effect on the absorption of fluconazole(8) or voriconazole.(9) Case reports and in-vivo studies have documented significant decreases in ketoconazole levels during concurrent therapy with H-2 antagonists, including cimetidine and ranitidine. Concurrent administration of itraconazole and famotidine resulted in a significant decrease in itraconazole levels, but no significant changes in famotidine levels. An interaction should be expected to occur between both ketoconazole or itraconazole and the other H-2 antagonists.(10-14) In randomized, open-labeled, cross-over study in 12 healthy subjects, simultaneous administration of an antacid decreased the area-under-curve (AUC) and maximum concentration (Cmax) of a single dose of itraconazole (200 mg) by 66% and 70%, respectively. Time to Cmax (Tmax) increased by 70%.(15) This interaction has also been reported in a case report.(16) In a study in 3 subjects, simultaneous administration of a combination aluminum hydroxide/magnesium hydroxide (30 ml) decreased the AUC of a single dose of ketoconazole (200 mg) by 41%.(172) In a case report, a patient receiving concurrent ketoconazole with aluminum hydroxide, cimetidine, and sodium bicarbonate did not respond to therapy until cimetidine was discontinued and the administration time of aluminum hydroxide and cimetidine was changed to 2 hours after ketoconazole. In a follow-up study in 2 subjects, concurrent cimetidine and sodium hydroxide lowered ketoconazole levels.(18) In a study in 14 subjects, simultaneous administration of aluminum hydroxide/magnesium hydroxide (20 ml, 1800 mg/1200 mg) had no significant effects on fluconazole pharmacokinetics.(3) In a randomized, open-label, cross-over study in 6 subjects, simultaneous administration of itraconazole with buffered didanosine tablets resulted in undetectable levels of itraconazole.(19) In a randomized cross-over study in 12 HIV-positive subjects, administration of buffered didanosine tablets 2 hours after ketoconazole had no effects on ketoconazole levels.(20) In a randomized, cross-over, open-label study in 24 healthy subjects, simultaneous administration of enteric-coated didanosine had no effect on ketoconazole pharmacokinetics.(21) One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
ITRACONAZOLE, ITRACONAZOLE MICRONIZED, KETOCONAZOLE, SPORANOX, TOLSURA |
| Thyroid Preparations/Calcium; Iron; Sucralfate SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The mechanism by which malabsorption of thyroid preparations occurs from calcium-containing products is presumed to be a binding of the medication to the thyroid hormone, forming an insoluble or nonabsorbable complex.(1-3) Iron may form a ferric-thyroxine complex with thyroid agents, preventing their absorption from the gastrointestinal tract.(1,4) Sucralfate binds to other agents in the gastrointestinal tract and alters absorption of other drugs, including thyroid agents.(1,5) CLINICAL EFFECTS: The simultaneous administration of thyroid preparations with calcium, iron, or sucralfate may result in decreased levels and clinical effects of thyroid preparations.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Instruct patients to separate the administration time of thyroid preparations from calcium or iron by as much time as possible, preferably by at least four hours.(1) Administer thyroid preparations at least 2 hours before sucralfate.(5) Patients taking thyroid preparations and calcium- or iron-containing products or sucralfate should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased. Separating the administration times of the thyroid preparation and the calcium- or iron-containing products or sucralfate may decrease the effects of the interaction.(1-5) DISCUSSION: In a pharmacokinetic study 8 healthy, euthyroid adults were given levothyroxine alone and levothyroxine coadministered with calcium carbonate, calcium citrate, or calcium acetate in doses containing 500 mg elemental calcium. The coadministration of each of the three calcium preparations significantly reduced levothyroxine absorption by about 20%-25% compared with levothyroxine given alone.(3) In a study in 14 subjects, the simultaneous administration of thyroxine with ferrous sulfate for 12 weeks resulted in an increase in the mean level of thyroid stimulating hormone (TSH) from 1.6+/-0.4 mU/L to 5.4+/-2.8 mU/L. Mixing thyroxine with ferrous sulfate in vitro resulted in a poorly soluble complex.(4) In a study in 20 hypothyroid patients, the simultaneous administration of levothyroxine and calcium carbonate (1200 mg) daily for three months resulted in reductions in the mean free T4 and total T4 levels. These values increased in most patients following the discontinuation of calcium carbonate. A concurrent in-vitro study found that calcium carbonate adsorbed levothyroxine in solution at a pH of 2, gastric pH, but not at a pH of 7.4.(6) One author reported three cases of decreased levothyroxine efficacy following the addition of calcium carbonate to therapy.(7) In a study in 5 healthy subjects, levothyroxine (five 200 mcg tablets) was administered in 3 different dosing regimens: after an overnight fast, with the fifth and final dose of sucralfate (1 gram every 6 hours) and 8 hours after the second and final dose of sucralfate (2 grams every 12 hours). When administered alone, 80% of levothyroxine was absorbed within 6 hours of administration, compared to 23% when administered concurrently with sucralfate. There was no difference in levothyroxine absorption when administered alone or 8 hours after sucralfate.(8) There are several case reports documenting decreased effects of thyroid supplementation as the result of simultaneous administration of sucralfate.(9,10) One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
ADTHYZA, ARMOUR THYROID, CYTOMEL, ERMEZA, EUTHYROX, LEVO-T, LEVOTHYROXINE SODIUM, LEVOTHYROXINE SODIUM DILUTION, LEVOXYL, LIOTHYRONINE SODIUM, NIVA THYROID, NP THYROID, PCCA T3 SODIUM DILUTION, PCCA T4 SODIUM DILUTION, RENTHYROID, SYNTHROID, THYQUIDITY, THYROID, TIROSINT, TIROSINT-SOL, UNITHROID |
| Orlistat/Fat Soluble Vitamins SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The acetate ester forms of vitamin A and vitamin E must undergo hydrolysis for absorption from the gastrointestinal tract.(1) The enzyme responsible for this hydrolysis is inhibited by orlistat.(2) CLINICAL EFFECTS: Orlistat may reduce absorption of fat soluble vitamins, leading to a deficiency state. PREDISPOSING FACTORS: A pre-existing deficiency of fat soluble vitamins (A,D,E and K) or chronic malabsorption syndrome. PATIENT MANAGEMENT: The inhibition of fat soluble vitamin absorption by orlistat should be borne in mind during implementation of a vitamin supplementation strategy. Patients should be strongly encouraged to take a multivitamin supplement which contains fat soluble vitamins, particularly Vitamin D as it appears most susceptible to this interaction.(4,5) Multivitamin supplements should be taken at least two hours before or after the dose of orlistat, or at bedtime.(4) Patients with chronic malabsorption syndromes should not receive orlistat.(4) DISCUSSION: Adult patients taking orlistat without supplementation showed a greater reduction in vitamin A,D,E and beta-carotene levels compared to placebo during two or more consecutive visits in studies of 1-2 years duration; these patients had normal baseline values prior to orlistat therapy. Low vitamin values in orlistat patients were as follows: low Vitamin D 12%, low beta-carotene 6.1%, low Vitamin E 5.8%, low Vitamin A 2.2%.(4) A pharmacokinetic interaction study showed a 30% reduction in beta-carotene supplement absorption and a 60% decreased in vitamin E acetate absorption with concomitant orlistat.(4) In a study, orlistat produced the vitamin net concentration by approximately 43%.(1) In a study, no statistically significant decrease in vitamin A absorption was observed with concurrent orlistat.(2) In a study, mean vitamin D levels were significantly reduced compared with baseline after one month of orlistat therapy despite multivitamin supplementation.(5) |
ORLISTAT, XENICAL |
| Chloroquine; Hydroxychloroquine/Di-; Trivalent Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Di- and trivalent cations such as aluminum, calcium, lanthanum, and magnesium may adsorb chloroquine and hydroxychloroquine; preventing their absorption.(1-5) The adsorption may also limit the effectiveness of the di- or trivalent cation.(1) CLINICAL EFFECTS: Simultaneous administration of di- or trivalent cations may result in decreased levels and effectiveness of chloroquine and hydroxychloroquine(2-5) and decreased effectiveness of the di- or trivalent cation.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Instruct patients to separate the administration times of these medicines by 2 to 4 hours.(2,3) DISCUSSION: Adsorption of chloroquine by magnesium trisilicate was found to decrease hydrochloric acid uptake and decrease the amount of magnesium released in an acidic environment.(1) In a study, calcium carbonate, kaolin, and magnesium trisilicate were found to decrease the absorption of chloroquine by 52.8%, 46.5%, and 31.3%, respectively.(3) Magnesium trisilicate and magnesium oxide have been shown to decrease the release of chloroquine from tablets and to adsorb chloroquine after its release.(4) In a study in 6 subjects, magnesium trisilicate and kaolin decreased the area-under-curve (AUC) of chloroquine by 18.2% and 28.6%, respectively.(5) |
CHLOROQUINE PHOSPHATE, HYDROXYCHLOROQUINE SULFATE, PLAQUENIL, SOVUNA |
| Oral Iron Supplements/Antacids and Selected Minerals SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Some antacids may bind to iron, preventing its absorption. Alterations in gastric pH by antacids may also play a role. Iron may bind to other minerals such as calcium, manganese, tin, and zinc in the GI tract. CLINICAL EFFECTS: Simultaneous administration of an antacid or minerals may decrease the absorption of orally administered iron. PREDISPOSING FACTORS: The interaction with some combinations may be affected by the presence or absence of food. PATIENT MANAGEMENT: Iron supplements should not be taken within 1 hour before or 2 hours after antacids, calcium, manganese, or zinc.(1) Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: Magnesium hydroxide has been shown to inhibit the absorption of elemental iron,(2) although other studies have shown conflicting results.(3,4) Sodium bicarbonate has been shown to decrease the absorption of iron by 50%.(3) In a study in 61 healthy subjects, calcium citrate, calcium carbonate, and calcium phosphate inhibited iron absorption when taken with food. However, in the fasted state, calcium carbonate had no effect on iron absorption. In the fasted state, calcium citrate and calcium phosphate decreased iron absorption by 49% and 62%, respectively,(6) In a study in 23 healthy subjects, calcium acetate and calcium carbonate decreased the area-under-curve (AUC) of elemental iron (65 mg) by 27% and 19%, respectively.(7) In a study, manganese decreased iron absorption. A ratio of 5:1 of zinc:iron decreased iron absorption by 56%.(8) In a study, inorganic iron decreased zinc absorption.(9) In another study, ferrous sulfate decreased the absorption of zinc sulfate in a concentration dependent manner; however, heme chloride had no effect on zinc sulfate.(10) In a study in premature infants, administration of liquid zinc and iron supplements between feedings decreased iron uptake; however, no effect was seen when the supplements were mixed with feedings.(11) One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
ACCRUFER, AUROVELA 24 FE, AUROVELA FE, AURYXIA, BALCOLTRA, BLISOVI 24 FE, BLISOVI FE, CHARLOTTE 24 FE, FEIRZA, FERRIC CITRATE, FINZALA, GEMMILY, HAILEY 24 FE, HAILEY FE, JOYEAUX, JUNEL FE, JUNEL FE 24, KAITLIB FE, LARIN 24 FE, LARIN FE, LAYOLIS FE, LEVONORG-ETH ESTRAD-FE BISGLYC, LO LOESTRIN FE, LOESTRIN FE, MERZEE, MIBELAS 24 FE, MICROGESTIN FE, MINZOYA, NORETHIN-ETH ESTRA-FERROUS FUM, NORETHINDRONE-E.ESTRADIOL-IRON, TARINA 24 FE, TARINA FE, TARINA FE 1-20 EQ, TAYTULLA, TILIA FE, TRI-LEGEST FE, VELPHORO, WYMZYA FE, XARAH FE, XELRIA FE |
| Phenytoin/Aluminum-Magnesium Hydroxide; Oral Calcium SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Aluminum hydroxide; magnesium hydroxide, and oral calcium may bind to phenytoin, preventing its absorption.(1-4) CLINICAL EFFECTS: Simultaneous ingestion of aluminum-magnesium hydroxide and/or calcium-containing products may result in decreased levels and effectiveness of phenytoin.(1-4) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of phenytoin recommends that administration times of phenytoin and antacids being staggered.(1) DISCUSSION: In a study in 8 healthy subjects, simultaneous administration of phenytoin (600 mg) with calcium carbonate significantly decreased the area-under-curve (AUC) of phenytoin.(2) In a study in 8 healthy subjects, simultaneous administration of aluminum-magnesium hydroxide or calcium carbonate significantly decreased the AUC of phenytoin.(3) In a study in 6 patients with epilepsy, concurrent administration of an aluminum-magnesium hydroxide antacid resulted in a small but statistically significant decrease in phenytoin AUC.(4) |
DILANTIN, DILANTIN-125, PHENYTEK, PHENYTOIN, PHENYTOIN SODIUM, PHENYTOIN SODIUM EXTENDED |
| Eltrombopag/Polyvalent Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Eltrombopag chelates polyvalent cations such as aluminum, calcium, iron, magnesium, selenium, and zinc.(1) CLINICAL EFFECTS: Simultaneous administration of eltrombopag and polyvalent cations may decrease the absorption and clinical effects of eltrombopag. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of eltrombopag states that it should be administered at least 2 hours before or 4 hours after any medications or products containing polyvalent cations such as antacids or mineral supplements.(1) DISCUSSION: In a crossover study in 25 healthy subjects, administration of eltrombopag with an antacid (1524 mg aluminum hydroxide/1425 mg magnesium carbonate/sodium alginate) decreased eltrombopag levels by 70%.(1,2) |
ALVAIZ, PROMACTA |
| Selected Oral Quinolones/Selected Oral Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Aluminum, calcium, iron, lanthanum, magnesium, and zinc may form chelation compounds with the quinolones.(1-39) CLINICAL EFFECTS: Simultaneous administration or administration of products containing aluminum, calcium, iron, lanthanum, magnesium, and/or zinc close to the administration time of an oral quinolone may result in decreased absorption and clinical effectiveness of the quinolone. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: If possible, avoid concurrent therapy with quinolones and cation-containing products. If it is necessary to administer these agents concurrently, follow the manufacturers' recommendations regarding timing of administration of the quinolone and cation-containing products. Manufacturer recommendations regarding the separation of administration times of quinolones and products containing aluminum, calcium, iron, lanthanum, magnesium, and/or zinc vary: ---Do not give ciprofloxacin for at least 2 hours before or 6 hours after oral cations.(1) ---Do not give delafloxacin for at least 2 hours before or 6 hours after oral cations.(2) ---Do not give enoxacin for at least 2 hours before or 8 hours after oral cations.(3) ---Do not give levofloxacin for at least 2 hours before or 2 hours after oral cations.(4) ---Do not give nalidixic acid for at least 2 hours before or 2 hours after oral cations.(5) ---Do not give norfloxacin for at least 2 hours before or 2 hours after oral cations.(6) ---Do not give ofloxacin for at least 2 hours before or 2 hours after oral cations.(7) ---Do not give sparfloxacin for at least 4 hours before oral cations.(8) The US manufacturer of lanthanum recommends that quinolones be taken at least 1 hour before or 4 hours after lanthanum;(9) however, it would be prudent to follow the specific quinolone manufacturers' recommendations regarding concurrent administration of cations. For quinolones not listed above, separate their administration from oral cations by as much time as feasible. DISCUSSION: Aluminum, calcium, iron, magnesium, and zinc products have been shown to form chelation compounds with quinolone antibiotics, resulting in decreased absorption of the quinolone.(1-38) Treatment failures have been reported.(10-12) In a study in 12 healthy subjects, simultaneous administration of didanosine chewable tablets, which contain aluminum and magnesium, decreased ciprofloxacin area-under-curve (AUC) and maximum concentration (Cmax) by 92% and 98%, respectively.(13) The administration of ciprofloxacin 2 hours prior to Videx chewable/dispersible tablets decreased ciprofloxacin concentrations by 26%.(14,15) In a study in healthy subjects, pretreatment with an antacid containing aluminum-magnesium hydroxide at 5-10 minutes, 2 hours, and 4 hours before a single dose of ciprofloxacin decreased ciprofloxacin AUC by 84.9%, 76.8%, and 30%, respectively. There was no effect when the antacid was administered 6 hours before or 2 hours after.(16) In a study in 12 healthy subjects, aluminum hydroxide decreased ciprofloxacin AUC by 85%.(17) In a study in patients on continuous ambulatory peritoneal dialysis, peak levels of ciprofloxacin were decreased by 67% to 92% in patients receiving aluminum-containing antacids.(18) In a study in 15 healthy subjects, simultaneous administration of calcium acetate decreased the bioavailability of ciprofloxacin by 51%.(19) In a study in 6 healthy males, simultaneous administration of calcium carbonate decreased ciprofloxacin Cmax and AUC by 40% and 43%, respectively.(20) In a study in 12 healthy subjects, calcium carbonate decreased ciprofloxacin AUC by 40%.(17) In a study in 13 healthy males, calcium carbonate had no effect on ciprofloxacin bioavailability when administered 2 hours prior to the antibiotic.(21,22) In a study in healthy males, simultaneous administration of calcium polycarbophil decreased ciprofloxacin AUC by 50%.(23) In a study in 8 healthy males, simultaneous administration of ferrous fumarate (200 mg) decreased ciprofloxacin AUC by 70%.(24) In a study in healthy subjects, ferrous gluconate decreased ciprofloxacin bioavailability by 50%; however, no significant effects were seen with iron-ovotransferrin.(25) In a study in 8 healthy subjects, ferrous sulfate decreased the Cmax and AUC of simultaneously administered ciprofloxacin by 54% and 57%, respectively.(26) In a study in 8 healthy subjects, administration of ferrous sulfate decreased the Cmax and AUC of ciprofloxacin by 33% and 46%, respectively. Administration of ferrous gluconate decreased the Cmax and AUC of ciprofloxacin by 57% and 67%, respectively. Administration of a multivitamin product containing calcium, copper, iron, magnesium, manganese, and zinc decreased the Cmax and AUC of ciprofloxacin by 53% and 56%, respectively.(27) In a study in 12 healthy males, ferrous sulfate decreased ciprofloxacin AUC by 63%.(28) In a study in 12 healthy subjects, lanthanum carbonate decreased the area-under-curve (AUC) and maximum concentration (Cmax) of concurrently administered ciprofloxacin by 54% and 56%, respectively.(29) In a study in 12 healthy males, a multivitamin containing zinc decreased ciprofloxacin AUC by 22%.(28) In a study in 12 healthy subjects, an antacid containing aluminum-magnesium hydroxide had no effect on the pharmacokinetics of intravenous enoxacin.(30) In a study in 10 healthy subjects, administration of an aluminum-magnesium hydroxide antacid 0.5 hours or 2 hours before oral enoxacin (400 mg single dose) decreased the AUC of enoxacin by 73% and 43%, respectively. There were no significant effects on enoxacin AUC when the antacid was administered 8 hours before or 2 hours after enoxacin.(31) In a study in 9 healthy subjects, colloidal aluminum phosphate had no effect on the amount of enoxacin absorbed; however, ferrous sulfate (1050 mg) decreased the amount of enoxacin absorption by 10%.(32) In a study in 5 healthy subjects and 5 patients with cystic fibrosis, separation of levofloxacin (750 mg) and calcium carbonate (500 mg 3 times daily with meals) by 2 hours resulted in no interaction in healthy subjects; however, levofloxacin levels were not bioequivalent in patients with cystic fibrosis.(33) Concurrent magnesium-aluminum hydroxide or calcium have been shown to decrease the bioavailability of norfloxacin by 91.0% and 63.5%, respectively.(34) Concurrent zinc has been shown to decrease the bioavailability of norfloxacin.(35) In a study in 8 healthy subjects, ferrous sulfate decreased the Cmax and AUC of simultaneously administered norfloxacin by 75% and 73%, respectively.(26) Simultaneous aluminum phosphate was found to decrease the rate, but not the extent, of absorption of ofloxacin.(36) In a study in 8 healthy subjects, ferrous sulfate decreased the Cmax and AUC of simultaneously administered norfloxacin by 36% and 25%, respectively.(26) In an in vitro study, ferrous sulfate, aluminum hydroxide, and calcium carbonate decreased ofloxacin availability by 32.6%, 30.7%, and 26.2%, respectively. However, in vivo tests showed a significant effect with only aluminum hydroxide.(37) In a study in 9 healthy subjects, simultaneous administration colloidal aluminum phosphate had no effect on ofloxacin (200 mg) absorption; however, ferrous sulfate (1050 mg) decreased the ofloxacin fraction of dose absorbed by 10.85%.(32) In a study in 16 subjects, administration of either aluminum-magnesium hydroxide or calcium carbonate at least 2 hours before or after ofloxacin administration had no significant effects on ofloxacin levels.(38) The administration of an antacid containing aluminum hydroxide and magnesium hydroxide 2 hours before, 2 hours after, and 4 hours after sparfloxacin decreased sparfloxacin levels by 23%, 17%, and 5%, respectively.(39) One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
BAXDELA, CIPRO, CIPROFLOXACIN, CIPROFLOXACIN HCL, LEVOFLOXACIN, LEVOFLOXACIN HEMIHYDRATE, NALIDIXIC ACID, OFLOXACIN |
| Selected Cephalosporins/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Absorption of oral cefuroxime may be reduced in patients receiving concomitant treatment with acid reducing agents.(1,2) CLINICAL EFFECTS: Antibiotic efficacy against organisms with a high minimum inhibitory concentration (MIC) to cefuroxime could be decreased. PREDISPOSING FACTORS: Taking cefuroxime on an empty stomach magnifies this effect. PATIENT MANAGEMENT: Separate the administration of cefuroxime by at least 1-2 hours after administration of antacids. Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. Since concurrent use of H2 antagonists and proton pump inhibitors (PPIs) in patients taking cefuroxime should be avoided, these would not be alternatives to antacids in these patients. DISCUSSION: In a study performed prior to the introduction of PPIs, administration of ranitidine 300 mg and sodium bicarbonate followed by cefuroxime taken on a empty stomach lowered both Cmax and AUC of cefuroxime by approximately 40 per cent compared with administration of cefuroxime alone on an empty stomach. Postprandial administration of cefuroxime in subjects taking ranitidine was similar to that of subjects taking cefuroxime on an empty stomach.(2) |
CEFUROXIME |
| Elvitegravir/Selected Oral Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The exact mechanism is unknown, but aluminum, calcium, iron, magnesium, sucralfate, and zinc may bind to elvitegravir in GI tract. CLINICAL EFFECTS: Simultaneous administration or administration of products containing aluminum, calcium, iron, magnesium, and/or sucralfate may result in decreased levels and effectiveness of elvitegravir, as well as the development of resistance.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Separate the administration of elvitegravir and products containing aluminum, calcium, iron, magnesium, and/or sucralfate by at least 2 hours.(1) Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: Administration of an antacid (exact formulation not stated) 2 hours before elvitegravir (50 mg) decreased the maximum concentration (Cmax), area-under-curve (AUC), or minimum concentration (Cmin) of elvitegravir by 18%, 15%, and 10%, respectively.(1) Administration of an antacid 2 hours after elvitegravir (50 mg) decreased the Cmax, AUC, or Cmin of elvitegravir by 21%, 20%, and 20%, respectively.(1) Administration of an antacid 4 hours before elvitegravir (50 mg) decreased the Cmax and AUC of elvitegravir by 5%, and 4%, respectively.(1) Administration of an antacid 4 hours before elvitegravir (50 mg) decreased both the Cmax and AUC of elvitegravir by 2%.(1) |
GENVOYA, STRIBILD |
| Dolutegravir/Selected Oral Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Aluminum, calcium, iron, lanthanum, magnesium, sucralfate, and zinc may form chelation compounds with dolutegravir.(1) CLINICAL EFFECTS: Simultaneous administration or administration of products containing aluminum, calcium, iron, lanthanum, magnesium, and/or sucralfate close to the administration time of dolutegravir may result in decreased absorption and clinical effectiveness of dolutegravir.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: If possible, avoid concurrent therapy with dolutegravir and cation-containing products. If it is necessary to use these agents concurrently, dolutegravir should be administered 2 hours before or 6 hours after taking these medications.(1) Alternatively, dolutegravir and supplements containing calcium or iron can be taken together with food.(1) DISCUSSION: In a study in 16 subjects, the administration of an antacid (Maalox - aluminum and magnesium hydroxide) simultaneously with dolutegravir (50 mg single dose) decreased the maximum concentration (Cmax), area-under-curve (AUC), and minimum concentration (Cmin) of dolutegravir by 72%, 74%, and 74%, respectively.(1) In a study in 16 subjects, the administration of an antacid (Maalox - aluminum and magnesium hydroxide) 2 hours after dolutegravir (50 mg single dose) decreased dolutegravir Cmax, AUC, and Cmin by 18%, 26%, and 30%, respectively.(1) In a study in 16 subjects, the administration of a multiple vitamin (One-A-Day) simultaneously with dolutegravir (50 mg single dose) decreased dolutegravir Cmax, AUC, and Cmin by 35%, 33%, and 32%, respectively.(1) |
DOVATO, TIVICAY, TIVICAY PD, TRIUMEQ, TRIUMEQ PD |
| Riociguat/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The mechanism of interaction is not clear. Increased gastric pH is thought to decrease riociguat solubility and absorption.(1) CLINICAL EFFECTS: Simultaneous administration of riociguat with an antacid may result in decreased levels and effectiveness of riociguat.(1-2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Separate the administration of antacids and riociguat by at least 1 hour.(1) Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: Administration of 10 mL of an aluminum hydroxide-magnesium hydroxide containing antacid decreased the area-under-curve (AUC)and maximum concentration (Cmax)of riociguat by 34% and 56% respectively.(1) |
ADEMPAS |
| Ledipasvir; Velpatasvir/Antacids; H2 Antagonists SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The aqueous solubility of ledipasvir and velpatasvir is pH dependent. Higher gastric pH leads to lower solubility which may reduce ledipasvir and velpatasvir's absorption.(1-3) CLINICAL EFFECTS: Administration of antacids and H2 antagonists may reduce the bioavailability of ledipasvir and velpatasvir, leading to decreased systemic levels and effectiveness.(1-3) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: In order to assure systemic absorption and maximal effectiveness from use of this Hepatitis C treatment, counsel patient to separate products containing ledipasvir or velpatasvir from antacid administration by 4 hours.(1-3) H2 antagonists may be administered simultaneously or 12 hours apart from products containing ledipasvir or velpatasvir at a dose that does not exceed doses comparable to famotidine 40 mg twice daily (or a total daily dose comparable to famotidine 80 mg).(1-3) Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: In an interaction study, famotidine 40 mg, given with or 12 hours after a ledipasvir-sofosbuvir dose did not have significant effects on ledipasvir-sofosbuvir exposure.(1) In an interaction study, famotidine 40 mg, given with or 12 hours prior to a velpatasvir-sofosbuvir dose did not have a significant effect on velpatasvir-sofosbuvir exposure.(2) In an interaction study, famotidine (dosage not stated) did not have a significant effect on the pharmacokinetic of sofosbuvir, velpatasvir, or voxilaprevir.(3) |
EPCLUSA, HARVONI, LEDIPASVIR-SOFOSBUVIR, SOFOSBUVIR-VELPATASVIR, VOSEVI |
| Dolutegravir-Rilpivirine/Selected Oral Cations; Antacids; H2 Antagonists SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Aluminum, calcium, iron, lanthanum, magnesium, sucralfate, and zinc may form chelation compounds with dolutegravir.(1) Rilpivirine requires an acidic medium for absorption. Antacid or H2 antagonist induced decrease in gastric pH may result in decrease in rilpivirine absorption.(1) CLINICAL EFFECTS: Simultaneous administration or administration of products containing aluminum, calcium, iron, lanthanum, magnesium, and/or sucralfate close to the administration time of dolutegravir may result in decreased absorption and clinical effectiveness of dolutegravir.(1) Simultaneous administration of an antacid or a H2 antagonist may result in decreased levels and effectiveness of rilpivirine, as well as the development of resistance.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: If possible, avoid concurrent therapy with dolutegravir-rilpivirine and cation-containing products. If it is necessary to use these agents concurrently, dolutegravir-rilpivirine should be administered 4 hours before or 6 hours after taking these medications.(1) Alternatively, dolutegravir-rilpivirine and supplements containing calcium or iron can be taken together with food.(1) In patients maintained on dolutegravir-rilpivirine, administer dolutegravir-rilpivirine at least 4 hours before or 6 hours after antacids .(1) In patients maintained on dolutegravir-rilpivirine, administer dolutegravir-rilpivirine at least 4 hours before or 12 hours after H2 antagonists.(1) Concurrent use of proton pump inhibitors will dolutegravir-rilpivirine is contraindicated.(1) DISCUSSION: In a study in 16 subjects, the administration of an antacid (Maalox - aluminum and magnesium hydroxide) simultaneously with dolutegravir (50 mg single dose) decreased the maximum concentration (Cmax), area-under-curve (AUC), and minimum concentration (Cmin) of dolutegravir by 72%, 74%, and 74%, respectively.(1) In a study in 16 subjects, the administration of an antacid (Maalox - aluminum and magnesium hydroxide) 2 hours after dolutegravir (50 mg single dose) decreased dolutegravir Cmax, AUC, and Cmin by 18%, 26%, and 30%, respectively.(1) In a study in 16 subjects, the administration of a multiple vitamin (One-A-Day) simultaneously with dolutegravir (50 mg single dose) decreased dolutegravir Cmax, AUC, and Cmin by 35%, 33%, and 32%, respectively.(1) In a study in 16 subjects, omeprazole (20 mg daily) decreased the Cmax, AUC, and Cmin of rilpivirine (150 mg daily) by 40%, 40%, and 33%, respectively. The Cmax and AUC of omeprazole decreased by 14% and 14%, respectively.(1) In a study in 24 subjects, famotidine (40 mg single dose) administered 12 hours before a single dose of rilpivirine (150 mg) had no significant effect on rilpivirine Cmax or AUC.(1) In a study in 23 subjects, famotidine (40 mg single dose) administered 2 hours before a single dose of rilpivirine (150 mg) decreased the rilpivirine Cmax and AUC by 85% and 76%, respectively.(1) In a study in 24 subjects, famotidine (40 mg single dose) administered 4 hours before a single dose of rilpivirine (150 mg) increased the rilpivirine Cmax and AUC by 21% and 13%, respectively.(1) |
JULUCA |
| Bictegravir/Calcium & Iron Containing Supplements SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Calcium or iron containing supplements may bind to bictegravir in the GI tract, preventing its absorption.(1) CLINICAL EFFECTS: Calcium or iron containing supplements may reduce levels and clinical effectiveness of bictegravir.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Bictegravir and calcium or iron containing supplements may be taken together with food. Routine administration of bictegravir under fasting conditions simultaneously with, or within 2 hours after, calcium or iron containing supplements is not recommended.(1) In pregnant patients, if bictegravir is taken on an empty stomach, take bictegravir at least 2 hours before or 6 hours after calcium or iron containing supplements.(1) DISCUSSION: Simultaneous administration of aluminum and magnesium hydroxide (20 ml) in a fasted state with bictegravir (50 mg single dose) decreased bictegravir maximum concentration (Cmax) and area-under-curve (AUC) by 80% and 79%, respectively.(1) Administration of aluminum and magnesium hydroxide (20 ml) 2 hours after bictegravir (50 mg single dose) in a fasted state decreased bictegravir Cmax and AUC by 7% and 13%, respectively.(1) Administration of aluminum and magnesium hydroxide (20 ml) 2 hours before bictegravir (50 mg single dose) in a fasted state decreased bictegravir Cmax and AUC by 58% and 52%, respectively.(1) Simultaneous administration of aluminum and magnesium hydroxide (20 ml) in a fed state with bictegravir (50 mg single dose) decreased bictegravir Cmax and AUC by 49% and 47%, respectively.(1) Simultaneous administration of calcium carbonate (1200 mg single dose) in a fasted state with bictegravir (50 mg single dose) decreased bictegravir Cmax and AUC by 42% and 33%, respectively.(1) Simultaneous administration of calcium carbonate (1200 mg single dose) in a fed state with bictegravir (50 mg single dose) decreased bictegravir Cmax by 10% and increased AUC 3%, respectively.(1) Simultaneous administration of ferrous fumarate (324 mg single dose) in a fasted state with bictegravir (50 mg single dose) decreased bictegravir Cmax and AUC by 71% and 63%, respectively.(1) Simultaneous administration of ferrous fumarate (324 mg single dose) in a fed state with bictegravir (50 mg single dose) decreased bictegravir Cmax and AUC by 25% and 16%, respectively.(1) |
BIKTARVY |
| Baloxavir/Polyvalent Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Aluminum, calcium, iron, magnesium, selenium, and zinc may form chelation compounds with baloxavir.(1) CLINICAL EFFECTS: Simultaneous administration of products containing aluminum, calcium, iron, magnesium, selenium, and zinc may result in decreased levels of and clinical effects from baloxavir.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Avoid concurrent administration of baloxavir with cation-containing products.(1) DISCUSSION: A significant decrease in baloxavir exposure was observed when baloxavir was coadministered with calcium, aluminum, magnesium, or iron in monkeys. No studies have been conducted in humans.(1) |
XOFLUZA |
| Colesevelam/Fat Soluble Vitamins SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Colesevelam may decrease the absorption of fat-soluble vitamins A, D, E, and K.(1) CLINICAL EFFECTS: Colesevelam may reduce absorption of fat soluble vitamins, leading to a deficiency state. PREDISPOSING FACTORS: A pre-existing deficiency of fat soluble vitamins (A,D,E and K) or chronic malabsorption syndrome. PATIENT MANAGEMENT: The inhibition of fat soluble vitamin absorption by colesevelam should be borne in mind during implementation of a vitamin supplementation strategy. Oral multivitamin supplements should be taken at least four hours before the dose of colesevelam.(1) DISCUSSION: Colesevelam may decrease the absorption of fat-soluble vitamins A, D, E, and K.(1) |
COLESEVELAM HCL, WELCHOL |
| Trientine/Selected Minerals, Oral SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Mineral supplements may bind to trientine and block its absorption. CLINICAL EFFECTS: The levels and clinical effects of trientine may be decreased. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of trientine states that mineral supplements should not be given with trientine. If concomitant therapy is necessary, take trientine on an empty stomach and separate administration at least one hour apart from any other drug. Monitor clinical status for decreased effectiveness and adjust the trientine dose if necessary. DISCUSSION: Multivitamins with minerals may decrease trientine absorption so ensure patient is aware of the risks. |
CUVRIOR, SYPRINE, TRIENTINE HCL |
| Infigratinib; Selpercatinib/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The solubility of infigratinib and selpercatinib is pH dependent. Antacid-induced changes in gastric pH may decrease the absorption of infigratinib and selpercatinib.(1,2) CLINICAL EFFECTS: Simultaneous administration of antacids may result in decreased levels and effectiveness of infigratinib and selpercatinib.(1,2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Avoid the use of antacids, proton pump inhibitors (PPIs), and H2 antagonists, in patients receiving treatment with infigratinib or selpercatinib. If coadministration with antacids cannot be avoided, take infigratinib or selpercatinib at least 2 hours before or 2 hours after the antacid.(1,2) If the antacid is replaced with a H2 antagonist, take infigratinib or selpercatinib 2 hours before or 10 hours after the H2 antagonist.(1,2) If the antacid is replaced with a PPI, take selpercatinib with food.(2) DISCUSSION: Infigratinib is practically insoluble at pH 6.8.(1) Selpercatinib solubility is pH dependent.(2) Antacids may decrease the solubility and absorption of infigratinib and selpercatinib and decrease their effectiveness. |
RETEVMO |
| Cabotegravir/Polyvalent Cations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Cabotegravir chelates polyvalent cations such as aluminum, calcium, iron, magnesium, selenium, and zinc.(1) CLINICAL EFFECTS: Simultaneous administration of cabotegravir and polyvalent cations may decrease the absorption and clinical effects of cabotegravir.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of cabotegravir states that it should be administered at least 2 hours before or 4 hours after any medications or products containing polyvalent cations such as antacids or mineral supplements.(1) DISCUSSION: Clinical studies have not been conducted. Prescribing information states cabotegravir levels may be decreased when coadministered with antacids containing polyvalent cations (examples include aluminum or magnesium hydroxide, calcium carbonate) suggesting cabotegravir is susceptible to chelation.(1) |
VOCABRIA |
| Sotorasib/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The aqueous solubility of sotorasib is pH dependent. Higher gastric pH leads to lower solubility which may reduce sotorasib absorption.(1) CLINICAL EFFECTS: Coadministration of antacids may reduce the bioavailability of sotorasib, leading to decreased systemic levels and effectiveness.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Coadministration of sotorasib with proton pump inhibitors, H2 antagonists, and antacids should be avoided. If coadministration with an acid-reducing agent is unavoidable, take sotorasib 4 hours before or 10 hours after a locally acting antacid.(1) DISCUSSION: The solubility of sotorasib in the aqueous media decreases over the range pH 1.2 to 6.8 from 1.3 mg/mL to 0.03 mg/mL. In an interaction study, coadministration of repeat doses of omeprazole with a single dose of sotorasib decreased sotorasib maximum concentration (Cmax) by 65% and area-under-curve (AUC) by 57% under fed conditions, and decreased sotorasib Cmax by 57% and AUC by 42% under fasted conditions. Coadministration of a single dose of famotidine given 10 hours prior to and 2 hours after a single dose of sotorasib under fed conditions decreased sotorasib Cmax by 35% and AUC by 38%.(1) |
LUMAKRAS |
| Levoketoconazole/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The aqueous solubility of levoketoconazole is pH dependent. Higher gastric pH leads to lower solubility. Antacids increase gastric pH and may decrease the absorption of levoketoconazole.(1) CLINICAL EFFECTS: Coadministration of antacids may reduce the bioavailability of levoketoconazole, leading to decreased systemic levels and effectiveness.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Coadministration of levoketoconazole with proton pump inhibitors and H2 antagonists should be avoided. If coadministration with an acid-reducing agent is unavoidable, take the antacid 2 hours before levoketoconazole.(1) DISCUSSION: Levoketoconazole is very slightly soluble in water but soluble below pH 2. Antacids raise gastric pH and may impair dissolution and absorption of levoketoconazole.(1) |
RECORLEV |
| Sparsentan/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The aqueous solubility of sparsentan is pH dependent. Higher gastric pH leads to lower solubility. Antacids increase gastric pH and may decrease the absorption of sparsentan.(1) CLINICAL EFFECTS: Coadministration of antacids may reduce the bioavailability of sparsentan, leading to decreased systemic levels and effectiveness.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: If coadministration with an acid-reducing agent is unavoidable, take an antacid 2 hours before or 2 hours after sparsentan. Coadministration of sparsentan with proton pump inhibitors and H2 antagonists should be avoided.(1) DISCUSSION: Sparsentan is practically insoluble in water but has intrinsic solubility of 1.48 mg/mL and 0.055 mg/mL below pH 1.2 and 6.8, respectively. Antacids raise gastric pH and may impair dissolution and absorption of sparsentan.(1) |
FILSPARI |
| Nirogacestat/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The aqueous solubility of nirogacestat is pH dependent. Higher gastric pH leads to lower solubility which may reduce nirogacestat absorption.(1) CLINICAL EFFECTS: Coadministration of antacids may reduce the bioavailability of nirogacestat, leading to decreased systemic levels and effectiveness.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Coadministration of nirogacestat with proton pump inhibitors, H2 antagonists, and antacids should be avoided. If coadministration with an acid-reducing agent is unavoidable, take nirogacestat 2 hours before or 2 hours after a locally acting antacid.(1) DISCUSSION: The solubility of nirogacestat is poor at a pH >= 6.(1) Concomitant use of proton pump inhibitors, H2 antagonists, or antacids are expected to reduce concentrations of nirogacestat.(1) |
OGSIVEO |
| Vadadustat/Polyvalent Cations and Phosphate Binders SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Vadadustat may form a chelate with iron supplements, phosphate binders, and other medicinal products whose primary component consists of polyvalent cations such as aluminum, calcium, magnesium, selenium, and zinc.(1) CLINICAL EFFECTS: Simultaneous administration of vadadustat and polyvalent cations and phosphate binders decreases the exposure and effectiveness of vadadustat.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturer of vadadustat states that it should be administered at least 1 hour before or 2 hours after any medications or products whose primary component consists of iron, phosphate binders and polyvalent cations.(1) DISCUSSION: Two studies evaluating the pharmacokinetics, safety, and tolerability of a single oral dose of vadadustat coadministered with a phosphate binder or iron supplement were conducted in healthy adult participants. Vadadustat exposure was reduced by coadministration with sevelamer carbonate, calcium acetate, ferric citrate, and ferrous sulfate. Geometric least squares mean ratios for area under the concentration-time curve (AUC) were reduced 37% to 55% by phosphate binders and 46% by ferrous sulfate. However, when vadadustat was administered 1 hour before phosphate binders, 90% confidence intervals for vadadustat exposure were within the no-effect boundaries of +50% to -33%, indicating that drug-drug interactions can be reduced by administering vadadustat 1 hour before phosphate binders.(2) |
VAFSEO |
| Cefpodoxime/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Absorption of oral cefpodoxime may be reduced in patients receiving concomitant treatment with acid reducing agents.(1-3) CLINICAL EFFECTS: Antibiotic efficacy against organisms with a high minimum inhibitory concentration (MIC) to cefpodoxime could be decreased. PREDISPOSING FACTORS: Taking cefpodoxime on an empty stomach magnifies this effect. PATIENT MANAGEMENT: Separate the administration of cefpodoxime by at least 1-2 hours after administration of antacids. Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. Since concurrent use of H2 antagonists and proton pump inhibitors (PPIs) in patients taking cefpodoxime should be avoided, these would not be alternatives to antacids in these patients. DISCUSSION: In a study of ten subjects, administration of cefpodoxime after single dose famotidine 40 mg decreased both maximum concentration (Cmax) and area-under-curve (AUC) by approximately 40% compared with administration of cefpodoxime on an empty stomach.(2) In a study of 17 subjects, administration of cefpodoxime after single dose ranitidine 150 mg decreased Cmax and AUC by approximately 40% compared with administration of cefpodoxime on an empty stomach.(3) |
CEFPODOXIME PROXETIL |
The following contraindication information is available for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione):
Drug contraindication overview.
No enhanced Contraindications information available for this drug.
No enhanced Contraindications information available for this drug.
There are 1 contraindications.
Absolute contraindication.
| Contraindication List |
|---|
| Hypervitaminosis D |
There are 6 severe contraindications.
Adequate patient monitoring is recommended for safer drug use.
| Severe List |
|---|
| Constipation |
| Dehydration |
| Hypercalcemia |
| Hyperphosphatemia |
| Kidney stone |
| Sarcoidosis |
There are 3 moderate contraindications.
Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.
| Moderate List |
|---|
| Hyperparathyroidism |
| Kidney disease with reduction in glomerular filtration rate (GFr) |
| Sarcoidosis |
The following adverse reaction information is available for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione):
Adverse reaction overview.
No enhanced Common Adverse Effects information available for this drug.
No enhanced Common Adverse Effects information available for this drug.
There are 3 severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
| None. | None. |
| Rare/Very Rare |
|---|
|
Anorexia Hypercalcemia Kidney stone |
There are 5 less severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
|
Abdominal distension Flatulence |
Acute abdominal pain Constipation Nausea |
| Rare/Very Rare |
|---|
| None. |
The following precautions are available for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione):
No enhanced Pediatric Use information available for this drug.
Contraindicated
Severe Precaution
Management or Monitoring Precaution
Contraindicated
| None |
Severe Precaution
| None |
Management or Monitoring Precaution
| None |
Reproduction studies have not been conducted in animals, and it is not known if phytonadione has teratogenic effects. A characteristic physiognomy, possibly with aortic valvular stenosis, retinopathy, and mental and/or physical retardation, has occurred following prolonged hypercalcemia in infants and in neonates of mothers with hypercalcemia during pregnancy. Hypercalcemia during pregnancy may also lead to suppression of PTH concentrations in the neonate resulting in hypocalcemia, tetany, and seizures. Safe use of calcifediol, calcitriol, dihydrotachysterol (no longer commercially available in the US), paricalcitol, or ergocalciferol during pregnancy has not been established; however, the risks to the mother and fetus from untreated hypoparathyroidism or hypophosphatemia may be greater than those resulting from administration of vitamin D analogs.
Safe use of calcifediol, calcitriol, dihydrotachysterol, doxercalciferol, paricalcitol, or ergocalciferol during lactation has not been established; however, the risks to the mother and fetus from untreated hypoparathyroidism or hypophosphatemia may be greater than those resulting from administration of vitamin D analogs. Large doses of vitamin D analogs should not be administered to nursing women.
No enhanced Geriatric Use information available for this drug.
The following prioritized warning is available for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione):
No warning message for this drug.
No warning message for this drug.
The following icd codes are available for CITRACAL (calcium carbonate/cholecalciferol (vit d3)/phytonadione)'s list of indications:
| Hypocalcemia | |
| E20.810 | Autosomal dominant hypocalcemia |
| E83.51 | Hypocalcemia |
| P71.0 | Cow's milk hypocalcemia in newborn |
| P71.1 | Other neonatal hypocalcemia |
| Hypocalcemia prevention | |
| E58 | Dietary calcium deficiency |
| Osteoporosis | |
| M80 | Osteoporosis with current pathological fracture |
| M80.0 | Age-related osteoporosis with current pathological fracture |
| M80.00 | Age-related osteoporosis with current pathological fracture, unspecified site |
| M80.00xA | Age-related osteoporosis with current pathological fracture, unspecified site, initial encounter for fracture |
| M80.00xD | Age-related osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with routine healing |
| M80.00xG | Age-related osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with delayed healing |
| M80.00xK | Age-related osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with nonunion |
| M80.00xP | Age-related osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with malunion |
| M80.00xS | Age-related osteoporosis with current pathological fracture, unspecified site, sequela |
| M80.01 | Age-related osteoporosis with current pathological fracture, shoulder |
| M80.011 | Age-related osteoporosis with current pathological fracture, right shoulder |
| M80.011A | Age-related osteoporosis with current pathological fracture, right shoulder, initial encounter for fracture |
| M80.011D | Age-related osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with routine healing |
| M80.011G | Age-related osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with delayed healing |
| M80.011K | Age-related osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with nonunion |
| M80.011P | Age-related osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with malunion |
| M80.011S | Age-related osteoporosis with current pathological fracture, right shoulder, sequela |
| M80.012 | Age-related osteoporosis with current pathological fracture, left shoulder |
| M80.012A | Age-related osteoporosis with current pathological fracture, left shoulder, initial encounter for fracture |
| M80.012D | Age-related osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with routine healing |
| M80.012G | Age-related osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with delayed healing |
| M80.012K | Age-related osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with nonunion |
| M80.012P | Age-related osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with malunion |
| M80.012S | Age-related osteoporosis with current pathological fracture, left shoulder, sequela |
| M80.019 | Age-related osteoporosis with current pathological fracture, unspecified shoulder |
| M80.019A | Age-related osteoporosis with current pathological fracture, unspecified shoulder, initial encounter for fracture |
| M80.019D | Age-related osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with routine healing |
| M80.019G | Age-related osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with delayed healing |
| M80.019K | Age-related osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with nonunion |
| M80.019P | Age-related osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with malunion |
| M80.019S | Age-related osteoporosis with current pathological fracture, unspecified shoulder, sequela |
| M80.02 | Age-related osteoporosis with current pathological fracture, humerus |
| M80.021 | Age-related osteoporosis with current pathological fracture, right humerus |
| M80.021A | Age-related osteoporosis with current pathological fracture, right humerus, initial encounter for fracture |
| M80.021D | Age-related osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with routine healing |
| M80.021G | Age-related osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with delayed healing |
| M80.021K | Age-related osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with nonunion |
| M80.021P | Age-related osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with malunion |
| M80.021S | Age-related osteoporosis with current pathological fracture, right humerus, sequela |
| M80.022 | Age-related osteoporosis with current pathological fracture, left humerus |
| M80.022A | Age-related osteoporosis with current pathological fracture, left humerus, initial encounter for fracture |
| M80.022D | Age-related osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with routine healing |
| M80.022G | Age-related osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with delayed healing |
| M80.022K | Age-related osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with nonunion |
| M80.022P | Age-related osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with malunion |
| M80.022S | Age-related osteoporosis with current pathological fracture, left humerus, sequela |
| M80.029 | Age-related osteoporosis with current pathological fracture, unspecified humerus |
| M80.029A | Age-related osteoporosis with current pathological fracture, unspecified humerus, initial encounter for fracture |
| M80.029D | Age-related osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with routine healing |
| M80.029G | Age-related osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with delayed healing |
| M80.029K | Age-related osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with nonunion |
| M80.029P | Age-related osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with malunion |
| M80.029S | Age-related osteoporosis with current pathological fracture, unspecified humerus, sequela |
| M80.03 | Age-related osteoporosis with current pathological fracture, forearm |
| M80.031 | Age-related osteoporosis with current pathological fracture, right forearm |
| M80.031A | Age-related osteoporosis with current pathological fracture, right forearm, initial encounter for fracture |
| M80.031D | Age-related osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with routine healing |
| M80.031G | Age-related osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with delayed healing |
| M80.031K | Age-related osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with nonunion |
| M80.031P | Age-related osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with malunion |
| M80.031S | Age-related osteoporosis with current pathological fracture, right forearm, sequela |
| M80.032 | Age-related osteoporosis with current pathological fracture, left forearm |
| M80.032A | Age-related osteoporosis with current pathological fracture, left forearm, initial encounter for fracture |
| M80.032D | Age-related osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with routine healing |
| M80.032G | Age-related osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with delayed healing |
| M80.032K | Age-related osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with nonunion |
| M80.032P | Age-related osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with malunion |
| M80.032S | Age-related osteoporosis with current pathological fracture, left forearm, sequela |
| M80.039 | Age-related osteoporosis with current pathological fracture, unspecified forearm |
| M80.039A | Age-related osteoporosis with current pathological fracture, unspecified forearm, initial encounter for fracture |
| M80.039D | Age-related osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with routine healing |
| M80.039G | Age-related osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with delayed healing |
| M80.039K | Age-related osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with nonunion |
| M80.039P | Age-related osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with malunion |
| M80.039S | Age-related osteoporosis with current pathological fracture, unspecified forearm, sequela |
| M80.04 | Age-related osteoporosis with current pathological fracture, hand |
| M80.041 | Age-related osteoporosis with current pathological fracture, right hand |
| M80.041A | Age-related osteoporosis with current pathological fracture, right hand, initial encounter for fracture |
| M80.041D | Age-related osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with routine healing |
| M80.041G | Age-related osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with delayed healing |
| M80.041K | Age-related osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with nonunion |
| M80.041P | Age-related osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with malunion |
| M80.041S | Age-related osteoporosis with current pathological fracture, right hand, sequela |
| M80.042 | Age-related osteoporosis with current pathological fracture, left hand |
| M80.042A | Age-related osteoporosis with current pathological fracture, left hand, initial encounter for fracture |
| M80.042D | Age-related osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with routine healing |
| M80.042G | Age-related osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with delayed healing |
| M80.042K | Age-related osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with nonunion |
| M80.042P | Age-related osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with malunion |
| M80.042S | Age-related osteoporosis with current pathological fracture, left hand, sequela |
| M80.049 | Age-related osteoporosis with current pathological fracture, unspecified hand |
| M80.049A | Age-related osteoporosis with current pathological fracture, unspecified hand, initial encounter for fracture |
| M80.049D | Age-related osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with routine healing |
| M80.049G | Age-related osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with delayed healing |
| M80.049K | Age-related osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with nonunion |
| M80.049P | Age-related osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with malunion |
| M80.049S | Age-related osteoporosis with current pathological fracture, unspecified hand, sequela |
| M80.05 | Age-related osteoporosis with current pathological fracture, femur |
| M80.051 | Age-related osteoporosis with current pathological fracture, right femur |
| M80.051A | Age-related osteoporosis with current pathological fracture, right femur, initial encounter for fracture |
| M80.051D | Age-related osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with routine healing |
| M80.051G | Age-related osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with delayed healing |
| M80.051K | Age-related osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with nonunion |
| M80.051P | Age-related osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with malunion |
| M80.051S | Age-related osteoporosis with current pathological fracture, right femur, sequela |
| M80.052 | Age-related osteoporosis with current pathological fracture, left femur |
| M80.052A | Age-related osteoporosis with current pathological fracture, left femur, initial encounter for fracture |
| M80.052D | Age-related osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with routine healing |
| M80.052G | Age-related osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with delayed healing |
| M80.052K | Age-related osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with nonunion |
| M80.052P | Age-related osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with malunion |
| M80.052S | Age-related osteoporosis with current pathological fracture, left femur, sequela |
| M80.059 | Age-related osteoporosis with current pathological fracture, unspecified femur |
| M80.059A | Age-related osteoporosis with current pathological fracture, unspecified femur, initial encounter for fracture |
| M80.059D | Age-related osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with routine healing |
| M80.059G | Age-related osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with delayed healing |
| M80.059K | Age-related osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with nonunion |
| M80.059P | Age-related osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with malunion |
| M80.059S | Age-related osteoporosis with current pathological fracture, unspecified femur, sequela |
| M80.06 | Age-related osteoporosis with current pathological fracture, lower leg |
| M80.061 | Age-related osteoporosis with current pathological fracture, right lower leg |
| M80.061A | Age-related osteoporosis with current pathological fracture, right lower leg, initial encounter for fracture |
| M80.061D | Age-related osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with routine healing |
| M80.061G | Age-related osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with delayed healing |
| M80.061K | Age-related osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with nonunion |
| M80.061P | Age-related osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with malunion |
| M80.061S | Age-related osteoporosis with current pathological fracture, right lower leg, sequela |
| M80.062 | Age-related osteoporosis with current pathological fracture, left lower leg |
| M80.062A | Age-related osteoporosis with current pathological fracture, left lower leg, initial encounter for fracture |
| M80.062D | Age-related osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with routine healing |
| M80.062G | Age-related osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with delayed healing |
| M80.062K | Age-related osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with nonunion |
| M80.062P | Age-related osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with malunion |
| M80.062S | Age-related osteoporosis with current pathological fracture, left lower leg, sequela |
| M80.069 | Age-related osteoporosis with current pathological fracture, unspecified lower leg |
| M80.069A | Age-related osteoporosis with current pathological fracture, unspecified lower leg, initial encounter for fracture |
| M80.069D | Age-related osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with routine healing |
| M80.069G | Age-related osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with delayed healing |
| M80.069K | Age-related osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with nonunion |
| M80.069P | Age-related osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with malunion |
| M80.069S | Age-related osteoporosis with current pathological fracture, unspecified lower leg, sequela |
| M80.07 | Age-related osteoporosis with current pathological fracture, ankle and foot |
| M80.071 | Age-related osteoporosis with current pathological fracture, right ankle and foot |
| M80.071A | Age-related osteoporosis with current pathological fracture, right ankle and foot, initial encounter for fracture |
| M80.071D | Age-related osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with routine healing |
| M80.071G | Age-related osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with delayed healing |
| M80.071K | Age-related osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with nonunion |
| M80.071P | Age-related osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with malunion |
| M80.071S | Age-related osteoporosis with current pathological fracture, right ankle and foot, sequela |
| M80.072 | Age-related osteoporosis with current pathological fracture, left ankle and foot |
| M80.072A | Age-related osteoporosis with current pathological fracture, left ankle and foot, initial encounter for fracture |
| M80.072D | Age-related osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with routine healing |
| M80.072G | Age-related osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with delayed healing |
| M80.072K | Age-related osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with nonunion |
| M80.072P | Age-related osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with malunion |
| M80.072S | Age-related osteoporosis with current pathological fracture, left ankle and foot, sequela |
| M80.079 | Age-related osteoporosis with current pathological fracture, unspecified ankle and foot |
| M80.079A | Age-related osteoporosis with current pathological fracture, unspecified ankle and foot, initial encounter for fracture |
| M80.079D | Age-related osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with routine healing |
| M80.079G | Age-related osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with delayed healing |
| M80.079K | Age-related osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with nonunion |
| M80.079P | Age-related osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with malunion |
| M80.079S | Age-related osteoporosis with current pathological fracture, unspecified ankle and foot, sequela |
| M80.08 | Age-related osteoporosis with current pathological fracture, vertebra(e) |
| M80.08xA | Age-related osteoporosis with current pathological fracture, vertebra(e), initial encounter for fracture |
| M80.08xD | Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with routine healing |
| M80.08xG | Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with delayed healing |
| M80.08xK | Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with nonunion |
| M80.08xP | Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with malunion |
| M80.08xS | Age-related osteoporosis with current pathological fracture, vertebra(e), sequela |
| M80.0A | Age-related osteoporosis with current pathological fracture, other site |
| M80.0AxA | Age-related osteoporosis with current pathological fracture, other site, initial encounter for fracture |
| M80.0AxD | Age-related osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with routine healing |
| M80.0AxG | Age-related osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with delayed healing |
| M80.0AxK | Age-related osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with nonunion |
| M80.0AxP | Age-related osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with malunion |
| M80.0AxS | Age-related osteoporosis with current pathological fracture, other site, sequela |
| M80.0B | Age-related osteoporosis with current pathological fracture, pelvis |
| M80.0B1 | Age-related osteoporosis with current pathological fracture, right pelvis |
| M80.0B1A | Age-related osteoporosis with current pathological fracture, right pelvis, initial encounter for fracture |
| M80.0B1D | Age-related osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with routine healing |
| M80.0B1G | Age-related osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with delayed healing |
| M80.0B1K | Age-related osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with nonunion |
| M80.0B1P | Age-related osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with malunion |
| M80.0B1S | Age-related osteoporosis with current pathological fracture, right pelvis, sequela |
| M80.0B2 | Age-related osteoporosis with current pathological fracture, left pelvis |
| M80.0B2A | Age-related osteoporosis with current pathological fracture, left pelvis, initial encounter for fracture |
| M80.0B2D | Age-related osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with routine healing |
| M80.0B2G | Age-related osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with delayed healing |
| M80.0B2K | Age-related osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with nonunion |
| M80.0B2P | Age-related osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with malunion |
| M80.0B2S | Age-related osteoporosis with current pathological fracture, left pelvis, sequela |
| M80.0B9 | Age-related osteoporosis with current pathological fracture, unspecified pelvis |
| M80.0B9A | Age-related osteoporosis with current pathological fracture, unspecified pelvis, initial encounter for fracture |
| M80.0B9D | Age-related osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with routine healing |
| M80.0B9G | Age-related osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with delayed healing |
| M80.0B9K | Age-related osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with nonunion |
| M80.0B9P | Age-related osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with malunion |
| M80.0B9S | Age-related osteoporosis with current pathological fracture, unspecified pelvis, sequela |
| M80.8 | Other osteoporosis with current pathological fracture |
| M80.80 | Other osteoporosis with current pathological fracture, unspecified site |
| M80.80xA | Other osteoporosis with current pathological fracture, unspecified site, initial encounter for fracture |
| M80.80xD | Other osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with routine healing |
| M80.80xG | Other osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with delayed healing |
| M80.80xK | Other osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with nonunion |
| M80.80xP | Other osteoporosis with current pathological fracture, unspecified site, subsequent encounter for fracture with malunion |
| M80.80xS | Other osteoporosis with current pathological fracture, unspecified site, sequela |
| M80.81 | Other osteoporosis with pathological fracture, shoulder |
| M80.811 | Other osteoporosis with current pathological fracture, right shoulder |
| M80.811A | Other osteoporosis with current pathological fracture, right shoulder, initial encounter for fracture |
| M80.811D | Other osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with routine healing |
| M80.811G | Other osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with delayed healing |
| M80.811K | Other osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with nonunion |
| M80.811P | Other osteoporosis with current pathological fracture, right shoulder, subsequent encounter for fracture with malunion |
| M80.811S | Other osteoporosis with current pathological fracture, right shoulder, sequela |
| M80.812 | Other osteoporosis with current pathological fracture, left shoulder |
| M80.812A | Other osteoporosis with current pathological fracture, left shoulder, initial encounter for fracture |
| M80.812D | Other osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with routine healing |
| M80.812G | Other osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with delayed healing |
| M80.812K | Other osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with nonunion |
| M80.812P | Other osteoporosis with current pathological fracture, left shoulder, subsequent encounter for fracture with malunion |
| M80.812S | Other osteoporosis with current pathological fracture, left shoulder, sequela |
| M80.819 | Other osteoporosis with current pathological fracture, unspecified shoulder |
| M80.819A | Other osteoporosis with current pathological fracture, unspecified shoulder, initial encounter for fracture |
| M80.819D | Other osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with routine healing |
| M80.819G | Other osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with delayed healing |
| M80.819K | Other osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with nonunion |
| M80.819P | Other osteoporosis with current pathological fracture, unspecified shoulder, subsequent encounter for fracture with malunion |
| M80.819S | Other osteoporosis with current pathological fracture, unspecified shoulder, sequela |
| M80.82 | Other osteoporosis with current pathological fracture, humerus |
| M80.821 | Other osteoporosis with current pathological fracture, right humerus |
| M80.821A | Other osteoporosis with current pathological fracture, right humerus, initial encounter for fracture |
| M80.821D | Other osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with routine healing |
| M80.821G | Other osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with delayed healing |
| M80.821K | Other osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with nonunion |
| M80.821P | Other osteoporosis with current pathological fracture, right humerus, subsequent encounter for fracture with malunion |
| M80.821S | Other osteoporosis with current pathological fracture, right humerus, sequela |
| M80.822 | Other osteoporosis with current pathological fracture, left humerus |
| M80.822A | Other osteoporosis with current pathological fracture, left humerus, initial encounter for fracture |
| M80.822D | Other osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with routine healing |
| M80.822G | Other osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with delayed healing |
| M80.822K | Other osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with nonunion |
| M80.822P | Other osteoporosis with current pathological fracture, left humerus, subsequent encounter for fracture with malunion |
| M80.822S | Other osteoporosis with current pathological fracture, left humerus, sequela |
| M80.829 | Other osteoporosis with current pathological fracture, unspecified humerus |
| M80.829A | Other osteoporosis with current pathological fracture, unspecified humerus, initial encounter for fracture |
| M80.829D | Other osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with routine healing |
| M80.829G | Other osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with delayed healing |
| M80.829K | Other osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with nonunion |
| M80.829P | Other osteoporosis with current pathological fracture, unspecified humerus, subsequent encounter for fracture with malunion |
| M80.829S | Other osteoporosis with current pathological fracture, unspecified humerus, sequela |
| M80.83 | Other osteoporosis with current pathological fracture, forearm |
| M80.831 | Other osteoporosis with current pathological fracture, right forearm |
| M80.831A | Other osteoporosis with current pathological fracture, right forearm, initial encounter for fracture |
| M80.831D | Other osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with routine healing |
| M80.831G | Other osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with delayed healing |
| M80.831K | Other osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with nonunion |
| M80.831P | Other osteoporosis with current pathological fracture, right forearm, subsequent encounter for fracture with malunion |
| M80.831S | Other osteoporosis with current pathological fracture, right forearm, sequela |
| M80.832 | Other osteoporosis with current pathological fracture, left forearm |
| M80.832A | Other osteoporosis with current pathological fracture, left forearm, initial encounter for fracture |
| M80.832D | Other osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with routine healing |
| M80.832G | Other osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with delayed healing |
| M80.832K | Other osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with nonunion |
| M80.832P | Other osteoporosis with current pathological fracture, left forearm, subsequent encounter for fracture with malunion |
| M80.832S | Other osteoporosis with current pathological fracture, left forearm, sequela |
| M80.839 | Other osteoporosis with current pathological fracture, unspecified forearm |
| M80.839A | Other osteoporosis with current pathological fracture, unspecified forearm, initial encounter for fracture |
| M80.839D | Other osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with routine healing |
| M80.839G | Other osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with delayed healing |
| M80.839K | Other osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with nonunion |
| M80.839P | Other osteoporosis with current pathological fracture, unspecified forearm, subsequent encounter for fracture with malunion |
| M80.839S | Other osteoporosis with current pathological fracture, unspecified forearm, sequela |
| M80.84 | Other osteoporosis with current pathological fracture, hand |
| M80.841 | Other osteoporosis with current pathological fracture, right hand |
| M80.841A | Other osteoporosis with current pathological fracture, right hand, initial encounter for fracture |
| M80.841D | Other osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with routine healing |
| M80.841G | Other osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with delayed healing |
| M80.841K | Other osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with nonunion |
| M80.841P | Other osteoporosis with current pathological fracture, right hand, subsequent encounter for fracture with malunion |
| M80.841S | Other osteoporosis with current pathological fracture, right hand, sequela |
| M80.842 | Other osteoporosis with current pathological fracture, left hand |
| M80.842A | Other osteoporosis with current pathological fracture, left hand, initial encounter for fracture |
| M80.842D | Other osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with routine healing |
| M80.842G | Other osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with delayed healing |
| M80.842K | Other osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with nonunion |
| M80.842P | Other osteoporosis with current pathological fracture, left hand, subsequent encounter for fracture with malunion |
| M80.842S | Other osteoporosis with current pathological fracture, left hand, sequela |
| M80.849 | Other osteoporosis with current pathological fracture, unspecified hand |
| M80.849A | Other osteoporosis with current pathological fracture, unspecified hand, initial encounter for fracture |
| M80.849D | Other osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with routine healing |
| M80.849G | Other osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with delayed healing |
| M80.849K | Other osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with nonunion |
| M80.849P | Other osteoporosis with current pathological fracture, unspecified hand, subsequent encounter for fracture with malunion |
| M80.849S | Other osteoporosis with current pathological fracture, unspecified hand, sequela |
| M80.85 | Other osteoporosis with current pathological fracture, femur |
| M80.851 | Other osteoporosis with current pathological fracture, right femur |
| M80.851A | Other osteoporosis with current pathological fracture, right femur, initial encounter for fracture |
| M80.851D | Other osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with routine healing |
| M80.851G | Other osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with delayed healing |
| M80.851K | Other osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with nonunion |
| M80.851P | Other osteoporosis with current pathological fracture, right femur, subsequent encounter for fracture with malunion |
| M80.851S | Other osteoporosis with current pathological fracture, right femur, sequela |
| M80.852 | Other osteoporosis with current pathological fracture, left femur |
| M80.852A | Other osteoporosis with current pathological fracture, left femur, initial encounter for fracture |
| M80.852D | Other osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with routine healing |
| M80.852G | Other osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with delayed healing |
| M80.852K | Other osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with nonunion |
| M80.852P | Other osteoporosis with current pathological fracture, left femur, subsequent encounter for fracture with malunion |
| M80.852S | Other osteoporosis with current pathological fracture, left femur, sequela |
| M80.859 | Other osteoporosis with current pathological fracture, unspecified femur |
| M80.859A | Other osteoporosis with current pathological fracture, unspecified femur, initial encounter for fracture |
| M80.859D | Other osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with routine healing |
| M80.859G | Other osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with delayed healing |
| M80.859K | Other osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with nonunion |
| M80.859P | Other osteoporosis with current pathological fracture, unspecified femur, subsequent encounter for fracture with malunion |
| M80.859S | Other osteoporosis with current pathological fracture, unspecified femur, sequela |
| M80.86 | Other osteoporosis with current pathological fracture, lower leg |
| M80.861 | Other osteoporosis with current pathological fracture, right lower leg |
| M80.861A | Other osteoporosis with current pathological fracture, right lower leg, initial encounter for fracture |
| M80.861D | Other osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with routine healing |
| M80.861G | Other osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with delayed healing |
| M80.861K | Other osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with nonunion |
| M80.861P | Other osteoporosis with current pathological fracture, right lower leg, subsequent encounter for fracture with malunion |
| M80.861S | Other osteoporosis with current pathological fracture, right lower leg, sequela |
| M80.862 | Other osteoporosis with current pathological fracture, left lower leg |
| M80.862A | Other osteoporosis with current pathological fracture, left lower leg, initial encounter for fracture |
| M80.862D | Other osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with routine healing |
| M80.862G | Other osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with delayed healing |
| M80.862K | Other osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with nonunion |
| M80.862P | Other osteoporosis with current pathological fracture, left lower leg, subsequent encounter for fracture with malunion |
| M80.862S | Other osteoporosis with current pathological fracture, left lower leg, sequela |
| M80.869 | Other osteoporosis with current pathological fracture, unspecified lower leg |
| M80.869A | Other osteoporosis with current pathological fracture, unspecified lower leg, initial encounter for fracture |
| M80.869D | Other osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with routine healing |
| M80.869G | Other osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with delayed healing |
| M80.869K | Other osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with nonunion |
| M80.869P | Other osteoporosis with current pathological fracture, unspecified lower leg, subsequent encounter for fracture with malunion |
| M80.869S | Other osteoporosis with current pathological fracture, unspecified lower leg, sequela |
| M80.87 | Other osteoporosis with current pathological fracture, ankle and foot |
| M80.871 | Other osteoporosis with current pathological fracture, right ankle and foot |
| M80.871A | Other osteoporosis with current pathological fracture, right ankle and foot, initial encounter for fracture |
| M80.871D | Other osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with routine healing |
| M80.871G | Other osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with delayed healing |
| M80.871K | Other osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with nonunion |
| M80.871P | Other osteoporosis with current pathological fracture, right ankle and foot, subsequent encounter for fracture with malunion |
| M80.871S | Other osteoporosis with current pathological fracture, right ankle and foot, sequela |
| M80.872 | Other osteoporosis with current pathological fracture, left ankle and foot |
| M80.872A | Other osteoporosis with current pathological fracture, left ankle and foot, initial encounter for fracture |
| M80.872D | Other osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with routine healing |
| M80.872G | Other osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with delayed healing |
| M80.872K | Other osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with nonunion |
| M80.872P | Other osteoporosis with current pathological fracture, left ankle and foot, subsequent encounter for fracture with malunion |
| M80.872S | Other osteoporosis with current pathological fracture, left ankle and foot, sequela |
| M80.879 | Other osteoporosis with current pathological fracture, unspecified ankle and foot |
| M80.879A | Other osteoporosis with current pathological fracture, unspecified ankle and foot, initial encounter for fracture |
| M80.879D | Other osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with routine healing |
| M80.879G | Other osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with delayed healing |
| M80.879K | Other osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with nonunion |
| M80.879P | Other osteoporosis with current pathological fracture, unspecified ankle and foot, subsequent encounter for fracture with malunion |
| M80.879S | Other osteoporosis with current pathological fracture, unspecified ankle and foot, sequela |
| M80.88 | Other osteoporosis with current pathological fracture, vertebra(e) |
| M80.88xA | Other osteoporosis with current pathological fracture, vertebra(e), initial encounter for fracture |
| M80.88xD | Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with routine healing |
| M80.88xG | Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with delayed healing |
| M80.88xK | Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with nonunion |
| M80.88xP | Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with malunion |
| M80.88xS | Other osteoporosis with current pathological fracture, vertebra(e), sequela |
| M80.8A | Other osteoporosis with current pathological fracture, other site |
| M80.8AxA | Other osteoporosis with current pathological fracture, other site, initial encounter for fracture |
| M80.8AxD | Other osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with routine healing |
| M80.8AxG | Other osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with delayed healing |
| M80.8AxK | Other osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with nonunion |
| M80.8AxP | Other osteoporosis with current pathological fracture, other site, subsequent encounter for fracture with malunion |
| M80.8AxS | Other osteoporosis with current pathological fracture, other site, sequela |
| M80.8B | Other osteoporosis with current pathological fracture, pelvis |
| M80.8B1 | Other osteoporosis with current pathological fracture, right pelvis |
| M80.8B1A | Other osteoporosis with current pathological fracture, right pelvis, initial encounter for fracture |
| M80.8B1D | Other osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with routine healing |
| M80.8B1G | Other osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with delayed healing |
| M80.8B1K | Other osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with nonunion |
| M80.8B1P | Other osteoporosis with current pathological fracture, right pelvis, subsequent encounter for fracture with malunion |
| M80.8B1S | Other osteoporosis with current pathological fracture, right pelvis, sequela |
| M80.8B2 | Other osteoporosis with current pathological fracture, left pelvis |
| M80.8B2A | Other osteoporosis with current pathological fracture, left pelvis, initial encounter for fracture |
| M80.8B2D | Other osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with routine healing |
| M80.8B2G | Other osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with delayed healing |
| M80.8B2K | Other osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with nonunion |
| M80.8B2P | Other osteoporosis with current pathological fracture, left pelvis, subsequent encounter for fracture with malunion |
| M80.8B2S | Other osteoporosis with current pathological fracture, left pelvis, sequela |
| M80.8B9 | Other osteoporosis with current pathological fracture, unspecified pelvis |
| M80.8B9A | Other osteoporosis with current pathological fracture, unspecified pelvis, initial encounter for fracture |
| M80.8B9D | Other osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with routine healing |
| M80.8B9G | Other osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with delayed healing |
| M80.8B9K | Other osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with nonunion |
| M80.8B9P | Other osteoporosis with current pathological fracture, unspecified pelvis, subsequent encounter for fracture with malunion |
| M80.8B9S | Other osteoporosis with current pathological fracture, unspecified pelvis, sequela |
| M81 | Osteoporosis without current pathological fracture |
| M81.0 | Age-related osteoporosis without current pathological fracture |
| M81.8 | Other osteoporosis without current pathological fracture |
| Z87.310 | Personal history of (healed) osteoporosis fracture |
| Post-menopausal osteoporosis prevention | |
| Z78.0 | Asymptomatic menopausal state |
| Vitamin D deficiency | |
| E55 | Vitamin D deficiency |
| E55.0 | Rickets, active |
| E55.9 | Vitamin D deficiency, unspecified |
Formulary Reference Tool