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Drug overview for SODIUM BICARBONATE (sodium bicarbonate):
Generic name: SODIUM BICARBONATE (SOE-dee-um bye-KAR-bo-nate)
Drug class: Antacids
Therapeutic class: Gastrointestinal Therapy Agents
Antacids are inorganic salts that dissolve in acid gastric secretions Sodium bicarbonate is an alkalinizing agent. releasing anions that partially neutralize gastric hydrochloric acid.
Antacids are used as an adjunct to other drugs for the relief of peptic ulcer pain and to promote the healing of peptic ulcers. Antacids also are used for the relief of esophageal reflux, acid indigestion, heartburn, dyspepsia, and sour stomach; for the prevention of stress ulceration and GI bleeding; to reduce the risk associated with gastric aspiration; and for the management of hyperphosphatemia.
Generic name: SODIUM BICARBONATE (SOE-dee-um bye-KAR-bo-nate)
Drug class: Antacids
Therapeutic class: Gastrointestinal Therapy Agents
Antacids are inorganic salts that dissolve in acid gastric secretions Sodium bicarbonate is an alkalinizing agent. releasing anions that partially neutralize gastric hydrochloric acid.
Antacids are used as an adjunct to other drugs for the relief of peptic ulcer pain and to promote the healing of peptic ulcers. Antacids also are used for the relief of esophageal reflux, acid indigestion, heartburn, dyspepsia, and sour stomach; for the prevention of stress ulceration and GI bleeding; to reduce the risk associated with gastric aspiration; and for the management of hyperphosphatemia.
DRUG IMAGES
SODIUM BICARB 325 MG TABLET
SODIUM BICARB 650 MG TABLET
The following indications for SODIUM BICARBONATE (sodium bicarbonate) have been approved by the FDA:
Indications:
Dyspepsia
Professional Synonyms:
Functional dyspepsia
Indications:
Dyspepsia
Professional Synonyms:
Functional dyspepsia
The following dosing information is available for SODIUM BICARBONATE (sodium bicarbonate):
Antacids are administered orally. The dose of antacids should be expressed in terms of mEq of acid neutralizing capacity. Dose and frequency of administration depend on the acid secretory rate of the stomach, gastric emptying time, and the disorder being treated.
The duration of action of antacids is determined principally by gastric emptying time. In fasting subjects, antacids have a duration of action of 20-60 minutes. However, if the drugs are administered 1 hour after meals, acid neutralizing effects may persist up to 3 hours.
Sodium bicarbonate generally has a shorter duration of action than other antacids. Antacids should be used for longer than 2-week periods only under the management of a physician and as part of a carefully planned therapeutic regimen.
There is considerable variation in in vivo acid neutralizing capacity of equal volumes of different antacids and antacid products. Since suspensions are more rapidly and effectively solubilized than powders or tablets, antacid suspensions have a greater ability to react with and neutralize gastric acid. Antacid suspensions have a smaller particle size than do tablets and drying of antacid suspensions to prepare powders and tablets causes substantial loss of ability to neutralize acid.
In general, an antacid suspension is preferable to a tablet or powder; tablets should be reserved for chronic use in patients who refuse suspensions because they are inconvenient or unpalatable. Tablets should be thoroughly chewed before swallowing.
The US Food and Drug Administration (FDA) requires that antacids have a minimum in vitro acid neutralizing capacity of 5 mEq per dose and that antacid labeling contain the in vitro acid neutralizing capacity; however, this FDA in vitro test does not correlate with in vivo acid neutralizing capacity.
For peptic ulcer disease, dosages of antacids are empirical and various antacid dosages have been used. In patients with uncomplicated duodenal ulcers or gastric ulcers, an antacid is administered 1 and 3 hours postprandially and at bedtime. In patients with duodenal ulcers, antacids are usually given for 4-6 weeks, and in patients with gastric ulcers, antacids are administered until healing is complete.
If symptoms of duodenal ulcer recur, some clinicians recommend that antacids be administered 1 and 3 hours postprandially and at bedtime for 1 week and, if pain is relieved, less frequently for an additional 1-2 weeks; these patients should consult their physicians if pain worsens or is not relieved after the first week of therapy. Additional doses of antacids may be administered to relieve ulcer pain which occurs between regularly scheduled doses.
For the acute management of moderate or severe esophageal reflux, an antacid suspension is administered every hour; if symptoms persist, antacids may be given every 30 minutes. For long-term therapy of esophageal reflux, antacids are administered 1 and 3 hours postprandially and at bedtime and whenever symptoms recur.
In the management of GI bleeding and stress ulceration, antacids are usually administered every hour and, for GI bleeding, the antacid dosage should be titrated to maintain the nasogastric aspirate above pH 3.5. For severe symptoms, antacid suspensions may be diluted with water or milk and given by continuous intragastric infusion.
To reduce the risk of anesthesia-induced gastric acid aspiration, an antacid suspension has been given 30 minutes before anesthesia.
In conjunction with dietary phosphate restriction in the management of hyperphosphatemia, 30-40 mL of aluminum hydroxide or aluminum carbonate suspension is administered 3 or 4 times daily.
Dosage of sodium bicarbonate injection is determined by severity of the acidosis, appropriate laboratory determinations, and the patient's age, weight, and clinical condition. Frequent laboratory determinations and clinical evaluation of the patient are essential during therapy with sodium bicarbonate, especially during prolonged therapy, to monitor changes in fluid and electrolyte and acid-base balance.
Generally, full correction of bicarbonate deficit should not be attempted during the first 24 hours of sodium bicarbonate therapy, since this may result in precipitation of metabolic alkalosis because of delayed physiologic compensatory mechanisms. When total carbon dioxide content is returned to normal or beyond within the first day of therapy, substantially alkaline values for blood pH and subsequent adverse effects are likely to occur. When initial, rapid administration of the drug is considered necessary, it is generally recommended that no more than 33-50% of the calculated bicarbonate requirements be administered initially.
Several methods for estimating bicarbonate requirements in patients with metabolic acidosis have been suggested; specialized references on fluid and electrolyte and acid-base balance should be consulted for specific recommendations.
Sodium bicarbonate is not recommended for routine use in advanced cardiovascular life support (ACLS) during cardiac arrest (see Uses: Advanced Cardiovascular Life Support); however, if the drug is used in certain resuscitation situations (e.g., preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdosage), an IV dose of 1 mEq/kg is usually given initially in adults. Whenever possible, dosage of sodium bicarbonate should be guided by the bicarbonate concentration or by the calculated base deficit obtained from blood gas analysis or laboratory measurement. Complete correction of the base deficit is not recommended to minimize the risk of alkalosis.
For the management of cardiac arrest due to hyperkalemia in adults, 50 mEq of sodium bicarbonate has been administered IV over 5 minutes as adjunctive therapy to other standard ACLS measures.
If sodium bicarbonate is used for pediatric resuscitation, the guidelines for pediatric advanced life support (PALS) recommend a pediatric dose of 1 mEq/kg, administered slowly by IV or IO+ injection. If blood gas tensions and pH measurements are available, subsequent doses should be determined by the following equation:
In less urgent forms of metabolic acidosis, a 2-5 mEq/kg dose of sodium bicarbonate may be administered to older children or adults as a 4- to 8-hour IV infusion. Subsequent doses should be determined by the response of the patient and appropriate laboratory determinations. Sodium bicarbonate therapy should be planned in a stepwise manner, since the degree of response following a given dose is not always predictable.
Generally, the dose and frequency of administration should be reduced after severe symptoms have improved.
For the treatment of ventricular arrhythmias associated with cocaine toxicity in pediatric patients, 1-2 mEq/kg of IV sodium bicarbonate has been administered.
Although the specific role of sodium bicarbonate therapy in the treatment of diabetic ketoacidosis has not been established (see Uses: Diabetic Ketoacidosis), when IV sodium bicarbonate is administered, the acidosis should only partially be corrected, generally to an arterial pH of about 7.2, in order to avoid rebound alkalosis.
For the treatment of acidosis associated with chronic renal failure, oral sodium bicarbonate therapy is generally initiated when plasma bicarbonate concentration is less than 15 mEq/L. Therapy is usually initiated in adults with an oral sodium bicarbonate dosage of 20-36 mEq daily, given in divided doses. Dosage is then titrated to provide a plasma bicarbonate concentration of about 18-20 mEq/L.
Because of the sodium content of sodium bicarbonate, the fluid and electrolyte balance of the patient must be carefully monitored during therapy with the drug. To relieve symptoms and prevent or stabilize renal failure and osteomalacia in patients with renal tubular acidosis, higher dosages of sodium bicarbonate are necessary. In adults with distal (type 1) renal tubular acidosis, an initial oral dosage of 0.5-2
mEq/kg daily, given in 4 or 5 divided doses, has been suggested. Dosage is titrated until hypercalciuria and acidosis are controlled, and according to the response and tolerance of the patient. Alternatively, an adult dosage of 48-72 mEq (about 4-6 g) daily has been suggested.
Higher dosages are generally required in patients with proximal (type 2) renal tubular acidosis; oral dosages of 4-10 mEq/kg daily, given in divided doses, have been suggested.
The usual oral dosage of sodium bicarbonate for alkalinization of urine in adults is 48 mEq (4 g) initially, followed by 12-24 mEq (1-2 g) every 4 hours. Dosages of 30-48 mEq (2.5-4 g) every 4 hours, up to 192 mEq (16 g) daily, may be required in some patients. Dosage should be individually titrated to maintain the desired urinary pH. For alkalinization of urine in children, an oral dosage of 1-10 mEq (84-840 mg) per kg daily, adjusted according to response, has been suggested.
The duration of action of antacids is determined principally by gastric emptying time. In fasting subjects, antacids have a duration of action of 20-60 minutes. However, if the drugs are administered 1 hour after meals, acid neutralizing effects may persist up to 3 hours.
Sodium bicarbonate generally has a shorter duration of action than other antacids. Antacids should be used for longer than 2-week periods only under the management of a physician and as part of a carefully planned therapeutic regimen.
There is considerable variation in in vivo acid neutralizing capacity of equal volumes of different antacids and antacid products. Since suspensions are more rapidly and effectively solubilized than powders or tablets, antacid suspensions have a greater ability to react with and neutralize gastric acid. Antacid suspensions have a smaller particle size than do tablets and drying of antacid suspensions to prepare powders and tablets causes substantial loss of ability to neutralize acid.
In general, an antacid suspension is preferable to a tablet or powder; tablets should be reserved for chronic use in patients who refuse suspensions because they are inconvenient or unpalatable. Tablets should be thoroughly chewed before swallowing.
The US Food and Drug Administration (FDA) requires that antacids have a minimum in vitro acid neutralizing capacity of 5 mEq per dose and that antacid labeling contain the in vitro acid neutralizing capacity; however, this FDA in vitro test does not correlate with in vivo acid neutralizing capacity.
For peptic ulcer disease, dosages of antacids are empirical and various antacid dosages have been used. In patients with uncomplicated duodenal ulcers or gastric ulcers, an antacid is administered 1 and 3 hours postprandially and at bedtime. In patients with duodenal ulcers, antacids are usually given for 4-6 weeks, and in patients with gastric ulcers, antacids are administered until healing is complete.
If symptoms of duodenal ulcer recur, some clinicians recommend that antacids be administered 1 and 3 hours postprandially and at bedtime for 1 week and, if pain is relieved, less frequently for an additional 1-2 weeks; these patients should consult their physicians if pain worsens or is not relieved after the first week of therapy. Additional doses of antacids may be administered to relieve ulcer pain which occurs between regularly scheduled doses.
For the acute management of moderate or severe esophageal reflux, an antacid suspension is administered every hour; if symptoms persist, antacids may be given every 30 minutes. For long-term therapy of esophageal reflux, antacids are administered 1 and 3 hours postprandially and at bedtime and whenever symptoms recur.
In the management of GI bleeding and stress ulceration, antacids are usually administered every hour and, for GI bleeding, the antacid dosage should be titrated to maintain the nasogastric aspirate above pH 3.5. For severe symptoms, antacid suspensions may be diluted with water or milk and given by continuous intragastric infusion.
To reduce the risk of anesthesia-induced gastric acid aspiration, an antacid suspension has been given 30 minutes before anesthesia.
In conjunction with dietary phosphate restriction in the management of hyperphosphatemia, 30-40 mL of aluminum hydroxide or aluminum carbonate suspension is administered 3 or 4 times daily.
Dosage of sodium bicarbonate injection is determined by severity of the acidosis, appropriate laboratory determinations, and the patient's age, weight, and clinical condition. Frequent laboratory determinations and clinical evaluation of the patient are essential during therapy with sodium bicarbonate, especially during prolonged therapy, to monitor changes in fluid and electrolyte and acid-base balance.
Generally, full correction of bicarbonate deficit should not be attempted during the first 24 hours of sodium bicarbonate therapy, since this may result in precipitation of metabolic alkalosis because of delayed physiologic compensatory mechanisms. When total carbon dioxide content is returned to normal or beyond within the first day of therapy, substantially alkaline values for blood pH and subsequent adverse effects are likely to occur. When initial, rapid administration of the drug is considered necessary, it is generally recommended that no more than 33-50% of the calculated bicarbonate requirements be administered initially.
Several methods for estimating bicarbonate requirements in patients with metabolic acidosis have been suggested; specialized references on fluid and electrolyte and acid-base balance should be consulted for specific recommendations.
Sodium bicarbonate is not recommended for routine use in advanced cardiovascular life support (ACLS) during cardiac arrest (see Uses: Advanced Cardiovascular Life Support); however, if the drug is used in certain resuscitation situations (e.g., preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdosage), an IV dose of 1 mEq/kg is usually given initially in adults. Whenever possible, dosage of sodium bicarbonate should be guided by the bicarbonate concentration or by the calculated base deficit obtained from blood gas analysis or laboratory measurement. Complete correction of the base deficit is not recommended to minimize the risk of alkalosis.
For the management of cardiac arrest due to hyperkalemia in adults, 50 mEq of sodium bicarbonate has been administered IV over 5 minutes as adjunctive therapy to other standard ACLS measures.
If sodium bicarbonate is used for pediatric resuscitation, the guidelines for pediatric advanced life support (PALS) recommend a pediatric dose of 1 mEq/kg, administered slowly by IV or IO+ injection. If blood gas tensions and pH measurements are available, subsequent doses should be determined by the following equation:
In less urgent forms of metabolic acidosis, a 2-5 mEq/kg dose of sodium bicarbonate may be administered to older children or adults as a 4- to 8-hour IV infusion. Subsequent doses should be determined by the response of the patient and appropriate laboratory determinations. Sodium bicarbonate therapy should be planned in a stepwise manner, since the degree of response following a given dose is not always predictable.
Generally, the dose and frequency of administration should be reduced after severe symptoms have improved.
For the treatment of ventricular arrhythmias associated with cocaine toxicity in pediatric patients, 1-2 mEq/kg of IV sodium bicarbonate has been administered.
Although the specific role of sodium bicarbonate therapy in the treatment of diabetic ketoacidosis has not been established (see Uses: Diabetic Ketoacidosis), when IV sodium bicarbonate is administered, the acidosis should only partially be corrected, generally to an arterial pH of about 7.2, in order to avoid rebound alkalosis.
For the treatment of acidosis associated with chronic renal failure, oral sodium bicarbonate therapy is generally initiated when plasma bicarbonate concentration is less than 15 mEq/L. Therapy is usually initiated in adults with an oral sodium bicarbonate dosage of 20-36 mEq daily, given in divided doses. Dosage is then titrated to provide a plasma bicarbonate concentration of about 18-20 mEq/L.
Because of the sodium content of sodium bicarbonate, the fluid and electrolyte balance of the patient must be carefully monitored during therapy with the drug. To relieve symptoms and prevent or stabilize renal failure and osteomalacia in patients with renal tubular acidosis, higher dosages of sodium bicarbonate are necessary. In adults with distal (type 1) renal tubular acidosis, an initial oral dosage of 0.5-2
mEq/kg daily, given in 4 or 5 divided doses, has been suggested. Dosage is titrated until hypercalciuria and acidosis are controlled, and according to the response and tolerance of the patient. Alternatively, an adult dosage of 48-72 mEq (about 4-6 g) daily has been suggested.
Higher dosages are generally required in patients with proximal (type 2) renal tubular acidosis; oral dosages of 4-10 mEq/kg daily, given in divided doses, have been suggested.
The usual oral dosage of sodium bicarbonate for alkalinization of urine in adults is 48 mEq (4 g) initially, followed by 12-24 mEq (1-2 g) every 4 hours. Dosages of 30-48 mEq (2.5-4 g) every 4 hours, up to 192 mEq (16 g) daily, may be required in some patients. Dosage should be individually titrated to maintain the desired urinary pH. For alkalinization of urine in children, an oral dosage of 1-10 mEq (84-840 mg) per kg daily, adjusted according to response, has been suggested.
Sodium bicarbonate is administered by IV infusion. Sodium bicarbonate may be administered by rapid IV injection when initial immediate administration of the drug is considered necessary (e.g., during cardiac arrest). The drug also may be administered orally in the treatment of mild to moderately severe acidosis, in conditions (e.g., chronic renal failure) requiring prolonged therapy with an alkalinizing agent, and in conditions in which IV administration of the drug is not necessary (e.g., alkalinization of the urine).
The drug has also been administered by subcutaneous injection if diluted to isotonicity (1.5% sodium bicarbonate solution). Extravasation of hypertonic sodium bicarbonate injections must be avoided. (See Cautions: Adverse Effects.)Sodium bicarbonate also has been administered by intraosseous (IO) injection+ in the setting of pediatric advanced life support (PALS); onset of action and systemic concentrations are comparable to those achieved with venous administration.
However, acid-base balance analysis may be inaccurate after administration of sodium bicarbonate via the IO cannula. In neonates and children younger than 2 years of age, hypertonic sodium bicarbonate injections generally should be administered by slow IV infusion of a 4.2% solution up to 8 mEq/kg daily. (See Cautions: Pediatric Precautions.)
The drug has also been administered by subcutaneous injection if diluted to isotonicity (1.5% sodium bicarbonate solution). Extravasation of hypertonic sodium bicarbonate injections must be avoided. (See Cautions: Adverse Effects.)Sodium bicarbonate also has been administered by intraosseous (IO) injection+ in the setting of pediatric advanced life support (PALS); onset of action and systemic concentrations are comparable to those achieved with venous administration.
However, acid-base balance analysis may be inaccurate after administration of sodium bicarbonate via the IO cannula. In neonates and children younger than 2 years of age, hypertonic sodium bicarbonate injections generally should be administered by slow IV infusion of a 4.2% solution up to 8 mEq/kg daily. (See Cautions: Pediatric Precautions.)
No dosing information available.
No generic dosing information available.
The following drug interaction information is available for SODIUM BICARBONATE (sodium bicarbonate):
There are 0 contraindications.
There are 3 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 |
|---|---|
| Delayed-Release Cysteamine Bitartrate/Bicarbonate SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Bicarbonate increases gastric pH. As gastric pH increases, the solubility of delayed-release cysteamine bitartrate may increase.(1) The exact mechanism behind the interaction between delayed-release cysteamine bitartrate and bicarbonate is unknown. CLINICAL EFFECTS: Simultaneous administration of delayed-release cysteamine bitartrate and bicarbonate may result in an early release of cysteamine bitartrate and decreased effectiveness of cysteamine bitartrate.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturer of delayed-release cysteamine bitartrate states that delayed-release cysteamine bitartrate should be administered at least 1 hour before or 1 hour after administration of bicarbonate.(3) DISCUSSION: Interactions between delayed-release cysteamine bitartrate and other acid reducing agents including H2-receptor antagonists and proton pump inhibitors were not noted in the clinical trials.(1,2) The interaction was only documented with co-administration of delayed-release cysteamine bitartrate and bicarbonate.(2,3) |
PROCYSBI |
| Selected Mesalamine/Antacids SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Certain mesalamine formulations (namely Apriso) contain granules with an enteric coating that dissolves at pH 6 and above. Antacids may raise the intragastric pH, resulting in premature release of the drug in the stomach.(1) CLINICAL EFFECTS: Simultaneous administration of certain mesalamine formulations (namely Apriso) with an antacid may result in premature release of mesalamine in the stomach and decreased effectiveness in the intestines and colon.(1-2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturer of Apriso states that coadministration with antacids should be avoided.(1) Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: Dissolution of the enteric coating of mesalamine is pH-dependent. Coadministration of certain mesalamine formulations (namely Apriso) with antacids should be avoided.(1) |
APRISO, MESALAMINE ER |
| Dextroamphetamine Transdermal/Urinary Alkalinizers SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Urinary alkalinizers decrease the renal elimination of dextroamphetamine.(1) CLINICAL EFFECTS: Concurrent use of dextroamphetamine and urinary alkalinizers may result in increased dextroamphetamine levels and side effects. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Coadministration of dextroamphetamine with urinary alkalinizing agents should be avoided.(1) DISCUSSION: Concurrent use of alkalinizing agents with dextroamphetamine decreases the renal elimination of dextroamphetamine. Co-administration of these should be avoided because of the potential of increased actions of dextroamphetamine.(1) |
XELSTRYM |
There are 19 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 |
|---|---|
| Sympathomimetics/Urinary Alkalinizers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Unionized sympathomimetic amines will be reabsorbed into systemic circulation from the distal tubules of the kidneys. CLINICAL EFFECTS: Enhanced sympathomimetic activity and increased risk of sympathomimetic toxicity. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Watch patient for enhanced sympathomimetic side effects when urinary alkalinizers are concomitantly used. A lower dose of certain sympathomimetics may be required. DISCUSSION: Signs and symptoms of sympathomimetic toxicity include euphoria, confusion, delirium, hallucinations and nervousness. |
AKOVAZ, BENZPHETAMINE HCL, EMERPHED, EPHEDRINE HCL, EPHEDRINE SULFATE, EPHEDRINE SULFATE-0.9% NACL, EPHEDRINE SULFATE-NACL, LISDEXAMFETAMINE DIMESYLATE, MIDODRINE HCL, REZIPRES, VYVANSE |
| Quinidine/Urinary Alkalinizers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Quinidine elimination is impaired by urinary alkalinization. CLINICAL EFFECTS: Potentiation of quinidine effects may be observed. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Monitoring quinidine levels and cardiac function may be indicated. The quinidine dose may need to be adjusted when a urinary alkalinizer is started or stopped. DISCUSSION: Additional documentation is necessary to confirm this potential interaction. |
NUEDEXTA, QUINIDINE GLUCONATE, QUINIDINE SULFATE |
| 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 |
| Amprenavir; Atazanavir/Antacids; Buffered Formulations SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Antacids increase gastric pH. As gastric pH increases, the solubility of atazanavir decreases.(1,2) The exact mechanism behind the interaction between amprenavir and antacids is unknown. CLINICAL EFFECTS: Simultaneous administration of amprenavir or atazanavir with antacids or buffered formulations may result in decreased levels and effectiveness of amprenavir(3) and atazanavir.(1,2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturer of amprenavir states that amprenavir should be administered 1 hour before or after antacids or buffered formulations such as didanosine.(3) The manufacturer of atazanavir states that atazanavir should be administered 2 hours before or 1 hour after antacids or buffered formulations.(1,2) Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: Simultaneous administration of atazanavir with didanosine buffered tablets decreased atazanavir area-under-curve (AUC), maximum concentration (Cmax) and minimum concentration (Cmin) by 87%, 89% and 84%, respectively. Administration of atazanavir 1 hour after didanosine buffered tablets had no significant effect on atazanavir pharmacokinetics.(1) Other buffered formulations and antacids are expected to substantially decrease atazanavir concentrations and therapeutic effectiveness as well.(1,2) |
ATAZANAVIR SULFATE, EVOTAZ, REYATAZ |
| Selected Kinase Inhibitors/Antacids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The solubility of bosutinib,(1) dasatinib,(2) erlotinib,(3) gefitinib,(4) neratinib,(5) nilotinib(6), pazopanib,(7) and pexidartinib(8) is pH dependent. Antacid-induced changes in gastric pH may decrease the absorption of these agents.(1-8) CLINICAL EFFECTS: Simultaneous administration of antacids may result in decreased levels and effectiveness of bosutinib,(1) dasatinib,(2) erlotinib,(3) gefitinib,(4) neratinib,(5) nilotinib(6), pazopanib,(7) and pexidartinib.(8) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Antacid use should be considered in place of H2 blockers or proton pump inhibitors in patients receiving bosutinib,(1) dasatinib,(2) erlotinib,(3) gefitinib,(4) neratinib,(5) nilotinib(6), pazopanib,(7) and pexidartinib;(8) however, separation of administration times is required. If antacids are used, separate the administration times by several hours(1-8) but at least 2 hours for bosutinib,(1) dasatinib,(2) nilotinib,(6) and pexidartinib(8), 6 hours for gefitinib,(4) and 3 hours for neratinib.(5) 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 24 healthy subjects, lansoprazole (60 mg) decreased bosutinib (400 mg single dose) area-under-curve (AUC) and maximum concentration (Cmax) by 26% and 46%, respectively.(1) In a study in 24 healthy subjects, simultaneous administration of dasatinib (50 mg) with aluminum hydroxide/magnesium hydroxide (30 ml) decreased dasatinib AUC and Cmax by 55% and 58%, respectively. In the same subjects, administration of the antacid 2 hours before dasatinib decreased dasatinib Cmax by 26%, but had no effect on dasatinib AUC.(2) In a study in 24 healthy subjects, administration of a single dose of dasatinib (50 mg) 10 hours after famotidine decreased dasatinib AUC and Cmax by 61% and 63%, respectively.(2) In a study, concurrent omeprazole decreased the AUC and Cmax of erlotinib by 46% and 61%, respectively.3) In a study, concurrent esomeprazole decreased the AUC of nilotinib by 34%.(6) In a study in 15 healthy subjects, lansoprazole (30 mg at steady state) decreased the Cmax and AUC of a single dose of neratinib (240 mg) by 71% and 65%, respectively.(5) There were no significant changes in nilotinib pharmacokinetics when famotidine was administered 10 hours before or 2 hours after nilotinib.(6) There were no significant changes in nilotinib pharmacokinetics when an antacid (aluminum hydroxide/magnesium hydroxide/simethicone) was administered 2 hours before or after nilotinib.(6) Coadministration of esomeprazole decreased pexidartinib Cmax and AUC by 55% and 50%.(8) |
BOSULIF, DANZITEN, DASATINIB, ERLOTINIB HCL, GEFITINIB, IRESSA, NERLYNX, NILOTINIB HCL, PAZOPANIB HCL, SPRYCEL, TARCEVA, TASIGNA, TURALIO, VOTRIENT |
| 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 |
| Rilpivirine/Antacids; H2 Antagonists SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Rilpivirine requires an acidic medium for absorption. Antacid or H2 antagonist induced decrease in gastric pH may result in a decrease in rilpivirine absorption.(1) CLINICAL EFFECTS: 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: In patients maintained on rilpivirine, administer antacids at least 2 hours before or 4 hours after rilpivirine.(1) In patients maintained on rilpivirine, administer H2 antagonists at least 12 hours before or 4 hours after rilpivirine.(1) Concurrent use of proton pump inhibitors with rilpivirine is contraindicated.(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 16 subjects, omeprazole (20 mg daily) decreased the maximum concentration (Cmax), area-under-curve (AUC), and minimum concentration (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 after a single dose of rilpivirine (150 mg) increased the rilpivirine Cmax and AUC by 21% and 13%, respectively.(1) |
COMPLERA, EDURANT, ODEFSEY |
| 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 |
| 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 |
| Memantine; Amantadine/Urinary Alkalinizers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Memantine and amantadine elimination is impaired by urinary alkalinization.(1,2) CLINICAL EFFECTS: Potentiation of memantine or amantadine effects may be observed. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Monitor patient for adverse reactions such as dizziness, headache, or confusion if a urinary alkalinizer is required. The memantine or amantadine dose may need to be adjusted when a urinary alkalinizer is started or stopped.(1,2) DISCUSSION: The clearance of memantine was reduced by about 80% under alkaline urine conditions at pH 8. Urine alkalinization may lead to an accumulation of memantine with a possible increase in adverse effects. Urine pH is also altered by diet and clinical state of the patient (e.g., renal tubular acidosis or severe infections of the urinary tract). Hence, memantine should be used with caution under these conditions.(1) A study in rats showed that concomitant administration of sodium bicarbonate with amantadine caused a decrease in amantadine renal clearance (1.16 vs. 0.76). Amantadine's area-under-the-curve (AUC) was increased approximately 78%.(3) A study in 12 healthy subjects showed that plasma concentrations of memantine are dependent on urine pH. Alkaline urine pH caused a 79% reduction in renal clearance.(4) |
AMANTADINE, AMANTADINE HCL, GOCOVRI, MEMANTINE HCL, MEMANTINE HCL ER, MEMANTINE HCL-DONEPEZIL HCL ER, NAMENDA, NAMENDA XR, NAMZARIC, OSMOLEX ER |
| 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 |
| 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 |
| 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 |
| Amphetamines/Antacids; Urinary Alkalinizers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Antacids and urinary alkalinizers increase the absorption of amphetamines. CLINICAL EFFECTS: Concurrent use of amphetamines and antacids or urinary alkalinizers may result in increased amphetamine levels and side effects. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US and Canadian manufacturers state that coadministration of alkalinizing agents with amphetamines should be avoided.(1-3) The Canadian manufacturer states that concurrent use of proton pump inhibitors and amphetamines should be avoided.(3) The US manufacturer states that patients receiving concurrent therapy should be monitored for changes in clinical effects.(1) Monitor patients receiving concurrent therapy for changes in amphetamine effectiveness and side effects. If concurrent use cannot be avoided, separate the administration times of amphetamines and antacids. Some vitamin preparations may contain sufficient quantities of calcium and/or magnesium salts with antacid properties to interact as well. DISCUSSION: Concurrent use of alkalinizing agents with amphetamines increase the absorption of amphetamines. Co-administration of these should be avoided because of the potential of increased actions of the amphetamines.(1,2) |
ADDERALL, ADDERALL XR, ADZENYS XR-ODT, AMPHETAMINE SULFATE, DESOXYN, DEXEDRINE, DEXTROAMPHETAMINE SULFATE, DEXTROAMPHETAMINE SULFATE ER, DEXTROAMPHETAMINE-AMPHET ER, DEXTROAMPHETAMINE-AMPHETAMINE, DYANAVEL XR, EVEKEO, METHAMPHETAMINE HCL, MYDAYIS, PROCENTRA, ZENZEDI |
| 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 |
| 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 SODIUM BICARBONATE (sodium bicarbonate):
Drug contraindication overview.
No enhanced Contraindications information available for this drug.
No enhanced Contraindications information available for this drug.
There are 0 contraindications.
There are 0 severe contraindications.
There are 5 moderate contraindications.
Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.
| Moderate List |
|---|
| Chronic heart failure |
| Chronic kidney disease stage 4 (severe) GFR 15-29 ml/min |
| Chronic kidney disease stage 5 (failure) GFr<15 ml/min |
| Edema |
| Kidney disease with likely reduction in glomerular filtration rate (GFr) |
The following adverse reaction information is available for SODIUM BICARBONATE (sodium bicarbonate):
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 2 severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
| None. | None. |
| Rare/Very Rare |
|---|
|
Alkalosis Hypercalcemia |
There are 3 less severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
| None. |
Abdominal distension Flatulence |
| Rare/Very Rare |
|---|
|
Body fluid retention |
The following precautions are available for SODIUM BICARBONATE (sodium bicarbonate):
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 |
Animal reproduction studies have not been performed with sodium bicarbonate. It is also not known whether sodium bicarbonate can cause fetal harm when administered to pregnant women. Sodium bicarbonate should be used during pregnancy only when clearly needed.
No enhanced Lactation information available for this drug.
No enhanced Geriatric Use information available for this drug.
The following prioritized warning is available for SODIUM BICARBONATE (sodium bicarbonate):
No warning message for this drug.
No warning message for this drug.
The following icd codes are available for SODIUM BICARBONATE (sodium bicarbonate)'s list of indications:
| Dyspepsia | |
| K30 | Functional dyspepsia |
Formulary Reference Tool