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Dexlansoprazole: Pediatric drug information

Dexlansoprazole: Pediatric drug information
(For additional information see "Dexlansoprazole: Drug information" and see "Dexlansoprazole: Patient drug information")

For abbreviations, symbols, and age group definitions used in Lexicomp (show table)
Brand Names: US
  • Dexilant
Brand Names: Canada
  • Dexilant
Therapeutic Category
  • Proton Pump Inhibitor;
  • Substituted Benzimidazole
Dosing: Pediatric
Erosive esophagitis

Erosive esophagitis:

Healing: Children ≥12 years and Adolescents: Oral: 60 mg once daily for up to 8 weeks.

Maintenance of healing: Children ≥12 years and Adolescents: Oral: 30 mg once daily.

Gastroesophageal reflux disease, symptomatic

Gastroesophageal reflux disease (GERD), symptomatic: Note: Guidelines recommend a 4- to 8-week treatment course; if improvement seen after 4 to 8 weeks, consider possible wean; if no response after 4 to 8 weeks, reevaluate diagnosis and consider referral to pediatric GI specialist (Ref).

Children ≥12 years and Adolescents: Oral: 30 mg once daily.

Discontinuation of therapy: Oral: Based on experience in adults, some experts recommend a step-down approach in order to avoid worsening or rebound symptoms. One recommendation is to decrease the dose by 50% over 2 to 4 weeks. If the patient is already on the lowest possible dose, alternate day therapy may be considered. If symptoms worsen during treatment or after discontinuation, patient should be reevaluated (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Pediatric

Altered kidney function: There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); however, the pharmacokinetics of dexlansoprazole are not expected to be altered in patients with kidney impairment.

Hemodialysis: Dexlansoprazole is not expected to be removed by hemodialysis.

Dosing: Hepatic Impairment: Pediatric

Children ≥12 years and Adolescents:

Mild impairment: No dosage adjustment necessary.

Moderate impairment:

Healing of erosive esophagitis: Oral: 30 mg once daily for up to 8 weeks.

Gastroesophageal reflux disease or erosive esophagitis maintenance: There are no dosage adjustments provided in the manufacturer's labeling.

Severe impairment: Use is not recommended.

Dosing: Adult

(For additional information see "Dexlansoprazole: Drug information")

Dosage guidance:

Dosing: Doses >30 mg do not provide additional benefit during maintenance phase.

Eosinophilic esophagitis

Eosinophilic esophagitis (off-label use): Oral: 30 mg once daily for an 8-week trial (Ref). Some experts increase to 60 mg once daily after 4 weeks if symptoms fail to improve (Ref).

Gastroesophageal reflux disease, erosive or nonerosive

Gastroesophageal reflux disease, erosive or nonerosive: Note: For patients with alarm symptoms (eg, dysphagia), referral to a specialist is recommended (Ref). Maximal acid suppression is generally observed after ~3 days of continuous therapy (Ref).

Initial therapy:

Mild and intermittent symptoms (<2 episodes/week) without erosive esophagitis or Barrett esophagus:

Note: Some experts reserve proton pump inhibitors (PPIs) as alternatives to H2-receptor antagonists (H2RAs) for patients who have residual acid reflux symptoms despite twice-daily H2RA (Ref).

Oral: 30 mg once daily for 4 to 8 weeks (Ref). Note: Some experts continue therapy until asymptomatic for 8 weeks (Ref).

Severe or frequent symptoms (≥2 episodes/week) without erosive esophagitis or Barrett esophagus: Oral: 30 mg once daily for 8 weeks (Ref). Note: Some experts continue therapy until patient has been asymptomatic for 8 weeks (Ref).

Erosive esophagitis or Barrett esophagus: Oral: 60 mg once daily for 8 weeks (Ref) then 30 mg once daily indefinitely (Ref), or 30 mg once daily indefinitely (preferred by some experts) (Ref).

Residual symptoms despite 30 mg once daily:

Note: Referral to a specialist is recommended. Options include doubling the PPI dose, switching to a different PPI, or adding an H2RA (Ref). For patients requiring concomitant H2RA therapy, some experts administer the H2RA at bedtime (Ref); however, others advocate concurrent administration to ensure adherence (Ref).

Recurrent symptoms after discontinuing acid suppression:

Recurrent symptoms after ≥3 months: Repeat an 8-week course at the previously effective dose (Ref).

Recurrent symptoms after <3 months: Long-term maintenance at the lowest effective dose; referral to a specialist is recommended (Ref).

Missed doses: If a dose is missed, administer as soon as possible; however, if the next scheduled dose is due, take the next dose on time and do not take the missed dose (do not take 2 doses at one time to make up for a missed dose).

Discontinuation of therapy: Oral: In patients who have received continuous therapy for >6 months, some experts gradually taper therapy until discontinuation to avoid worsening or rebound symptoms. There is no single agreed upon discontinuation strategy. Some experts decrease the dose by 50% every week. Once patients are on the lowest dose for 1 week, discontinue therapy (Ref). An alternative strategy is to decrease the dose by 50% over 2 to 4 weeks, then discontinue. If the patient is already on the lowest possible dose, alternate day therapy may be considered (Ref). In addition, as-needed therapy with an H2RA or an antacid can be used during the taper (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); however, the pharmacokinetics of dexlansoprazole are not expected to be altered in patients with renal impairment.

Hemodialysis: Dexlansoprazole is not expected to be removed by hemodialysis.

Dosing: Hepatic Impairment: Adult

Mild impairment (Child-Pugh class A): No dosage adjustment necessary.

Moderate impairment (Child-Pugh class B): 30 mg once daily is recommended.

Severe impairment (Child-Pugh class C): Use is not recommended.

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Incidence reported for adults unless otherwise specified.

1% to 10%:

Cardiovascular: Acute myocardial infarction (<2%), angina pectoris (<2%), bradycardia (<2%), cardiac arrhythmia (<2%), chest pain (<2%), deep vein thrombosis (<2%), edema (<2%; including oral, facial edema, and pharyngeal edema), hypertension (<2%), palpitations (<2%), tachycardia (<2%)

Dermatologic: Acne vulgaris (<2%), dermatitis (<2%), erythema of skin (<2%), pruritus (<2%), skin lesion (<2%), skin rash (<2%), sunburn (<2%), urticaria (<2%)

Endocrine & metabolic: Change in libido (<2%), goiter (<2%), heavy menstrual bleeding (<2%), hot flash (<2%), hypercalcemia (<2%), hypokalemia (<2%), increased serum glucose (<2%), increased serum potassium (<2%), increased serum total protein (<2%), menstrual disease (<2%), weight gain (<2%)

Gastrointestinal: Abdominal distress (<2%), abdominal pain (adolescents: ≥5%), abdominal tenderness (<2%), abnormal bowel sounds (<2%), abnormal stools (<2%), anorectal pain (<2%), Barrett esophagus (<2%), bezoar formation (<2%), biliary colic (<2%), change in appetite (<2%), cholelithiasis (<2%), colitis (microscopic; <2%), colonic polyp (<2%), constipation (<2%), delayed gastric emptying (<2%), diarrhea (adolescents and adults: ≥5%), duodenitis (<2%), dysgeusia (<2%), dyspepsia (<2%), dysphagia (<2%), enteritis (<2%), eructation (<2%), esophagitis (<2%), flatulence (1% to 3%), gastric polyp (<2%; including fundic gland), gastritis (<2%), gastroenteritis (<2%), gastroesophageal reflux disease (<2%), gastrointestinal disease (<2%), gastrointestinal hypermotility (<2%), gastrointestinal perforation (<2%), gastrointestinal ulcer (<2%), halitosis (<2%), hematemesis (<2%), hematochezia (<2%), hemorrhoids (<2%), hiccups (<2%), increased gastrin (<2%), irritable bowel syndrome (<2%), mucosal swelling (<2%), mucus stools (<2%), oral bullae (<2%), oral herpes simplex infection (<2%), oral paresthesia (<2%), painful defecation (<2%), proctitis (<2%), rectal hemorrhage (<2%), retching (<2%), sore throat (<2%), vomiting (1% to 2%), xerostomia (<2%)

Genitourinary: Dysmenorrhea (<2%), dyspareunia (<2%), dysuria (<2%), urinary urgency (<2%), vulvovaginal infection (<2%)

Hematologic & oncologic: Anemia (<2%), decreased platelet count (<2%), lymphadenopathy (<2%)

Hepatic: Decreased serum bilirubin (<2%), hepatomegaly (<2%), increased serum alanine aminotransferase (<2%), increased serum alkaline phosphatase (<2%), increased serum aspartate aminotransferase (<2%), increased serum bilirubin (<2%)

Hypersensitivity: Hypersensitivity reaction (<2%)

Infection: Candidiasis (<2%), influenza (<2%), viral infection (<2%)

Nervous system: Abnormal dreams (<2%), anxiety (<2%), asthenia (<2%), chills (<2%), depression (<2%), dizziness (<2%), falling (<2%), feeling abnormal (<2%), headache (adolescents: ≥5%; adults: <2%), insomnia (<2%), memory impairment (<2%), migraine (<2%), pain (<2%), paresthesia (<2%), procedural pain (<2%), psychomotor agitation (<2%), seizure (<2%), tremor (<2%), trigeminal neuralgia (<2%), vertigo (<2%)

Neuromuscular & skeletal: Arthralgia (<2%), arthritis (<2%), bone fracture (<2%), joint sprain (<2%), muscle cramps (<2%), musculoskeletal pain (<2%), myalgia (<2%)

Ophthalmic: Eye irritation (<2%), swelling of eye (<2%)

Otic: Otalgia (<2%), tinnitus (<2%)

Renal: Increased serum creatinine (<2%)

Respiratory: Asthma (<2%), bronchitis (<2%), cough (<2%), dyspnea (<2%), hyperventilation (<2%), nasopharyngitis (adolescents: ≥5%; adults: <2%), oropharyngeal pain (adolescents: ≥5%), pharyngitis (<2%), pulmonary aspiration (<2%), respiratory congestion (<2%), sinusitis (<2%), upper respiratory tract infection (2% to 3%)

Miscellaneous: Fever (<2%), inflammation (<2%), nodule (<2%)

Postmarketing:

Dermatologic: Acute generalized exanthematous pustulosis, erythema multiforme, exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis

Endocrine & metabolic: Hypocalcemia, hypomagnesemia, hyponatremia

Gastrointestinal: Clostridioides difficile-associated diarrhea, pancreatitis

Genitourinary: Erectile dysfunction

Hematologic & oncologic: Autoimmune hemolytic anemia, immune thrombocytopenia

Hepatic: Hepatitis, hepatotoxicity (idiosyncratic) (Chalasani 2014)

Hypersensitivity: Anaphylactic shock, drug reaction with eosinophilia and systemic symptoms, hypersensitivity angiitis

Nervous system: Cerebrovascular accident, transient ischemic attacks

Ophthalmic: Blurred vision

Otic: Deafness

Renal: Acute kidney injury, chronic renal failure (Lazarus 2016)

Respiratory: Constriction of the pharynx

Contraindications

Known hypersensitivity (eg, anaphylaxis, anaphylactic shock, angioedema, bronchospasm, acute tubulointerstitial nephritis, urticaria) to dexlansoprazole or any component of the formulation; concomitant use with products that contain rilpivirine.

Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Warnings/Precautions

Concerns related to adverse effects:

• Carcinoma: No occurrences of enterochromaffin-like (ECL) cell carcinoids, dysplasia, or neoplasia (such as those seen in studies of rodents exposed to lansoprazole) have been reported in humans.

Clostridioides difficile-associated diarrhea (CDAD): Use of proton pump inhibitors (PPIs) may increase risk of CDAD, especially in hospitalized patients; consider CDAD diagnosis in patients with persistent diarrhea that does not improve. Use the lowest dose and shortest duration of PPI therapy appropriate for the condition being treated.

• Cutaneous and systemic lupus erythematosus: Has been reported as new onset or exacerbation of existing autoimmune disease; most cases were cutaneous lupus erythematosus (CLE), most commonly, subacute CLE (occurring within weeks to years after continuous therapy). Systemic lupus erythematosus (SLE) is less common (typically occurs within days to years after initiating treatment) and occurred primarily in young adults up to elderly patients. Discontinue therapy if signs or symptoms of CLE or SLE occur and refer to specialist for evaluation; most patients improve 4 to 12 weeks after discontinuation of dexlansoprazole.

• Dermatologic reactions: Severe cutaneous adverse reactions, including acute generalized exanthematous pustulosis, drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, and toxic epidermal necrolysis, have been reported.

• Fractures: Increased incidence of osteoporosis-related bone fractures of the hip, spine, or wrist may occur with PPI therapy. Patients on high-dose (multiple daily doses) or long-term therapy (≥1 year) should be monitored. Use the lowest effective dose for the shortest duration of time, use vitamin D and calcium supplementation, and follow appropriate guidelines to reduce risk of fractures in patients at risk.

• Fundic gland polyps: Use of PPIs increases risk of fundic gland polyps, especially with long term use (>1 year). May occur without symptoms but nausea, vomiting, or abdominal pain may occur; GI bleeding and/or anemia may occur with ulcerated polyps. Diagnosis of polyps may also increase risk for small intestinal blockage. Use the lowest dose and shortest duration of PPI therapy appropriate for the condition being treated.

• Hypomagnesemia: Reported rarely, usually with prolonged PPI use of ≥3 months (most cases >1 year of therapy). May be symptomatic or asymptomatic; severe cases may cause tetany, seizures, and cardiac arrhythmias. Hypomagnesemia may lead to or exacerbate hypocalcemia in patients at risk (eg, hypoparathyroidism). Hypomagnesemia may also lead to hypokalemia. Hypomagnesemia and hypocalcemia may be corrected by magnesium/calcium supplementation, although discontinuation of dexlansoprazole may be necessary.

• Tubulointerstitial nephritis: Acute tubulointerstitial nephritis has been observed in patients taking PPIs; may occur at any time during therapy. Patients may present with symptomatic hypersensitivity reaction to nonspecific symptoms of impaired renal function (eg, anorexia, malaise, nausea); may be diagnosed with biopsy and in the absence of extra-renal manifestations (eg, fever, rash, arthralgia). Discontinue and evaluate patients if acute tubulointerstitial nephritis is suspected.

• Vitamin B12 deficiency: Prolonged treatment (≥2 years) may lead to vitamin B12 malabsorption and subsequent vitamin B12 deficiency. The magnitude of the deficiency is dose related and the association is stronger in females and those younger in age (<30 years); prevalence is decreased after discontinuation of therapy (Lam 2013).

Disease-related concerns:

• Gastric malignancy: Relief of symptoms does not preclude the presence of a gastric malignancy.

• Gastrointestinal infection (eg, Salmonella, Campylobacter): Use of PPIs may increase risk of these infections.

• Hepatic impairment: Patients with moderate hepatic impairment (Child-Pugh class B) may require dosage reductions; use is not recommended in patients with severe hepatic impairment (Child-Pugh class C).

Concurrent drug therapy issues:

• Clopidogrel: PPIs may diminish the therapeutic effect of clopidogrel, thought to be due to reduced formation of the active metabolite of clopidogrel. The manufacturer of clopidogrel recommends either avoidance of both omeprazole (even when scheduled 12 hours apart) and esomeprazole or use of a PPI with comparatively less effect on the active metabolite of clopidogrel (eg, pantoprazole). Although lansoprazole exhibits the most potent CYP2C19 inhibition in vitro (Li 2004; Ogilvie 2011), an in vivo study of extensive CYP2C19 metabolizers showed less reduction of the active metabolite of clopidogrel when administered with lansoprazole/dexlansoprazole compared to esomeprazole/omeprazole (Frelinger 2012). In contrast to these warnings, others have recommended the continued use of PPIs, regardless of the degree of inhibition, in patients with a history of GI bleeding or multiple risk factors for GI bleeding who are also receiving clopidogrel since no evidence has established clinically meaningful differences in outcome; however, a clinically significant interaction cannot be excluded in those who are poor metabolizers of clopidogrel (Abraham 2010; Levine 2011). The manufacturer of dexlansoprazole states that no dosage adjustment is necessary for clopidogrel when used concurrently with approved doses.

Other warnings/precautions:

• Laboratory test interference: Serum chromogranin A (CgA) levels increase secondary to drug-induced decreases in gastric acid; may cause false-positive results in diagnostic investigations for neuroendocrine tumors. Temporarily stop dexlansoprazole treatment at least 14 days before CgA test; if CgA level is high, repeat test to confirm. Use same commercial laboratory for testing to prevent variable results.

Warnings: Additional Pediatric Considerations

Dexlansoprazole is the R-enantiomer of lansoprazole. Neonatal and infant animal models (rat) have shown mitral valve heart thickening with lansoprazole treatment in 2 nonclinical, oral toxicity studies. Heart valve thickening occurred at doses resulting in 2.5 and 1.8 times the expected dexlansoprazole exposure in children 1 to 2 years of age; duration of treatment associated with valve thickening ranged from 5 days to 8 weeks. Valve thickening reversed or trended towards reversibility 4 weeks after discontinuation. The risk of heart valve thickening does not appear to occur at ≥2 years of age.

Gastric acid suppression medications have been associated with an increase in Clostridioides difficile infection (CDI) and recurrent CDI in pediatric patients (Nylund 2014). In a retrospective, observational, case control study of pediatric patients 1 to 18 years of age who were hospitalized for diarrhea and abdominal pain, the use of proton pump inhibitors (PPIs) was significantly higher in patients who tested positive for C. difficile compared to patients who tested negative for C. difficile (22.1% vs 5.9%) (Turco 2010). Consider CDI diagnosis in patients with persistent diarrhea that does not improve. Use the lowest dose and shortest duration of PPI therapy appropriate for the condition being treated.

A large retrospective cohort study reviewed records for patients with a low baseline risk for fractures who were initiated on acid suppression therapy in the first year of life and evaluated the fracture risk in the first 5 years of life; a total of 97,286 patients were prescribed acid suppression therapy; 73% were prescribed H2 blockers, 9% were prescribed PPIs, and 18% were prescribed both. H2 blocker use alone was not associated with an increased fracture hazard; however, PPI use was associated with a 21% increase and use of PPI plus H2 blocker was associated with a 30% increase. Longer duration of therapy and earlier age at initiation seemed to also increase the fracture hazard. Study findings do not establish a causal relationship between PPI use and fractures. If acid suppression therapy is necessary in the first year of life, limiting therapy to a single drug and limiting the duration should be considered (Malchodi 2019). A second large cohort study reviewed records for 115,933 children <18 years initiated on a PPI. PPI initiation was associated with a statistically significant 11% relative increase in risk of any fracture in patients ≥6 years. The increased risk also seemed to be more pronounced with a longer cumulative duration of PPI use (Wang 2020).

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Capsule Delayed Release, Oral:

Dexilant: 30 mg, 60 mg [contains carrageenan, fd&c blue #2 (indigo carm) aluminum lake]

Generic: 30 mg, 60 mg

Generic Equivalent Available: US

Yes

Pricing: US

Capsule, delayed release (Dexilant Oral)

30 mg (per each): $12.34

60 mg (per each): $12.34

Capsule, delayed release (Dexlansoprazole Oral)

30 mg (per each): $10.49

60 mg (per each): $10.49

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Capsule Delayed Release, Oral:

Dexilant: 30 mg, 60 mg [contains fd&c blue #2 (indigo carm) aluminum lake]

Administration: Pediatric

Oral: Administer without regard to meals; capsules should be swallowed whole; do not chew. For patients with difficulty swallowing capsules, capsules may be opened and the intact granules sprinkled on 1 tablespoon of applesauce; the mixture should be swallowed immediately; do not chew granules. Do not save applesauce and granule mixture for later use.

Oral syringe: Open capsules and mix granules (not crushed) with 20 mL of water. Withdraw entire mixture into oral syringe; swirl syringe gently to prevent granules from settling and administer mixture immediately into the mouth. Refill syringe with 10 mL of water, swirl gently, and administer; fill syringe with an additional 10 mL of water, swirl gently, and administer. Do not save water and granule mixture for later use.

NG tube (≥16 French) administration: Open capsules and mix granules (not crushed) with 20 mL of water. Withdraw entire mixture into catheter-tip syringe; swirl syringe gently to prevent granules from settling and administer mixture immediately through NG tube into the stomach. Refill syringe with 10 mL of water, swirl gently, and flush NG tube; fill syringe with an additional 10 mL of water, swirl gently, and administer. Do not save water and granule mixture for later use.

Administration: Adult

Administer without regard to meals; capsules should be swallowed whole; do not chew. Alternatively, patients who are unable to swallow capsules may open the capsule, sprinkle the intact granules onto 1 tablespoon of applesauce, and swallow intact granules immediately (do not chew granules). Do not save applesauce and granule mixture for later use. Capsules may also be opened for administration via NG tube or oral syringe.

NG tube (≥16 French): Open capsules and mix granules (not crushed) with 20 mL of water. Withdraw entire mixture into catheter-tip syringe; swirl syringe gently to prevent granules from settling and administer mixture immediately through NG tube (≥16 French) into the stomach. Refill syringe with 10 mL of water, swirl gently, and flush NG tube; repeat (with a second rinse). Do not save water and granule mixture for later use.

Oral syringe: Open capsules and mix granules (not crushed) with 20 mL of water. Withdraw entire mixture into oral syringe; swirl syringe gently to prevent granules from settling and administer mixture immediately into the mouth. Refill syringe with 10 mL of water, swirl gently, and administer; repeat (with a second rinse). Do not save water and granule mixture for later use.

Storage/Stability

Store at 20°C to 25°C (68°F to 77°F); excursions are permitted to 15°C to 30°C (59°F to 86°F).

Medication Guide and/or Vaccine Information Statement (VIS)

An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/022287s037lbl.pdf#page=24, must be dispensed with this medication.

Use

Healing of all grades of erosive esophagitis; maintenance of healed erosive esophagitis and relief of heartburn; treatment of symptomatic nonerosive gastroesophageal reflux disease (All indications: FDA approved in ages ≥12 years and adults).

Medication Safety Issues
Sound-alike/look-alike issues:

Dexlansoprazole may be confused with aripiprazole, lansoprazole

Dexilant may be confused with DULoxetine

Kapidex [DSC] may be confused with Capex, Casodex, Kadian

International issues:

Kapidex [DSC] may be confused with Capadex which is a brand name for propoxyphene/acetaminophen combination product [Australia, New Zealand]

Older Adult: High-Risk Medication:

Beers Criteria: Dexlansoprazole is identified in the Beers Criteria as a potentially inappropriate medication to be avoided (as scheduled use for >8 weeks) in patients 65 years and older due to its risk of C. difficile infection, pneumonia, GI malignancies, and bone loss/fractures unless given for high-risk patients (eg, oral corticosteroid or chronic NSAID use), patients with erosive esophagitis, Barrett’s esophagitis, a pathological hypersecretory condition, or if the patient has demonstrated a need for maintenance therapy (eg, failure of drug discontinuation trial or failure of H2 blockers) (Beers Criteria [AGS 2023]).

Metabolism/Transport Effects

Substrate of CYP2C19 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.

Acalabrutinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Acalabrutinib. This interaction is only applicable to acalabrutinib capsules. Risk X: Avoid combination

Alcohol (Ethyl): May decrease the serum concentration of Dexlansoprazole. Risk X: Avoid combination

Amphetamine: Inhibitors of the Proton Pump (PPIs and PCABs) may increase the absorption of Amphetamine. Risk C: Monitor therapy

Atazanavir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Atazanavir. Management: Avoid use in treatment-experienced patients. In treatment-naive patients, administer boosted atazanavir 12 hours after the PPI and the PPI dose should not exceed the equivalent of 20 mg omeprazole. Monitor for reduced atazanavir efficacy. Risk D: Consider therapy modification

Belumosudil: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Belumosudil. Management: Increase the dose of belumosudil to 200 mg twice daily when coadministered with inhibitors of the proton pump (PPIs and PCABs). Risk D: Consider therapy modification

Bisphosphonate Derivatives: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the therapeutic effect of Bisphosphonate Derivatives. Risk C: Monitor therapy

Bosutinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Bosutinib. Management: Consider alternatives to proton pump inhibitors and potassium-competitive acid blockers, such as short-acting antacids or histamine-2 receptor antagonists. Administer alternative agents more than 2 hours before or after bosutinib. Risk D: Consider therapy modification

Capecitabine: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the therapeutic effect of Capecitabine. Risk C: Monitor therapy

Cefditoren: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Cefditoren. Risk X: Avoid combination

Cefpodoxime: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Cefpodoxime. Risk C: Monitor therapy

Cefuroxime: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the absorption of Cefuroxime. Risk X: Avoid combination

CYP2C19 Inducers (Strong): May decrease the serum concentration of Dexlansoprazole. Risk X: Avoid combination

CYP2C19 Inhibitors (Moderate): May increase the serum concentration of Dexlansoprazole. Risk C: Monitor therapy

CYP2C19 Inhibitors (Strong): May increase the serum concentration of Dexlansoprazole. Risk C: Monitor therapy

Cysteamine (Systemic): Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the therapeutic effect of Cysteamine (Systemic). Risk C: Monitor therapy

Dacomitinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Dacomitinib. Management: Avoid concurrent use of dacomitinib with PPIs and PCABs. Antacids may be used. Histamine H2-receptor antagonists (HR2A) may be used if dacomitinib is given at least 6 hours before or 10 hours after the H2RA. Risk X: Avoid combination

Dasatinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Dasatinib. Management: Antacids (taken 2 hours before or after dasatinib administration) can be used in place of PPIs or PCABs if some acid-reducing therapy is needed. Risk X: Avoid combination

Delavirdine: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Delavirdine. Management: Chronic therapy with PPIs or PCABs should be avoided in patients treated with delavirdine. The clinical significance of short-term PPI or PCAB therapy with delavirdine is uncertain, but such therapy should be undertaken with caution. Risk X: Avoid combination

Dextroamphetamine: Inhibitors of the Proton Pump (PPIs and PCABs) may increase the absorption of Dextroamphetamine. Specifically, the dextroamphetamine absorption rate from mixed amphetamine salt extended release (XR) capsules may be increased in the first hours after dosing. Risk C: Monitor therapy

Doxycycline: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the bioavailability of Doxycycline. Risk C: Monitor therapy

Enoxacin: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the absorption of Enoxacin. Risk C: Monitor therapy

Erlotinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Erlotinib. Risk X: Avoid combination

Gefitinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Gefitinib. Management: Avoid use of inhibitors of the proton pump (PPIs or PCABs) with gefitinib when possible. If required, administer gefitinib 12 hours after the PPI/PCAB or 12 hours before the next dose of the PPI/PCAB. Closely monitor clinical response to gefitinib. Risk D: Consider therapy modification

Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies): Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the therapeutic effect of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Risk C: Monitor therapy

Indinavir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Indinavir. Risk C: Monitor therapy

Infigratinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentrations of the active metabolite(s) of Infigratinib. Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Infigratinib. Risk X: Avoid combination

Itraconazole: Inhibitors of the Proton Pump (PPIs and PCABs) may increase the serum concentration of Itraconazole. This specifically applies to the super bioavailable itraconazole products (eg, Tolsura brand). Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Itraconazole. This specifically applies to the non-super bioavailable itraconazole products (eg, Sporanox brand and its generics). Management: Exposure to Tolsura brand itraconazole may be increased by PPIs or PCABs ; consider itraconazole dose reduction. Exposure to Sporanox brand itraconazole may be decreased. Give Sporanox brand itraconazole at least 2 hrs before or 2 hrs after PPIs or PCABs. Risk D: Consider therapy modification

Ketoconazole (Systemic): Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the absorption of Ketoconazole (Systemic). Ketoconazole (Systemic) may increase the serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). Management: Administer ketoconazole with an acidic beverage, such as non-diet cola, to increase gastric acidity and improve absorption if concomitant use with proton pump inhibitors or potassium-competitive acid blockers is necessary. Risk D: Consider therapy modification

Ledipasvir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Ledipasvir. Management: PPI or PCAB doses equivalent to omeprazole 20 mg or lower may be given with ledipasvir under fasted conditions. Use of ledipasvir with higher doses or with food, or 2 hours after a these agents, may reduce ledipasvir bioavailability. Risk D: Consider therapy modification

Levoketoconazole: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the absorption of Levoketoconazole. Levoketoconazole may increase the serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). Risk X: Avoid combination

Lumacaftor and Ivacaftor: May decrease the serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). Risk C: Monitor therapy

Methotrexate: Inhibitors of the Proton Pump (PPIs and PCABs) may increase the serum concentration of Methotrexate. Management: Consider temporarily interrupting PPI or PCAB therapy in patients receiving high-dose methotrexate. If coadministered, monitor for increased methotrexate toxicity (eg, mucositis, myalgias) and/or delayed methotrexate elimination. Risk D: Consider therapy modification

Multivitamins/Minerals (with ADEK, Folate, Iron): Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Multivitamins/Minerals (with ADEK, Folate, Iron). Specifically, the absorption of iron may be decreased. Risk C: Monitor therapy

Mycophenolate: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Mycophenolate. Specifically, concentrations of the active mycophenolic acid may be reduced. Risk C: Monitor therapy

Nelfinavir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentrations of the active metabolite(s) of Nelfinavir. Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Nelfinavir. Management: Due to potentially significant reductions in nelfinavir exposure, avoid concurrent use of nelfinavir with a PPI or PCAB when possible. If unavoidable, consider PPI or PCAB use for a short duration (less than 30 days) and closely monitor viral load. Risk D: Consider therapy modification

Neratinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Neratinib. Specifically, proton pump inhibitors may reduce neratinib absorption. Risk X: Avoid combination

Nilotinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Nilotinib. Management: Avoid this combination. Histamine H2 receptor antagonists (H2RAs) given 10 hours before or 2 hours after nilotinib, or antacids given 2 hours before or 2 hours after nilotinib are acceptable alternatives. Risk D: Consider therapy modification

Nirogacestat: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Nirogacestat. Risk X: Avoid combination

Octreotide: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Octreotide. Risk C: Monitor therapy

Palbociclib: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the therapeutic effect of Palbociclib. Specifically, this has been reported with the use of palbociclib capsules. Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Palbociclib. Specifically, this may occur with the use of palbociclib capsules, and to the greatest extent when taken without food. Management: Carefully evaluate potential risks and benefits of coadministration of palbociclib capsules and proton pump inhibitors or potassium-competitive acid blockers due to the risk of reduced palbociclib efficacy. Palbociclib capsules should be taken with food. Risk D: Consider therapy modification

PAZOPanib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of PAZOPanib. Risk X: Avoid combination

Pexidartinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Pexidartinib. Management: Avoid this combination. If acid-reduction is needed, consider administering an antacid 2 hours before or after pexidartinib, or administer pexidartinib 2 hours before or 10 hours after an H2 receptor antagonist. Risk X: Avoid combination

Posaconazole: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Posaconazole. Management: Avoid coadministration of PPIs or PCABs and posaconazole oral suspension. Posaconazole delayed-release tablets do not appear to be sensitive to this interaction and do not required dose adjustment if coadministered with PPIs or PCABs. Risk D: Consider therapy modification

Rilpivirine: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Rilpivirine. Risk X: Avoid combination

Riociguat: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Riociguat. Risk C: Monitor therapy

Risedronate: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the therapeutic effect of Risedronate. Inhibitors of the Proton Pump (PPIs and PCABs) may increase the serum concentration of Risedronate. This applies specifically to use of delayed-release risedronate. Management: Coadministration of PPIs or PCABs with delayed-release risedronate formulations is not recommended. Limit PPI/PCAB dose and duration during coadministration with risedronate as possible. Patients over age 70 are at higher risk of adverse effects. Risk D: Consider therapy modification

Saquinavir: Inhibitors of the Proton Pump (PPIs and PCABs) may increase the serum concentration of Saquinavir. Risk C: Monitor therapy

Secretin: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the diagnostic effect of Secretin. Specifically, use of PPIs may cause a hyperresponse in gastrin secretion in response to secretin stimulation testing, falsely suggesting gastrinoma. Management: Avoid concomitant use of PPIs or PCABs and secretin, and discontinue PPI or PCAB several weeks prior to secretin administration, with the duration of separation determined by the specific acid suppressant. See full monograph for details. Risk D: Consider therapy modification

Selpercatinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Selpercatinib. Management: Coadministration of selpercatinib and PPIs or PCABs should be avoided. If coadministration cannot be avoided, selpercatinib and PPIs or PCABs should be administered simultaneously with food. Risk D: Consider therapy modification

SORAfenib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the absorption of SORAfenib. Risk C: Monitor therapy

Sotorasib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Sotorasib. Risk X: Avoid combination

Sparsentan: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Sparsentan. Risk X: Avoid combination

St John's Wort: May decrease the serum concentration of Dexlansoprazole. Risk X: Avoid combination

Tacrolimus (Systemic): Inhibitors of the Proton Pump (PPIs and PCABs) may increase the serum concentration of Tacrolimus (Systemic). Risk C: Monitor therapy

Technetium Tc 99m Sestamibi: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the diagnostic effect of Technetium Tc 99m Sestamibi. Management: Consider holding/stopping proton pump inhibitor therapy for at least 3 days prior to the use technetium Tc 99m sestamibi in cardiac imaging procedures. Risk D: Consider therapy modification

Technetium Tc 99m Tetrofosmin: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the diagnostic effect of Technetium Tc 99m Tetrofosmin. Risk C: Monitor therapy

Thiazolidinediones: Inhibitors of the Proton Pump (PPIs and PCABs) may enhance the adverse/toxic effect of Thiazolidinediones. Specifically, the risk of osteoporosis or fracture may be increased. Risk C: Monitor therapy

Tipranavir: May decrease the serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). These data are derived from studies with Ritonavir-boosted Tipranavir. Risk C: Monitor therapy

Velpatasvir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Velpatasvir. Management: Sofosbuvir/velpatasvir should be administered with food and taken 4 hours before omeprazole 20 mg. Sofosbuvir/velpatasvir/voxilaprevir can be administered with omeprazole 20 mg. Use with other PPIs or PCABs has not been studied. Risk D: Consider therapy modification

Vitamin K Antagonists (eg, warfarin): Dexlansoprazole may increase the serum concentration of Vitamin K Antagonists. Risk C: Monitor therapy

Voriconazole: May increase the serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). Inhibitors of the Proton Pump (PPIs and PCABs) may increase the serum concentration of Voriconazole. Risk C: Monitor therapy

Food Interactions

Prolonged treatment (≥2 years) may lead to malabsorption of dietary vitamin B12 and subsequent vitamin B12 deficiency (Lam 2013).

Pregnancy Considerations

Outcome data following use of proton pump inhibitors (PPIs) during pregnancy are available (Choi 2023; Hussain 2022; Peron 2023).

Recommendations for the treatment of gastroesophageal reflux disease in pregnant patients are available. When initiating treatment during pregnancy, a step-up approach, starting with diet and lifestyle modifications, is recommended. PPIs are considered acceptable for use during pregnancy when other medications are not effective (Ali 2022; Dunbar 2022; Thélin 2020).

Monitoring Parameters

Magnesium levels (baseline and periodically thereafter) in patients on long-term treatment or those taking digoxin or drugs that cause hypomagnesemia (eg, diuretics); calcium (baseline and periodically in patients at risk [eg, hypoparathyroidism]).

Mechanism of Action

Proton pump inhibitor; decreases acid secretion in gastric parietal cells through inhibition of (H+, K+)-ATPase enzyme system, blocking the final step in gastric acid production

Pharmacokinetics (Adult Data Unless Noted)

Distribution: Vd: Symptomatic GERD: 40 L

Protein binding: 96% to 99%

Metabolism: Hepatic (extensive) via CYP2C19-mediated hydroxylation and CYP3A4-mediated oxidation; followed by reduction to sulfate, glucuronide, and glutathione conjugates (inactive)

Bioavailability: May be increased when administered with food

Half-life, elimination: ~1 to 2 hours

Time to peak, serum: Two distinct peaks secondary to dual release formulation: Initial peak between 1 and 2 hours and a second higher peak between 4 and 5 hours.

Excretion: Urine (~51% as metabolites); feces (~48%)

Note: CYP2C19 polymorphism is expected to affect dexlansoprazole exposure. In a study involving Japanese men following a single dose of dexlansoprazole, Cmax and AUC were up to 2 times greater in intermediate metabolizers compared to extensive metabolizers. In addition, mean Cmax and mean AUC were up to 4 times greater and up to 12 times greater, respectively, in poor metabolizers compared to extensive metabolizers.

Pharmacokinetics: Additional Considerations (Adult Data Unless Noted)

Hepatic function impairment: Plasma exposure to the drug is ~2 times greater in patients with moderate hepatic impairment (Child-Pugh class B) compared with subjects with normal hepatic function.

Pediatric: Systemic exposures in children and adolescents 12 to 17 years of age were similar to those observed in adults.

Older adult: The elimination half-life is increased and AUC is higher in the elderly.

Sex: Systemic exposure is 43% higher in females than in males.

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Dexilant;
  • (AR) Argentina: Apatrix | Arigastril | Dexopral | Ibepral;
  • (BD) Bangladesh: Delanix | Dexila | Dexilend | Dexoprex | Dlp;
  • (CO) Colombia: Dexlansoprazol | Dexlanzopral | Dexopral;
  • (DO) Dominican Republic: Dexlansoprazol ethical | Dexlanzopral;
  • (EC) Ecuador: Dexilant | Dexlanzopral;
  • (EG) Egypt: Dexilant | Doxirazol | Lantopep | Protolans | Ulcezole;
  • (IN) India: Deltone;
  • (IT) Italy: Gladexa;
  • (JO) Jordan: Dexilant;
  • (KE) Kenya: Dolgina;
  • (KR) Korea, Republic of: Dexirazole;
  • (LB) Lebanon: Dexilant;
  • (LT) Lithuania: Dexilant;
  • (MX) Mexico: Dexivant;
  • (PE) Peru: Dexilant | Dexlanzopral;
  • (PK) Pakistan: Daplazole | Ddr | Delanzo | Dexiva | Dextol | Dolgina | Dudex | Dxl | Kapdex | Kewdex | Redexa | Remit dr | Stomdex | Werdex | Wilsop | Xanilo;
  • (PL) Poland: Dexilant;
  • (QA) Qatar: Dexilant;
  • (SA) Saudi Arabia: Dexilant;
  • (UA) Ukraine: Dexilant;
  • (ZA) South Africa: Dexilant
  1. 2023 American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2023;71(7):2052-2081. doi:10.1111/jgs.18372 [PubMed 37139824]
  2. Abdul-Hussein M, Freeman J, Castell D. Concomitant administration of a histamine2 receptor antagonist and proton pump inhibitor enhances gastric acid suppression. Pharmacotherapy. 2015;35(12):1124-1129. doi:10.1002/phar.1665 [PubMed 26621819]
  3. Abraham NS, Hlatky MA, Antman EM, et al. ACCF/ACG/AHA 2010 Expert Consensus Document on the Concomitant Use of Proton Pump Inhibitors and Thienopyridines: A Focused Update of the ACCF/ACG/AHA 2008 Expert Consensus Document on Reducing the Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use: A Report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents. Circulation. 2010;122(24):2619-2633. [PubMed 21060077]
  4. Ali RAR, Hassan J, Egan LJ. Review of recent evidence on the management of heartburn in pregnant and breastfeeding women. BMC Gastroenterol. 2022;22(1):219. doi:10.1186/s12876-022-02287-w [PubMed 35508989]
  5. Bell AD, Roussin A, Cartier R, et al. The Use of Antiplatelet Therapy in the Outpatient Setting: Canadian Cardiovascular Society Guidelines. Can J Cardiol. 2011;27(suppl A):1-59. [PubMed 21640290]
  6. Bonis PAL, Gupta SK. Treatment of eosinophilic esophagitis. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed October 25, 2021.
  7. Chalasani NP, Hayashi PH, Bonkovsky HL, et al. ACG Clinical Guideline: the diagnosis and management of idiosyncratic drug-induced liver injury. Am J Gastroenterol. 2014;109(7):950-966. [PubMed 24935270]
  8. Choi A, Noh Y, Jeong HE, et al. Association between proton pump inhibitor use during early pregnancy and risk of congenital malformations. JAMA Netw Open. 2023;6(1):e2250366. doi:10.1001/jamanetworkopen.2022.50366 [PubMed 36626173]
  9. de Jager CP, Wever PC, Gemen EF, et al, “Proton Pump Inhibitor Therapy Predisposes to Community-Acquired Streptococcus pneumoniae Pneumonia,” Aliment Pharmacol Ther, 2012, 36(10):941-9. [PubMed 23034135]
  10. DeVault KR and Castell DO, “Updated Guidelines for the Diagnosis and Treatment of Gastroesophageal Reflux Disease,” Am J Gastroenterol, 2005, 100(1):190-200. [PubMed 15654800]
  11. Dexilant (dexlansoprazole) [prescribing information]. Lexington, MA: Takeda Pharmaceuticals America Inc; March 2022.
  12. Dexilant (dexlansoprazole) [prescribing information]. Lexington, MA: Takeda Pharmaceuticals America Inc; April 2023.
  13. Dexilant (dexlansoprazole) [prescribing information]. Lexington, MA: Takeda Pharmaceuticals America Inc; July 2023.
  14. DiGiovanni EL, Champeaux AL, Arroyo MR, Richter JE. Esophageal eosinophilia treated with long-duration proton pump inhibitor therapy. ACG Case Rep J. 2016;3(2):95-97. doi:10.14309/crj.2016.11 [PubMed 26958557]
  15. Dunbar K, Yadlapati R, Konda V. Heartburn, nausea, and vomiting during pregnancy. Am J Gastroenterol. 2022;117(10S):10-15. doi:10.14309/ajg.0000000000001958 [PubMed 36194028]
  16. Earnest DL, Dorsch E, Jones J, Jennings DE, Greski-Rose PA. A placebo-controlled dose-ranging study of lansoprazole in the management of reflux esophagitis. Am J Gastroenterol. 1998;93(2):238-243. doi:10.1111/j.1572-0241.1998.00238.x [PubMed 9468251]
  17. Fallone CA, Chiba N, van Zanten SV, et al. The Toronto consensus for the treatment of Helicobacter pylori infection in adults. Gastroenterology. 2016;151(1):51-69.e14. [PubMed 27102658]
  18. Fändriks L, Lönroth H, Pettersson A, Vakil N. Can famotidine and omeprazole be combined on a once-daily basis? Scand J Gastroenterol. 2007;42(6):689-694. doi:10.1080/00365520601026665 [PubMed 17505990]
  19. Fass R. Approach to refractory gastroesophageal reflux disease in adults. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed October 12, 2022.
  20. Fass R, Chey WD, Zakko SF, et al. Clinical trial: the effects of the proton pump inhibitor dexlansoprazole MR on daytime and nighttime heartburn in patients with non-erosive reflux disease. Aliment Pharmacol Ther. 2009;29(12):1261-1272. doi:10.1111/j.1365-2036.2009.04013.x [PubMed 19392864]
  21. Frelinger AL 3rd, Lee RD, Mulford DJ, et al, “A Randomized, 2-Period, Crossover Design Study to Assess the Effects of Dexlansoprazole, Lansoprazole, Esomeprazole, and Omeprazole on the Steady-State Pharmacokinetics and Pharmacodynamics of Clopidogrel in Healthy Volunteers,” J Am Coll Cardiol, 2012, 59(14):1304-11. [PubMed 22464259]
  22. Haastrup P, Paulsen MS, Begtrup LM, Hansen JM, Jarbøl DE. Strategies for discontinuation of proton pump inhibitors: a systematic review. Fam Pract. 2014;31(6):625-630. doi:10.1093/fampra/cmu050 [PubMed 25192903]
  23. Hirano I, Chan ES, Rank MA, et al; AGA Institute Clinical Guidelines Committee; Joint Task Force on Allergy-Immunology Practice Parameters. AGA Institute and the Joint Task Force on Allergy-Immunology Practice Parameters clinical guidelines for the management of eosinophilic esophagitis. Gastroenterology. 2020;158(6):1776-1786. doi:10.1053/j.gastro.2020.02.038 [PubMed 32359562]
  24. Hussain S, Singh A, Antony B, et al. Proton pump inhibitors use and risk of preeclampsia: a meta- analysis. J Clin Med. 2022;11(16):4675. doi:10.3390/jcm11164675 [PubMed 36012913]
  25. Kahrilas PJ. Medical management of gastroesophageal reflux disease in adults. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed October 12, 2022.
  26. Kahrilas PJ, Shaheen NJ, Vaezi MF, et al. American Gastroenterological Association Medical Position Statement on the Management of Gastroesophageal Reflux Disease. Gastroenterology. 2008;135(4):1383-1391. [PubMed 18789939]
  27. Katz PO, Dunbar KB, Schnoll-Sussman FH, Greer KB, Yadlapati R, Spechler SJ. ACG clinical guideline for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol. 2022;117(1):27-56. doi:10.14309/ajg.0000000000001538 [PubMed 34807007]
  28. Kavitt RT, Ates F, Slaughter JC, et al. Randomized controlled trial comparing esophageal dilation to no dilation among adults with esophageal eosinophilia and dysphagia. Dis Esophagus. 2016;29(8):983-991. doi:10.1111/dote.12398 [PubMed 26228516]
  29. Kim J, Blackett JW, Jodorkovsky D. Strategies for effective discontinuation of proton pump inhibitors. Curr Gastroenterol Rep. 2018;20(6):27. doi:10.1007/s11894-018-0632-y [PubMed 29767318]
  30. Lam JR, Schneider JL, Zhao W, Corley DA. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA. 2013;310(22):2435-2422. [PubMed 24327038]
  31. Lanza FL, Chan FK, Quigley EM. Guidelines for Prevention of NSAID-Related Ulcer Complications. Am J Gastroenterol. 2009;140(3):728-738. [PubMed 19240698]
  32. Laserna-Mendieta EJ, Casabona S, Guagnozzi D, et al; EUREOS EoE CONNECT research group. Efficacy of proton pump inhibitor therapy for eosinophilic oesophagitis in 630 patients: results from the EoE connect registry. Aliment Pharmacol Ther. 2020;52(5):798-807. doi:10.1111/apt.15957 [PubMed 32677040]
  33. Lazarus B, Chen Y, Wilson FP, et al. Proton pump inhibitor use and the risk of chronic kidney disease. JAMA Intern Med. 2016;238-246. [PubMed 26752337]
  34. Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation. 2011;124(23):e574-e651. [PubMed 22064601]
  35. Li XQ, Andersson TB, Ahalström M, et al. Comparison of Inhibitory Effects of the Proton Pump-Inhibiting Drugs Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole and Rabeprazole on Human Cytochrome P450 Activities. Drug Metab Dispo. 2004;32(8):821-827. [PubMed 15258107]
  36. Lucendo AJ, Arias Á, Molina-Infante J. Efficacy of proton pump inhibitor drugs for inducing clinical and histologic remission in patients with symptomatic esophageal eosinophilia: a systematic review and meta-analysis. Clin Gastroenterol Hepatol. 2016;14(1):13-22.e1. doi:10.1016/j.cgh.2015.07.041 [PubMed 26247167]
  37. Malchodi L, Wagner K, Susi A, Gorman G, Hisle-Gorman E. Early acid suppression therapy exposure and fracture in young children. Pediatrics. 2019;144(1):e20182625. [PubMed 31175146]
  38. Nylund CM, Eide M, Gorman GH. Association of Clostridium difficile infections with acid suppression medications in children. J Pediatr. 2014;165(5):979-984. [PubMed 25112692]
  39. Ogilvie BW, Yerino P, Kazmi F, et al. The Proton Pump Inhibitor, Omeprazole, but not Lansoprazole or Pantoprazole, is a Metabolism-Dependent Inhibitor of CYP2C19: Implications for Coadministration With Clopidogrel. Drug Metab Dispos. 2011;39(11):2020-2033. [PubMed 21795468]
  40. Peron A, Ripoche E, Picot C, Ajiji P, Cucherat M, Cottin J. Use of proton pump inhibitors during pregnancy: a systematic review and meta-analysis of congenital malformations. Reprod Toxicol. 2023;119:108419. doi:10.1016/j.reprotox.2023.108419 [PubMed 37269915]
  41. Philpott H, Nandurkar S, Royce SG, Thien F, Gibson PR. A prospective open clinical trial of a proton pump inhibitor, elimination diet and/or budesonide for eosinophilic oesophagitis. Aliment Pharmacol Ther. 2016;43(9):985-993. doi:10.1111/apt.13576 [PubMed 26939578]
  42. Refer to manufacturer's labeling.
  43. Rosen R, Vandenplas Y, Singendonk M, et al. Pediatric gastroesophageal reflux clinical practice guidelines: joint recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. 2018;66(3):516-554. [PubMed 29470322]
  44. Shaheen NJ, Falk GW, Iyer PG, et al. Diagnosis and management of Barrett's esophagus: an updated ACG guideline. Am J Gastroenterol. 2022;117(4):559-587. doi:10.14309/ajg.0000000000001680 [PubMed 35354777]
  45. Sharma P, Shaheen NJ, Perez MC, et al, “Healing of Erosive Oesophagitis With TAK-390MR, a Proton Pump Inhibitor With a Novel Dual Delayed-Release Formulation: Results From Two Randomized Controlled Studies,” Aliment Pharmacol Ther, 2009, 29(7):731-41. [PubMed 19183157]
  46. Shin JM, Kim N. Pharmacokinetics and pharmacodynamics of the proton pump inhibitors. J Neurogastroenterol Motil. 2013;19(1):25-35. doi:10.5056/jnm.2013.19.1.25 [PubMed 23350044]
  47. Sugimoto M, Furuta T, Shirai N, Ikuma M, Hishida A, Ishizaki T. Initial 48-hour acid inhibition by intravenous infusion of omeprazole, famotidine, or both in relation to cytochrome P450 2C19 genotype status. Clin Pharmacol Ther. 2006;80(5):539-548. doi:10.1016/j.clpt.2006.08.010 [PubMed 17112810]
  48. Talley NJ and Vakil N, “Practice Parameters Committee of the American College of Gastroenterology. Guidelines for the Management of Dyspepsia,” Am J Gastroenterol, 2005, 100(10):2324-37. [PubMed 16181387]
  49. Talley NJ, Zand Irani M. Optimal management of severe symptomatic gastroesophageal reflux disease. J Intern Med. 2021;289(2):162-178. doi:10.1111/joim.13148 [PubMed 32691466]
  50. Targownik LE, Fisher DA, Saini SD. AGA clinical practice update on de-prescribing of proton pump inhibitors: expert review. Gastroenterology. 2022;162(4):1334-1342. doi:10.1053/j.gastro.2021.12.247 [PubMed 35183361]
  51. Thélin CS, Richter JE. Review article: the management of heartburn during pregnancy and lactation. Aliment Pharmacol Ther. 2020;51(4):421-434. doi:10.1111/apt.15611 [PubMed 31950535]
  52. Turco R, Martinelli M, Miele E, et al. Proton pump inhibitors as a risk factor for paediatric Clostridium difficile infection. Aliment Pharmacol Ther. 2010;31(7):754-759. [PubMed 20047577]
  53. Vazquez-Elizondo G, Ngamruengphong S, Khrisna M, Devault KR, Talley NJ, Achem SR. The outcome of patients with oesophageal eosinophilic infiltration after an eight-week trial of a proton pump inhibitor. Aliment Pharmacol Ther. 2013;38(10):1312-1319. doi:10.1111/apt.12513 [PubMed 24117619]
  54. Wang Y, Pan T, Wang Q, Guo Z. Additional bedtime H2-receptor antagonist for the control of nocturnal gastric acid breakthrough. Cochrane Database Syst Rev. 2009;(4):CD004275. doi:10.1002/14651858.CD004275.pub3 [PubMed 19821323]
  55. Wang YH, Wintzell V, Ludvigsson JF, Svanström H, Pasternak B. Association between proton pump inhibitor use and risk of fracture in children. JAMA Pediatr. 2020;174(6):543-551. doi:10.1001/jamapediatrics.2020.0007 [PubMed 32176276]
  56. Wolfe MM and Sachs G, “Acid Suppression: Optimizing Therapy for Gastroduodenal Ulcer Healing, Gastroesophageal Reflux Disease, and Stress-Related Erosive Syndrome,” Gastroenterology, 2000,118(2 Suppl 1):9-31. [PubMed 10868896]
  57. Wolfe MM. Proton pump inhibitors: overview of use and adverse effects in the treatment of acid related disorders. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed January 27, 2023.
  58. Wu JCY, Sheu BS, Wu MS, Lee YC, Choi MG. Phase 4 study in patients from Asia with gastroesophageal reflux disease treated with dexlansoprazole. J Neurogastroenterol Motil. 2020;26(1):85-95. doi:10.5056/jnm19031 [PubMed 31597230]
  59. Zheng RN. Comparative study of omeprazole, lansoprazole, pantoprazole and esomeprazole for symptom relief in patients with reflux esophagitis. World J Gastroenterol. 2009;15(8):990-995. doi:10.3748/wjg.15.990 [PubMed 19248200]
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