Version July 2023
Note: Doses >30 mg do not provide additional benefit during maintenance phase.
Eosinophilic esophagitis (off-label use): Oral: 30 mg once daily for an 8-week trial (Bonis 2021; manufacturer's labeling). Some experts increase to 60 mg once daily after 4 weeks if symptoms fail to improve (Bonis 2021; DiGiovanni 2016; Kavitt 2016).
Gastroesophageal reflux disease, erosive or nonerosive: Note: For patients with alarm symptoms (eg, dysphagia), referral to a specialist is recommended (ACG [Katz 2022]). Maximal acid suppression is generally observed after ~3 days of continuous therapy (Shin 2013).
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 (Kahrilas 2022).
Oral: 30 mg once daily for 4 to 8 weeks (ACG [Katz 2022]; Wu 2020). Note: Some experts continue therapy until asymptomatic for 8 weeks (Kahrilas 2022).
Severe or frequent symptoms (≥2 episodes/week) without erosive esophagitis or Barrett esophagus: Oral: 30 mg once daily for 8 weeks (ACG [Katz 2022]; Zheng 2009). Note: Some experts continue therapy until patient has been asymptomatic for 8 weeks (Kahrilas 2022).
Erosive esophagitis or Barrett esophagus: Oral: 60 mg once daily for 8 weeks (manufacturer's labeling) then 30 mg once daily indefinitely, (ACG [Shaheen 2022]; AGA [Targownik 2022]) or 30 mg once daily indefinitely (preferred by some experts) (Kahrilas 2022).
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 (Talley 2021). For patients requiring concomitant H2RA therapy, some experts administer the H2RA at bedtime (Fass 2022; Wang 2009); however, others advocate concurrent administration to ensure adherence (Abdul-Hussein 2015; Fandriks 2007; Sugimoto 2006).
Recurrent symptoms after discontinuing acid suppression:
Recurrent symptoms after ≥3 months: Repeat an 8-week course at the previously effective dose (Kahrilas 2022).
Recurrent symptoms after <3 months: Long-term maintenance at the lowest effective dose; referral to a specialist is recommended (ACG [Katz 2022]; Kahrilas 2022).
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 (Wolfe 2023). 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 (Kim 2018). In addition, as-needed therapy with an H2RA or an antacid can be used during the taper (Haastrup 2014).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
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.
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.
(For additional information see "Dexlansoprazole: Pediatric drug information")
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 (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 (NASPGHAN/ESPGHAN [Rosen 2018]).
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 (Kim 2018).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
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.
Children ≥12 years and Adolescents:
Mild impairment (Child-Pugh class A): No dosage adjustment necessary.
Moderate impairment (Child-Pugh class B):
Healing of erosive esophagitis: 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 (Child-Pugh class C): Use is not recommended.
Refer to adult dosing.
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
Yes
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]
An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2022/022287s035lbl.pdf#page=24, must be dispensed with this medication.
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.
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.
Gastroesophageal reflux disease, erosive or nonerosive:
Erosive esophagitis: Healing of all grades of erosive esophagitis in patients ≥12 years of age for up to 8 weeks; to maintain healing of erosive esophagitis and relief of heartburn for up to 6 months in adults and 16 weeks in patients 12 to 17 years of age.
Symptomatic and nonerosive: Treatment of heartburn associated with symptomatic nonerosive gastroesophageal reflux disease in patients ≥12 years of age for 4 weeks.
Eosinophilic esophagitis
Dexlansoprazole may be confused with aripiprazole, lansoprazole
Dexilant may be confused with DULoxetine
Kapidex [DSC] may be confused with Capex, Casodex, Kadian
Kapidex [DSC] may be confused with Capadex which is a brand name for propoxyphene/acetaminophen combination product [Australia, New Zealand]
Beers Criteria: Proton pump inhibitors are identified in the Beers Criteria as potentially inappropriate medications to be avoided (as scheduled use for more than 8 weeks) in patients 65 years and older due to their risk of C. difficile infection 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 2019]).
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 gastrin (<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 polyps (<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%), irritable bowel syndrome (<2%), mucosal swelling (<2%), mucus stools (<2%), oral bullae (<2%), oral herpes simplex infection (<2%), oral paresthesia (<2%), proctitis (<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%), rectal hemorrhage (<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%), 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%), painful defecation (<2%), paresthesia (<2%), procedural pain (<2%), psychomotor agitation (<2%), seizure (<2%), trigeminal neuralgia (<2%), vertigo (<2%)
Neuromuscular & skeletal: Arthralgia (<2%), arthritis (<2%), asthenia (<2%), bone fracture (<2%), joint sprain (<2%), muscle cramps (<2%), musculoskeletal pain (<2%), myalgia (<2%), tremor (<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:
Cardiovascular: Cerebrovascular accident, hypersensitivity angiitis, transient ischemic attacks
Dermatologic: Acute generalized exanthematous pustulosis, drug reaction with eosinophilia and systemic symptoms, exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis
Endocrine & metabolic: Hypocalcemia, hypomagnesemia, hyponatremia
Gastrointestinal: Clostridioides difficile associated diarrhea, pancreatitis
Genitourinary: Chronic renal failure (Lazarus 2016)
Hematologic & oncologic: Autoimmune hemolytic anemia, immune thrombocytopenia
Hepatic: Hepatitis, hepatotoxicity (idiosyncratic) (Chalasani 2014)
Hypersensitivity: Anaphylactic shock
Ophthalmic: Blurred vision
Otic: Deafness
Renal: Acute kidney injury
Respiratory: Constriction of the pharynx
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.
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.
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).
Substrate of CYP2C19 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
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. 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: Inhibitors of the Proton Pump (PPIs and PCABs) may diminish the therapeutic effect of Immune Checkpoint Inhibitors. 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. Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Itraconazole. 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
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. Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Palbociclib. 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 PPIs several weeks prior to secretin administration, with the duration of separation determined by the specific PPI. 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
Prolonged treatment (≥2 years) may lead to malabsorption of dietary vitamin B12 and subsequent vitamin B12 deficiency (Lam 2013).
Adverse events have not been observed in animal reproduction studies.
Recommendations for the treatment of GERD in pregnancy are available. As in nonpregnant patients, lifestyle modifications followed by other medications are the initial treatments (Body 2016; Huerta-Iga 2016; Katz 2013; van der Woude 2014). Based on available data, PPIs may be used when clinically indicated (use of agents with more available data may be preferred) (Body 2016; Matok 2012; Pasternak 2010; van der Woude 2014).
It is not known if dexlansoprazole is present in breast milk. According to the manufacturer, the decision to continue or discontinue breastfeeding during therapy should take into account the risk of infant exposure, the benefits of breastfeeding to the infant, and benefits of treatment to the mother.
Magnesium (baseline and periodically thereafter; especially if taking concomitant digoxin, diuretics, or other drugs known to cause hypomagnesemia) and calcium (baseline and periodically in patients at risk [eg, hypoparathyroidism]).
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
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.
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.
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
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