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Omeprazole: Pediatric drug information

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

For abbreviations, symbols, and age group definitions used in Lexicomp (show table)
Brand Names: US
  • Acid Reducer [OTC];
  • PriLOSEC;
  • PriLOSEC OTC [OTC]
Brand Names: Canada
  • APO-Omeprazole;
  • BIO-Omeprazole;
  • DOM-Omeprazole DR [DSC];
  • JAMP-Omeprazole DR;
  • Losec;
  • Losec Mups;
  • NAT-Omeprazole DR;
  • NRA-Omeprazole [DSC];
  • Omeprazole-20;
  • PMS-Omeprazole;
  • PMS-Omeprazole DR [DSC];
  • Priva-Omeprazole [DSC];
  • RAN-Omeprazole [DSC];
  • RIVA-Omeprazole DR;
  • SANDOZ Omeprazole;
  • SANDOZ Omperazole;
  • TEVA-Omeprazole;
  • VAN-Omeprazole [DSC]
Therapeutic Category
  • Gastric Acid Secretion Inhibitor;
  • Gastrointestinal Agent, Gastric or Duodenal Ulcer Treatment;
  • Proton Pump Inhibitor
Dosing: Neonatal
Gastroesophageal reflux disease

Gastroesophageal reflux disease (GERD): Note: Routine use is not recommended in preterm neonates (Ref). Limited data available: Term and preterm neonates: Oral: 0.7 mg/kg/dose once daily reduced the percentage of time gastric and esophageal pH <4, as well as the number of reflux episodes in 10 infants (mean PMA: 36.1 weeks; range: 34 to 40 weeks) in a randomized, double-blind, placebo-controlled trial (Ref). In a dose-finding study of neonates with PMA ≥35 weeks (n=54, GA: 24 to 41 weeks, PNA: 6 to 85 days), higher doses of 1 to 2.5 mg/kg once daily were reported. Based on intraesophageal pH monitoring, this study found that neonates with GA <32 weeks generally required doses up to 2.5 mg/kg/day and neonates with GA ≥32 weeks required lower doses of 1 mg/kg/day (Ref).

Dosing: Pediatric
Erosive esophagitis

Erosive esophagitis:

Treatment: Note: Duration of therapy is dependent on age: Infant duration is up to 6 weeks and children and adolescent duration is 4 to 8 weeks. In children and adolescents with no response at 8 weeks, treatment may continue to an additional 4 weeks. For recurrence of erosive esophagitis or gastroesophageal reflux disease (GERD) symptoms (eg, heartburn), an additional 4- to 8-week course may be considered.

Infants, Children, and Adolescents: Oral:

3 to <5 kg: 2.5 mg once daily.

5 kg to <10 kg: 5 mg once daily.

10 kg to <20 kg: 10 mg once daily.

≥20 kg: 20 mg once daily.

Maintenance of healing: Children and Adolescents: Oral:

5 kg to <10 kg: 5 mg once daily.

10 kg to <20 kg: 10 mg once daily.

≥20 kg: 20 mg once daily.

Gastroesophageal reflux disease

Gastroesophageal reflux disease (GERD): 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).

Fixed dosing: Children and Adolescents: Oral:

5 kg to <10 kg: 5 mg once daily.

10 kg to <20 kg: 10 mg once daily.

≥20 kg: 20 mg once daily.

Weight-based dosing: Infants, Children, and Adolescents: Oral: 0.7 to 4 mg/kg/day (Ref); the dose most frequently reported to provide healing of esophagitis and relief of GERD symptoms is 1 mg/kg/day (Ref); maximum daily dose: 40 mg/day (Ref).

Helicobacter pylori eradication

Helicobacter pylori eradication (Ref): Oral: Children and Adolescents: Note: Usual duration of therapy is 14 days as part of triple therapy; use in combination with 2 antimicrobials (eg, clarithromycin, metronidazole, amoxicillin); preferred agents determined by susceptibility. Bismuth may be added to regimens as an alternative if resistance is present or susceptibility is unknown.

15 to <25 kg: 20 mg twice daily.

25 to 34 kg: 30 mg twice daily.

>34 kg: 40 mg twice 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: Infants, Children, and Adolescents: Oral:

Mild to severe: No dosage adjustment necessary.

Hemodialysis, intermittent: Poorly dialyzed. There are no dosing adjustments provided in the manufacturer's labeling; however, based on adult data, no supplemental dosage or adjustment necessary (Ref).

Dosing: Hepatic Impairment: Pediatric

Infants, Children, and Adolescents: There are no dosage adjustments provided in the manufacturer's labeling. However, based on increased bioavailability, dosage adjustment should be considered, especially for maintenance healing of erosive esophagitis. Specific guidelines are not available.

Dosing: Adult

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

Note: Do not administer concomitantly with other antisecretory agents, such as H2-receptor antagonists (H2RAs), prostaglandin analogues (eg, misoprostol), or somatostatin analogues (eg, octreotide), due to decreased acid-inhibitory effects; if another antisecretory agent is needed, allow a sufficient time interval between administration (ie, morning omeprazole and bedtime H2RA) (Ref).

Aspiration prophylaxis in patients undergoing anesthesia

Aspiration prophylaxis in patients undergoing anesthesia (off-label use):

Note: May be considered in patients at high risk for aspiration (Ref).

Oral: 40 mg given the night before surgery and 40 mg given the morning of surgery (Ref).

Barrett esophagus

Barrett esophagus (off-label use):

Oral: 20 mg once daily; may increase the dose (eg, to 20 mg twice daily) if needed to eliminate gastroesophageal reflux disease symptoms or heal reflux esophagitis. Long-term maintenance therapy is recommended (Ref).

Dyspepsia, functional

Dyspepsia, functional (idiopathic or non-ulcer) (off-label use):

Note: For patients who test negative for H. pylori infection or have persistent symptoms following H. pylori eradication (Ref).

Oral: 20 mg once daily for a 4- to 8-week trial (Ref); can be continued for a longer duration in patients with symptom improvement. Some experts recommend attempting to discontinue every 6 to 12 months to minimize the long-term risk of therapy (Ref).

Eosinophilic esophagitis

Eosinophilic esophagitis (off-label use):

Oral: 20 mg twice daily for an 8-week trial (Ref). Once 8-week trial is complete and remission is achieved, the dose may be gradually lowered to an individualized maintenance level (Ref). Some experts initiate with 20 mg once daily and increase to twice daily dosing after 4 weeks if symptoms fail to improve (Ref).

Gastroesophageal reflux disease, erosive or nonerosive

Gastroesophageal reflux disease, erosive or nonerosive:

Initial therapy:

Mild/intermittent disease (<2 episodes/week) and no evidence of erosive esophagitis:

Note: Some experts reserve proton pump inhibitors (PPIs) for patients who have residual acid reflux symptoms despite twice-daily H2RA (Ref).

Oral: 10 mg once daily; can increase to 20 mg once daily after 4 to 8 weeks if necessary. Discontinue once asymptomatic for 8 weeks (Ref).

Severe and/or frequent symptoms (≥2 episodes/week) and/or erosive esophagitis:

Oral: 20 to 40 mg once daily; once symptoms are controlled, continue for at least 8 weeks (Ref). Subsequently, patients without erosive esophagitis or Barrett esophagus can taper to the lowest dose necessary to control symptoms (and/or switch to an H2RA blocker) then discontinue acid suppression once asymptomatic. Patients with erosive esophagitis or Barrett esophagus should continue long-term maintenance therapy with 20 mg once daily (Ref).

Residual symptoms despite 40 mg once daily therapy:

Note: Referral to a specialist is recommended.

Oral: Options include splitting the dose to 20 mg twice daily, increasing the dose to 40 mg twice daily, or switching to another PPI (Ref).

OTC labeling (patient-guided therapy):Heartburn, frequent symptoms (≥2 episodes/week):

Oral: 20 mg once daily for 14 days (maximum: 20 mg/day); may repeat a 14-day course every 4 months if needed. Seek medical referral if symptoms do not resolve within 14 days of treatment; do not take for >14 days or more often than every 4 months unless directed by a physician (Ref).

Helicobacter pylori eradication

Helicobacter pylori eradication:

Oral: 20 mg or 40 mg twice daily as part of an appropriate combination regimen with antibiotics. Dose depends on the selected regimen (Ref).

Nonsteroidal anti-inflammatory drug–induced ulcers, primary prevention

Nonsteroidal anti-inflammatory drug (including aspirin)–induced ulcers, primary prevention (off-label use):

Note: For select patients at moderate or high risk for GI toxicity. These include patients with a history of GI ulcer, on dual antiplatelet therapy (eg, aspirin plus a P2Y12 inhibitor), on concurrent anticoagulant therapy, or with multiple additional risk factors (eg, corticosteroid use, high nonsteroidal anti-inflammatory drug [NSAID] dose, H. pylori infection) (Ref). For patients on dual antiplatelet therapy, some experts reserve prophylaxis for those with additional risk factors (Ref). Due to a potential drug-drug interaction with clopidogrel, the manufacturer and some experts recommend avoiding concurrent omeprazole use (Ref); however, some studies have not identified a clinically meaningful interaction (Ref). If present, H. pylori infection should be treated first (Ref).

Oral: 20 mg once daily for the duration of high-risk NSAID use (Ref).

Peptic ulcer disease, treatment and secondary prevention

Peptic ulcer disease, treatment and secondary prevention:

Note: For patients on NSAIDs (including aspirin), the NSAID should be discontinued, if possible (Ref). If present, H. pylori infection should be treated first; uncomplicated H. pylori–associated ulcers may not need PPI treatment beyond that included in the eradication regimen (Ref).

Uncomplicated ulcer:

Oral: 20 to 40 mg once daily. Duration depends on the size, location, and cause of the ulcer and ranges from 4 to 8 weeks. In patients with refractory or recurrent disease, may increase the dose to 20 to 40 mg twice daily (Ref).

Complicated ulcer (perforation, penetration, or gastric outlet obstruction) (off-label use):

Oral: 40 mg twice daily for 4 weeks, followed by 40 mg once daily. Duration depends on the location and etiology of ulcer (Ref).

Bleeding ulcer:

Oral (preferably following initial use of an IV proton pump inhibitor): Note: Optimal preendoscopic PPI therapy is uncertain. Some experts suggest initiating high-dose IV PPI with continuous or intermittent dosing in patients with suspected active upper GI bleed prior to endoscopy (Ref). Following endoscopy, for patients with high-risk stigmata of recent bleeding (eg, active bleed, visible vessel, adherent clot), a continuous infusion of an IV PPI for at least 72 hours before transitioning to an oral PPI is recommended (Ref). Patients without high-risk stigmata of recent bleeding can be switched to an oral PPI immediately after endoscopy (Ref).

Patients with high-risk stigmata of recent bleeding on endoscopy (following IV proton pump inhibitor therapy): 40 mg twice daily for 14 days, followed by 40 mg once daily (Ref).

Patients with no high-risk stigmata of recent bleeding on endoscopy: 20 mg once daily (Ref).

Duration: The total duration of treatment depends on size, location, and cause of the ulcer, and ranges from 4 to 12 weeks (Ref).

Maintenance therapy/secondary prevention (off-label use):

Note: For select high-risk patients (eg, idiopathic ulcers, frequently recurrent ulcers, need for continued NSAID use).

Oral: 20 mg once daily (Ref).

Stress ulcer prophylaxis in select critically ill patients

Stress ulcer prophylaxis in select critically ill patients (off-label use):

Note: Used in critically ill patients with risk factors for GI bleeding (eg, coagulopathy, mechanical ventilation for >48 hours, traumatic brain injury, history of GI ulceration or bleeding within past year, extensive burns) (Ref).

Oral or via NG tube: 40 mg once daily (Ref) or 40 mg initially, then another 40 mg dose given 6 to 8 hours later, followed by 40 mg once daily (Ref). Discontinue prophylaxis once risk factors have resolved (Ref).

Zollinger-Ellison syndrome

Zollinger-Ellison syndrome:

Oral: Initial: 40 mg twice daily; if needed, may titrate upward early in therapy to a maximum of 180 mg/day; once acid output has been controlled, gradual dose reductions are usually possible; reported maintenance dosage range: 10 to 180 mg/day (mean: 60 to 70 mg/day); daily doses >80 mg are usually given in 2 divided doses; continue therapy as long as clinically indicated (Ref).

Discontinuation of therapy: 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. If the patient is receiving 40 mg once or twice daily, some experts decrease the dose by 50% every week. For patients receiving twice-daily dosing, the first dose reduction can be achieved by decreasing to once-daily AM dosing. 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

The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.

Altered kidney function: Mild to severe impairment: No dosage adjustment necessary (Ref).

Hemodialysis, intermittent (thrice weekly): Poorly dialyzed: No supplemental dose or dosage adjustment necessary (Ref).

Peritoneal dialysis: No dosage adjustment necessary (Ref).

CRRT: No dosage adjustment necessary (Ref).

PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).

Dosing: Hepatic Impairment: Adult

Mild to severe impairment (Child-Pugh class A, B, or C): 10 mg once daily when used for maintenance of healing of erosive esophagitis. There are no dosage adjustments provided for the other indications. Alternatively, a maximum dose of 20 mg/day regardless of indication, has been recommended (Ref). In a very small study, omeprazole systemic exposure and half-life increased ~2- and ~3-fold respectively, in patients with mild to severe hepatic impairment.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Capsule Delayed Release, Oral:

Generic: 10 mg, 20 mg, 40 mg

Capsule Delayed Release, Oral, as magnesium [strength expressed as base]:

Generic: 20 mg

Packet, Oral, as magnesium [strength expressed as base]:

PriLOSEC: 2.5 mg (30 ea); 10 mg (30 ea)

Tablet Delayed Release, Oral:

Generic: 20 mg, 20 mg [DSC]

Tablet Delayed Release, Oral, as magnesium [strength expressed as base]:

Acid Reducer: 20 mg [contains corn starch]

PriLOSEC OTC: 20 mg

PriLOSEC OTC: 20 mg [contains fd&c blue #2 (indigo carm) aluminum lake, fd&c red #40(allura red ac)aluminum lake, saccharin sodium; wild berry flavor]

Generic: 20 mg

Generic Equivalent Available: US

May be product dependent

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Capsule Delayed Release, Oral:

Losec: 20 mg

Generic: 10 mg, 20 mg, 40 mg [DSC]

Tablet Delayed Release, Oral:

Losec: 10 mg [DSC]

Generic: 10 mg

Tablet Delayed Release, Oral, as magnesium [strength expressed as base]:

Losec: 20 mg [DSC]

Losec Mups: 20 mg

Generic: 20 mg

Dosage Forms Considerations

First-Omeprazole oral suspension is a compounding kit. Refer to manufacturer's labeling for compounding instructions.

Medication Guide and/or Vaccine Information Statement (VIS)

An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:

Prilosec capsules: https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/022056s022lbl.pdf#page=35

Prilosec granules for oral suspension: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/022056s023lbl.pdf#page=35

Administration: Pediatric

Oral: Should be taken before meals; best if taken 30 minutes before a meal (Ref); may be administered with antacids.

Capsule: Should be swallowed whole; do not chew or crush. Delayed-release capsule may be opened and contents added to 1 tablespoon of applesauce; use immediately after adding to applesauce; do not chew or crush. Follow with a cool glass of water. Applesauce should not be heated; do not store mixture for future use.

Oral suspension: Empty the contents of the 2.5 mg packet into 5 mL of water or 10 mg packet into 15 mL of water and stir; allow the suspension to sit for 2 to 3 minutes to thicken; stir and administer within 30 minutes. If any material remains after administration, add more water, stir, and administer immediately.

Tablet: Should be swallowed whole; do not crush or chew.

Nasogastric or gastric tube administration:

Capsule: The manufacturer of Prilosec does not give recommendations for extemporaneous preparation of omeprazole capsules for NG/OG administration. Consider using the packets for oral suspension. If packets are unavailable, methods of preparation of capsules for NG/OG administration have been described (Ref). An extemporaneously prepared suspension with extended stability may also be used (Ref).

Oral suspension: Add 5 mL of water to a catheter-tipped syringe and then add the contents of a 2.5 mg packet (or 15 mL of water for the 10 mg packet), shake the suspension well, and leave to thicken for 2 to 3 minutes. Shake the syringe and administer through nasogastric or gastric tube (French size 6 or greater) within 30 minutes of reconstitution. Refill syringe with an equal amount (5 mL or 15 mL) of water, shake, and flush remaining contents through NG or gastric tube.

Administration: Adult

Oral: For most indications, administer 30 to 60 minutes before a meal; best if taken before breakfast (Ref). If administering twice daily, first dose should be administered before breakfast and the second dose before dinner (Ref).

Capsule: Swallow whole; do not chew or crush. Capsule may be opened and contents mixed with 1 tablespoon of applesauce (soft enough to swallow without chewing). Swallow immediately with a glass of cool water; mixture should not be chewed, crushed, warmed, or saved for future use.

Oral suspension: Following reconstitution, the suspension should be left to thicken for 2 to 3 minutes and administered within 30 minutes. If any material remains after administration, add more water, stir, and administer immediately.

Tablet: Swallow whole with a glass of water before morning meal; do not crush or chew.

Bariatric surgery: Tablet, delayed release: Some institutions may have specific protocols that conflict with these recommendations; refer to institutional protocols as appropriate. Oral capsule and suspension formulations are available. If safety and efficacy can be effectively monitored, no change in formulation or administration is required after bariatric surgery; however, for patients with refractory acid reflux, esophagitis, Barrett esophagus, or ulcer, it is advised to open contents of the capsule and mix with 1 tablespoon of applesauce. Swallow immediately without chewing, crushing, warming, or saving for future use. If there is inadequate response to omeprazole consider escalation of therapy to twice a day, or conversion to food independent proton pump inhibitor (omeprazole/sodium bicarbonate or dexlansoprazole).

NG/Gastric tube:

Oral suspension (using packets): Add 5 mL of water to a catheter tipped syringe and then add contents of a 2.5 mg packet (or 15 mL of water for the 10 mg packet). Immediately shake syringe and leave to thicken for 2 to 3 minutes; shake syringe again and within 30 minutes administer via NG or gastric tube (French size 6 or larger). Refill syringe with an equal amount of water, shake, and flush remaining contents through NG or gastric tube

Oral suspension (using capsules): The manufacturer of Prilosec does not give recommendations for extemporaneous preparation of omeprazole capsules for NG/OG administration. Consider using the packets for oral suspension. If packets are unavailable, methods of preparation of capsules for NG/OG administration have been described (Ref). An extemporaneously prepared suspension with extended stability may also be used (Ref).

Storage/Stability

Capsules, tablets: Store at 15°C to 30°C (59°F to 86°F). Protect from light and moisture.

Granules for oral suspension: Store at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F).

Powder for suspension (compounding kits): Refer to manufacturer's labeling.

OTC capsules: Store at 20°C to 25°C (68°F to 77°F); protect from moisture.

Use

Short-term treatment (up to 6 weeks) of erosive esophagitis due to acid-mediated gastroesophageal reflux disease (GERD) (FDA approved in ages 1 month to <1 year); short-term treatment (4 to 8 weeks) of erosive esophagitis due to acid-mediated GERD diagnosed by endoscopy (FDA approved in ages ≥1 year and adults); maintenance of healing of erosive esophagitis due to acid-mediated GERD (FDA approved in ages ≥1 year and adults); treatment of heartburn and other symptoms associated with GERD (FDA approved in ages ≥1 year and adults); short-term treatment (4 to 8 weeks) of active duodenal ulcers and active benign gastric ulcers (FDA approved in adults); treatment (in combination with clarithromycin ± amoxicillin) for Helicobacter pylori eradication in patients with duodenal ulcer disease (active or up to 1-year history) to reduce recurrence of duodenal ulcer (FDA approved in adults); long-term treatment of pathological hypersecretory conditions (eg, Zollinger-Ellison syndrome, multiple endocrine adenomas, systemic mastocytosis) (FDA approved in adults); relief of frequent (≥2 days per week) heartburn (OTC products: FDA approved in adults)

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

Omeprazole may be confused with aripiprazole, esomeprazole, fomepizole

PriLOSEC may be confused with Plendil, Prevacid, predniSONE, prilocaine, Prinivil, Pristiq, Proventil, PROzac

Older Adult: High-Risk Medication:

Beers Criteria: Proton pump inhibitors (omeprazole) 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]).

International issues:

Losec [multiple international markets] may be confused with Lasix brand name for furosemide [US, Canada, and multiple international markets]

Medral [Mexico] may be confused with Medrol brand name for methylprednisolone [US., Canada, and multiple international markets]

Norpramin: Brand name for omeprazole [Spain], but also the brand name for desipramine [US, Canada] and enalapril/hydrochlorothiazide [Portugal]

Protonix: Brand name for omeprazole [Philippines] but also the brand name for pantoprazole [US]

Adverse Reactions (Significant): Considerations
Cutaneous and systemic lupus erythematosus

Cutaneous lupus erythematosus, most often subacute cutaneous lupus erythematosus (SCLE), has been reported with use of proton pump inhibitors (PPIs), including omeprazole (Ref). SCLE is reversible (resolution ~3 months following discontinuation [range: 4 weeks to 8 months]), and cross-reactivity between PPIs has been reported (Ref). SCLE may present as a widespread skin rash which may include bullous lesions and focal skin necrosis (Ref). In addition, systemic lupus erythematosus (SLE) secondary to PPIs may occur, although less often as compared to SCLE. Presentation often includes rash, however, arthralgia or cytopenia may also occur.

Mechanism: Non-dose-related; immunologic. SCLE is typically associated with positive antinuclear antibodies (ANA), anti-Ro/SSA and anti-La/SSB antibodies (Ref).

Onset: Varied.

Cutaneous lupus erythematosus: ~8 months following treatment initiation (range: 3 days to 3.5 years) (Ref).

Systemic lupus erythematosus: According to the manufacturer, may occur within days to years after initiating treatment.

Risk factors:

• Prior history or family history of SCLE, especially secondary to PPIs (Ref)

• Presence of risk factors for SCLE (eg, female of childbearing age, periods of female hormone changes, prior history of drug allergies, sun-reactive skin, exposure to UV radiation) (Ref)

Enteric infections

Use of proton pump inhibitors (PPIs), including omeprazole, may increase risk of enteric infections in adult and pediatric patients, including gastroenteritis and Clostridioides difficile associated diarrhea (CDAD); however data are conflicting, especially with regard to CDAD (Ref). Diarrhea, which may be a result of enteric infection, is the most common adverse effect secondary to long-term PPI use and often results in treatment discontinuation (Ref). Consider CDAD diagnosis in patients with persistent diarrhea that does not improve, especially in hospitalized patients.

Mechanism: Dose-related (Ref); related to the pharmacologic action. The increase in gastric pH secondary to PPI administration leads to changes in intestinal microbial environment which may allow for intestinal germination and growth of C. difficile spores as well as colonization by other bacteria responsible for enteric infections (eg, Salmonella, Campylobacter, Shigella, norovirus) (Ref).

Onset: Varied; hospitalized patients receiving high doses may experience CDAD within days of treatment initiation (Ref) whereas others develop gastroenteritis with long-term therapy in the community setting (Ref).

Risk factors:

• High doses of PPIs (eg, daily or more frequently than daily use) (Ref)

• Hospitalized patients (Ref)

• Infants and children with defective immune systems or indwelling catheters (Ref)

Fractures

Use of proton pump inhibitors (PPIs), including omeprazole, may increase the risk of bone fracture in children, young adults, and older adults, including osteoporosis-related fractures (Ref). However, data regarding the impact of PPIs on fractures, as well as bone mineral density (BMD), are inconclusive and some have concluded that any association with fracture may be related to other independent risk factors (Ref).

Mechanism: Dose-related; related to the pharmacologic action (hypergastrinemia and hypochlorhydria). Hypergastrinemia causes secondary hyperparathyroidism which can increase bone resorption and subsequent decreased BMD. Hypochlorhydria results in decreased absorption of calcium, magnesium, and vitamin B12. Impaired calcium absorption may cause secondary hyperparathyroidism and decreased BMD. Decreased vitamin B12 absorption may decrease osteoblastic activity leading to decreased BMD, as well as decreased collagen cross-linking leading to weakened bone structure (Ref).

Onset: Delayed (≥1 year) (Ref).

Risk factors:

• Presence of risk factors for fractures and/or osteoporosis (Ref)

• Duration of therapy (eg, ≥1 year) (Ref)

• High doses of PPIs (≥1.5 doses per day) (Ref)

• Pediatric: Initiation of therapy at age <1 year or ≥6 years (Ref)

• Pediatric: Concurrent use of PPI plus H2 blocker (Ref)

Fundic gland polyps

Long-term use of proton pump inhibitors (PPIs), including omeprazole, has been associated with the development of reversible gastric polyp (fundic gland) (Ref). Most PPI users who developed fundic gland polyps were asymptomatic. Symptomatic patients may report nausea, vomiting, or abdominal pain. GI bleeding and/or anemia may occur with ulcerated polyp. Clinicians should note that Helicobacter pylori infection may be protective against fundic gland polyps as bacterial proteases help glandular outflow by breaking down blockages (Ref).

Mechanism: Time-related; long-term use of PPIs is associated with an increase in the prevalence of parietal cell protrusions which cause outflow blockage of the isthmus and subsequent formation of fundic gland cysts. As therapy continues, fundic gland cysts may enlarge and develop into fundic gland polyps (Ref).

Onset: Delayed (>1 year) (Ref).

Risk factors:

• Patients with familial adenomatous polyposis (Ref)

• Duration of treatment (>1 year and especially ≥5 years) (Ref)

Hypersensitivity reactions (immediate and delayed)

Immediate hypersensitivity reactions secondary to proton pump inhibitors (PPIs) are rare and range from urticaria and angioedema to anaphylaxis (Ref). Delayed hypersensitivity reactions include maculopapular rash (Ref) as well as rare severe cutaneous adverse reactions (SCARs) such as acute generalized exanthematous pustulosis, drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, and toxic epidermal necrolysis (Ref).

Mechanism: Non-dose-related; immunologic.

Immediate hypersensitivity reactions (eg, anaphylaxis, urticaria): IgE-mediated (Ref)

Delayed hypersensitivity reactions (including maculopapular rash and SCARs): T-cell-mediated (Ref).

Onset:

Immediate hypersensitivity reactions: Rapid; occurs within 1 hour of administration but may occur up to 6 hours after exposure (Ref).

Delayed hypersensitivity reactions:

Maculopapular reactions: Intermediate; generally occurs 7 to 10 days after initiation, but may occur up to 1 month following initiation of therapy (Ref).

Other reactions (including SCARs): Varied; occurs after 7 to 14 days up to 3 months following initiation of therapy (Ref).

Risk factors:

• Prior history of hypersensitivity reaction to PPIs (Ref)

• Cross-reactivity has been noted with PPIs, although cross-reactivity patterns have been variable (Ref)

Hypomagnesemia

Long-term use of proton pump inhibitors (PPIs), including omeprazole, has resulted in reversible hypomagnesemia (Ref). Symptoms may be severe (eg, tetany, cardiac arrhythmias, cerebellar syndrome, seizures) and resistant to treatment with supplementation (Ref). May require discontinuation of PPI in addition to magnesium supplementation in ~25% of patients. Following discontinuation, magnesium normalizes after ~1 week (Ref). Hypomagnesemia may recur if PPI therapy is restarted (Ref).

Mechanism: Time-related; the specific mechanism is unknown; however, long-term use of PPIs may be associated with changes in intestinal absorption of magnesium (Ref).

Onset: Delayed; hypomagnesemia occurs most often after 1 year of therapy but may occur as early as 3 months (Ref). In patients with prior PPI-induced hypomagnesemia, re-initiation may result in recurrence within 2 weeks (Ref).

Risk factors:

• Duration of therapy (≥3 months and especially >1 year) (Ref)

• Concurrent use of other drugs that cause hypomagnesemia (eg, digoxin, loop diuretics, thiazide diuretics) (Ref)

• Patients who have undergone kidney transplantation (Ref)

Interstitial nephritis

Acute interstitial nephritis (AIN) may occur rarely (Ref), with renal biopsy showing diffuse interstitial infiltrate and tubulitis (Ref). Patients generally achieve complete or partial recovery by 6 months following treatment of AIN (Ref). Signs of systemic hypersensitivity (fever, rash, eosinophilia) often seen in other cases of drug-induced AIN are not typically observed in proton pump inhibitor (PPI)-induced AIN (Ref). Clinicians should note that there appears to be no correlation between duration of exposure to PPI and duration or severity of acute kidney failure after resolution of AIN (Ref).

Mechanism: Non-dose-related; unknown although may be immunologic (Ref) or idiosyncratic, with direct toxic effect of omeprazole on tubular cells (Ref).

Onset: Varied; usually occurs within 3 months (Ref) although has been reported to occur up to 10 months (Ref). Upon reexposure symptoms often present more rapidly, often within 12 hours (Ref).

Risk factors:

• Older adults; although this may be due to increased use of PPIs (Ref)

• Cross-reactions among PPIs in patients who developed AIN is not known

Vitamin B12 deficiency

Long-term use of acid suppressive therapies, including omeprazole, may result in reversible vitamin B12 deficiency; however, data regarding the clinical significance of these changes and causality are conflicted (Ref).

Mechanism: Dose- and time-related; acid suppressive therapies interfere with acid-activated proteolytic digestion of dietary protein-bound vitamin B12 in the stomach, thereby resulting in malabsorption of vitamin B12 (Ref).

Onset: Delayed (Ref).

Risk factors:

• Duration of therapy (≥2 to 3 years); the association between ≥2 years of proton pump inhibitor (PPI) use and vitamin B12 deficiency was stronger among people <30 years of age and in females (Ref)

• High doses of PPIs (≥1.5 pills per day) (Ref)

• Presence of risk factors for vitamin B12 deficiency (eg, malnourished patients, vegan diet) (Ref)

Adverse Reactions

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

>10%: Respiratory: Respiratory system disorder (infants: 42%; children 1 to <2 years: 75%; children ≥2 years and adolescents: 19%)

1% to 10%:

Dermatologic: Skin rash (2%)

Gastrointestinal: Abdominal pain (5%), constipation (2%), diarrhea (4%), flatulence (3%), nausea (4%), vomiting (3%)

Nervous system: Dizziness (2%), headache (7%)

Neuromuscular & skeletal: Asthenia (1%), back pain (1%)

Respiratory: Cough (1%), upper respiratory infection (2%)

Postmarketing:

Cardiovascular: Acute coronary syndrome (Kounis syndrome) (Gázquez 2010), angina pectoris, bradycardia, chest pain, increased blood pressure, palpitations, peripheral edema (Brunner 2001), tachycardia

Dermatologic: Acute generalized exanthematous pustulosis, alopecia (Borum 1997), cutaneous lupus erythematosus (Toms-Whittle 2011), dermatitis (Jurakić Tončić 2019, Rebuck 1998), hyperhidrosis (Mamun 1999), hypertrichosis (Elosua-González 2018), maculopapular rash (Chularojanamontri 2012), pruritus (Bose 2013), skin photosensitivity, Stevens-Johnson syndrome (Lin 2018; Van Tendeloo 2020), toxic epidermal necrolysis (Lin 2018; Thakor 2009), urticaria (Bose 2013; Bowlby 1994), xeroderma

Endocrine & metabolic: Glycosuria, gynecomastia (Convens 1991), hypocalcemia (Shabajee 2008), hypoglycemia, hypokalemia (Maeda 2011), hypomagnesemia (Shabajee 2008), hyponatremia (Shiba 1996), vitamin B12 deficiency (Lam 2013), weight gain

Gastrointestinal: Abdominal swelling, anorexia, Clostridioides difficile associated diarrhea (Li 2017), colitis (microscopic) (Wilcox 2009), dysgeusia (Markitiziu 1996), esophageal candidiasis (Larner 1992, Sood 1995), fecal discoloration, gastric polyp (fundic gland; with chronic use [>1 year]: common: ≥10%) (Jalving 2006), gastroenteritis (adult and pediatric patients) (Canani 2006, Houben 2017, Wei 2017), irritable bowel syndrome, pancreatitis (Youssef 2005), sore throat, stomatitis, tongue mucosa atrophy, xerostomia (Teare 1995)

Genitourinary: Hematuria (Myers 2001), microscopic pyuria (Myers 2001), proteinuria (Myers 2001), testicular pain, urinary frequency, urinary tract infection

Hematologic & oncologic: Agranulocytosis (Ottervanger 1995), anemia (iron deficiency) (Imai 2018), benign polyp of the stomach (Miyamoto 2017), hemolytic anemia (Marks 1991), leukocytosis, leukopenia (Odou 1999), neutropenia (Gouraud 2010, Holt 1999), pancytopenia, petechia, thrombocytopenia (Kallam 2015)

Hepatic: Cholestatic hepatitis, hepatic encephalopathy, hepatic failure (Jochem 1992), hepatic necrosis, hepatocellular hepatitis, hepatotoxicity (idiosyncratic) (Chalasani 2014)

Hypersensitivity: Anaphylactic shock (González-Rubio 2017), anaphylaxis (Bose 2013; Galindo 1999), angioedema (Bose 2013; Bowlby 1994)

Immunologic: Drug reaction with eosinophilia and systemic symptoms (Lin 2018)

Nervous system: Abnormal dreams, aggressive behavior, agitation, anterior ischemic optic neuropathy (Schonhofer 1997), anxiety, apathy, confusion, dementia (Gomm 2016), depression, drowsiness, fatigue, hallucination (Sebastián Domingo 2018), insomnia, myasthenia, nervousness, pain, paresthesia, sleep disturbance, vertigo

Neuromuscular & skeletal: Arthralgia (Beutler 1994), bone fracture (Nassar 2018), lower leg pain, muscle cramps, myalgia, systemic lupus erythematosus, tremor

Ophthalmic: Blurred vision, diplopia, dry eye syndrome, eye irritation, optic atrophy, optic neuritis

Otic: Tinnitus

Renal: Acute interstitial nephritis (Klassen 2013; Yip 1997), renal disease (chronic; Lazarus 2016)

Respiratory: Bronchospasm, epistaxis, pneumonia (community-acquired; in pediatric patients 4 to 36 months of age) (Canani 2006)

Miscellaneous: Fever

Contraindications

Hypersensitivity (eg, anaphylaxis, anaphylactic shock, angioedema, bronchospasm, acute tubulointerstitial nephritis, urticaria) to omeprazole, other substituted benzimidazole proton pump inhibitors, or any component of the formulation; concomitant use with products that contain rilpivirine

OTC labeling: When used for self-medication (OTC), do not use if trouble or pain when swallowing food; vomiting with blood, or bloody or black stools; heartburn with lightheadedness, dizziness, or sweating; chest pain or shoulder pain with shortness of breath, sweating, pain spreading to arms, neck or shoulders, or lightheadedness; frequent chest pain.

Warnings/Precautions

Concerns related to adverse effects:

• Carcinoma: In long-term (2-year) studies in rats, omeprazole produced a dose-related increase in gastric carcinoid tumors. While available endoscopic evaluations and histologic examinations of biopsy specimens from human stomachs have not detected a risk from short-term exposure to omeprazole, further human data on the effect of sustained hypochlorhydria and hypergastrinemia are needed to rule out the possibility of an increased risk for the development of tumors in humans receiving long-term therapy.

Disease-related concerns:

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

• Hepatic impairment: In patients with hepatic impairment (Child-Pugh class A, B, or C) exposure to omeprazole is increased; dosage reduction is recommended.

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). 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).

Special populations:

• Asian ethnicity: Bioavailability is increased in patients of Asian descent; dosage reduction is recommended for maintenance healing of erosive esophagitis.

• Older adult: Bioavailability may be increased in older adults.

Dosage form specific issues:

• Benzyl alcohol and derivatives: Some dosage forms may contain benzyl alcohol; large amounts of benzyl alcohol (≥99 mg/kg/day) have been associated with a potentially fatal toxicity (“gasping syndrome”) in neonates; the “gasping syndrome” consists of metabolic acidosis, respiratory distress, gasping respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension, and cardiovascular collapse (AAP ["Inactive" 1997]; CDC 1982); some data suggests that benzoate displaces bilirubin from protein binding sites (Ahlfors 2001); avoid or use dosage forms containing benzyl alcohol with caution in neonates. See manufacturer's labeling.

Other warnings/precautions:

• Appropriate use: Helicobacter pylori eradication: Short-term combination therapy (≤7 days) has been associated with a higher incidence of treatment failure. The American College of Gastroenterology recommends 10 to 14 days of therapy (triple or quadruple) for eradication of H. pylori (Chey 2017).

• 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 omeprazole treatment at least 14 days before CgA test; if initial CgA levels are high, repeat test to confirm. Use same commercial laboratory for testing to prevent variable results.

• Self-medication (OTC use): When used for self-medication (OTC), notify health care provider before use if any of the following are present: heartburn for >3 months; frequent wheezing, particularly with heartburn; unexplained weight loss; nausea or vomiting; or stomach pain. Discontinue use and notify health care provider if heartburn continues or worsens; diarrhea occurs; if >14 days of therapy is needed; or if >1 course of therapy is needed every 4 months.

Warnings: Additional Pediatric Considerations

Routine use in preterm infants is not recommended (AAP [Eichenwald 2018]).

Metabolism/Transport Effects

Substrate of CYP2A6 (minor), CYP2C19 (major), CYP2C9 (minor), CYP2D6 (minor), CYP3A4 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits CYP2C19 (weak), OAT1/3

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.

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

Acalabrutinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease the serum concentration of Acalabrutinib. 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

Cilostazol: Omeprazole may increase serum concentrations of the active metabolite(s) of Cilostazol. Omeprazole may increase the serum concentration of Cilostazol. Management: Reduce the cilostazol dose to 50 mg twice daily in patients who are also receiving omeprazole. Monitor clinical response to cilostazol closely. Risk D: Consider therapy modification

Citalopram: Omeprazole may increase the serum concentration of Citalopram. Management: Limit citalopram dose to a maximum of 20 mg/day if used with omeprazole. Monitor for evidence of citalopram toxicity (eg, serotonin syndrome, QT prolongation) in patients receiving this combination. Risk D: Consider therapy modification

CloBAZam: CYP2C19 Inhibitors (Weak) may increase serum concentrations of the active metabolite(s) of CloBAZam. CYP2C19 Inhibitors (Weak) may increase the serum concentration of CloBAZam. Risk C: Monitor therapy

Clofarabine: OAT1/3 Inhibitors may increase the serum concentration of Clofarabine. Risk C: Monitor therapy

Clopidogrel: Omeprazole may diminish the antiplatelet effect of Clopidogrel. Omeprazole may decrease serum concentrations of the active metabolite(s) of Clopidogrel. Risk X: Avoid combination

CloZAPine: Omeprazole may decrease the serum concentration of CloZAPine. Omeprazole may increase the serum concentration of CloZAPine. Risk C: Monitor therapy

CycloSPORINE (Systemic): Omeprazole may increase the serum concentration of CycloSPORINE (Systemic). Risk C: Monitor therapy

CYP2C19 Inducers (Moderate): May decrease the serum concentration of Omeprazole. Risk C: Monitor therapy

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

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

CYP2C19 Inhibitors (Strong): May increase the serum concentration of Omeprazole. 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

Darunavir: May decrease the serum concentration of Omeprazole. Risk C: Monitor therapy

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

Dichlorphenamide: OAT1/3 Inhibitors may increase the serum concentration of Dichlorphenamide. 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

Escitalopram: Omeprazole may increase the serum concentration of Escitalopram. Risk C: Monitor therapy

Fosphenytoin-Phenytoin: CYP2C19 Inhibitors (Weak) may increase the serum concentration of Fosphenytoin-Phenytoin. Risk C: Monitor therapy

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

Gliclazide: Omeprazole may increase the serum concentration of Gliclazide. Risk C: Monitor therapy

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 CYP2C19 Substrates (High risk with Inducers). Risk C: Monitor therapy

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

Mavacamten: CYP2C19 Inhibitors (Weak) may increase the serum concentration of Mavacamten. Management: Start mavacamten at 5 mg/day if stable on a weak CYP2C19 inhibitor. For those stable on mavacamten who are initiating a weak CYP2C19 inhibitor, reduce mavacamten dose by one dose level. Risk D: Consider therapy modification

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

Moclobemide: May increase the serum concentration of Omeprazole. Omeprazole may increase the serum concentration of Moclobemide. Risk C: Monitor therapy

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

St John's Wort: May decrease the serum concentration of Omeprazole. 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): Omeprazole may increase the serum concentration of Vitamin K Antagonists. Risk C: Monitor therapy

Voriconazole: Omeprazole may increase the serum concentration of Voriconazole. Voriconazole may increase the serum concentration of Omeprazole. 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

Available data have not shown an increased risk of major birth defects following maternal use of omeprazole during pregnancy.

Recommendations for the treatment of GERD in pregnancy are available. As in nonpregnant patients, lifestyle modifications followed by other medications are the initial treatments (ACG [Katz 2013]; Body 2016; Huerta-Iga 2016; van der Woude 2014). Based on available data, PPIs may be used when clinically indicated (Body 2016; Matok 2012; Pasternak 2010; van der Woude 2014).

Mechanism of Action

Proton pump inhibitor; suppresses gastric basal and stimulated acid secretion by inhibiting the parietal cell H+/K+ ATP pump

Pharmacokinetics (Adult data unless noted)

Note: Half-life and AUC were significantly reduced for omeprazole suspension when compared with an equivalent dose via the commercially available capsule in 7 adults (Song 2001).

Onset of action: Antisecretory: ~1 hour

Peak effect: Within 2 hours

Duration: Up to 72 hours; 50% of maximum effect at 24 hours; after stopping treatment, secretory activity gradually returns over 3 to 5 days

Maximum secretory inhibition: 4 days

Absorption: Rapid

Protein binding: ~95%

Metabolism: Hepatic via CYP2C19 primarily and (to a lesser extent) via 3A4 to hydroxy, desmethyl, and sulfone metabolites (all inactive); saturable first-pass effect

Bioavailability: Oral: ~30% to 40%; Hepatic dysfunction: ~100%; Asians: AUC increased up to fourfold compared to Caucasians

Half-life elimination: 0.5 to 1 hour; hepatic impairment: ~3 hours

Time to peak, plasma: 0.5 to 3.5 hours

Excretion: Urine (~77% as metabolites, very small amount as unchanged drug); feces

Clearance: 500-600 mL/minute; chronic hepatic disease: 70 mL/minute

Pharmacokinetics: Additional Considerations

Altered kidney function: There is slight increase in bioavailability in patients whose CrCl ranged between 10 and 62 mL/minute/1.73 m2.

Hepatic function impairment: In patients with hepatic impairment (Child-Pugh class A, B, or C), bioavailability is increased ~100%, plasma half-life is increased, and plasma clearance is decreased.

Older adult: The elimination rate is decreased; bioavailability is increased.

Race/ethnicity: AUC is increased ~4-fold in Asian patients.

Extemporaneous Preparations

Note: A more palatable omeprazole (2 mg/mL) suspension is commercially available as a compounding kit (First-Omeprazole).

2 mg/mL Oral Solution

A 2 mg/mL oral omeprazole solution (Simplified Omeprazole Solution) may be made with five omeprazole 20 mg delayed release capsules and 50 mL sodium bicarbonate 8.4%. Empty capsules into beaker. Add sodium bicarbonate solution. Gently stir (about 15 minutes) until a white suspension forms. Transfer to amber-colored syringe or bottle. Stable for 14 days at room temperature or for 30 days refrigerated.

DiGiacinto JL, Olsen KM, Bergman KL, et al, “Stability of Suspension Formulations of Lansoprazole and Omeprazole Stored in Amber-Colored Plastic Oral Syringes,” Ann Pharmacother, 2000, 34(5):600-5.10852086
Quercia R, Fan C, Liu X, et al, “Stability of Omeprazole in an Extemporaneously Prepared Oral Liquid,” Am J Health Syst Pharm, 1997, 54(16):1833-6.9269520
Sharma V, “Comparison of 24-hour Intragastric pH Using Four Liquid Formulations of Lansoprazole and Omeprazole,” Am J Health Syst Pharm, 1999, 56(23 Suppl 4):18-21.10597120
Pricing: US

Capsule, delayed release (Omeprazole Magnesium Oral)

20.6 (20 Base) mg (per each): $0.59 - $0.77

Capsule, delayed release (Omeprazole Oral)

10 mg (per each): $3.01 - $3.99

20 mg (per each): $0.27 - $4.45

40 mg (per each): $6.69 - $7.40

Pack (PriLOSEC Oral)

2.5 mg (per each): $16.61

10 mg (per each): $16.61

Tablet, EC (Omeprazole Magnesium Oral)

20 mg (per each): $0.60 - $0.81

Tablet, EC (Omeprazole Oral)

20 mg (per each): $0.62 - $0.94

Tablet, EC (PriLOSEC OTC Oral)

20 mg (per each): $0.86

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.

Brand Names: International
  • Acidcare (BE);
  • Acifre (PH);
  • Acimax (AU);
  • Aleprozil (MX);
  • Amelxess (EG);
  • Antra (AT, IT);
  • Arapride (ES);
  • Aulcer (ES);
  • Azoran (MX);
  • Baromezole (VN);
  • Benzol (MT);
  • Crismel (HU);
  • Desec (TH);
  • Domer (MX);
  • Dudencer (HK);
  • Duogas (TH);
  • Epirazole (AE, CY, EG, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Eucid (TH);
  • Eupept (BR);
  • Ezrazole (PH);
  • Gasec (BB, BM, BS, BZ, EC, GY, HK, JM, MY, SR, TT, UA);
  • Gasec Gastrocaps (BF, BJ, CI, ET, GH, GM, GN, KE, LR, MA, ML, MR, MU, MW, NE, NG, SC, SD, SL, SN, TN, TZ, UG, ZM);
  • Gastec (AR);
  • Gastop (PE);
  • Gastracid (DE);
  • Gastrofer (ID);
  • Gemzole (PH);
  • Getzone (VN);
  • Healor (BD);
  • Helizol (EC);
  • Hyposec (AE, CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Inhibitron (CR, DO, GT, HN, MX, NI, PA, SV);
  • Lensor (LU);
  • Locid (ET);
  • Logastric (BE);
  • Lokev (ID);
  • Lokit (ET);
  • Lomac (IN);
  • Lomex (PY);
  • Lopraz (IE);
  • Losamel (IE);
  • Losec (AE, AR, AT, AU, BB, BE, BF, BH, BJ, BM, BR, BS, BZ, CI, CY, CZ, DK, EE, EG, ES, ET, FI, GB, GH, GM, GN, GR, GY, HK, HU, IE, IL, IQ, IR, IS, IT, JM, JO, KE, KW, LB, LR, LU, LY, MA, ML, MR, MT, MU, MW, MX, MY, NE, NG, NL, NZ, OM, PH, PK, PL, PT, PY, QA, RO, RU, SA, SC, SD, SE, SL, SN, SR, SY, TN, TR, TZ, UG, UY, VE, VN, YE, ZM);
  • Losec MUPS (CO, EG, MY, PH);
  • Loseprazol (SI);
  • Luodan (CN);
  • Madiprazole (TH);
  • Maxor (AU);
  • Medoprazole (BF, BJ, CI, ET, GH, GM, GN, KE, LR, MA, ML, MR, MT, MU, MW, MY, NE, NG, SC, SD, SL, SN, TN, TZ, UG, ZM);
  • Mepha Gasec (CR, DO, GT, HN, NI, PA, SV);
  • Mepracid (PH);
  • Minisec (BH);
  • Miracid (TH);
  • Mopral (FR, MX);
  • Nexium Control (HR);
  • Nocid (HK, TH);
  • Ocid (ET, IN, LK, SG);
  • Ogal (CO, PE);
  • Olexin (MX);
  • Olit (SG);
  • Om (BD);
  • Omed (BF, BJ, CH, CI, ET, GH, GM, GN, ID, IN, KE, KR, LR, MA, ML, MR, MU, MW, NE, NG, SC, SD, SL, SN, TN, TZ, UG, ZM);
  • Omedar (AE, CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Omegut (PH);
  • Omelon (MY, TW);
  • Omep (BD, HK, UA);
  • OMEP (DE);
  • Omepra (IL);
  • Omepradex (IL);
  • Omepradex-Z (IL);
  • Omepral (AU, JP);
  • Omeprazon (JP);
  • Omepril (EC);
  • Omeq (KR);
  • Omesec (HK, MY, SG);
  • Omesel (VN);
  • Omex (CO);
  • Omezol (AE, CY, IN, IQ, IR, JO, KW, LB, LY, NZ, OM, SA, SY, YE);
  • Omezole (HK, SG, TW);
  • Omezzol (EC);
  • Omicap (ZW);
  • Omilock (MY);
  • Omipin (PH);
  • Omisec (AE, CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Omiz (BH, QA);
  • Omizac (IN, ZW);
  • Omizec (HK);
  • OMP (KR);
  • Ompranyt (MT);
  • Omprazole (KR);
  • OMZ (ID);
  • Onic (ID);
  • Opal (PE);
  • Opel (PH);
  • Oprax (PE);
  • Oprazole (AE, BH, JO, KW, LB, QA, SA);
  • Orazole (CR, DO, GT, HN, NI, PA, SV);
  • Ortanol (HR);
  • Ozmep (AU);
  • Parizac (ES);
  • Penrazole (SG);
  • Peptaz (LK);
  • Peptizole (TH);
  • Prazidec (MX);
  • Prazole (TH);
  • Prenome (BE);
  • Probitor (AU, BG, MY, SG, ZW);
  • Proceptin (SG);
  • Promezol (ID);
  • Protonix (PH);
  • Pumpitor (ID, LK, SG);
  • Pumpitor DI (ID);
  • Qrazol (KR);
  • Ramezol (KR);
  • Reglacid (BE);
  • Result (KR);
  • Risek (AE, BH, ET, JO, KW, LB, MY, PH, QA, SA);
  • Romep (IE);
  • Sedacid (BE);
  • Siozole (IN);
  • Stomacer (ID);
  • Stomec (TH);
  • Suifac (MX);
  • Trisec (LK);
  • Ulceral (QA);
  • Ulcozol (EC, PE);
  • Ulnor (DE);
  • Ulpraz (ID);
  • Ulsen (MX);
  • Ultop (HR, UA);
  • Ulzec (ZA);
  • Ulzol (ID);
  • Vescomecid (TH);
  • Viprazo (PH);
  • Vulcasid (MX);
  • Wonmp (KR);
  • Xeldrin (BD);
  • Xoprin (PE);
  • Zatrol (CL);
  • Zefxon (MY, TH);
  • Zenpro (MY, SG);
  • Zenprol (HK);
  • Zimor (MY, SG);
  • Ziom (LK);
  • Zpmacid (ZW)


For country code abbreviations (show table)
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  67. FDA Drug Safety Communication. Low magnesium levels can be associated with long-term use of Proton Pump Inhibitor drugs (PPIs). https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-low-magnesium-levels-can-be-associated-long-term-use-proton-pump. March 2, 2011.
  68. Feldman M. NSAIDs (including aspirin): Secondary prevention of gastroduodenal toxicity. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed August 28, 2019b.
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