Version July 2025
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).
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 (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 (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.
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).
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.
(For additional information see "Omeprazole: Drug information")
Dosage guidance:
Clinical considerations: Avoid coadministration with other antisecretory agents 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).
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 (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 (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:
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:
Oral: 20 or 40 mg twice daily for 14 days as part of an appropriate combination regimen with antibiotics. Dose depends on the selected regimen (Ref).
NSAID (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:
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 critically ill patients (off-label use):
Oral: 40 mg once daily; discontinue prophylaxis once risk factors have resolved (Ref).
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.
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).
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.
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 (median time to resolution: 4 weeks following discontinuation [range: 3 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: Median time to onset has been reported between 6 weeks and ~8 months following treatment initiation in PPI-naive patients (range: 3 days to 12 years) (Ref). A more rapid onset (median: 2 weeks; range: 0.43 to 4 weeks) has been reported in patients with a prior history of PPI-induced SCLE (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)
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); recurrent CDAD may occur with continued PPI use (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). An increased risk for the development of CDAD may persist for months following discontinuation of PPI therapy (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)
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)
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)
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 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). A more rapid onset of DRESS (4 days) has been reported with omeprazole (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)
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 2 to 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, loop diuretics, thiazide diuretics) (Ref)
• Patients who have undergone kidney transplantation (Ref)
Acute interstitial nephritis (AIN) may occur rarely with proton-pump inhibitors (PPIs) (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 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 after years of treatment (Ref). Upon reexposure symptoms often present more rapidly, often within 12 hours (Ref).
Risk factors:
• Older adults (Ref); although this may be due to increased use of PPIs (Ref). An analysis of cases of PPI-associated acute kidney injury within the Food and Drug Administration Adverse Event Reporting System (FAERS) found that middle-aged patients (45 to 64 years of age) were affected more often than patients >65 years of age (Ref).
• Concomitant use of other nephrotoxic drugs may be associated with an increased risk of PPI-induced acute kidney injury (AKI) (Ref)
• Cross-reactions among PPIs in patients who developed AIN is not known
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). A stronger association between long-term proton-pump inhibitor (PPI) use and vitamin B12 deficiency has been observed in patients <40 years of age as compared to older patients (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)
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: Asthenia (1%), dizziness (2%), headache (7%)
Neuromuscular & skeletal: Back pain (1%)
Respiratory: Cough (1%), upper respiratory infection (2%)
Postmarketing:
Cardiovascular: Acute coronary syndrome (Kounis syndrome) (Ref), angina pectoris, bradycardia, chest pain, increased blood pressure, palpitations, peripheral edema (Ref), tachycardia
Dermatologic: Acute generalized exanthematous pustulosis, alopecia (Ref), cutaneous lupus erythematosus (Ref), dermatitis (Ref), hyperhidrosis (Ref), hypertrichosis (Ref), maculopapular rash (Ref), pruritus (Ref), skin photosensitivity, Stevens-Johnson syndrome (Ref), toxic epidermal necrolysis (Ref), urticaria (Ref), xeroderma
Endocrine & metabolic: Galactorrhea not associated with childbirth (Ref), gynecomastia (Ref), hypocalcemia (Ref), hypoglycemia, hypokalemia (Ref), hypomagnesemia (Ref), hyponatremia (Ref), vitamin B12 deficiency (Ref), weight gain
Gastrointestinal: Abdominal swelling, anorexia, benign polyp of the stomach (Ref), Clostridioides difficile-associated diarrhea (Ref), colitis (microscopic) (Ref), dysgeusia (Ref), esophageal candidiasis (Ref), fecal discoloration, gastric polyp (fundic gland; with chronic use [>1 year]) (Ref), gastroenteritis (Ref), irritable bowel syndrome, pancreatitis (Ref), stomatitis, tongue mucosa atrophy, xerostomia (Ref)
Genitourinary: Erectile dysfunction, glycosuria, hematuria (Ref), microscopic pyuria (Ref), proteinuria (Ref), testicular pain, urinary frequency, urinary tract infection
Hematologic & oncologic: Agranulocytosis (Ref), anemia (including iron deficiency anemia) (Ref), hemolytic anemia (Ref), leukocytosis, leukopenia (Ref), neutropenia (Ref), pancytopenia, petechia, thrombocytopenia (Ref)
Hepatic: Cholestatic hepatitis, hepatic encephalopathy, hepatic failure (Ref), hepatic necrosis, hepatocellular hepatitis, hepatotoxicity (idiosyncratic) (Ref)
Hypersensitivity: Anaphylactic shock (Ref), anaphylaxis (Ref), angioedema (Ref), drug reaction with eosinophilia and systemic symptoms (Ref)
Nervous system: Abnormal dreams, aggressive behavior, agitation, anxiety, apathy, confusion, dementia (Ref), depression, drowsiness, fatigue, hallucination (Ref), insomnia, myasthenia, nervousness, pain, paresthesia, sleep disturbance, tremor, vertigo
Neuromuscular & skeletal: Arthralgia (Ref), bone fracture (Ref), lower leg pain, muscle cramps, myalgia, systemic lupus erythematosus
Ophthalmic: Anterior ischemic optic neuropathy (Ref), blurred vision, diplopia, dry eye syndrome, eye irritation, optic atrophy, optic neuritis
Otic: Tinnitus
Renal: Acute interstitial nephritis (Ref), acute kidney injury (Ref), kidney disease (chronic, including progression) (Ref)
Respiratory: Bronchospasm, epistaxis, pharyngitis, pneumonia (community-acquired; in pediatric patients 4 to 36 months of age) (Ref)
Miscellaneous: Fever
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.
Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
OTC labeling: When used for self-medication (OTC), do not use if hypersensitive to omeprazole or any component of the formulation; 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.
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.
• Bariatric surgery: Presurgical assessment of the indication for use, symptoms, and goals of therapy should be documented to enable postsurgical assessment. Small pharmacokinetic studies show wide interpatient variability in bioavailability and absorption of omeprazole in the first 6 months following Roux-en-Y gastric bypass (Ref). Monitor for continued efficacy after bariatric surgery and consider switching to an alternative medication if symptoms worsen.
• 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:
• 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.
Routine use in preterm infants is not recommended (AAP [Eichenwald 2018]).
First-Omeprazole oral suspension is a compounding kit. Refer to manufacturer's labeling for compounding instructions.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
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:
FT Omeprazole: 20 mg
FT Omeprazole: 20 mg [contains carmine (cochineal extract), fd&c blue #2 (indigo carm) aluminum lake, menthol; berry flavor]
Generic: 20 mg
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
May be product dependent
Capsule, delayed release (Omeprazole Magnesium Oral)
20.6 (20 Base) mg (per each): $0.46 - $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): $18.10
10 mg (per each): $18.10
Tablet, EC (Omeprazole Magnesium Oral)
20 mg (per each): $0.60 - $0.81
Tablet, EC (Omeprazole Oral)
20 mg (per each): $0.26 - $0.94
Tablet, EC (PriLOSEC OTC Oral)
20 mg (per each): $0.86
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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:
Generic: 10 mg
Tablet Delayed Release, Oral, as magnesium [strength expressed as base]:
Losec: 20 mg [DSC]
Losec Mups: 20 mg
Generic: 20 mg
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.
The following recommendations are based upon the best available evidence and clinical expertise. Senior editorial team: Joseph I. Boullata, PharmD, RPh, CNS-S, FASPEN, FACN; Peggi A. Guenter, PhD, RN, FASPEN; Kathleen Gura, PharmD, BCNSP, FASHP, FASPEN, FPPA, FMSHP; Mark G. Klang, MS, RPh, BCNSP, PhD, FASPEN; Linda Lord, NP, ACNP-BC, CNSC, FASPEN; Lucas E. Orth, PharmD, BCPPS; Russel J. Roberts, PharmD, BCCCP, FCCM.
Note: Recommendations may not account for differences in inactive ingredients, osmolality, or other formulation properties that may vary among products from different manufacturers.
Oral: Should be taken before meals; best if taken 30 minutes before a meal (Ref); may be administered with antacids.
Capsule, delayed release: Should be swallowed whole; do not chew or crush.
Oral administration in applesauce: Open capsule and sprinkle contents on 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.
Administration via feeding tube: Not recommended: Opening capsules could lead to degradation of granules and decreased efficacy (Ref); the size of granules within capsules is variable and may increase the risk of feeding tube occlusion (Ref). Both water and acidic juice (eg, apple juice) may cause granules to become sticky and occlude enteral feeding tubes (Ref). Note: An extemporaneously compounded mixture using delayed-release capsules and sodium bicarbonate as a diluent has been suggested and may be considered when alternatives are not available (Ref).
Oral packet for 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.
Administration via feeding tube:
Gastric (eg, NG, G-tube) or post-pyloric (eg, J-tube) tubes (≥6 French): To optimize effectiveness, omeprazole should be separated from enteral nutrition (Ref). If using a 2.5 mg packet, add 5 mL of purified water to enteral dosing syringe, then add granules from packet. If using a 10 mg packet, add 15 mL of purified water to an enteral dosing syringe, then add granules from packet. Immediately shake syringe and leave to thicken for 2 to 3 minutes; shake syringe again and administer via feeding tube within 30 minutes. Refill the syringe with an equal amount of purified water (eg, 5 mL for a 2.5 mg packet; 15 mL for a 10 mg packet), shake syringe and flush enteral feeding tube to ensure delivery of entire dose (Ref).
General guidance: Hold enteral nutrition 30 to 60 minutes prior to omeprazole administration (Ref). Flush feeding tube with the lowest volume of purified water necessary to clear the tube prior to administration based on size of patient and/or feeding tube (eg, neonates: 1 to 3 mL; infants and children: 2 to 5 mL; adolescents: 15 mL); refer to institutional policies and procedures (Ref). Following administration process described above, flush feeding tube with an appropriate volume of purified water and restart enteral nutrition (Ref).
Tablet, delayed release (OTC product): Should be swallowed whole; do not crush or chew.
Administration via feeding tube: NOT recommended: Crushing delayed-release omeprazole tablets may cause gastric degradation of the active ingredient and decreased bioavailability. Additionally, enteric coating may clump and cause enteral feeding tube obstruction (Ref).
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: Omeprazole is available as delayed-release formulations. Bariatric surgery may significantly alter the release characteristics in an unknown manner. Providers should determine if the condition being treated can be safely monitored or if a switch to an alternative medication is necessary (Ref).
Enteral feeding tube:
The following recommendations are based upon the best available evidence and clinical expertise. Senior editorial team: Joseph I. Boullata, PharmD, RPh, CNS-S, FASPEN, FACN; Peggi A. Guenter, PhD, RN, FASPEN; Kathleen Gura, PharmD, BCNSP, FASHP, FASPEN, FPPA, FMSHP; Mark G. Klang, MS, RPh, BCNSP, PhD, FASPEN; Linda Lord, NP, ACNP-BC, CNSC, FASPEN; Lucas E. Orth, PharmD, BCPPS; Russel J. Roberts, PharmD, BCCCP, FCCM.
Oral capsule, delayed release: Enteral feeding tube administration utilizing delayed-release, enteric-coated omeprazole is not recommended (Ref). Opening capsules could lead to degradation of granules and decreased efficacy (Ref); the size of granules within capsules are variable and may increase the risk of feeding tube occlusion (Ref). Both water and acidic juice (eg, apple juice) may cause granules to become sticky and occlude enteral feeding tubes (Ref). Note: An extemporaneously compounded mixture using delayed-release capsules and sodium bicarbonate as a diluent has been suggested and may be considered when alternatives are not available (Ref).
Oral packet for suspension:
Gastric (eg, NG, G-tube ) or postpyloric (eg, J-tube) tubes (≥6 French): To optimize effectiveness, omeprazole should be separated from enteral nutrition (EN) (Ref). If using a 2.5 mg packet, add 5 mL of purified water to enteral dosing syringe, then add granules from packet. If using a 10 mg packet, add 15 mL of purified water to an enteral dosing syringe, then add granules from packet. Immediately shake syringe and leave to thicken for 2 to 3 minutes; shake syringe again and administer via feeding tube within 30 minutes (Ref).
General guidance: Hold EN 30 to 60 minutes prior to omeprazole administration (Ref). Flush feeding tube with an appropriate volume of purified water (eg, 15 mL) before administration (Ref). Following administration, rinse enteral dosing syringe used for preparation with an equal amount of purified water (eg, 5 mL for a 2.5 mg packet; 15 mL for a 10 mg packet), shake the syringe, and administer contents to ensure delivery of entire dose (Ref). Flush feeding tube with an appropriate volume of purified water (eg, 15 mL) and restart EN (Ref).
Oral tablet, delayed release: Enteral feeding tube administration utilizing omeprazole delayed-release tablets is not recommended (Ref). Crushing delayed-release omeprazole tablets may cause gastric degradation of the active ingredient and decreased bioavailability. Additionally, enteric coating may clump and cause enteral feeding tube obstruction (Ref).
Oral tablet, disintegrating, delayed release:
Gastric (eg, NG, G-tube) or postpyloric (eg, J-tube) tubes (≥16 French): To optimize effectiveness, omeprazole should be separated from EN (Ref). Remove plunger from an empty enteral dosing syringe and place orally disintegrating omeprazole tablet(s) into syringe barrel. Replace the syringe plunger and draw up 10 to 20 mL purified water. Cap the end of the syringe and allow tablet to disintegrate, shaking gently as needed; administer via feeding tube (Ref).
Dosage form information: Tablets disintegrate into small granules, which may occlude enteral dosing syringes and/or enteral feeding tubes, especially small-bore feeding tubes (Ref).
General guidance: Hold EN 30 to 60 minutes prior to omeprazole administration (Ref). Flush feeding tube with an appropriate volume of purified water (eg, 15 mL) before administration (Ref). Following administration, rinse enteral dosing syringe used for preparation with purified water (eg, 10 to 20 mL); administer contents to ensure delivery of entire dose (Ref). Flush feeding tube with an appropriate volume of purified water (eg, 15 mL) and restart EN (Ref).
Note: Recommendations may not account for differences in inactive ingredients, osmolality, or other formulation properties that may vary among products from different manufacturers.
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.
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/2023/022056s026lbl.pdf#page=34
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)
Omeprazole may be confused with ARIPiprazole, esomeprazole, fomepizole
PriLOSEC may be confused with Plendil, Prevacid, predniSONE, prilocaine, Prinivil, Pristiq, Proventil, PROzac
Omeprazole is identified in the Beers Criteria as a potentially inappropriate medication to be avoided (as scheduled use for >8 weeks) in patients 65 years and older due to its risk of C. difficile infection, pneumonia, GI malignancies, and bone loss/fractures unless given for high-risk patients (eg, oral corticosteroid or chronic NSAID use), patients with erosive esophagitis, Barrett’s esophagitis, a pathological hypersecretory condition, or if the patient has demonstrated a need for maintenance therapy (eg, failure of drug discontinuation trial or failure of H2 blockers) (Beers Criteria [AGS 2023]).
Omeprazole is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication in older adults (≥65 years of age) at a full therapeutic dosage for longer than 8 weeks for the treatment of uncomplicated peptic ulcer disease (O’Mahony 2023).
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]
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;
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 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 drug interactions program
Acalabrutinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Acalabrutinib. This interaction is only applicable to acalabrutinib capsules. Risk X: Avoid
Afatinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease therapeutic effects of Afatinib. Risk C: Monitor
Amphetamines: Inhibitors of the Proton Pump (PPIs and PCABs) may increase absorption of Amphetamines. Specifically, the amphetamine absorption rate may be increased in the first hours after dosing. Risk C: Monitor
Atazanavir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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 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 decrease therapeutic effects of Bisphosphonate Derivatives. Risk C: Monitor
Bosutinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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 decrease therapeutic effects of Capecitabine. Risk C: Monitor
CarBAMazepine: May decrease serum concentration of Omeprazole. Omeprazole may increase serum concentration of CarBAMazepine. Risk C: Monitor
Cefditoren: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Cefditoren. Risk X: Avoid
Cefpodoxime: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Cefpodoxime. Risk C: Monitor
Cefuroxime: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease absorption of Cefuroxime. Management: Avoid concomitant use of oral cefuroxime axetil and proton pump inhibitors (PPIs) or potassium-competitive acid blockers (PCABs) when possible. If combined, ensure oral cefuroxime axetil is taken with food to minimize the magnitude of this interaction. Risk D: Consider Therapy Modification
Cilostazol: Omeprazole may increase serum concentration of Cilostazol. Omeprazole may increase active metabolite exposure 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 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 concentration of CloBAZam. CYP2C19 Inhibitors (Weak) may increase active metabolite exposure of CloBAZam. Risk C: Monitor
Clofarabine: OAT1/3 Inhibitors may increase serum concentration of Clofarabine. Risk C: Monitor
Clopidogrel: Omeprazole may decrease antiplatelet effects of Clopidogrel. Omeprazole may decrease active metabolite exposure of Clopidogrel. Risk X: Avoid
CloZAPine: Omeprazole may decrease serum concentration of CloZAPine. Omeprazole may increase serum concentration of CloZAPine. Risk C: Monitor
CycloSPORINE (Systemic): Omeprazole may increase serum concentration of CycloSPORINE (Systemic). Risk C: Monitor
CYP2C19 Inducers (Moderate): May decrease serum concentration of Omeprazole. Risk C: Monitor
CYP2C19 Inducers (Strong): May decrease serum concentration of Omeprazole. Risk X: Avoid
CYP2C19 Inhibitors (Moderate): May increase serum concentration of Omeprazole. Risk C: Monitor
CYP2C19 Inhibitors (Strong): May increase serum concentration of Omeprazole. Risk C: Monitor
Cysteamine (Systemic): Inhibitors of the Proton Pump (PPIs and PCABs) may decrease therapeutic effects of Cysteamine (Systemic). Risk C: Monitor
Dacomitinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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
Darunavir: May decrease serum concentration of Omeprazole. Risk C: Monitor
Dasatinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Dasatinib. Management: Do not administer PPIs/PCABs with dasatinib. Antacids (taken 2 hours before or after dasatinib) can be used instead if some acid-reducing therapy is needed. No interaction is expected with the Phyrago brand of dasatinib. Risk X: Avoid
Dichlorphenamide: OAT1/3 Inhibitors may increase serum concentration of Dichlorphenamide. Risk C: Monitor
Doxycycline: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease bioavailability of Doxycycline. Risk C: Monitor
Erlotinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Erlotinib. Risk X: Avoid
Escitalopram: Omeprazole may increase serum concentration of Escitalopram. Risk C: Monitor
Fosphenytoin-Phenytoin: CYP2C19 Inhibitors (Weak) may increase serum concentration of Fosphenytoin-Phenytoin. Risk C: Monitor
Gefitinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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 serum concentration of Gliclazide. Risk C: Monitor
Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies): Inhibitors of the Proton Pump (PPIs and PCABs) may decrease therapeutic effects of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Risk C: Monitor
Indinavir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Indinavir. Risk C: Monitor
Itraconazole: Inhibitors of the Proton Pump (PPIs and PCABs) may increase serum concentration of Itraconazole. This specifically applies to the super bioavailable itraconazole products (eg, Tolsura brand). Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Itraconazole. This specifically applies to the non-super bioavailable itraconazole products (eg, Sporanox brand and its generics). Management: Exposure to Tolsura brand itraconazole may be increased by PPIs or PCABs ; consider itraconazole dose reduction. Exposure to Sporanox brand itraconazole may be decreased. Give Sporanox brand itraconazole at least 2 hrs before or 2 hrs after PPIs or PCABs. Risk D: Consider Therapy Modification
Ketoconazole (Systemic): May increase serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). Inhibitors of the Proton Pump (PPIs and PCABs) may decrease absorption of Ketoconazole (Systemic). 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 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 absorption of Levoketoconazole. Levoketoconazole may increase serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). Risk X: Avoid
Lumacaftor and Ivacaftor: May decrease serum concentration of CYP2C19 Substrates (High risk with Inducers). Risk C: Monitor
Lumacaftor and Ivacaftor: May decrease serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). Risk C: Monitor
Mavacamten: CYP2C19 Inhibitors (Weak) may increase serum concentration of Mavacamten. Management: Start mavacamten at 5 mg/day if stable on a weak CYP2C19 inhibitor, and reduce the mavacamten dose by one dose level if initiating a weak CYP2C19 inhibitor. Avoid initiating weak CYP2C19 inhibitors in patients on mavacamten 2.5 mg/day. Risk D: Consider Therapy Modification
Methotrexate: Inhibitors of the Proton Pump (PPIs and PCABs) may increase 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 serum concentration of Omeprazole. Omeprazole may increase serum concentration of Moclobemide. Risk C: Monitor
Multivitamins/Minerals (with ADEK, Folate, Iron): Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Multivitamins/Minerals (with ADEK, Folate, Iron). Specifically, the absorption of iron may be decreased. Risk C: Monitor
Mycophenolate: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Mycophenolate. Specifically, concentrations of the active mycophenolic acid may be reduced. Risk C: Monitor
Nelfinavir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Nelfinavir. Inhibitors of the Proton Pump (PPIs and PCABs) may decrease active metabolite exposure 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 serum concentration of Neratinib. Specifically, proton pump inhibitors may reduce neratinib absorption. Risk X: Avoid
Nilotinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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 X: Avoid
Nirogacestat: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Nirogacestat. Risk X: Avoid
Octreotide: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Octreotide. Risk C: Monitor
Palbociclib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease therapeutic effects of Palbociclib. Specifically, this has been reported with the use of palbociclib capsules. Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Palbociclib. Specifically, this may occur with the use of palbociclib capsules, and to the greatest extent when taken without food. Management: Carefully evaluate potential risks and benefits of coadministration of palbociclib capsules and proton pump inhibitors or potassium-competitive acid blockers due to the risk of reduced palbociclib efficacy. Palbociclib capsules should be taken with food. Risk D: Consider Therapy Modification
PAZOPanib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of PAZOPanib. Risk X: Avoid
PEMEtrexed: Inhibitors of the Proton Pump (PPIs and PCABs) may increase adverse/toxic effects of PEMEtrexed. Specifically, the risk of hematological toxicities may be increased. Risk C: Monitor
Pexidartinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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
Posaconazole: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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 serum concentration of Rilpivirine. Risk X: Avoid
Riociguat: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Riociguat. Risk C: Monitor
Risedronate: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease therapeutic effects of Risedronate. Inhibitors of the Proton Pump (PPIs and PCABs) may increase 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 serum concentration of Saquinavir. Risk C: Monitor
Secretin: Coadministration of Inhibitors of the Proton Pump (PPIs and PCABs) and Secretin may alter diagnostic results. Specifically, use of PPIs may cause a hyperresponse in gastrin secretion in response to secretin stimulation testing, falsely suggesting gastrinoma. Management: Avoid concomitant use of PPIs or PCABs and secretin, and discontinue PPI or PCAB several weeks prior to secretin administration, with the duration of separation determined by the specific acid suppressant. See full monograph for details. Risk D: Consider Therapy Modification
Seladelpar: OAT1/3 Inhibitors may increase serum concentration of Seladelpar. Risk X: Avoid
Selpercatinib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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 absorption of SORAfenib. Risk C: Monitor
Sotorasib: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Sotorasib. Risk X: Avoid
Sparsentan: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Sparsentan. Risk X: Avoid
St John's Wort: May decrease serum concentration of Omeprazole. Risk X: Avoid
Sulopenem Etzadroxil: OAT1/3 Inhibitors may increase serum concentration of Sulopenem Etzadroxil. Risk C: Monitor
Sulpiride: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease serum concentration of Sulpiride. Management: Consider alternatives to this combination due to the possibility of reduced sulpiride absorption and efficacy. If gastric acid suppressing therapy is required, consider use of antacids administered at least 2 hours after sulpiride. Risk D: Consider Therapy Modification
Tacrolimus (Systemic): Inhibitors of the Proton Pump (PPIs and PCABs) may increase serum concentration of Tacrolimus (Systemic). Risk C: Monitor
Technetium Tc 99m Sestamibi: Coadministration of Inhibitors of the Proton Pump (PPIs and PCABs) and Technetium Tc 99m Sestamibi may alter diagnostic results. 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: Coadministration of Inhibitors of the Proton Pump (PPIs and PCABs) and Technetium Tc 99m Tetrofosmin may alter diagnostic results. Risk C: Monitor
Thiazolidinediones: Inhibitors of the Proton Pump (PPIs and PCABs) may increase adverse/toxic effects of Thiazolidinediones. Specifically, the risk of osteoporosis or fracture may be increased. Risk C: Monitor
Tipranavir: May decrease serum concentration of Inhibitors of the Proton Pump (PPIs and PCABs). These data are derived from studies with Ritonavir-boosted Tipranavir. Risk C: Monitor
Vadadustat: OAT1/3 Inhibitors may increase serum concentration of Vadadustat. Risk C: Monitor
Velpatasvir: Inhibitors of the Proton Pump (PPIs and PCABs) may decrease 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: Omeprazole may increase serum concentration of Vitamin K Antagonists. Risk C: Monitor
Voriconazole: Omeprazole may increase serum concentration of Voriconazole. Voriconazole may increase serum concentration of Omeprazole. Risk C: Monitor
Prolonged treatment (≥2 years) may lead to malabsorption of dietary vitamin B12 and subsequent vitamin B12 deficiency (Lam, 2013).
Outcome data following use of proton pump inhibitors (PPIs) during pregnancy are available (Choi 2023; Hussain 2022; Peron 2023). An increased risk of major congenital malformations has not been observed in available studies.
Recommendations for the treatment of gastroesophageal reflux disease in pregnant patients are available. When initiating treatment during pregnancy, a step-up approach, starting with diet and lifestyle modifications is recommended. PPIs are considered acceptable for use during pregnancy when other medications are not effective (Ali 2022; Dunbar 2022; Thélin 2020).
Proton pump inhibitor; suppresses gastric basal and stimulated acid secretion by inhibiting the parietal cell H+/K+ ATP pump
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
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.
