Gastroesophageal Reflux Disease (GERD)
Clinical Snapshot
Gastroesophageal reflux disease (GERD) is defined as reflux of stomach contents that causes troublesome symptoms and/or complications.[1] The underlying mechanism is incompetence of the gastroesophageal junction — the lower esophageal sphincter (LES) together with the surrounding diaphragmatic crura — most often driven by frequent transient LES relaxations, and often worsened by a hiatal hernia. The severity of symptoms and the degree of esophageal mucosal injury generally correlate with how long the esophageal mucosa is exposed to acid (pH under 4) over a 24-hour period, not with symptom intensity alone.[2]
GERD matters clinically for two separate reasons: its direct effect on quality of life through heartburn and regurgitation, and the potential for long-term esophageal complications — erosive esophagitis, peptic stricture, and Barrett esophagus, which carries a risk of progression to esophageal adenocarcinoma. Most patients who report reflux symptoms have no visible mucosal injury on endoscopy.
The GERD spectrum
Non-erosive reflux disease (NERD)
Troublesome reflux symptoms with a normal-appearing esophagus on endoscopy, but abnormal esophageal acid exposure on ambulatory pH monitoring. This is the most common GERD phenotype.
Erosive esophagitis
Endoscopically visible mucosal breaks in the distal esophagus, graded by severity (Los Angeles classification), which can progress to ulceration, bleeding, or stricture formation if untreated.
Barrett esophagus
Metaplastic columnar epithelium replacing the normal squamous lining, developing through repeated injury-and-repair cycles in chronic esophagitis — the clinically important precursor lesion for esophageal adenocarcinoma.
Functional heartburn and reflux hypersensitivity
Heartburn-like symptoms without objective evidence of abnormal acid reflux or esophagitis (functional heartburn), or symptoms triggered by physiological, normal-range reflux episodes (reflux hypersensitivity). These are technically distinct from true GERD and generally do not respond to escalating acid suppression — see Assessment & Diagnosis for how to distinguish them.[3]
Recognize the Condition
Typical presentation
Heartburn (a retrosternal burning sensation, often worse after meals, when lying flat, or when bending forward) and regurgitation of acid or bile are the two hallmark symptoms; hypersalivation ("water brash") and noncardiac chest pain also occur. Heartburn and regurgitation are highly specific for GERD when present, but their absence does not reliably exclude it — pathological acid reflux can occur without classic symptoms.[2]
Globus versus dysphagia — a distinction that changes management
Globus (a continuous lump-in-the-throat sensation that does not interfere with swallowing) is a minor, common feature of reflux that does not require investigation and usually responds to effective acid suppression. Dysphagia (actual difficulty swallowing) is a different symptom entirely and is an alarm feature requiring endoscopic evaluation — see Red Flags & Refer.
Montreal classification: esophageal vs. extraesophageal GERD syndromes
Typical reflux syndrome
Heartburn and/or regurgitation, with or without a reflux chest pain syndrome resembling cardiac pain — the presentation most people mean by "GERD."
Esophageal syndromes with tissue injury
Reflux esophagitis, reflux-related stricture, Barrett esophagus, and esophageal adenocarcinoma — objective mucosal or structural damage from chronic reflux.
Extraesophageal syndromes — established association
Reflux cough syndrome, reflux laryngitis syndrome, reflux asthma syndrome, and reflux dental erosion syndrome. These can occur with or without accompanying typical heartburn/regurgitation.
Extraesophageal syndromes — proposed association
Pharyngitis, sinusitis, idiopathic pulmonary fibrosis, and recurrent otitis media — plausibly linked to reflux, but with less consistent evidence than the established-association group.[1]
Practically, extraesophageal manifestations include airway symptoms (cough, wheezing), oropharyngeal symptoms (hoarse voice, sore throat, globus sensation, oropharyngeal ulceration), dental enamel erosion, and burning mouth syndrome. These can occur even when typical heartburn/regurgitation is minimal or absent, which is why a purely symptom-based approach can miss extraesophageal GERD.
Risk Factors
- Hiatal hernia.
- Obesity — BMI over 30 kg/m2, or a recent significant weight gain, even without a high baseline BMI.
- Pregnancy.
- Esophageal dysmotility (e.g., scleroderma).
- Smoking.
- Alcohol use.
Medications that promote reflux (reduce LES tone or impair esophageal motility)
Review the medication list for the following classes whenever GERD is new, worsening, or refractory, and eliminate or substitute where clinically appropriate:
- Alpha-adrenergic agonists.
- Anticholinergic agents.
- Beta-adrenergic agonists.
- Calcium channel blockers.
- Estrogen.
- Nitrates.
- Opioids.
- Theophylline.
- Tricyclic antidepressants.
Additional risk factors for progression to Barrett esophagus
- Chronic GERD itself is the major risk factor.
- Male sex.
- White race or ethnicity.
- Age 50 years or older.
- Abdominal obesity.
- Family history of Barrett esophagus or esophageal adenocarcinoma.
- Smoking.
Red Flags & Refer
Any of the following "alarm features" warrants referral for upper endoscopy rather than continued empiric drug therapy — they suggest a possible upper GI malignancy or another diagnosis that a reflux-focused trial would miss.[2]
- Dysphagia, especially for solid food.
- Odynophagia (pain on swallowing).
- Unintentional weight loss.
- Evidence of GI bleeding (hematemesis, melena) or iron-deficiency anemia.
- A palpable epigastric mass.
- Persistent vomiting.
- Family history of upper GI cancer.
- New onset of reflux symptoms at age 60 or older.
- Symptoms that persist despite an optimized twice-daily PPI trial (see Treatment Failure & Next Step) — refractory symptoms need investigation, not further empiric drug escalation.
Assessment & Diagnosis
Differentiating GERD from its common mimics
Reflux-type symptoms and noncardiac chest pain have several distinct causes that can present similarly but need different management — differentiate before committing to escalating acid suppression.[3][4]
| Feature | GERD | Functional heartburn | Eosinophilic esophagitis | Pill-induced esophagitis | Cardiac chest pain |
|---|---|---|---|---|---|
| Typical trigger/pattern | Meals, recumbency, bending forward | No consistent trigger; reflux-like burning without a demonstrable acid cause | Solid-food dysphagia and food-bolus impaction, often in a younger adult with an atopic history | A recent causative medication (e.g., a bisphosphonate, tetracycline, NSAID, or potassium chloride) taken with little water or right before lying down | Exertional; radiates to arm/jaw/back; associated diaphoresis or dyspnea |
| Response to an adequate PPI trial | Symptoms improve | No meaningful improvement, by definition | Dysphagia persists even if some symptom overlap improves | Odynophagia resolves once the causative drug/technique is corrected, not because of acid suppression | No relationship to acid suppression |
| Ambulatory pH/impedance testing | Abnormal esophageal acid exposure | Normal acid exposure despite ongoing symptoms | Typically normal | Not indicated | Not indicated |
| Endoscopy/biopsy finding | Erosive esophagitis, or a normal-appearing esophagus in NERD | Normal mucosa | Esophageal eosinophilia on biopsy; rings, furrows, or strictures | A discrete ulcer at the site of pill impaction (classically mid-esophagus, at the level of aortic arch compression) | Normal esophagus — the diagnosis lies outside the GI tract |
| Key next step | Treat with lifestyle measures and acid suppression per this chapter | Low-dose neuromodulator therapy — escalating acid suppression further is not the answer | Endoscopy with biopsies; allergy/dietary and topical corticosteroid workup | Counsel proper pill-taking technique (upright, full glass of water, remain upright afterward) and switch or reformulate the causative drug | Urgent cardiac workup (ECG, troponin) before attributing symptoms to a GI cause, especially with an exertional pattern or cardiac risk factors |
History
- History alone is usually sufficient for diagnosis when symptoms are typical: heartburn, regurgitation of acid or bile, hypersalivation ("water brash"), and noncardiac chest pain.
- Ask specifically about extraesophageal manifestations — cough, wheezing, hoarse voice, sore throat, globus sensation or ulceration, dental enamel erosion, burning mouth syndrome.
- Ask about esophageal complications — dysphagia (suggesting a peptic stricture), or odynophagia/GI bleeding (suggesting esophageal ulceration).
- Identify predisposing/associated conditions — hiatal hernia, obesity, pregnancy, esophageal dysmotility (e.g., scleroderma).
- Screen for every alarm feature in Red Flags & Refer before starting empiric therapy.
When to order upper endoscopy
Upper endoscopy is generally not required when GERD features are typical and no alarm feature is present — an empiric PPI trial is both treatment and, if symptoms respond, diagnostic confirmation.[2]
Order upper endoscopy for any of the following:
- Any alarm feature (see Red Flags & Refer).
- Refractory GERD — heartburn and reflux symptoms that persist despite an optimized twice-daily PPI trial (dosed 30-60 minutes before meals) for 4-8 weeks.
- Suspicion of a different cause of esophagitis — eosinophilic, pill-induced, or infectious esophagitis.
- To confirm the diagnosis when response to an empiric trial is unclear or when planning long-term management, since endoscopy also stages any erosive esophagitis present (Los Angeles grade) and identifies Barrett esophagus if present.
Chronic GERD is the major risk factor for Barrett esophagus, but current Canadian guidance recommends against routine endoscopic screening for esophageal adenocarcinoma or Barrett esophagus in adults with chronic GERD who do not have alarm features — this recommendation does not apply to patients who already have alarm features or a confirmed diagnosis of Barrett esophagus/dysplasia, who need endoscopic follow-up on its own schedule.[5]
Ambulatory pH and impedance monitoring
Indicated for atypical reflux symptoms where the diagnosis is unclear, and for patients who fail standard medical therapy. It can detect abnormal acid reflux even when esophagitis is absent (as in NERD), correlate symptom episodes with actual reflux events, and determine whether therapy is adequately controlling reflux. The Lyon Consensus 2.0 (2024) update to modern GERD diagnostic criteria now allows Los Angeles grade B esophagitis (previously grade C or higher was required) to independently confirm a GERD diagnosis on endoscopy, alongside acid-exposure-time thresholds on pH/impedance testing.[3]
Testing not indicated
Testing for Helicobacter pylori is not necessary in GERD patients. H. pylori infection has an inverse relationship with GERD complications — the associated chronic gastritis may lower gastric acidity — so eradication is not part of routine GERD management, though it remains indicated for its own reasons (e.g., confirmed peptic ulcer disease).
Treatment Targets
- Relieve symptoms — particularly heartburn and regurgitation — and improve quality of life.
- Promote healing of erosive esophagitis when present.
- Prevent complications: stricture formation, bleeding, and progression to Barrett esophagus or extraesophageal problems.
- Prevent recurrence once symptom control is achieved.
Choose Initial Treatment
Severity-based initial therapy
Trivial/mild GERD — infrequent (under 3 times weekly), low-intensity, non-nocturnal symptoms without complications — start with an antacid, an alginate, or an H2RA used on demand.
Moderate-to-severe GERD, or endoscopy-confirmed erosive esophagitis — start a once-daily PPI, taken 30 minutes before a meal (usually breakfast), for 8 weeks. This is the most effective and most common initial approach once symptoms are more than trivial.[2]
Partial response to an adequate once-daily PPI trial — increase to twice-daily dosing (30-60 minutes before meals) or switch to a delayed-release formulation (dexlansoprazole) for improved 24-hour coverage.
Do not use a PPI "as needed" or sporadically (e.g., once or twice weekly) — onset is not immediate, so this dosing pattern does not provide adequate acid inhibition; a scheduled trial is required to properly assess response.
Maintenance strategy once initial symptom control is achieved
Severe erosive esophagitis (Los Angeles grade C or D), Barrett esophagus, or a history of GI bleeding on therapy — continue long-term maintenance PPI therapy at the lowest effective dose; do not attempt discontinuation in these groups.
NERD or milder erosive disease, once symptom-free — attempt step-down therapy: gradually reduce the intensity of acid suppression (e.g., twice-daily to once-daily, then to half the once-daily dose) until the lowest dose that maintains symptom control is found; some patients can transition to an H2RA without loss of symptom control. On-demand therapy (daily PPI dosing until symptoms resolve, then stopping, and resuming only when symptoms recur) is an alternative maintenance strategy, particularly for NERD — in most patients, continuous PPI therapy still provides better symptom control, quality of life, and mucosal protection than on-demand dosing, so reserve on-demand for patients who specifically prefer it once initial control is confirmed.
Anyone who has completed at least 4 weeks of PPI therapy for heartburn or mild-to-moderate GERD/esophagitis and whose symptoms have resolved — attempt an annual trial of dose reduction, on-demand dosing, or discontinuation, per current Canadian deprescribing guidance, except in Barrett esophagus, severe erosive esophagitis (LA grade C/D), or a history of GI bleeding, where long-term maintenance therapy is appropriate instead.[6][7]
Non-Pharmacologic Treatment
- Modify diet — avoid chocolate, caffeine, acidic citrus juices, and large, fatty meals.
- Reduce body weight if BMI is over 30 kg/m2, or following a recent weight gain, even without a high baseline BMI.
- Avoid eating within 3 hours of bedtime.
- Avoid lying down right after meals.
- Elevate the head of the bed by 10-20 cm, particularly for nocturnal or laryngeal reflux symptoms — best achieved with a block under the bed frame's legs, not with extra pillows or a wedge, which raises only the upper body rather than the whole thorax.
- Stop smoking.
- Avoid alcohol.
- Avoid tight-fitting clothing around the abdomen.
- Review the medication list for drugs that lower LES tone or impair esophageal motility (see Risk Factors) and eliminate or substitute where clinically appropriate.
These lifestyle measures have the best supporting evidence when applied together rather than individually.[2] Counsel patients that antacids and alginates provide fast but short-lived relief and do not heal esophagitis or prevent complications — appropriate for mild, infrequent symptoms, but not a substitute for scheduled acid-suppressing therapy in moderate-to-severe disease.
Special Populations
Breastfeeding: Antacids are not concentrated in breast milk and are considered safe. Alginates are also safe. H2RAs and PPIs are both considered compatible with breastfeeding — any small amount of a PPI passing into breast milk is likely destroyed in the infant's stomach by acid hydrolysis, and famotidine is preferred over other H2RAs given its minimal interaction profile and more established safety data.
Pediatrics
Physiologic reflux (frequent "spitting up" without other concerning features) is extremely common in infancy and typically resolves on its own by 12-18 months of age without treatment. Poor weight gain or failure to thrive, forceful or bilious vomiting, blood in the stool or vomitus, and respiratory symptoms in an infant are red flags warranting pediatric GI referral rather than empiric acid suppression. Empiric acid-suppressing therapy for infant fussiness or crying without other reflux features is not supported by evidence and exposes the infant to unnecessary risk. Pediatric GERD in older children, and pharmacologic treatment when genuinely indicated, is managed per separate pediatric-specific dosing and guidance — this chapter's recommendations are written for adult GERD.
Older adults
Older adults are more likely to have atypical presentations (dyspepsia, dysphagia, or respiratory symptoms without prominent heartburn), and new-onset reflux symptoms at age 60 or older is itself an alarm feature warranting endoscopy rather than an empiric trial (see Red Flags & Refer). Older adults are also more susceptible to the long-term risks of chronic PPI therapy and are frequently on multiple interacting medications, making an annual deprescribing review particularly valuable in this group.[6]
Renal and hepatic impairment
Omeprazole should not exceed 20 mg/day in significant hepatic impairment. H2RAs require renal dose reduction — reduce famotidine, nizatidine, and ranitidine doses (or extend the dosing interval) in significant renal impairment, and reduce cimetidine dosing in renal impairment given its already extensive interaction profile. Avoid regular, high-dose aluminum- or magnesium-containing antacids/alginates in significant renal impairment because of accumulation risk, and avoid regular high-dose calcium carbonate in renal impairment given hypercalcemia risk.
Monitoring & Follow-Up
Reassess symptom response at 4-8 weeks after starting an 8-week PPI trial. If well controlled, decide between continuing maintenance therapy (severe erosive esophagitis, Barrett esophagus, GI bleeding history) versus attempting step-down, on-demand dosing, or discontinuation (NERD, milder disease).
For anyone remaining on long-term PPI therapy, reassess the ongoing indication at least annually — through an actual trial of dose reduction or discontinuation, not simply a chart review — except in Barrett esophagus, severe erosive esophagitis (LA grade C/D), or a history of GI bleeding, where long-term maintenance is appropriate and an annual discontinuation attempt is not indicated.[6][7]
For patients remaining on long-term PPI therapy, periodically review the real, evidence-associated risks of prolonged acid suppression and counsel accordingly — this is informational counselling, not a reason to withhold indicated therapy: vitamin B12 deficiency (reduced absorption of protein-bound B12 — check levels if symptoms of deficiency develop, particularly in older adults or after several years of continuous use), hypomagnesemia (can present with fatigue, muscle cramps, arrhythmia, or seizures — consider checking magnesium periodically in patients on other magnesium-wasting drugs, such as diuretics, or after prolonged therapy), increased fracture risk (counsel on adequate calcium/vitamin D intake and weight-bearing exercise; do not withhold PPI therapy from a patient who needs it, but do not continue it indefinitely without an ongoing indication either), and increased risk of Clostridioides difficile and other enteric infections (reinforce standard infection-prevention counselling, and reconsider ongoing PPI necessity in a patient with recurrent C. difficile).[8]
Community-acquired pneumonia and other associations raised in epidemiological literature (chronic kidney disease, cardiovascular events, dementia) do not have an established causal relationship with PPI use — mention them as part of a balanced long-term risk discussion without overstating certainty.[8]
Common Errors to Avoid
- Using a PPI "as needed" or sporadically — onset is not immediate (meaningful relief can take more than a single dose), so as-needed dosing does not provide adequate acid inhibition; a scheduled trial is required to properly assess response.
- Taking a PPI with or after food, rather than 30 minutes before a meal — this significantly reduces effectiveness, since PPIs require an activated proton pump to bind.
- Combining a PPI and an H2RA on the same schedule — taking them together can blunt the PPI's effect rather than adding to it.
- Using an H2RA continuously as long-term maintenance therapy — tachyphylaxis develops quickly; H2RAs are best used intermittently, on-demand, or as a bedtime add-on.
- Attempting deprescribing or a discontinuation trial in a patient with Barrett esophagus, severe erosive esophagitis (LA grade C/D), or a GI bleeding history — these patients need long-term maintenance PPI therapy, not an annual step-down attempt.
- Never attempting a discontinuation or step-down trial in a patient who has been on stable, effective PPI therapy for years by default — long-term PPI use should be reassessed at least annually, not simply continued indefinitely without review.
- Missing an alarm feature and treating empirically instead of referring for endoscopy — new dysphagia, GI bleeding, unintentional weight loss, or new-onset symptoms at age 60 or older need investigation, not a longer empiric trial.
- Recommending or dispensing ranitidine or nizatidine without checking current Health Canada recall status — most ranitidine products were recalled over nitrosamine (NDMA) contamination, and famotidine is preferred where an H2RA is needed.[9]
- Missing a reversible drug-induced contributor — a medication that lowers LES tone or impairs esophageal motility (see Risk Factors) — when GERD is new or worsening.
- Discussing long-term PPI risks (B12 deficiency, hypomagnesemia, fracture risk, C. difficile) in a way that frightens a patient with a genuine ongoing indication into stopping therapy inappropriately — these are real counselling points for periodic review and monitoring, not a reason to withhold indicated therapy.
- Ordering endoscopic screening for Barrett esophagus in a patient with chronic GERD who has no alarm features — current Canadian guidance recommends against this.
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.
Relative efficacy by drug class
| Drug class | Symptom relief | Esophagitis healing | Prevention of recurrence |
|---|---|---|---|
| Antacids | Some proven benefit | Not established | Not established |
| Alginates/antacids | Some proven benefit | Not established | Not established |
| Histamine H2-receptor antagonists | Good benefit | Some proven benefit | Conflicting data |
| Proton pump inhibitors | Most effective | Most effective | Most effective |
Qualitative grading based on controlled-trial evidence, adapted for teaching purposes.[2]
Proton Pump Inhibitors
Prodrugs requiring an activated proton pump for optimal efficacy — take 30 minutes before a meal (usually breakfast). Effective at standard once-daily doses in most patients; escalate to twice-daily dosing or a delayed-release formulation for partial response. At equivalent doses, all PPIs offer similar symptom relief, healing, and safety — agent selection is mainly about individual response and formulary coverage, not clinically meaningful differences in potency.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Omeprazole | Standard dose: 20 mg PO once daily, 30 min before breakfast, for 8 weeks If partial response: 20 mg PO BID, 30 min before breakfast and dinner Maintenance/step-down: Reduce to the lowest effective dose (e.g., every-other-day or half-dose) once symptom-free | Headache, nausea, diarrhea, abdominal pain, rash | Not to exceed 20 mg/day in hepatic impairment. May decrease absorption of drugs requiring gastric acidity (e.g., atazanavir, ketoconazole, iron salts). |
| Esomeprazole | Standard dose: 20-40 mg PO once daily, 30 min before food If partial response: Usual dose PO BID | Headache, nausea, diarrhea, rash | The (S)-enantiomer of omeprazole; commonly used at 40 mg daily; only modestly more effective than other PPIs at healing erosive esophagitis. Inhibits CYP2C19 — may increase levels of drugs cleared through this pathway (e.g., increased levels with clarithromycin). |
| Lansoprazole | Standard dose: 15-30 mg PO once daily, 30 min before food If partial response: Usual dose PO BID | Headache, nausea, diarrhea, rash | May decrease theophylline levels and increase tacrolimus levels. Half the usual dose can be useful for maintenance in patients with milder disease who have achieved remission. |
| Dexlansoprazole | Standard dose: 30-60 mg PO once daily, without regard to food timing | Headache, nausea, diarrhea, rash | Delayed-release dual-release formulation (an enantiomer of lansoprazole) that prolongs the plasma half-life for extended 24-hour coverage; marketed at a higher dose than lansoprazole. Can be taken without regard to food timing. A reasonable option for refractory or nocturnal breakthrough symptoms, or when adherence to twice-daily dosing of another PPI is a barrier. |
| Pantoprazole | Standard dose (magnesium salt): 40 mg PO once daily, 30 min before food Standard dose (sodium salt): 20-40 mg PO once daily, 30 min before food If partial response: Usual dose PO BID | Headache, nausea, diarrhea, rash | Available as the magnesium or sodium salt — clinically equivalent. May decrease theophylline levels and increase tacrolimus levels. |
| Rabeprazole | Standard dose: 10-20 mg PO once daily, 30 min before food If partial response: Usual dose PO BID | Headache, nausea, diarrhea, rash | Digoxin levels may increase moderately in some patients. |
Histamine H2-Receptor Antagonists
Onset is faster than PPIs, making them useful for on-demand use in mild, infrequent GERD, or as a bedtime add-on for nocturnal acid breakthrough on a PPI. Not reliably effective for healing erosive esophagitis — do not use as monotherapy for confirmed erosive disease. Regular, continuous use leads to rapid tachyphylaxis — best used intermittently or on-demand for maintenance.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Famotidine | Prescription dose: 20-40 mg PO BID OTC dose: 10-20 mg PRN, up to twice daily (maximum 40 mg/24h) | Headache, dizziness, constipation, diarrhea | Preferred H2RA — minimal drug-interaction profile compared with cimetidine. Antacids may be given concomitantly if needed. |
| Cimetidine | Standard dose: 800 mg PO once daily at bedtime, or 300 mg PO QID | Diarrhea, constipation, headache, fatigue, confusion (more likely in older adults or renal impairment), rare gynecomastia/impotence with prolonged use | Extensive CYP450 (1A2/2C/2D6/3A) interaction profile — increases levels of warfarin, phenytoin, theophylline, and other substrates. Reserve for when other H2RAs are not suitable. |
| Nizatidine | Standard dose: 150 mg PO BID | Headache, diarrhea, constipation, fatigue, confusion (more likely in older adults or renal impairment) | No significant CYP450 interaction profile. |
| Ranitidine | Standard dose: 150 mg PO BID-QID | Headache, diarrhea, constipation, fatigue, confusion (more likely in older adults or renal impairment) | Most ranitidine products were recalled from the Canadian market in 2019-2020 over nitrosamine (NDMA) contamination; current availability is limited to specific reformulated products passing batch NDMA testing. Confirm current Health Canada recall status before dispensing, and prefer famotidine where an H2RA is indicated.[9] |
Antacids
Neutralize gastric acid directly for rapid, short-lived relief. Do not heal esophagitis or prevent complications — reserved for mild, infrequent symptoms or as an adjunct between scheduled doses of a scheduled medication.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Calcium carbonate | Standard dose: 500-1000 mg PO PRN | Constipation, belching, gas; milk-alkali syndrome (hypercalcemia, metabolic alkalosis, acute kidney injury) with chronic excessive use | Also functions as a calcium supplement — count toward total daily elemental calcium intake in regular users. Reduces absorption of tetracyclines, quinolones, iron salts, levothyroxine, and bisphosphonates — separate dosing by at least 2 hours. |
| Aluminum hydroxide / magnesium hydroxide | Standard dose: 10-30 mL, or 1-4 chewable tablets, PO PRN after meals and at bedtime | Constipation (aluminum) or diarrhea (magnesium) — the combination is formulated to reduce the net bowel-habit effect | Avoid regular, high-dose use in significant renal impairment because of aluminum/magnesium accumulation risk. Reduces absorption of digoxin, tetracyclines, and quinolones — separate dosing by at least 2 hours. |
Alginates
Alginate precipitates into a near-neutral-pH gel raft on contact with gastric acid, physically floating over the postprandial acid pocket and displacing it away from the gastroesophageal junction, so the gel — rather than acid — is what refluxes. More effective than a plain antacid for reflux-specific symptoms, though it still does not heal esophagitis.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Alginate / aluminum hydroxide | Standard dose: 10-20 mL PO after meals and at bedtime, PRN | Nausea, belching, flatulence | Contains aluminum — avoid regular high-dose use in significant renal impairment. Reduces absorption of digoxin, tetracyclines, and quinolones — separate dosing by at least 2 hours. |
| Alginate / magnesium carbonate | Standard dose: 2-4 tablets chewed, PO after meals and at bedtime, PRN, followed by a drink of water | Nausea, belching, flatulence | Aluminum-free alternative to the aluminum-hydroxide combination. Reduces absorption of digoxin, tetracyclines, and quinolones — separate dosing by at least 2 hours. |
Mucosal Protectant (pregnancy-specific niche use)
Minimal systemic absorption; an option in pregnancy/breastfeeding when a non-systemic option beyond antacids/alginates is wanted, though it is not considered effective GERD therapy in general use.
| Drug | Dosage | Adverse effects | Comments |
|---|---|---|---|
| Sucralfate | Standard dose: 1 g PO QID, on an empty stomach | Constipation; aluminum accumulation with prolonged use in renal impairment | Not considered effective monotherapy for GERD outside of this specific pregnancy/breastfeeding niche role. Reduces absorption of many drugs (e.g., fluoroquinolones, levothyroxine) — separate dosing by at least 2 hours. |
References
- The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus — American Journal of Gastroenterology (Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R). Am J Gastroenterol 2006;101(8):1900-1920
- ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease — American College of Gastroenterology (Katz PO, Dunbar KB, Schnoll-Sussman FH, Greer KB, Yadlapati R, Spechler SJ). Am J Gastroenterol 2022;117(1):27-56
- Updates to the modern diagnosis of GERD: Lyon consensus 2.0 — Gut (Gyawali CP, Yadlapati R, Fass R, et al.). Gut 2024;73(2):361-371
- AGA clinical practice update on functional heartburn: expert review — Gastroenterology (Fass R, Zerbib F, Gyawali CP). Gastroenterology 2020;158(8):2286-2293
- Guideline on screening for esophageal adenocarcinoma in patients with chronic gastroesophageal reflux disease — CMAJ, Canadian Task Force on Preventive Health Care (Groulx S, Limburg H, Doull M, et al.). CMAJ 2020;192(27):E768-E777
- AGA Clinical Practice Update on De-Prescribing of Proton Pump Inhibitors: Expert Review — Gastroenterology, American Gastroenterological Association (Targownik LE, Fisher DA, Saini SD). Gastroenterology 2022;162(4):1334-1342
- Appropriate prescribing and deprescribing of proton pump inhibitors: New Choosing Wisely Canada toolkit — Canadian Family Physician (Bland E, Veldhuyzen van Zanten S, Thompson W). Can Fam Physician 2026;72(3):179-183
- The risks and benefits of long-term use of proton pump inhibitors: expert review and best practice advice from the American Gastroenterological Association — Gastroenterology (Freedberg DE, Kim LS, Yang YX). Gastroenterology 2017;152(4):706-715
- Status of ranitidine drugs in Canada — Health Canada Recalls and Safety Alerts. Health Canada, updated 2025
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.