Reflux (GERD) and functional dyspepsia — recognising it, testing smartly, treating properly

About this guide

Reflux and dyspepsia are two of the commonest things we see. They also happen to be two of the most under-recognised — many patients have been living with classic symptoms for years, attributing them to “gas,” a “sensitive stomach,” or “that’s just how I am after eating.” Others know something is wrong but have been on an antacid or proton pump inhibitor (PPI) for a decade without anyone re-examining whether that’s still the right plan.

Three things drive this guide:

1. Recognition matters. A lot of what we call “reflux” or “dyspepsia” doesn’t look the way textbooks describe. Throat clearing, chronic cough, a lingering sour taste in the morning, early fullness at meals, a chest pressure that keeps prompting heart workups — all of these can be driven by the same process.
2. Testing for Helicobacter pylori needs to be done properly. The bacterium is common in Singapore, is a curable driver of dyspepsia and ulcer disease, and is linked to gastric cancer — but the test you use matters. Antibody blood tests and “rapid antibody” kits (ART/IgG) are genuinely unhelpful for most clinical questions, and the Urea Breath Test (which we do at KTMC) is the preferred method.
3. We take gastric cancer seriously in Singapore. Gastric cancer incidence in East and Southeast Asian populations is meaningfully higher than Western benchmarks. Patients with warning features, strong family history, or persistent symptoms despite treatment often benefit from an endoscopy earlier rather than later.

This guide covers: what GERD is, what functional dyspepsia is, how to tell them apart, when we look further, how we test for H. pylori (and why some tests are no longer recommended), and how we treat it all sustainably — including the “when can I stop my PPI?” conversation that patients often want to have but rarely raise.

Do any of these sound familiar?

Symptom recognition is one of the hardest parts of this area. Patients often don’t connect their complaints to reflux or dyspepsia until someone explicitly asks. A few patterns worth recognising:

“I get this burning feeling behind my breastbone after meals, especially dinner. Sometimes at night I wake up with a sour taste at the back of my throat. I thought it was indigestion from eating late.”

“I’ve been coughing for months. My GP has tried two courses of antibiotics. My chest X-ray is clear. The cough is worse after dinner and when I lie down.”

“I can’t seem to eat a full meal anymore — I feel full after a few bites. Then there’s a bloated, uncomfortable feeling for an hour or two afterward. I’ve started avoiding lunch out with colleagues.”

“I keep clearing my throat and my voice goes hoarse by the end of the day. The ENT said my vocal cords look irritated. Nothing for infection.”

“I wake up with this pressure behind my breastbone and wonder if it’s my heart. I’ve had a stress test and an ECG. Everything’s fine. But the pressure is still there, every few mornings.”

The common thread in all of these is gastric contents — acid, bile, or both — going where they shouldn’t, either up into the oesophagus (reflux), or irritating the stomach lining, or producing abnormal sensations of fullness and pain that don’t match how much you’ve eaten.

If any of those stories felt like yours, this guide is written for you.

GERD and functional dyspepsia — they’re related, but different

The two conditions often get lumped together, and many patients do have elements of both. But the treatment and investigation pathways are different, so it’s worth separating them.

Gastro-oesophageal reflux disease (GERD)

GERD is reflux of stomach contents upward into the oesophagus, producing symptoms or damage. The hallmark symptoms:

• Heartburn — a burning sensation behind the breastbone, classically after meals or when lying down
• Acid regurgitation — a sour or bitter taste in the mouth, sometimes with small amounts of food coming back up
• Water brash — excess watery saliva, often with a sour taste

GERD also has a substantial list of atypical and extra-oesophageal presentations that are easy to miss:

• Chronic cough — particularly worse at night or after meals
• Hoarseness, throat clearing, globus (the sensation of something stuck in the throat) — often called laryngopharyngeal reflux (LPR) or “silent reflux”; patients may have little or no heartburn
• Non-cardiac chest pain — pressure or pain behind the breastbone that can mimic heart symptoms, often prompting repeated cardiac workups
• Dental erosion — particularly on the inner surfaces of the teeth
• Sleep disturbance — waking at night with cough, throat irritation, or sour regurgitation
• Asthma — severe or difficult-to-control asthma is sometimes driven partly by reflux

The underlying mechanism is usually the lower oesophageal sphincter (LOS) — the ring of muscle that separates the stomach from the oesophagus — relaxing when it shouldn’t, often combined with increased intra-abdominal pressure, a hiatal hernia (part of the stomach pushing up through the diaphragm), or delayed stomach emptying.

Functional dyspepsia

Functional dyspepsia is a cluster of chronic upper abdominal symptoms without a structural disease to explain them. The “functional” label reflects the fact that investigations (endoscopy, ultrasound, labs) typically don’t find a specific abnormality — but the symptoms are very real.

The internationally-used (Rome IV) criteria require at least one of:

• Bothersome postprandial fullness — feeling uncomfortably full for longer than expected after normal-sized meals
• Early satiety — feeling full after only a few bites
• Epigastric pain — pain or ache in the upper middle abdomen
• Epigastric burning — burning in the same area, without the retrosternal character of heartburn

These need to be present for at least 3 months, with onset at least 6 months before diagnosis, with no evidence of structural disease on investigation.

Two patterns are recognised, and patients often have both:

• Postprandial distress syndrome (PDS) — dominated by postprandial fullness and early satiety
• Epigastric pain syndrome (EPS) — dominated by epigastric pain and burning

Functional dyspepsia and GERD can coexist, and treatment overlaps substantially — but there are also specific interventions that favour one over the other.

Red flags — when we look further

Most reflux and dyspepsia is straightforward. A few features, though, change the approach and warrant earlier investigation:

• New onset dyspepsia at age 45 or above, particularly in patients of East or Southeast Asian background
• Progressive difficulty swallowing (dysphagia) — food or liquid getting “stuck”
• Pain on swallowing (odynophagia)
• Unintentional weight loss — more than about 5% of body weight over 6 months without trying
• Iron deficiency anaemia on blood tests
• Vomiting blood, coffee-ground vomitus, black tarry stools, or any visible GI bleeding
• Persistent vomiting
• A palpable lump in the upper abdomen
• A first-degree relative (parent, sibling, child) with stomach or oesophageal cancer
• Previous stomach ulcer or stomach surgery
• Severe or rapidly worsening symptoms despite standard treatment

Any of these features triggers a lower threshold for investigating further — usually with an upper endoscopy (gastroscopy, “OGD”).

When we’d refer for endoscopy

Singapore has a higher background rate of gastric cancer than Western benchmarks, particularly in Chinese populations and in older adults. The difference is clinically meaningful: while Western guidelines often recommend endoscopy only in patients over 55–60 with alarm features, local practice typically has a lower threshold.

We’d usually discuss an endoscopy referral to a gastroenterologist or general surgeon when:

• You have any alarm feature from the list above, regardless of age
• You have new-onset dyspepsia over age 45 (some colleagues use 40) without a clear trigger
• You have a strong family history of gastric cancer or Barrett’s oesophagus
• You have persistent symptoms despite 4–8 weeks of appropriate treatment (e.g. a PPI trial, or H. pylori eradication)
• Helicobacter pylori testing is positive and we want to assess for ulcer disease, gastric atrophy, or intestinal metaplasia while treating
• You have long-standing reflux (more than 5 years) and would benefit from a one-time check for Barrett’s oesophagus — a precancerous change that warrants surveillance if found

Endoscopy isn’t a minor investigation, but it is the single most useful tool for settling whether the upper gut looks normal, whether H. pylori is present, and whether there’s anything more concerning going on. We’d always discuss it as a shared decision rather than a default.

Our usual pathway: For patients at KTMC who need endoscopy, we’ll recommend a specific gastroenterologist or general surgeon (both Joo Chiat and Punggol have preferred referral partners), give you a referral letter that includes the reason, and follow up with you after the report so we can plan next steps together.

Helicobacter pylori — the one reversible cause worth ruling out

Helicobacter pylori (often abbreviated H. pylori) is a bacterium that colonises the stomach lining. It is curable with antibiotic treatment, and clearing it can:

• Cure a large proportion of dyspepsia in people who harbour it
• Heal gastric and duodenal ulcers and prevent their recurrence
• Reduce the long-term risk of gastric cancer, MALT lymphoma, and iron-deficiency anaemia

Local prevalence has fallen over the last few decades — it used to be present in well over half of adults, and is now closer to 20–30% depending on the population — but it remains common enough that testing is usually worth it in patients with dyspepsia, ulcer-type pain, or recurrent reflux that isn’t settling.

Testing for H. pylori — why the method matters

This is one of the most common areas where patients have been mis-tested. Several test modalities exist, but they aren’t interchangeable.

What we offer at KTMC — Urea Breath Test and stool antigen test

Both the Urea Breath Test (UBT) and the stool antigen test are offered at KTMC. International consensus (Maastricht VI / Florence Report 2022, ACG 2024, Asian-Pacific Consensus) positions them as equivalent first-line non-invasive tests for both diagnosis and test-of-cure, and local Singapore validation supports the same position. Both detect active, current infection (not past exposure) with sensitivity and specificity around 95%. Serology (blood antibody testing) performs substantially worse on both counts.

Urea Breath Test (UBT). You swallow a small amount of urea labelled with a harmless isotope of carbon. If H. pylori is present, the bacterium’s own enzyme (urease) breaks down the urea, releasing labelled carbon dioxide — which you then breathe out and we measure. Around 30 minutes in clinic, two breath samples, a small drink in between.

Stool antigen test. A single stool sample is collected (usually at home, dropped to the clinic) and analysed for H. pylori antigen. No in-clinic time required for the test itself. Particularly useful when the UBT logistics are difficult — children, patients with swallowing difficulty, patients travelling, or patients who can’t easily come in for the breath test.

Which we’d recommend for you depends on practicalities. For most adults the UBT is efficient (one clinic visit, result available the same day). For children, patients who’d rather avoid the small in-clinic procedure, or patients whose schedules make an appointment harder, the stool antigen test is equally valid.

What you need to do first — applies to both tests. The preparation rules are identical because both tests measure the bacterium’s active presence, which is suppressed by acid-suppressing medications and antibiotics:

• Stop proton pump inhibitors (PPIs) for at least 2 weeks before the test — PPIs suppress the bacterium and can produce a false-negative result
• Stop antibiotics and bismuth-containing medications for at least 4 weeks — same reason
• Stop H2 blockers (e.g. famotidine) for 24 hours before the test
• Fast for at least 4–6 hours before a UBT (no food; small sips of water OK); no fasting required for stool collection

If you’re on a PPI for a reason that makes stopping difficult, we’d discuss the trade-off — usually a short planned stop is fine, but we’d plan it rather than just pause the medication.

Testing done at endoscopy — rapid urease test and histology

When an endoscopy is being performed for another reason, the gastroenterologist will usually take small biopsies of the stomach lining and test them in two ways:

• Rapid urease test (CLO test) — similar principle to UBT, result within hours
• Histology — the biopsy is examined under the microscope, which also assesses for gastritis, atrophy, intestinal metaplasia, ulcer, or malignancy

These are the most useful tests when endoscopy is being done anyway.

What we don’t use — serology and “rapid antibody” tests

Blood tests for H. pylori antibodies — sometimes offered as part of a general wellness panel, or available as a “rapid antibody test” (ART) that gives an answer in minutes — are no longer recommended for routine clinical use, and international consensus groups (Maastricht VI, ACG, Asian-Pacific) all agree on this. Two reasons:

1. They can’t distinguish active infection from past infection. Once you’ve been exposed to H. pylori, IgG antibodies remain positive for years — sometimes for life — even after the bacterium has been successfully eradicated. A positive serology does not mean you need treatment. A negative serology in a patient who has had H. pylori before is also hard to interpret.
2. Low positive predictive value in populations where prevalence is falling. As local prevalence has come down, the probability that any given positive antibody test reflects a current, treatable infection has also come down. Antibody tests make sense in research and epidemiology; they rarely make sense for day-to-day clinical decisions.

The practical implication: if you’ve been told you have H. pylori based on a blood antibody test, and you’ve either never been treated or were treated long ago, this warrants a proper active-infection test (UBT or stool antigen) before committing to antibiotic therapy. The opposite also holds — if you’ve had treatment and a blood antibody test stays positive, that’s expected and does not mean treatment failed.

The test-of-cure — 4 weeks after treatment

Successful eradication needs to be confirmed after treatment. The standard is to repeat the UBT (or stool antigen test) at least 4 weeks after completing antibiotics, and 2 weeks off any PPI. Earlier testing risks a false-negative result. We routinely schedule this.

Treating H. pylori

Treatment requires a combination of antibiotics plus acid suppression — monotherapy doesn’t work, and short courses don’t work.

What you’ll typically be prescribed

The current options, adjusted for local availability and resistance patterns:

• Concomitant therapy (10–14 days) — a PPI + amoxicillin + clarithromycin + metronidazole, all taken together. This is our usual first-line choice in Singapore: it works well against most local strains and doesn’t depend on bismuth.
• Triple therapy (14 days) — a PPI + amoxicillin + clarithromycin. Still used in selected patients with no previous macrolide exposure, but clarithromycin resistance is rising locally and influences the choice.
• Bismuth quadruple therapy (10–14 days) — a PPI + bismuth + metronidazole + tetracycline. Works well even where resistance to clarithromycin is suspected, and is the standard first-line in several countries — but bismuth is not routinely available in community pharmacies in Singapore, so this regimen is usually arranged at specialist or hospital level when it’s needed (typically after first-line failure or in patients with specific resistance concerns).
• Levofloxacin-based therapy — a PPI + amoxicillin + levofloxacin, usually reserved for second-line after a failed concomitant or triple course.

Key points for the course:

• Complete the full course, not half. Eradication rates fall substantially if even a day or two is missed. Set reminders if you need to.
• Take medications at the right times — some need to be with food, others on an empty stomach. Follow the pharmacy labels precisely.
• Side effects are common — a metallic taste (from metronidazole), nausea, loose stools, occasional rash. These are almost always manageable with dose-timing tweaks. If you’re on a bismuth-containing regimen, dark stools and a dark tongue are expected and harmless.
• No alcohol during treatment — metronidazole causes an unpleasant reaction with alcohol.
• Probiotics during and after the course may reduce GI side effects and slightly improve eradication rates.

If the first-line course fails — about 10–15% of courses do — we switch to a different antibiotic combination rather than repeating the same one. This is where knowing that the bug is genuinely still present (via UBT or stool antigen, not serology) becomes essential.

Managing GERD — lifestyle foundation

For most patients, lifestyle measures produce meaningful improvement even before any medication. They also reduce how much long-term medication you actually need.

Weight

For patients who carry extra weight, particularly around the abdomen, weight reduction of even 5–10% often improves reflux substantially. Visceral fat increases intra-abdominal pressure and mechanically promotes reflux. See our medical weight management guide for the detail.

Meal size and timing

• Smaller, more frequent meals are generally easier on the lower oesophageal sphincter than large infrequent ones
• Don’t lie down within 3 hours of a meal — gravity is a significant ally in keeping stomach contents where they belong
• Avoid late-night dinners if reflux is worse at night
• Eat slowly, chew thoroughly — improves satiety and reduces swallowed air

Trigger foods

Common triggers vary between patients; the point is to notice which apply to you rather than follow a blanket list. The usual suspects:

• Fatty and fried foods — delay gastric emptying
• Spicy food — particularly chilli-based
• Tomato-based foods and citrus
• Chocolate, mint (including peppermint tea) — paradoxically relax the lower oesophageal sphincter
• Coffee (caffeinated and sometimes decaffeinated)
• Carbonated drinks
• Alcohol — particularly beer and wine
• Very hot or very cold foods

Keep a short symptom-and-food diary for 2–3 weeks if triggers aren’t obvious. Rather than eliminate everything, identify the 2–3 things that reliably trigger you.

Sleep position

For night-time reflux specifically:

• Elevate the head of the bed by 15–20 cm using blocks under the bed legs (not just extra pillows, which bend the body and worsen reflux)
• Sleep on your left side — anatomy favours this side for reflux reduction

Smoking

Smoking reduces lower oesophageal sphincter tone and reduces salivary protection against reflux. Stopping helps meaningfully — see our guidance on asthma for the local smoking-cessation services that apply equally here.

Tight clothing

High-waisted tight clothing, shapewear, and heavy belts can worsen reflux by raising intra-abdominal pressure. A small thing, but worth noticing.

Exercise — helpful overall, but timing and technique matter

Exercise and reflux have a more nuanced relationship than most patients realise:

• Regular moderate-intensity activity helps, mainly through weight management and general metabolic benefit. Walking, cycling on flat ground, swimming, and general aerobic work usually don’t provoke reflux.
• Intense exercise within 2–3 hours of a meal — running, high-intensity cycling, vigorous gym work — often worsens reflux in the short term. Leave a reasonable gap after eating.
• Movements that raise intra-abdominal pressure can trigger reflux episodes: heavy compound lifts done with Valsalva (squats, deadlifts with held breath), crunches and sit-ups, and yoga positions that invert the body (shoulder stands, headstands, downward dog for extended periods). For patients with significant reflux these are worth modifying — e.g. swap heavy deadlifts for goblet squats, swap sit-ups for planks and dead bugs, swap inversions for gentler hip-opening poses.
• “Core strengthening” in the conventional abdominal-compression sense isn’t the useful bit.

The specific exercise that genuinely helps — diaphragmatic breathing. Randomised trial evidence (Eherer 2012 in Am J Gastroenterol and subsequent studies) supports a daily diaphragmatic breathing practice as a real adjunct treatment for GERD. The proposed mechanism is strengthening the crural diaphragm, which wraps around the lower oesophagus and acts as an external reinforcement to the lower oesophageal sphincter.

The simple technique, 5–10 minutes daily:

1. Lie on your back or sit comfortably
2. Place one hand on your chest and one on your abdomen just below the ribs
3. Breathe in slowly through the nose, directing the breath so that the abdominal hand rises while the chest hand stays relatively still
4. Breathe out slowly through the mouth or nose
5. Aim for a rhythm of around 6 breaths per minute — slower than your usual rate

Consistency matters more than duration. Most patients who benefit notice a meaningful reduction in reflux symptom frequency over 4–8 weeks of daily practice, sometimes allowing a PPI step-down. It won’t work for every patient, but it is free, low-risk, and supported by the evidence base — worth a try.

GERD medications

A stepped approach usually works well.

Antacids — for occasional symptoms

Simple antacids (calcium carbonate — Gaviscon calcium, Eno, Gelusil, Mylanta) neutralise acid for short periods (30–60 minutes). Useful for occasional breakthrough symptoms; not effective as primary long-term therapy.

Alginates — a genuinely useful adjunct

Alginate-containing preparations (Gaviscon Double Action, Gaviscon Advance) form a physical “raft” floating on top of stomach contents, which suppresses reflux for 3–4 hours. Especially useful:

• After meals, particularly dinner, in patients with night-time reflux
• In pregnancy, where other options are limited
• As an adjunct to PPI when breakthrough symptoms remain

Alginates are safer than antacids for long-term use; the main caveat is sodium content for patients with significant heart failure or on strict sodium restriction.

H2 blockers — a useful middle step

Famotidine (Pepcidine) and similar H2 blockers reduce acid production, with onset within an hour and effect lasting several hours. Useful for:

• Mild-to-moderate GERD
• Occasional breakthrough on a PPI
• Night-time reflux, taken before bed in addition to a morning PPI
• Patients who prefer not to be on a daily PPI

Ranitidine (Zantac) — formerly the most widely used H2 blocker — was withdrawn globally from 2020 due to concerns about the contamination of the drug with N-nitrosodimethylamine (NDMA). Famotidine is the current alternative.

Proton pump inhibitors (PPIs) — effective, sometimes overused

PPIs are the most effective acid-suppressing medications. They include:

• Omeprazole (Losec, generic)
• Esomeprazole (Nexium)
• Pantoprazole (Pantoloc, Controloc)
• Rabeprazole (Pariet)
• Lansoprazole (Takepron)

When PPIs are appropriate:

• Moderate-to-severe reflux, including erosive oesophagitis
• Peptic ulcer disease
• H. pylori eradication (as part of the combination)
• Barrett’s oesophagus
• Long-term high-dose NSAID or steroid use (gastroprotection)
• Severe gastritis
• High bleeding risk with antiplatelet medications

Points worth knowing:

• Take PPIs 30–60 minutes before breakfast (for once-daily dosing) or before meals (for twice-daily dosing). They work best when the proton pumps are actively being switched on by eating. Taking a PPI at bedtime or randomly during the day substantially reduces its effect.
• Effect is not instant — PPIs reach full effect over about 4–5 days of regular use.
• Efficacy differs between agents slightly — if one isn’t working, switching within the class is reasonable before concluding a PPI doesn’t suit you.

Long-term safety — the honest picture:

PPIs are broadly safe medications, but long-term use (typically measured in years rather than weeks) has been associated with modest increases in several risks:

• Vitamin B12 deficiency — screening is worthwhile after several years of continuous use
• Low magnesium — occasionally significant, particularly with diuretic use
• Bone fracture risk — small but real signal in observational studies, particularly in older adults and with long duration
• Kidney problems — an uncommon but recognised risk of acute interstitial nephritis, and a modest signal for chronic kidney disease progression
• Clostridioides difficile infection — modest increased risk
• Pneumonia — small signal in some populations
• Rebound acid hypersecretion when stopping — short-term increase in symptoms for 2–4 weeks after stopping a long-term PPI, which can be mistaken for “my reflux coming back” and prompt unnecessary restart

These risks are genuinely modest for most patients taking PPIs for a clear clinical reason. They are a reason not to remain on a PPI without a clear clinical reason.

The “when can I stop my PPI?” conversation

A conversation we want to have more often than we usually do:

• If you were started on a PPI for a specific short-term indication (NSAID course, ulcer healing, H. pylori course) and the indication has passed, step-down is usually appropriate — either to on-demand use, to an H2 blocker, or to stopping entirely.
• If you’re on a PPI for long-standing reflux, a step-down trial is reasonable: reduce to half the current dose for 2–4 weeks, then to alternate days, then to as-needed. Expect some rebound and ride it out with an alginate or H2 blocker.
• If you have Barrett’s oesophagus, erosive oesophagitis on endoscopy, or severe symptoms that reliably return with stopping, long-term PPI is the right plan — with periodic review of dose and indication.

A lifetime PPI that no one reviews is usually not the right plan. Please raise it at your next visit if we haven’t discussed it.

Managing functional dyspepsia

Functional dyspepsia is often harder to treat than GERD, because there’s rarely a single structural fix. A stepped approach usually works.

Test and treat for H. pylori first

In Singapore’s population prevalence, this is a worthwhile first step for anyone presenting with dyspepsia without alarm features. A proportion of patients have their symptoms resolve entirely after successful eradication.

A PPI trial

A 4–8 week trial of a PPI helps a meaningful proportion of patients, particularly those with epigastric pain or burning symptoms. If symptoms settle, we’d typically try stepping down. If there’s no response after 8 weeks, the PPI is probably not the answer and we’d move on rather than continue indefinitely.

A prokinetic

For postprandial distress (fullness, early satiety, bloating) — where impaired stomach emptying is often the driver — a prokinetic is sometimes useful. Options:

• Domperidone — used short-term; the HSA has noted cardiac rhythm concerns with prolonged use at higher doses, so we’d review regularly
• Metoclopramide — used for acute episodes; long-term use is limited by the risk of extrapyramidal side effects (movement disorders)

Prokinetics aren’t a long-term solution for most patients and are usually adjuncts.

Neuromodulation — low-dose antidepressants for dyspepsia

For patients with persistent dyspepsia despite the above, low-dose amitriptyline (typically 10–25 mg at night) or mirtazapine (useful when appetite and weight are low) can meaningfully improve symptoms. These aren’t being used as antidepressants — the doses are much lower than treatment for depression — but they modulate the heightened visceral sensitivity that often underlies functional dyspepsia.

This is a well-evidenced option that patients sometimes resist when offered (“I’m not depressed”) — worth discussing with an open mind. Many patients report substantial improvement.

Dietary adjustment

• Small, frequent meals rather than large ones
• Chew thoroughly, eat slowly
• Identify individual trigger foods — commonly fatty or spicy meals, excessive tea or coffee, alcohol
• STW-5 (Iberogast) — a herbal prokinetic preparation available locally — has some evidence for functional dyspepsia, reasonable adjunct if you prefer a non-pharmacological option

Stress and sleep

Functional dyspepsia symptoms often fluctuate with stress, sleep quality, and mood. This doesn’t mean “it’s in your head” — it reflects a real interplay between the nervous system and the gut. A basic sleep and stress audit is often part of the conversation.

A brief note on pregnancy

Reflux is very common in pregnancy, driven by hormonal relaxation of the LOS and mechanical pressure from the growing uterus. The usual approach:

• Lifestyle first — small meals, avoid late eating, elevate head of bed, identify triggers
• Alginates (Gaviscon) — generally considered safe throughout pregnancy and often sufficient
• Famotidine — the H2 blocker with the most reassuring pregnancy safety data
• PPIs — omeprazole has the largest body of pregnancy safety data; generally considered acceptable where symptoms warrant it

Symptoms usually settle soon after delivery. H. pylori testing and treatment are usually deferred until after pregnancy unless a specific indication arises.

The Singapore context

• Healthier SG — for enrolled chronic-disease patients, reflux and dyspepsia review can be integrated into the chronic-care plan, with preferred long-term review cadence rather than episodic visits
• CHAS and MediSave — consultations and many PPIs / H2 blockers are subsidised where applicable; H. pylori eradication antibiotics vary
• Urea Breath Test at KTMC — we offer this in both Joo Chiat and Punggol clinics; results are discussed on the day or at the next visit
• Specialist referrals — we work with a small number of trusted gastroenterologists and general surgeons for endoscopy and onward care; we’ll suggest the most appropriate match based on your clinical picture and preference

Get in touch

Joo Chiat — 172 Joo Chiat Road, #01-01, Singapore 427443 · Tel 6920 1952

Punggol — 658 Punggol East, #01-04, Singapore 820658 · Tel 6312 4589

Email — admin@ktmc.sg

References

Guidelines and consensus statements

• Katz PO, Dunbar KB, Schnoll-Sussman FH, et al. ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol. 2022;117(1):27–56.
• Malfertheiner P, Megraud F, Rokkas T, et al. Management of Helicobacter pylori infection: the Maastricht VI / Florence consensus report. Gut. 2022;71:1724–1762.
• Chey WD, Howden CW, Moss SF, et al. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2024;119(9):1730–1753.
• Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ. Functional dyspepsia. Lancet. 2020;396:1689–1702.
• Stanghellini V, Chan FKL, Hasler WL, et al. Gastroduodenal Disorders. Gastroenterology. 2016;150(6):1380–1392. (Rome IV criteria)

Singapore context

• Ang TL, Fock KM, Dhamodaran S, Teo EK, Tan J. Evaluation of the Utility of Serology, Urea Breath Test, and Stool Antigen Test for the Detection of H. pylori in Singapore. J Gastroenterol Hepatol. — locally-adapted diagnostic recommendations.
• Ministry of Health, Singapore. Singapore Cancer Registry — annual reports on gastric cancer incidence.

PPI safety

• Freedberg DE, Kim LS, Yang YX. The Risks and Benefits of Long-term Use of Proton Pump Inhibitors: Expert Review and Best Practice Advice From the American Gastroenterological Association. Gastroenterology. 2017;152(4):706–715.
• Targownik LE, Fisher DA, Saini SD. AGA Clinical Practice Update on De-Prescribing of Proton Pump Inhibitors: Expert Review. Gastroenterology. 2022;162(4):1334–1342.

Diaphragmatic breathing for GERD

• Eherer AJ, Netolitzky F, Högenauer C, et al. Positive effect of abdominal breathing exercise on gastroesophageal reflux disease: a randomized, controlled study. Am J Gastroenterol. 2012;107(3):372–378.
• Casale M, Sabatino L, Moffa A, et al. Breathing training on lower esophageal sphincter as a complementary treatment of gastroesophageal reflux disease (GERD): a systematic review. Eur Rev Med Pharmacol Sci. 2016;20(21):4547–4552.

National programmes

• Ministry of Health, Singapore. Healthier SG and Chronic Tier information. healthiersg.gov.sg
• Community Health Assist Scheme. chas.sg

This information is for general education only and is not a substitute for medical advice. Reflux and dyspepsia management should be individualised based on your specific symptoms, risk factors, test results, and preferences — please speak with our team about what’s right for you. v1.0 · April 2026 · Review due April 2028.