Stomach and Digestive Treatments from UK Doctors

Acid-related disorders encompass gastro-oesophageal reflux disease (GORD), peptic ulcer disease, functional dyspepsia, and Barrett's oesophagus.

These conditions share overlapping symptoms — heartburn, epigastric pain, regurgitation, nausea — but differ in pathophysiology and management strategy.

GORD results from excessive reflux of gastric acid into the oesophagus, driven by transient lower oesophageal sphincter relaxation, hiatus hernia, or impaired oesophageal clearance.

Typical symptoms include heartburn (burning retrosternal discomfort worsened by bending or lying flat) and acid regurgitation.

Atypical presentations include chronic cough, hoarseness, dental erosion, and chest pain mimicking angina.

Prevalence in the UK is approximately 20-30% for monthly reflux symptoms and 5-7% for daily symptoms. Risk factors include obesity (relative risk 2.

5 for BMI above 30), smoking, alcohol, pregnancy, and medications that relax the lower oesophageal sphincter (calcium channel blockers, nitrates, anticholinergics).

Peptic ulcer disease affects 5-10% of the population over a lifetime. H. pylori infection accounts for 60-70% of gastric ulcers and 90% of duodenal ulcers. NSAID use is the second major cause.

Eradication of H. pylori heals 90% of infected ulcers and reduces recurrence from 70% to under 5% per year.

Functional dyspepsia is diagnosed when upper GI symptoms persist without an identifiable structural cause on endoscopy. It affects 10-15% of adults and is subclassified into:

• Epigastric pain syndrome (localised burning or pain)
• Postprandial distress syndrome (fullness, early satiation, bloating)

Alarm features warranting urgent endoscopy referral include dysphagia, unintentional weight loss exceeding 3% in 6 months, persistent vomiting, GI bleeding (haematemesis or melaena), iron deficiency anaemia, and new dyspepsia in patients over 55.

Proton pump inhibitors irreversibly block the H+/K+ ATPase enzyme in gastric parietal cells, reducing acid secretion by 90-95% at steady state.

They are the most effective class of acid-suppressing medication and the mainstay of GORD, peptic ulcer, and dyspepsia treatment.

Omeprazole 20 mg daily is the standard first-line PPI per NICE CG184 and the most widely prescribed. It heals erosive oesophagitis in 80-85% of patients within 4 weeks and 95% within 8 weeks.

Higher doses (40 mg) are reserved for severe oesophagitis (Los Angeles grade C/D) or Zollinger-Ellison syndrome.

Lansoprazole 30 mg daily is an equivalent alternative with marginally faster onset of action. It is preferred in some patients due to fewer CYP2C19-mediated drug interactions than omeprazole.

Esomeprazole (the S-enantiomer of omeprazole) at 40 mg provides slightly greater acid suppression, though the clinical difference is modest.

It is sometimes trialled when omeprazole at full dose provides incomplete relief.

Pantoprazole and rabeprazole are alternatives with varying interaction profiles.

Pantoprazole has the least CYP2C19 interaction, making it preferable for patients on clopidogrel where PPI co-prescription is indicated.

Prescribing strategy follows NICE guidance:

• Initial full-dose PPI for 4-8 weeks
• Step down to the lowest effective dose or switch to as-needed (PRN) dosing
• H2 receptor antagonists (ranitidine was withdrawn; famotidine 20 mg is available) provide an alternative for mild intermittent symptoms
• Antacids and alginates (Gaviscon Advance) offer on-demand symptom relief and are suitable adjuncts

H. pylori testing should precede PPI therapy in patients with uninvestigated dyspepsia under 55 without alarm features. A positive stool antigen test or urea breath test triggers eradication therapy:

• First-line: PPI + amoxicillin 1 g + clarithromycin 500 mg, all twice daily for 7 days (85% eradication)
• Penicillin allergy: PPI + metronidazole 400 mg + clarithromycin 500 mg twice daily for 7 days
• Confirm eradication with a repeat test 4 weeks after completing antibiotics and 2 weeks off PPI

PPIs are among the most overprescribed medications globally, with an estimated 25-70% of long-term users lacking a documented indication for continued therapy.

While PPIs are safe for most patients, prolonged use raises several evidence-based concerns that justify regular clinical review.

Fracture risk: A meta-analysis of 18 observational studies found a modest increase in hip fracture risk (OR 1.26) with PPI use exceeding 12 months.

The absolute risk increase is small (approximately 1 additional hip fracture per 1,200 patient-years), but patients with pre-existing osteoporosis or other fracture risk factors should have their bone health assessed.

Hypomagnesaemia: Symptomatic magnesium depletion occurs in approximately 1-2% of long-term PPI users.

The MHRA advises checking magnesium levels before starting long-term PPI therapy and periodically thereafter, particularly in patients taking digoxin or diuretics.

Vitamin B12 deficiency: Acid suppression impairs release of protein-bound B12 from food. Studies show a 25-65% increased risk of B12 deficiency with PPI use beyond 2 years.

Annual B12 measurement is prudent for patients on continuous therapy.

Clostridioides difficile infection: PPIs increase C. difficile risk by approximately 1.7-fold, likely by reducing the gastric acid barrier to spore survival.

This is particularly relevant in elderly patients, those recently treated with antibiotics, and hospitalised individuals.

Other associations under investigation:

• Community-acquired pneumonia: modest risk increase (OR 1.3) due to bacterial overgrowth in hypochlorhydric stomach
• Chronic kidney disease: observational data suggest small absolute risk increase with prolonged use
• Dementia: early epidemiological associations have not been confirmed in subsequent large studies

Deprescribing strategy: NICE recommends reviewing PPI therapy at least annually.

Gradual dose reduction over 4-8 weeks (halving the dose, then switching to alternate-day, then stopping) minimises rebound acid hypersecretion, which peaks 2-4 weeks after abrupt withdrawal and can mimic symptom recurrence.

Lifestyle modification is the first-line intervention for GORD and functional dyspepsia and remains important even when pharmacotherapy is required.

Multiple clinical guidelines endorse these measures as foundational to management.

Weight management is the most impactful modifiable factor for reflux.

A prospective study of over 10,000 women in the Nurses' Health Study found that each unit increase in BMI raised GORD symptom risk by 35%.

Losing 5-10% of body weight reduces reflux episodes by 40-50% and may allow PPI dose reduction or cessation.

Meal timing and composition directly influence reflux frequency:

• Eat at least 3 hours before lying down
• Smaller, more frequent meals reduce gastric distension and transient LOS relaxation
• High-fat meals delay gastric emptying by 30-40%, prolonging acid exposure
• Reduce intake of known reflux-provoking foods: coffee, chocolate, mint, citrus, tomatoes, spicy dishes

Positional therapy is effective for nocturnal reflux.

Elevating the head of the bed by 15-20 cm (using bed blocks, not extra pillows) reduces oesophageal acid exposure time by 67% in pH monitoring studies.

Left lateral decubitus sleeping position further reduces reflux due to anatomical positioning of the gastro-oesophageal junction.

Smoking cessation reduces transient lower oesophageal sphincter relaxation frequency and improves oesophageal acid clearance.

Smokers have a 70% higher risk of reflux symptoms compared with non-smokers.

Stress reduction benefits functional dyspepsia in particular, where visceral hypersensitivity is driven by the gut-brain axis.

Gut-directed hypnotherapy has Level 1 evidence for functional GI disorders, with 70-80% response rates in specialist centres.

Additional practical measures:

• Limit alcohol to under 14 units per week; spirits cause more reflux than beer or wine
• Avoid tight-fitting clothing that increases intra-abdominal pressure
• Chew food thoroughly to reduce aerophagia and improve mechanical digestion
• Peppermint oil capsules (enteric-coated) may help with IBS-overlap symptoms but can worsen reflux if the coating fails