Peptic Ulcer Disease

Meet the patient

A 66-year-old man on long-term ibuprofen for his knees wakes at 2 a.m. with epigastric burning that is eased by a glass of milk and a couple of antacids. He has noticed the pain between meals for weeks, and his weight has crept up because eating settles it. Tonight he vomits what looks like dark coffee-grounds, then passes black tarry stool and feels faint on standing.[4][8]

Two questions are now live and they govern the next hour: is he bleeding or perforating? (the haematemesis, melaena, and postural drop say bleeding) and what caused the ulcer, so you can stop it happening again? (the NSAID plus an unasked H. pylori history). Everything below exists to answer both at consultant depth.[1][5]

What an ulcer is — and what it is not

A peptic ulcer is a break through the muscularis mucosae. Stop there; the depth is the definition. It is distinct from an erosion, which is a shallow epithelial break that heals without scarring. The distinction matters because depth decides the complication — a deep crater can sit on a visible artery (bleeding) or erode the full wall (perforation).[4]

PUD arises when aggressive factors (acid, pepsin, H. pylori, NSAIDs) overwhelm mucosal defence (the mucus-bicarbonate barrier, mucosal blood flow, prostaglandins, rapid epithelial turnover). The two dominant causes together account for the great majority of ulcers; the remainder are Zollinger-Ellison, stress ulcers in the critically ill, and malignancy.[1][4]

The clinical task is not to heal the ulcer — a PPI does that in weeks — but to find and remove the cause. After successful H. pylori eradication, ulcer recurrence falls from roughly 60 percent to under 10 percent; with acid suppression alone, the ulcer recurs in most patients within a year. That single statistic is the whole argument for eradication.[1]

Duodenal versus gastric — the face-off that earns the marks

The DU-GU split drives the symptoms, the cancer risk, and the follow-up — learn it as a face-off with one discriminator.[4]

[4]

The discriminator line: food eases duodenal pain and worsens gastric pain. Add "wakes at night" (classic DU) and "weight loss with eating" (classic GU) and you can call it at the bedside before the scope.[4]

How common, and the patient who bleeds

PUD is common — lifetime prevalence about 10 percent, though it has fallen in the developed world as H. pylori carriage declines and acid suppression improves. H. pylori infects roughly half the world's population, acquired in childhood by the faecal-oral and oral-oral routes; prevalence is far higher in developing regions (over 80 percent in some Indian and African cohorts).[3][4]

The cause split examiners quote: H. pylori causes about 90 percent of duodenal ulcers and 60 to 70 percent of gastric ulcers; NSAIDs are the second commonest cause and the leading cause of bleeding ulcers wherever H. pylori is declining. About 20 to 30 percent of chronic NSAID users develop an endoscopic ulcer, though most are silent — which is exactly why the first sign is often a complication.[8]

[4] [8]

Risk factors for an ulcer — and more importantly for a complication (bleeding, perforation): H. pylori and NSAID or aspirin use (dose-dependent and synergistic), age over 60, a prior ulcer or bleed, smoking (impairs healing, doubles recurrence), alcohol excess, and the concurrent drugs — anticoagulants, antiplatelets (clopidogrel), SSRIs, corticosteroids, spironolactone.[1]

The single most dangerous combination is an NSAID plus H. pylori in an older patient on an anticoagulant — this is the patient who arrives in resus with massive haematemesis at 3 a.m. Find them before they bleed: test and eradicate H. pylori before starting a long-term NSAID, co-prescribe a PPI, and use the lowest dose for the shortest time.[8]

Two roads to an ulcer — the mechanism an examiner probes

Normal mucosal defence rests on a mucus-bicarbonate layer (a near-neutral pH at the epithelial surface), mucosal blood flow, prostaglandins (PGE2, PGI2) that drive mucus and bicarbonate secretion, and rapid epithelial renewal. An ulcer forms when that balance tips toward acid-peptic injury — and the pathogenesis differs by site.[4]

Gastric ulcer — weak defence, often normal acid. H. pylori-induced corpus-predominant atrophic gastritis shrinks parietal cell mass and acid output, and the damaged mucosa is injured even by modest acid. NSAIDs reproduce the picture by depleting prostaglandins. The exception is Zollinger-Ellison, where a gastrinoma drives acid hypersecretion through the defence — a hyper-acid gastric ulcer.[3][4]

Duodenal ulcer — acid hypersecretion with H. pylori. The pattern is antral-predominant gastritis: somatostatin-secreting D cells are damaged, gastrin release is unchecked, and acid output rises. The excess acid reaches the duodenum, the mucosa undergoes gastric metaplasia, and H. pylori colonises that metaplastic epithelium, causing ulceration. This is why H. pylori causes about 90 percent of duodenal ulcers.[3][4]

H. pylori virulence — the molecules examiners name

Helicobacter pylori is a spiral, microaerophilic, urease-producing Gram-negative bacterium that lives in the gastric mucus layer. Its virulence factors are high-yield and each one maps to a clinical fact:[3]

• Urease — hydrolyses urea to ammonia, alkalinising its microenvironment and surviving gastric acid. This is the basis of the rapid urease (CLO) test and the urea breath test.
• CagA (cytotoxin-associated gene A) — injected into epithelial cells via a type IV secretion system; drives inflammation and ulcer risk, and is strongly linked to gastric adenocarcinoma. Strains carrying the cag pathogenicity island are more virulent.
• VacA (vacuolating cytotoxin A) — forms pores in epithelial membranes, induces apoptosis and vacuolation.
• BabA (blood-group antigen-binding adhesin) — binds the Lewis-b blood-group antigen on gastric epithelium, enabling tight adherence and more severe disease.[1]

NSAIDs and the rest — COX inhibition and the special ulcers

NSAIDs inhibit cyclo-oxygenase. Blockade of the constitutive COX-1 cuts mucosal prostaglandin (PGE2, PGI2) synthesis, so mucus and bicarbonate secretion fall, mucosal blood flow drops, and epithelial turnover slows — the mucosa is stripped of its defences. Weakly acidic NSAIDs (aspirin) also cause direct topical injury in an acid stomach. Selective COX-2 inhibitors (celecoxib, etoricoxib) spare COX-1 and reduce — but do not abolish — gastrointestinal toxicity, at the cost of more cardiovascular risk.[4][8]

Zollinger-Ellison syndrome — a gastrin-secreting tumour (usually pancreatic or duodenal, part of MEN-1 in a quarter of cases) drives massive acid hypersecretion, producing multiple, recurrent, or distal (jejunal) ulcers refractory to standard PPI doses, with diarrhoea and a markedly raised fasting serum gastrin (check while off PPI).[4]

Stress ulcers in the critically ill arise from splanchnic hypoperfusion and mucosal ischaemia rather than acid — hence prophylaxis is targeted at the ICU patient with specific risk factors: Curling ulcer (major burns) and Cushing ulcer (severe head injury, direct vagal stimulation with massive acid and a high perforation risk).[4]

Clinical presentation — the pain, the silence, the complication

Classic symptom — epigastric burning or gnawing, episodic and periodic (clusters over days to weeks, then remits). The food relationship is the discriminator examiners test:[4]

• Duodenal ulcer — pain relieved by food (and antacids or milk), occurs 2 to 5 hours after eating, and classically wakes the patient at night (often 1 to 2 a.m.). Weight may rise because eating eases the pain.
• Gastric ulcer — pain worsened by food, soon after eating, with nausea, early satiety, and weight loss.[1]

The silence trap. Many ulcers — especially in the elderly and in chronic NSAID users — are silent, and declare themselves as a complication: haematemesis or melaena, sudden perforation, or unexplained iron-deficiency anaemia. Up to half of NSAID-related bleeds occur with no warning symptoms, which is why gastroprotection is a prevention strategy, not a wait-and-see.[8]

How complications present (the way many ulcers first declare themselves):[4][5]

• Bleeding — haematemesis (vomiting blood; "coffee-ground" if altered) and/or melaena (black, tarry, foul-smelling stool); syncope and postural dizziness with significant volume loss.
• Perforation — sudden, severe, generalised abdominal pain with peritonism (rigidity, guarding, rebound, absent bowel sounds) and free gas under the diaphragm on an erect chest X-ray.
• Penetration — a posterior DU boring into the pancreas gives severe boring back pain unresponsive to antacids, with raised amylase or lipase; no free gas, so it is often missed.
• Gastric outlet obstruction — non-bilious projectile vomiting of undigested food, early satiety, a succussion splash, and visible peristalsis.[1]

Alarm features — the trigger for urgent OGD

Apply these to any patient with dyspepsia. Their presence moves the patient straight to urgent oesophagogastroduodenoscopy and away from an empirical trial of acid suppression.[1]

[1]

The differential — and the surgical mimics

Recurrent or acute epigastric pain is not always a peptic ulcer. The key mimics, each with a one-line discriminator:[4]

• GORD — retrosternal burning and regurgitation, worse lying down or after large meals; no ulcer on OGD.
• Functional (non-ulcer) dyspepsia — dyspepsia with a normal OGD; the commonest cause after H. pylori is excluded.
• Gastric cancer — weight loss, dysphagia, early satiety, anaemia, a palpable mass; biopsy every gastric ulcer.
• Biliary colic or cholecystitis — right-upper-quadrant pain worse after fatty food; Murphy sign.
• Acute pancreatitis — severe epigastric pain radiating to the back, eased by sitting forward; raised lipase.
• Myocardial infarction (inferior) — epigastric pain in the elderly or diabetic; do an ECG.
• Mesenteric ischaemia — pain out of proportion to examination, postprandial.[1]

Always look for the alarm features above; their presence moves the patient straight to urgent OGD.[1]

Bedside assessment — seek the complication, not the diagnosis

In uncomplicated PUD the examination is often unremarkable apart from epigastric tenderness. The job at the bedside is to detect the complications:[4][5]

• Peritonism (rigidity, guarding, rebound, absent bowel sounds) — perforation until proven otherwise.
• Signs of volume loss (tachycardia, hypotension, postural drop, cool peripheries, oliguria) — bleeding.
• Melaena on rectal examination; a succussion splash and visible gastric peristalsis — gastric outlet obstruction.
• Pallor of anaemia; signs of chronic liver disease (varices, not PUD, may be the bleeder).
• An epigastric mass or Virchow (left supraclavicular) node — gastric cancer.[1]

Bedside observations (heart rate, blood pressure, respiratory rate, oxygen saturation, temperature, urine output, GCS) define severity in bleeding or complicated PUD. A postural drop in systolic blood pressure (over 20 mmHg) or a rise in pulse (over 30 bpm on standing) signals significant volume loss (over 1 litre).[5]

Investigations — OGD first, then the tests that guide the cure

The gold standard — oesophagogastroduodenoscopy

OGD localises the ulcer, identifies stigmata of recent haemorrhage (spurting vessel, non-bleeding visible vessel, adherent clot, oozing, clean base), treats bleeding (injection, thermal, clips), and biopsies — for H. pylori and to exclude malignancy in every gastric ulcer. Gastric ulcers are re-endoscoped at 8 to 12 weeks to confirm healing and exclude cancer. A duodenal ulcer is essentially always benign and does not mandate biopsy for malignancy, though biopsies are taken for H. pylori.[4][5]

Tests for H. pylori — the critical exam area

The tests divide into invasive (biopsy at OGD) and non-invasive, and into those that detect active infection versus those that cannot.[1][3]

[1] [3]

The crucial pre-test rule: stop PPIs for at least 2 weeks and antibiotics for at least 4 weeks before a urea breath test, stool antigen, or biopsy-based urease test — these agents suppress H. pylori and cause false negatives. (Serology is unaffected.)[1][3]

Bloods and other tests

FBC for anaemia of chronic bleeding (MCV and ferritin for iron deficiency). U&E, LFTs, coagulation, group and crossmatch in bleeding — a raised urea with normal creatinine is a bedside pointer to upper-GI bleeding (digested blood protein converted to urea). Fasting serum gastrin, off PPI, if Zollinger-Ellison is suspected. An erect chest X-ray or CT abdomen for free intra-abdominal gas indicates perforation.[1]

Risk-stratification scores in upper GI bleeding

Glasgow-Blatchford score (GBS) — a pre-endoscopy score predicting the need for intervention (transfusion, endoscopic or surgical treatment). Components: blood urea, systolic blood pressure, heart rate, haemoglobin, the presence of melaena or syncope, and major cardiac or hepatic disease. A score of 0 identifies low-risk patients suitable for outpatient management.[5]

Rockall score — a post-endoscopy score predicting rebleeding and mortality, combining pre-endoscopy components (age, shock, comorbidity) with endoscopic findings (diagnosis, stigmata of recent haemorrhage). A total score of 0 to 2 carries low risk; 3 or more is high risk. The pre-endoscopy Rockall (age plus shock plus comorbidity, maximum 7) is used before OGD.[5]

The bleeding peptic ulcer — resuscitation precedes the scope[1]

For the bleeding peptic ulcer — the commonest life-threatening presentation — resuscitation precedes definitive treatment. Humour is off here; this is a resuscitation problem with a protocol.[5]

[1] [5] [6]

The single trial to cite for the IV PPI infusion is Lau et al., NEJM 2000 — in bleeding peptic ulcers with endoscopically controlled bleeding, omeprazole 80 mg IV bolus then 8 mg per hour for 72 hours reduced rebleeding, surgery and repeat endoscopy versus placebo. It is the basis of the post-endoscopy IV PPI infusion that is now universal.[6]

Definitive management — find and remove the cause

The definitive ladder addresses the cause, heals the ulcer, and prevents recurrence. Get the cause wrong and the ulcer comes back.[1]

1. Eradicate H. pylori — the regimen is regional

The cure for H. pylori-associated ulcers. The first-line regimen is regional, driven by local clarithromycin resistance:[1][3]

2. Test of cure — mandatory

Confirm eradication with a urea breath test or stool antigen at least 4 weeks after completing antibiotics and at least 2 weeks after stopping the PPI. (Serology cannot be used for cure — it stays positive.) Test of cure is essential after every eradication course because resistance-driven failure is common.[1][3]

3. Acid suppression for healing

A PPI for 4 weeks (duodenal ulcer) to 6 to 8 weeks (gastric ulcer): omeprazole 20 to 40 mg once daily, or pantoprazole 40 mg, lansoprazole 30 mg, esomeprazole 20 to 40 mg, rabeprazole 20 mg. If a PPI is unavailable or contraindicated, an H2-receptor antagonist (famotidine 40 mg at night) or a mucosal protectant (sucralfate 1 g four times daily) is an alternative.[1][4]

4. NSAID-induced ulcer

Stop the NSAID where possible (switch to paracetamol, up to 1 g four times daily). Give a PPI — omeprazole 20 to 40 mg once daily for 4 to 8 weeks — to heal the ulcer. Misoprostol 200 micrograms four times daily is a prostaglandin analogue that restores defence (abortifacient — contraindicated in pregnancy). Test and eradicate H. pylori if co-existent, as the combination markedly raises risk.[4][8]

5. Confirm gastric ulcer healing

Gastric ulcers must be re-endoscoped at 8 to 12 weeks to confirm healing and exclude malignancy; a non-healing ulcer demands re-biopsy and surgical referral. Duodenal ulcers are benign and need no routine repeat OGD once H. pylori is eradicated.[4]

[1]

The perforated ulcer — and why you eradicate afterwards

Perforation is a surgical emergency: free gas, peritonitis, and an emergency laparotomy. The patch closure (Graham omental patch for a DU; resection for a GU) stops the leak — but the single trial to cite is Ng et al., Annals of Surgery 2000: after simple closure of a perforated DU, H. pylori eradication prevented ulcer recurrence at one year versus acid suppression alone. So the operation fixes the hole, and the eradication fixes the disease — both are mandatory.[7]

The special ulcers and scenarios

• Stress ulcer prophylaxis (ICU) — indicated for patients on mechanical ventilation for over 48 hours, coagulopathy, shock or sepsis, major burns (Curling ulcer), and severe head injury (Cushing ulcer). Use an enteral PPI (or an H2-blocker such as famotidine IV 20 mg twice daily); stop when the patient resumes oral intake and risk factors resolve. Do not prescribe prophylaxis to every ward patient — it raises C. difficile and pneumonia risk.[4]
• Zollinger-Ellison syndrome — suspect with multiple, jejunal, or refractory ulcers with diarrhoea and acid hypersecretion. Confirm with a raised fasting serum gastrin (off PPI) and a positive secretin stimulation test (gastrin paradoxically rises); localise the gastrinoma with CT, MRI, endoscopic ultrasound or somatostatin receptor scintigraphy. Treat with a high-dose PPI (omeprazole 60 to 80 mg daily or more) and surgical resection if localised; metastatic disease uses somatostatin analogues, everolimus, or sunitinib.
• Curling ulcer — acute stress ulceration within 72 hours of major burns (over 30 percent body surface area) from hypovolaemia and splanchnic hypoperfusion; prevent with early enteral feeding and acid suppression.[4]
• Cushing ulcer — stress ulcer after severe head injury or raised intracranial pressure, from direct vagal stimulation causing massive acid hypersecretion; high perforation risk.
• Marginal (anastomotic) ulcer — at a gastrojejunostomy after partial gastrectomy or Roux-en-Y; driven by acid on jejunal mucosa plus H. pylori; smoking and NSAIDs are cofactors.
• Refractory ulcer — failure to heal after 8 (DU) to 12 (GU) weeks of PPI. Reconsider: ongoing NSAID use, persistent H. pylori (adherence or resistance), Zollinger-Ellison, malignancy (re-biopsy), Crohn disease, cocaine, ischaemia, and non-adherence to the PPI.[1]

Complications and the classic pitfalls

The four complications (and a fifth for gastric ulcers):[4][5]

• Bleeding — the commonest complication; the leading cause of non-variceal upper GI bleeding; managed by endoscopic therapy plus high-dose IV PPI infusion.
• Perforation — sudden severe peritonitis with free gas; emergency surgical repair (Graham patch for DU; resection for GU).
• Penetration — a posterior DU into the pancreas (back pain, raised amylase or lipase); no free gas, so it is often missed.
• Gastric outlet obstruction — from oedema and scarring of a pyloric-channel or DU; non-bilious projectile vomiting, succussion splash; decompress with an NG tube, correct the hypokalaemic hypochloraemic metabolic alkalosis from vomiting, then balloon dilatation or surgery.
• Malignant transformation (gastric ulcer only) — the reason every GU is biopsied and re-endoscoped.[1]

The classic pitfalls every candidate must name: failing to test and eradicate H. pylori; not performing a test of cure; relying on serology to confirm active infection; giving a PPI before a urea breath test (false negative); not biopsying a gastric ulcer; not re-endoscoping a gastric ulcer at 8 to 12 weeks; and missing perforation in an elderly painless NSAID ulcer presenting as vague sepsis. A further trap: over-transfusing a bleeding patient raises splanchnic venous pressure and precipitates rebleeding — stay restrictive.[1][4][5]

How PUD patients come to harm — the preventable list

• The older patient on an NSAID plus an anticoagulant who was never tested for H. pylori and bleeds torrentially.[8]
• A gastric ulcer treated with a PPI and never biopsied or re-endoscoped, presenting later as cancer.[4]
• A H. pylori eradication given with no test of cure, recurring within the year.[1]
• A bleeding patient over-transfused, rebleeding from a raised portal pressure.[5]
• A urea breath test done on a PPI, read as negative, and the patient sent home to bleed.[1]
• Aspirin for secondary prevention stopped and forgotten after a bleed, with an early thrombotic event.[5]

Special populations

• NSAID or aspirin users — give gastroprotection with a PPI; test and eradicate H. pylori before starting long-term NSAID therapy. Aspirin for secondary cardiovascular prevention is usually continued through a bleed once haemostasis is secure (stop during active bleeding, restart early — within 7 days — to avoid thrombotic events).[5][8]
• The elderly — present atypically (painless bleed or perforation), have more comorbidity, and bleed more often on NSAIDs; lower threshold for OGD and PPI prophylaxis.
• Anticoagulated patients — bleeding ulcers are commoner and more severe; reverse anticoagulation per agent and re-start early (within 7 days) once haemostasis is secured, balancing thrombotic against rebleeding risk.[5]
• Pregnancy — PUD is uncommon; aluminium or magnesium antacids and sucralfate are first-line (safe); H2-blockers (except near term) and PPIs (omeprazole — the most data) are second-line; avoid bismuth and tetracycline. Eradication is deferred until after delivery unless bleeding.
• Immunocompromised — consider CMV (giant ulcers, intranuclear inclusions on biopsy) and HSV ulcers; treat the underlying virus.
• Chronic kidney disease — higher ulcer and bleed risk; dose-adjust the PPI; avoid NSAIDs.[1]

Prevention — the high-risk patient before the ulcer

Prevention targets the two dominant causes and the high-risk patient before the ulcer or its complication occurs.[4][8]

• Search-and-treat for H. pylori — screen and eradicate before starting long-term NSAID or aspirin, in those with a prior ulcer or bleed, and in first-degree relatives of gastric-cancer patients. Population-level screen-and-treat in high-prevalence regions reduces gastric-cancer incidence.[3]
• Gastroprotect NSAIDs — for any chronic NSAID, co-prescribe a PPI (omeprazole 20 mg daily); use the lowest effective dose for the shortest time; avoid combining NSAIDs; prefer a COX-2 selective agent (celecoxib) only when cardiovascular risk is low. Misoprostol 200 micrograms four times daily is a prostaglandin-replacement alternative.[8]
• Lifestyle — smoking cessation (roughly doubles recurrence if continued), moderate alcohol, stress management. Diet has modest symptomatic benefit but does not heal ulcers.
• Stress ulcer prophylaxis in ICU — restrict to genuine indications; stop on ward transfer or resumption of oral intake to limit C. difficile and pneumonia risk.[4]

The evidence — guidelines and the trials to cite

The three guideline pillars — NICE (UK), ACG (US, Chey 2017), and Maastricht VI/Florence (2022) — agree on the principles (eradicate H. pylori, heal with a PPI, gastroprotect NSAIDs, treat complications endoscopically) but differ on the first-line regimen and duration, driven by clarithromycin resistance. Duration matters: 14 days consistently outperforms 7 to 10; NICE retains 7 days on cost and adherence grounds.[1][3]

[1] [4]

The mantra: heal the ulcer with a PPI, but cure the disease by removing the cause — eradicate H. pylori and prove it, stop or gastroprotect the NSAID, and biopsy every gastric ulcer.[1][4]

Ward-round test — three stems

Stem 1 — the man from the top of the topic (answer)

A 66-year-old on ibuprofen wakes with night pain eased by milk, then vomits coffee-grounds and passes melaena with a postural drop. What is the first 12 hours? Model: This is a bleeding peptic ulcer — the commonest life-threatening presentation. Resuscitate first: ABCDE, two large-bore cannulae, balanced crystalloid, group-and-crossmatch, restrictive transfusion to Hb about 70 to 80 g/L (avoid over-transfusion, which raises splanchnic pressure and rebleeding), reverse any anticoagulant. Risk-stratify with the Glasgow-Blatchford score at the front door. Proceed to OGD within 24 hours for dual endoscopic haemostasis (adrenaline injection plus thermal coagulation or a clip on high-risk stigmata), then an IV PPI infusion — omeprazole 80 mg bolus then 8 mg per hour for 72 hours (Lau 2000). After haemostasis, find the cause: test for H. pylori (stop the PPI 2 weeks before a urea breath test or stool antigen), review the NSAID, and biopsy any gastric ulcer. Eradicate H. pylori if positive and confirm cure at 4 weeks; re-endoscope a gastric ulcer at 8 to 12 weeks.[5][6]

Stem 2 — the duodenal-versus-gastric discriminator (answer)

An examiner asks: "How does the pain of a duodenal ulcer differ from a gastric ulcer, and what does that tell you about the acid?" Model: Duodenal pain is eased by food and wakes the patient at night; gastric pain is worsened by food. The mechanism is the acid story: a DU is driven by antral-predominant gastritis, hypergastrinaemia and acid hypersecretion — so food (which buffers acid) relieves the pain, and the empty stomach at 2 a.m. brings it back. A GU sits on corpus-predominant atrophic gastritis with normal or low acid, so eating stimulates the little acid there is and worsens the pain. That is why H. pylori — the same organism — makes a DU through acid excess and a GU through acid depletion, and why a DU is essentially never malignant while a GU must always be biopsied.[4]

Stem 3 — the perforated DU and what you do after the patch (answer)

A 45-year-old smoker presents with sudden severe generalised abdominal pain, a rigid silent abdomen, and free gas under the diaphragm. At laparotomy a perforated DU is closed with an omental patch. What must happen next, and why? Model: The operation closes the hole; the disease is H. pylori, and it must be eradicated. Ng et al., Annals of Surgery 2000 showed that after simple closure of a perforated DU, H. pylori eradication prevented ulcer recurrence at one year versus acid suppression alone. So the post-operative plan is: test for H. pylori (biopsy-based urease at surgery, or urea breath test or stool antigen after stopping the PPI for 2 weeks and antibiotics for 4 weeks), eradicate with a regional regimen, and confirm cure — plus smoking cessation (smoking roughly doubles recurrence) and NSAID avoidance.[7]

References

1. [1]Chey WD, Leontiadis GI, Howden CW, et al. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection Am J Gastroenterol, 2017.PMID 28071659
2. [2]Yan TL, Wang JH, He XJ, et al. Ten-Day Vonoprazan-Amoxicillin Dual Therapy vs Standard 14-Day Bismuth-Based Quadruple Therapy for First-Line Helicobacter pylori Eradication: A Multicenter Randomized Clinical Trial Am J Gastroenterol, 2024.PMID 37975609
3. [3]Malfertheiner P, Megraud F, Rokkas T, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report Gut, 2022.PMID 35944925
4. [4]Lanas A, Chan FKL. Peptic ulcer disease Lancet, 2017.PMID 28242110
5. [5]Laine L, Barkun AN, Saltzman JR, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding Am J Gastroenterol, 2021.PMID 33929377
6. [6]Lau JY, Sung JJ, Lee KK, et al. Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers N Engl J Med, 2000.PMID 10922420
7. [7]Ng EK, Lam YH, Sung JJ, et al. Eradication of Helicobacter pylori prevents recurrence of ulcer after simple closure of duodenal ulcer perforation: randomized controlled trial Ann Surg, 2000.PMID 10674604
8. [8]Sostres C, Carrera-Lasfuentes P, Lanas A. Non-steroidal anti-inflammatory drug related upper gastrointestinal bleeding: types of drug use and patient profiles in real clinical practice Curr Med Res Opin, 2017.PMID 28569554