Write a short note on peptic ulcer disease, Helicobacter pylori and Zollinger-Ellison syndrome.

Definition

Peptic ulcer disease (PUD) is a break in the mucosa of the stomach or duodenum extending through the muscularis mucosae, arising from an imbalance between aggressive factors (acid, pepsin, *H. pylori*, NSAIDs) and defensive factors (mucus and bicarbonate layer, mucosal blood flow, prostaglandins, epithelial regeneration).

Duodenal ulcers are commoner than gastric ulcers and occur in a younger age group.

Aetiology

*helicobacter Pylori*

A Gram-negative, spiral, microaerophilic, flagellated bacillus that colonises the gastric mucus layer. Its survival mechanism is urease production, which splits urea into ammonia and CO2, neutralising gastric acid locally — and this same property is exploited by every diagnostic test for it (urea breath test, rapid urease test).

It causes chronic gastritis; the pattern determines the outcome — antral-predominant gastritis increases gastrin and acid, causing duodenal ulcer, while corpus-predominant gastritis causes atrophy, hypochlorhydria, gastric ulcer and increased cancer risk.

*H. pylori* is a WHO class I carcinogen, associated with gastric adenocarcinoma and gastric MALT lymphoma — the latter frequently regressing completely with eradication alone.

Clinical Features

Other features: epigastric tenderness, nausea, bloating and early satiety. Alarm ("red flag") features requiring urgent endoscopy: age over 45–50 with new-onset dyspepsia, weight loss, anaemia, dysphagia, persistent vomiting, gastrointestinal bleeding, epigastric mass, or a family history of gastric cancer.

Complications: haemorrhage (the commonest — haematemesis and melaena), perforation (sudden severe pain, board-like rigidity, free gas under the diaphragm), gastric outlet obstruction (from chronic scarring — vomiting of undigested food, succussion splash, hypochloraemic hypokalaemic metabolic alkalosis), and penetration into the pancreas causing back pain.

Investigations

For *H. pylori*:

Endoscopy: indicated for alarm features, older patients with new dyspepsia, and treatment failure. All gastric ulcers MUST be biopsied (multiple biopsies from the edge) to exclude malignancy, and re-scoped after treatment to confirm healing. Duodenal ulcers do not require biopsy.

Management

• 1. *H.
• pylori* eradication — the definitive treatment for *H. pylori*-associated ulcers, curing the disease rather than suppressing it. Standard therapy combines a proton pump inhibitor with two or three antibiotics (clarithromycin-based triple therapy, or bismuth-based quadruple therapy) for 14 days.
• Clarithromycin resistance is high in India, which increasingly favours bismuth quadruple or concomitant regimens.
• Confirm eradication with a urea breath test or stool antigen at least 4 weeks after completing treatment, particularly after complicated ulcer disease.

2. Acid suppression — proton pump inhibitors for symptom relief and healing; continued after eradication in complicated ulcers, and long-term where NSAIDs cannot be stopped.

3. NSAID-related ulcers — stop the NSAID if possible; if not, use the lowest effective dose, prefer a COX-2 selective agent in high-risk patients (weighing cardiovascular risk), and co-prescribe a proton pump inhibitor for gastroprotection in those at risk (age > 65, previous ulcer, concurrent anticoagulant, antiplatelet or steroid).

4. Lifestyle — stop smoking (which delays healing and increases recurrence), reduce alcohol, and avoid foods that provoke symptoms; the old bland "ulcer diet" is unnecessary.

5. Surgery — now rare, reserved for complications: perforation (omental patch repair), uncontrolled bleeding, and gastric outlet obstruction (after endoscopic dilatation fails).

Zollinger–ellison Syndrome

Definition: a gastrin-secreting neuroendocrine tumour (gastrinoma) causing gastric acid hypersecretion with severe, refractory peptic ulceration.

Features:

• Multiple, refractory ulcers, or ulcers in unusual locations — distal duodenum and jejunum
• Ulcers that recur despite eradication and adequate acid suppression, or that recur after surgery
• DIARRHOEA and STEATORRHOEA — from the massive acid load inactivating pancreatic lipase and damaging the small bowel mucosa; diarrhoea may be the presenting complaint and characteristically improves with acid suppression
• Gastro-oesophageal reflux, often severe
• About 25% occur as part of MEN 1 (with parathyroid and pituitary tumours) — so check serum calcium and PTH in every patient
• Most gastrinomas arise in the "gastrinoma triangle" (the confluence of the cystic and common bile ducts, the second and third parts of the duodenum, and the neck and body of the pancreas); over half are malignant, with liver metastases determining prognosis

Investigations:

• markedly raised fasting serum gastrin (measured off proton pump inhibitors, which themselves raise gastrin — a critical pitfall), with gastric pH < 2 (a raised gastrin with achlorhydria indicates atrophic gastritis instead)
• secretin stimulation test (paradoxical rise in gastrin)
• localisation with CT, MRI, endoscopic ultrasound and somatostatin receptor imaging (Ga-68 DOTATATE PET)
• screening for MEN 1.

Management:

• high-dose proton pump inhibitors to control acid (often at several times the standard dose)
• surgical resection of the tumour where localised and non-metastatic
• for metastatic disease, somatostatin analogues, chemotherapy, targeted agents and liver-directed therapy.