Peptic Ulcer Disease Treatment in Mumbai

Every peptic ulcer has a cause - and at Shree Hospitals, identifying and eliminating that cause is the foundation of our five-step management approach. Symptomatic treatment with antacids suppresses pain but does not heal the ulcer or prevent it from returning. Permanent resolution requires accurate endoscopic diagnosis, causative factor identification, targeted eradication therapy where H. pylori is confirmed, optimised acid suppression during healing, and structured follow-up to confirm that the ulcer has healed and that the causative pathogen has been eliminated. For complicated ulcers presenting with haemorrhage or perforation, rapid emergency intervention is life-saving.

Step 1 - Endoscopic Diagnosis: Visualising the Ulcer and Its Characteristics

Upper GI endoscopy (OGD) is the gold standard for peptic ulcer diagnosis - directly visualising the ulcer, measuring its size and depth, characterising its base and margins, taking biopsies to exclude malignancy in gastric ulcers, and simultaneously testing for H. pylori infection using the Campylobacter-like organism (CLO) rapid urease test on antral biopsy. All gastric ulcers - without exception - require biopsy to exclude gastric adenocarcinoma, which can appear macroscopically identical to a benign peptic ulcer on visual inspection alone. Duodenal ulcers in the classic position are almost universally benign and biopsy is not routinely required. In patients who cannot undergo endoscopy, non-invasive H. pylori testing by urea breath test or stool antigen test provides confirmation of infection status.

Step 2 - Identifying the Cause: H. pylori, NSAIDs, and Rare Aetiologies

1. pylori infection and NSAID use together account for over 90% of peptic ulcers. H. pylori - a gram-negative spiral bacterium that colonises the gastric antrum - disrupts mucosal defence by producing urease, which generates ammonia from urea, directly damaging the mucous layer and triggering an inflammatory response that causes mucosal breakdown. NSAIDs inhibit cyclo-oxygenase (COX) enzymes, reducing prostaglandin synthesis and imparing the mucosal protective barrier - both locally and systemically after oral absorption. Patients taking daily aspirin for cardiovascular protection, prescribed NSAIDs for musculoskeletal pain, or self-medicating with ibuprofen for headaches are all at risk. Rarer causes - Zollinger-Ellison syndrome (a gastrin-secreting pancreatic tumour causing multiple refractory ulcers), Crohn's disease of the upper GI tract, and systemic mastocytosis - are excluded when standard causes are absent or when ulcers fail to heal with standard therapy.
   

Step 3 - H. pylori Eradication Therapy

When H. pylori is confirmed by CLO test, urea breath test, or stool antigen, eradication therapy is the definitive treatment. Standard first-line therapy in India is 14-day triple therapy: a full-dose PPI (esomeprazole 40mg or pantoprazole 40mg twice daily) combined with clarithromycin 500mg and amoxicillin 1g, both twice daily. Clarithromycin resistance is rising in many Indian urban populations, making bismuth-based quadruple therapy - adding bismuth subcitrate and metronidazole - an increasingly important alternative first-line option. Eradication is confirmed by urea breath test or stool antigen test no sooner than 4 weeks after completing therapy and 2 weeks after stopping PPI. Confirmation of successful eradication is not optional - it is essential for ensuring the ulcer does not recur.

Step 4 - Continued PPI Therapy and Ulcer Healing Confirmation
 

1. pylori eradication alone is sufficient treatment for uncomplicated duodenal ulcers - the ulcer will heal once the infectious stimulus is removed and the standard 14-day eradication PPI course is completed. For gastric ulcers, PPI therapy is continued for 4–8 weeks after completing eradication therapy to ensure complete mucosal healing, followed by a mandatory repeat endoscopy at 6–8 weeks to confirm healing and repeat biopsy if initial biopsies were inadequate. For NSAID-induced ulcers, the NSAID is stopped where possible, or switched to a selective COX-2 inhibitor with a PPI added where continued NSAID use is unavoidable for the management of an underlying condition.
    

Step 5 - Managing Complications: Haemorrhage, Perforation & Refractory Ulcers

Bleeding peptic ulcers are the most common cause of upper GI haemorrhage requiring emergency endoscopy. At Shree Hospitals, emergency endoscopy is available 24 hours a day for patients presenting with haematemesis or melaena. Active bleeding ulcers are treated with endoscopic combination therapy - adrenaline injection followed by mechanical clipping or thermal coagulation - which achieves haemostasis in over 90% of cases, avoiding emergency surgery. Bleeding stigmata are graded using the Forrest Classification to predict rebleed risk and guide the intensity of monitoring. Perforated peptic ulcers - presenting with sudden severe upper abdominal pain and peritonism - are a surgical emergency treated with laparoscopic or open primary closure. Ulcers that fail to heal despite optimised medical therapy and confirmed H. pylori eradication require malignancy exclusion, reassessment for rare aetiologies, and surgical consideration.