Understanding Your Gastroscopy Results: A Complete Guide

Overview.

A gastroscopy (upper endoscopy, OGD/EGD) examines the oesophagus, stomach, and duodenum. Your report may mention gastritis, H. pylori, Barrett's oesophagus, ulcers, or hiatal hernia — terms that can be alarming without context. This guide explains common findings, when biopsy results change the picture, and which findings need treatment versus simple reassurance.

Context: Most gastroscopy findings are benign and manageable. However, some — Barrett's oesophagus, gastric intestinal metaplasia, and certain ulcers — require surveillance or treatment to prevent progression to cancer. Understanding your results helps you follow through on surveillance recommendations and avoid unnecessary anxiety about common, low-risk findings.

Key takeaways.

• Mild gastritis (non-atrophic) is extremely common and usually benign
• H. pylori found on biopsy always requires eradication therapy
• Barrett's oesophagus requires surveillance endoscopy at defined intervals
• Gastric/duodenal ulcers need H. pylori testing and usually PPI therapy
• Hiatal hernia is common and usually doesn't need treatment unless causing severe reflux
• Biopsy results (pathology) determine the management plan, not visual appearance alone

Normal Gastroscopy.

A normal examination shows healthy mucosa throughout the oesophagus, stomach, and duodenum with no ulcers, masses, or significant inflammation.

Completely normal

No further testing or surveillance needed for the upper GI tract. Symptoms (if they prompted the test) may be functional (functional dyspepsia).

Normal with biopsies taken

Biopsies are often taken routinely (e.g., to check for H. pylori or microscopic inflammation not visible to the eye). Wait for pathology results before drawing conclusions.

Gastritis.

Gastritis (inflammation of the stomach lining) is the most common finding. The biopsy determines the type and cause.

Non-atrophic (superficial) gastritis

Mild inflammation of the surface mucosa. Extremely common. Usually caused by H. pylori, NSAIDs, or alcohol. If H. pylori-negative and no concerning features, typically benign.

H. pylori gastritis

Gastritis caused by H. pylori infection (confirmed on biopsy via CLOtest, histology, or staining). Always requires eradication therapy. Test of cure 4+ weeks after treatment.

Atrophic gastritis

Loss of specialised gastric glands. More concerning — associated with pernicious anaemia (B12 deficiency), iron deficiency, and increased gastric cancer risk. May be autoimmune or post-H. pylori. Requires B12/iron monitoring and gastric cancer surveillance.

Intestinal metaplasia (stomach)

The stomach lining transforms to resemble intestinal lining. A precancerous condition, especially if extensive or incomplete type. Surveillance gastroscopy recommended per BSG/ESGE guidelines. More aggressive surveillance if family history of gastric cancer.

Chemical/reactive gastropathy

Caused by bile reflux, NSAIDs, or alcohol. Not an infection. Management: remove the offending agent (stop NSAIDs, reduce alcohol). Usually resolves.

Barrett's Oesophagus.

Barrett's oesophagus is the replacement of normal squamous oesophageal lining with columnar (intestinal-type) epithelium, caused by chronic gastro-oesophageal reflux (GORD). It is the primary risk factor for oesophageal adenocarcinoma.

Barrett's without dysplasia

Precancerous change but low risk of progression (~0.3-0.5% per year). Requires ongoing PPI therapy and surveillance endoscopy every 3-5 years (per BSG/AGA guidelines).

Barrett's with low-grade dysplasia

Cells are beginning to show abnormal changes. Increased progression risk (~0.7-1% per year). Confirm with a second expert pathologist. Options: enhanced surveillance every 6-12 months or endoscopic ablation (radiofrequency ablation).

Barrett's with high-grade dysplasia

Pre-invasive cancer. Significant progression risk (~5-8% per year). Endoscopic treatment (radiofrequency ablation, endoscopic mucosal resection) is recommended. This is treatable and curable at this stage.

Short-segment vs long-segment Barrett's

Short-segment (<3cm) has lower cancer risk than long-segment (≥3cm). Segment length affects surveillance intervals and treatment decisions.

Ulcers.

Ulcers are breaks in the mucosal lining. The two most important questions: Is H. pylori present? And for gastric ulcers, is the biopsy benign?

Duodenal ulcer

Almost always benign. Most commonly caused by H. pylori or NSAIDs. Treat with PPI + H. pylori eradication if positive. Rarely requires follow-up endoscopy unless symptoms persist.

Gastric ulcer

Must always be biopsied to rule out gastric cancer. If biopsies show benign ulcer + H. pylori: eradicate and repeat gastroscopy in 6-8 weeks to confirm healing. Unhealed gastric ulcers require rebiopsy.

Oesophageal ulcer

Usually from severe reflux or pill oesophagitis. Biopsy to rule out eosinophilic oesophagitis or infection (immunocompromised patients). PPI therapy and medication review.

Other Common Findings.

These findings frequently appear in gastroscopy reports and usually require minimal intervention.

Hiatal hernia

Part of the stomach protrudes through the diaphragm into the chest. Very common (>30% of adults over 50). Small sliding hiatal hernias usually don't require treatment unless causing significant reflux symptoms.

Oesophagitis (Los Angeles Classification A-D)

Inflammation/erosions of the oesophageal lining from acid reflux. Grade A (mild) to D (severe). PPI therapy typically resolves it. Grade C-D may need repeat endoscopy to confirm healing and rule out Barrett's.

Duodenitis

Inflammation of the duodenum. May be caused by H. pylori, NSAIDs, or celiac disease. If celiac disease is suspected, biopsies should include assessment for villous atrophy (Marsh classification).

Gastric polyps

Fundic gland polyps (most common in PPI users) are benign. Hyperplastic polyps are usually benign but >10mm should be removed. Adenomatous polyps are precancerous and require removal + surveillance.

FAQs.