Table of contents · 7 sections
Peptic ulcer disease of the stomach and duodenum is a chronic relapsing condition characterized by the formation of an ulcer defect in the mucosa. The two main causes—Helicobacter pylori and NSAIDs—determine the treatment strategy. This article provides a comprehensive overview of pathogenesis, diagnostics, treatment, and complications.
Etiology and pathogenesis
An ulcer forms when the balance between aggressive factors and protective mechanisms is disrupted:
| Aggressive factors | Protective factors |
|---|---|
| Hydrochloric acid (HCl) | Mucus-bicarbonate barrier |
| Pepsin | Prostaglandins (PGE₂ — stimulate mucus and bicarbonate secretion) |
| Helicobacter pylori | Adequate mucosal blood supply |
| NSAIDs (block COX-1 → ↓ PGE₂) | Epithelial regeneration |
| Bile acids (reflux) | Epidermal growth factor (EGF) |
Formula: "No acid, no ulcer" (Schwarz, 1910) is still relevant today. However, Marshall and Warren added: "No Helicobacter, no relapse" (Nobel Prize 2005).
Helicobacter pylori: key pathogen
- Gram-negative spiral bacterium residing beneath the mucous layer on the epithelial surface
- Urease — hydrolyzes urea → NH₃ → neutralizes HCl surrounding the bacterium (ensuring survival in acid). The basis of the breath test!
- CagA and VacA — virulence factors that damage the epithelium
- Associated with: gastritis (100%), duodenal ulcer (90-95%), gastric ulcer (70-80%), MALT lymphoma, gastric adenocarcinoma
Clinical presentation: differences between gastric and duodenal ulcers
| Sign | Gastric ulcer | Duodenal ulcer |
|---|---|---|
| Age | Over 40 years old | 20-40 years old |
| Pain | 30-60 minutes after eating (early) | 2-3 hours after eating, on an empty stomach, nighttime (late) |
| Relation to food | Eating exacerbates pain | Eating relieves pain |
| H. pylori prevalence | 70-80 % | 90-95 % |
| HCl secretion | Normal or ↓ | ↑ (hypersecretion) |
| Malignant transformation | Possible (2-5%) | Extremely rare |
Diagnostics
- EGD (esophagogastroduodenoscopy) — the gold standard. Visualization of the ulcer, biopsy (to rule out cancer + rapid urease test for H. pylori)
- H. pylori diagnostics:
| Method | Type | Sensory function | When to use |
|---|---|---|---|
| Rapid urease test (CLO test) | Invasive (biopsy specimen) | 90-95 % | During EGD |
| Histological examination of biopsy | Invasive | 95 % | Gold standard + morphology of gastritis |
| ¹³C-urea breath test | Non-invasive | 95-97 % | Initial diagnostics + test of cure |
| H. pylori stool antigen | Non-invasive | 90-95 % | Alternative to the breath test |
| Serology (IgG) | Non-invasive | 85-90 % | Screening. Not for test of cure! (IgG persist for months) |
Treatment: H. pylori eradication
Standard first-line triple therapy (14 days):
- PPI (omeprazole 20 mg b.i.d.) — suppression of HCl secretion
- Clarithromycin 500 mg b.i.d.
- Amoxicillin 1000 mg b.i.d. (or metronidazole 500 mg b.i.d.)
In case of inefficacy — quadruple therapy (PPI + bismuth + tetracycline + metronidazole) or a levofloxacin-containing regimen.
Check eradication — ≥4 weeks after the end of treatment: ¹³C-urea breath test or stool antigen. No earlier than 2 weeks after stopping PPIs!
Complications of peptic ulcer disease
| Complication | Manifestations | Tactics |
|---|---|---|
| Hemorrhage (15-20 %) | Melena (black stools), "coffee-ground" emesis, hemodynamic instability | Emergency EGD + endoscopic hemostasis, IV PPI bolus + infusion |
| Perforation (5-10 %) | "Knife-like" pain, board-like rigidity of the abdomen, free gas under the diaphragm | Emergency surgery (closure of the perforation) |
| Penetration | Extension into an adjacent organ (pancreas — girdle pain, ↑ amylase) | Surgical treatment (if conservative management fails) |
| Pyloric stenosis | Vomiting of undigested food, "succussion splash" on an empty stomach, weight loss | Endoscopic balloon dilation or surgery |
| Malignant transformation | Gastric ulcer not healing for >8 weeks | Repeat biopsy, resection |
Frequently asked questions
Why do NSAIDs cause ulcers?
NSAIDs inhibit cyclooxygenase (COX-1 and COX-2). COX-1 in the gastric mucosa synthesizes prostaglandin E₂, which stimulates the secretion of protective mucus and bicarbonate, and maintains blood flow. COX-1 blockade → decreased PGE₂ → weakened mucosal defense → ulcer. Selective COX-2 inhibitors (celecoxib) are less gastrotoxic, but not completely safe.
When is surgery indicated in peptic ulcer disease?
Absolute indications: perforation, profuse bleeding (not controlled endoscopically), decompensated pyloric stenosis, suspected malignant transformation (non-healing gastric ulcer). Elective surgery for recurrences after 2-3 eradication courses is now extremely rare due to the efficacy of medical therapy.
Study gastroenterology through interactive lessons on the platform. Related topics: acute abdomen, NSAIDs, antibiotics. Use clinical calculators for gastroenterological scales.