Stomach Ulcer (Peptic Ulcer) – Comprehensive Medical Guide

Overview

A stomach ulcer, more formally called a peptic ulcer, is a break in the lining of the stomach (gastric ulcer) or the first part of the small intestine (duodenal ulcer). The ulcer occurs when the protective mucus layer that coats the gut is eroded, allowing stomach acid to damage the underlying tissue.

Who it affects: Peptic ulcers can develop at any age, but they are most common in adults between 30‑60 years. Men have historically had a slightly higher incidence, though the gender gap has narrowed as risk factors such as NSAID use become more common among women.

Prevalence: In the United States, about 5‑10 % of the population will experience a peptic ulcer at some point in their lives. Worldwide, an estimated 4‑5 million new cases are diagnosed each year, with a higher burden in low‑ and middle‑income countries where *Helicobacter pylori* infection is more prevalent.^{[1] WHO, 2023}

Symptoms

Symptoms can be subtle or severe and may vary between gastric and duodenal ulcers. Common signs include:

• Burning or gnawing pain in the upper abdomen – often described as a “hunger‑type” pain that improves with food (duodenal) or worsens after eating (gastric).
• Early satiety – feeling full after a small amount of food.
• Nausea or vomiting – occasionally with bile or a sour taste.
• Bloating and belching.
• Heartburn or acid reflux – may coexist with ulcer pain.
• Loss of appetite and unintended weight loss.
• Dark, tar‑like stools (melena) – indicating digested blood.
• Vomiting of blood (hematemesis) – may appear bright red or coffee‑ground‑like.
• Fatigue – secondary to chronic blood loss.

Because symptoms overlap with other gastrointestinal conditions (e.g., gastritis, gastro‑esophageal reflux disease), accurate diagnosis is essential.

Causes and Risk Factors

Primary causes

1. Helicobacter pylori infection – This gram‑negative bacterium weakens the mucosal lining and stimulates excess acid production. Approximately 70‑80 % of duodenal ulcers and 50‑60 % of gastric ulcers are linked to *H. pylori*.^{[2] Mayo Clinic}
2. Non‑steroidal anti‑inflammatory drugs (NSAIDs) – Regular use of aspirin, ibuprofen, naproxen, or prescription COX‑2 inhibitors interferes with prostaglandin synthesis, reducing mucus and bicarbonate secretion.^{[3] NIH}
3. Excess gastric acid – Conditions such as Zollinger‑Ellison syndrome cause hyper‑secretion of acid, increasing ulcer risk.

Additional risk factors

• Age > 60 years (reduced mucosal regeneration)
• Smoking – nicotine impairs mucosal blood flow and promotes *H. pylori* colonization.
• Heavy alcohol consumption – irritates the mucosa and can increase acid output.
• Chronic stress – may exacerbate acid production, though it is not a direct cause.
• Family history of peptic ulcer disease.
• Use of corticosteroids in combination with NSAIDs.

Diagnosis

Because symptoms are non‑specific, physicians rely on a combination of history, physical exam, and targeted tests.

Initial evaluation

• Medical history – medication use (especially NSAIDs), alcohol, smoking, prior *H. pylori* infection, and family history.
• Physical exam – may reveal tenderness in the epigastrium.

Diagnostic tests

1. Upper gastrointestinal (GI) endoscopy (esophagogastroduodenoscopy, EGD) – Gold standard. Allows direct visualization, biopsy for *H. pylori* or malignancy, and therapeutic interventions (e.g., hemostasis). Recommended for patients > 55 years, those with alarm symptoms, or NSAID users.
2. Non‑invasive *H. pylori* testing:
   • Urea breath test – highly sensitive (> 95 %).
   • Stool antigen test – useful after treatment.
   • Serology – indicates past exposure but not active infection.
3. Radiographic studies – Barium swallow or upper GI series can detect large ulcers but are less sensitive than endoscopy.
4. Laboratory tests – CBC for anemia, serum electrolytes if vomiting is severe, and liver function tests if dyspepsia is atypical.

Treatment Options

Medication therapy

• Proton‑pump inhibitors (PPIs) – Omeprazole, esomeprazole, pantoprazole. Reduce acid secretion and promote healing. Typical course: 4‑8 weeks.
• H2‑receptor antagonists – Ranitidine (withdrawn in many markets), famotidine. Less potent than PPIs but useful for mild disease.
• Antibiotic regimens for *H. pylori*** – Triple therapy (PPI + clarithromycin + amoxicillin or metronidazole) for 10‑14 days. Bismuth‑based quadruple therapy is an alternative where resistance is common.
• Protective agents – Sucralfate forms a protective barrier; misoprostol (a prostaglandin analogue) especially for NSAID‑induced ulcers.
• Analgesic management – Acetaminophen is preferred for pain; avoid NSAIDs unless necessary and combined with a PPI.