H. Pylori Infection

Helicobacter pylori is a spiral bacterium uniquely adapted to survive the stomach's acid, colonising the gastric mucosa in roughly half the world's population. Most carriers never develop symptoms, but infection causes chronic gastritis in all of them and progresses to disease in a minority: it accounts for the majority of duodenal and gastric ulcers, and is classified as a group 1 carcinogen — the single largest risk factor for gastric cancer and for MALT lymphoma, which can regress with eradication alone. Symptoms, when present, include burning upper abdominal pain often relieved or provoked by eating, bloating, nausea and early fullness. Testing is straightforward with a urea breath test or stool antigen test, both of which require stopping proton pump inhibitors for two weeks and antibiotics for four weeks beforehand or they produce false negatives — a common practical pitfall. Treatment is a combination of two or three antibiotics plus a proton pump inhibitor for 10-14 days. Rising clarithromycin resistance has made regimen choice locally dependent, and quadruple therapy with bismuth is increasingly first-line. Confirming eradication at least four weeks after finishing treatment is essential, because failure rates are meaningful and untreated persistence carries the cancer risk.

• •Burning or gnawing upper abdominal pain, sometimes relieved by food or antacids
• •Pain that wakes you at night
• •Bloating and excessive belching
• •Nausea and early fullness with meals
• •Loss of appetite and unintentional weight loss
• •No symptoms at all in the majority of carriers
• •Black tarry stools or vomiting blood — bleeding ulcer, an emergency
• •Iron deficiency anaemia without an obvious cause

• •Acquisition in childhood via oral-oral or faecal-oral transmission
• •Household crowding and shared living conditions
• •Poor sanitation and unsafe drinking water historically
• •Family members with the infection
• •Higher prevalence in certain regions and migrant populations
• •Lower socioeconomic conditions during childhood

H. pylori neutralises its microenvironment by producing urease, which converts urea to ammonia — the basis of the breath test used to detect it. It burrows into the protective mucus layer and adheres to gastric epithelium, provoking chronic inflammation. Depending on the pattern of colonisation, it either increases acid output (favouring duodenal ulcers) or causes atrophic gastritis with reduced acid (the pathway toward gastric cancer). Transmission is oral-oral or faecal-oral, usually acquired in childhood within households, which is why it clusters in families and in crowded living conditions.