Helicobacter Pylori Antigen Test

Helicobacter pylori is a Gram-negative, spiral-shaped bacterium adapted to live in the stomach’s mucus layer. It survives acid by producing urease, an enzyme that splits urea into ammonia to buffer acid around the organism. Colonization usually occurs in childhood within families and can persist for decades. Most people never develop symptoms, yet the bacterium is the main cause of chronic gastritis, peptic ulcer disease, and mucosa-associated lymphoid tissue (MALT) lymphoma, and it is a Group I carcinogen for noncardia gastric cancer. The long latency between infection and cancer reflects a progression from chronic inflammation to atrophy, intestinal metaplasia, dysplasia, and finally malignancy. Prevalence differs by region and socioeconomic status, ranging from about one-third of people in developed regions to most of the population in many developing regions, with higher rates in crowded households and where sanitation is limited.

Diagnosis can be invasive or non-invasive. Endoscopy with biopsy allows histology, rapid urease testing, and culture with antibiotic susceptibility, which guides therapy when resistance is likely. Non-invasive tests include the urea breath test, which detects urease activity, and stool antigen assays that identify bacterial proteins; both are suitable for initial diagnosis and for confirming cure. Blood antibody tests show exposure but cannot confirm active infection or cure. Because rising resistance to clarithromycin, levofloxacin, and metronidazole has reduced the success of older triple therapies, current guidelines favor bismuth quadruple therapy or other non-clarithromycin regimens as first line in many settings, with treatment tailored to local resistance data or molecular susceptibility testing when available. Everyone treated should have a test of cure four weeks after antibiotics and two weeks off acid suppressants to avoid false negatives.

For prevention and long-term health, the actionable steps are straightforward. If you have a current or past ulcer, have gastric precancerous changes, or live with someone who is infected, testing and eradication reduce ulcer recurrence and lower gastric cancer risk. Family-based strategies help in high-prevalence settings because transmission often occurs among household members. After cure, stomach cancer risk falls but does not drop to zero if intestinal metaplasia is already present, so periodic surveillance may still be recommended.