Helicobacter pylori is a major contributor to ulcer disease and can also causedyspepsia. H.Pylori is transmitted person to person from gastric-oral and fecaloral routes. Most infections are acquired by age 10 and socio economics is the strongest risk factor. H.Pylori can cause peptic ulcer, gastric adenocarcinoma, gastric MALT lymphoma, gastritis, or dyspepsia.
The presence of H. pylori can be detected by using urea breath testing, stool antigen testing, or serology testing for the presence of antibodies to H.Pylori. Active infection can be demonstrated by the UBT because H. Pylori uniquely has urease so radiolabeled urea is cleaved releasing radiolabeled carbon 13 in the presence of urease. Serologic antibody formation is less sensitive, may not reflect active infection and is dependent on the prevalence of H.Pylori in the population.
H.Pylori is treated by proton pump inhibitors and antibiotics. The most common regimens are triple therapy: PPI, clarithromycin and either amoxicillin or metronidazole; or quadruple therapy: PPI, bismuth, tetracycline and metronidazole. Because 20% of those treated still have H. Pylori confirmatory tests for eradication 4 weeks after treatment is recommended.