Clinical Information

Helicobacter pylori is the main cause of peptic ulcer disease and a risk factor for gastric cancer when left untreated. Traditionally, H pylori diagnosis has included noninvasive tests (eg, urea breath test, fecal antigen test) or invasive tests (eg, gastric biopsy). Antimicrobial resistance in H pylori is poorly studied but is rising, challenging its treatment. In 2012, an international clinical consortium study group recommended monitoring of clarithromycin resistance rates and ceasing its use at a threshold range of 15% to 20%.(1) Local monitoring has been practically impossible as not all patients undergo invasive testing, which yields a culture isolate that can be subjected to susceptibility testing. Even if invasive testing is performed, the organism can be difficult to isolate in culture and is highly fastidious once isolated, oftentimes not being amenable to phenotypic susceptibility testing. Further, there are only a handful of specialized clinical microbiology laboratories that perform H pylori susceptibility testing. In an internal study of local and referred isolates, clarithromycin resistance was observed to be most commonly due to A2143G (70/88 isolates, 79.6%), followed by A2142G (12/88 isolates, 13.6%) and A2142C (3/88 isolates, 3.4%) alterations in the 23S ribosomal RNA gene.(2) Overall, one of these alterations was found in 97% of clarithromycin-resistant H pylori isolates studied.