This study aims to determine primary Helicobacter pylori resistance and its effect on eradication of the organism. Ninety-two patients with dyspeptic symptoms were enrolled. H. pylori was cultured and antibiotic sensitivity was determined by the Epsilometer test (Etest) for clarithromycin (CLR), amoxicillin (AMX) and metronidazole (MTR). 23S ribosomal RNA (rRNA) point mutations associated with clarithromycin resistance were also detected. Patients were treated with omeprazole (40 mg daily), CLR (500 mg) and AMX (1g twice a day) for 14 days. A 14C-urea breath test (14C-UBT) was repeated four weeks after completion of treatment to confirm eradication. Triple therapy failure was seen in 30(33%) patients. The resistance rates were: CLR 33% (30/92), MTR 48% (44/92) and AMX 2% (2/92). Clarithromycin resistance (CLR-R) was present in the 16-39 age group in 21 (47%) (P=0.007) compared to nine (19%)in the 40-79 age group. CLR resistance was seen in 30 H. pylori isolates, 20 (67%) from patients with non-ulcer dyspepsia (NUD), six (20%) with gastric ulcer (GU) and four (13%) with duodenal ulcer (DU). Triple therapy failure was associated with CLR-R in 28 (93%) (P<0.001). CLR-R mutations were present in 30 (33%) and were associated with treatment failure in 27 (90%; P<0.001). They were present in 20 (44%) isolates obtained from patients in the 16-39 age group (P=0.018). Treatment failure was associated with A2142G mutation in 20 (67%; P<0.001), A2143G mutation in 12 (40%; P<0.001) and A2142C mutation in five (17%; P=0.003). In conclusion, triple therapy failure was associated with CLR-R. Metronidazole resistance exceeded that of CLR, hence it cannot be substituted for CLR in a triple therapy.
- Drug resistance, microbial
- Helicobacter pylori