Detection of Helicobacter pylori resistance to clarithromycin and fluoroquinolones in Brazil : a national survey

• Autor(a) principal: Sanches, Bruno Squárcio Fernandes
• Data de Publicação: 2016
• Outros Autores: Martins, Gustavo Miranda, Lima, Karine Sampaio, Cota, Bianca Della Croce Vieira, Moretzsohn, Luciana Dias, Ribeiro, Laércio Tenório, Breyer, Helenice Pankowski, Maguilnik, Ismael, Maia, Alinne Lais Bessa, Rezende Filho, Joffre, Meira, Ana Carolina, Pinto, Henrique, Alves, Edson J., Mascarenhas, Ramiro Robson Fernandes, Passos, Raissa Iglesias Fernandes Angelo, Souza, Julia Duarte de, Trindade, Osmar Reni, Coelho, Luiz Gonzaga Vaz
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/168881
• topic: Antibacterianos; Claritromicina; Farmacorresistência bacteriana; Fluoroquinolonas; Infecções por Helicobacter; Testes de sensibilidade microbiana; Helicobacter pylori; Microbial drug resistence; Clarithromycin; Fluoroquinolones; Molecular diagnostic techniques

AIM To evaluate bacterial resistance to clarithromycin and fluoroquinolones in Brazil using molecular methods. METHODS The primary antibiotic resistance rates of Helicobacter pylori (H. pylori) were determined from November 2012 to March 2015 in the Southern, South-Eastern, Northern, North-Eastern, and Central-Western regions of Brazil. Four hundred ninety H. pylori patients [66% female, mean age 43 years (range: 18-79)] who had never been previously treated for this infection were enrolled. All patients underwent gastroscopy with antrum and corpus biopsies and molecular testing using GenoType HelicoDR (Hain Life Science, Germany). This test was performed to detect the presence of H. pylori and to identify point mutations in the genes responsible for clarithromycin and fluoroquinolone resistance. The molecular procedure was divided into three steps: DNA extraction from the biopsies, multiplex amplification, and reverse hybridization. RESULTS Clarithromycin resistance was found in 83 (16.9%) patients, and fluoroquinolone resistance was found in 66 (13.5%) patients. There was no statistical difference in resistance to either clarithromycin or fluoroquinolones (p = 0.55 and p = 0.06, respectively) among the different regions of Brazil. Dual resistance to clarithromycin and fluoroquinolones was found in 4.3% (21/490) of patients. The A2147G mutation was present in 90.4% (75/83), A2146G in 16.9% (14/83) and A2146C in 3.6% (3/83) of clarithromycin-resistant patients. In 10.8% (9/83) of clarithromycin-resistant samples, more than 01 mutation in the 23S rRNA gene was noticed. In fluoroquinolone-resistant samples, 37.9% (25/66) showed mutations not specified by the GenoType HelicoDR test. D91N mutation was observed in 34.8% (23/66), D91G in 18.1% (12/66), N87K in 16.6% (11/66) and D91Y in 13.6% (9/66) of cases. Among fluoroquinolone-resistant samples, 37.9% (25/66) showed mutations not specified by the GenoType HelicoDR test. CONCLUSION The H. pylori clarithromycin resis­tance rate in Brazil is at the borderline (15%-20%) for applying the standard triple therapy. The fluoroqui­nolone resistance rate (13.5%) is equally concerning.