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1.
Am J Gastroenterol ; 119(4): 646-654, 2024 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-37983769

RESUMO

INTRODUCTION: Antibiotic resistance is one of the main factors that determine the efficacy of treatments to eradicate Helicobacter pylori infection. Our aim was to evaluate the effectiveness of first-line and rescue treatments against H. pylori in Europe according to antibiotics resistance. METHODS: Prospective, multicenter, international registry on the management of H. pylori (European Registry on H. pylori Management). All infected and culture-diagnosed adult patients registered in the Spanish Association of Gastroenterology-Research Electronic Data Capture from 2013 to 2021 were included. RESULTS: A total of 2,852 naive patients with culture results were analyzed. Resistance to clarithromycin, metronidazole, and quinolones was 22%, 27%, and 18%, respectively. The most effective treatment, regardless of resistance, were the 3-in-1 single capsule with bismuth, metronidazole, and tetracycline (91%) and the quadruple with bismuth, offering optimal cure rates even in the presence of bacterial resistance to clarithromycin or metronidazole. The concomitant regimen with tinidazole achieved an eradication rate of 99% (90/91) vs 84% (90/107) with metronidazole. Triple schedules, sequential, or concomitant regimen with metronidazole did not achieve optimal results. A total of 1,118 non-naive patients were analyzed. Resistance to clarithromycin, metronidazole, and quinolones was 49%, 41%, and 24%, respectively. The 3-in-1 single capsule (87%) and the triple therapy with levofloxacin (85%) were the only ones that provided encouraging results. DISCUSSION: In regions where the antibiotic resistance rate of H. pylori is high, eradication treatment with the 3-in-1 single capsule, the quadruple with bismuth, and concomitant with tinidazole are the best options in naive patients. In non-naive patients, the 3-in-1 single capsule and the triple therapy with levofloxacin provided encouraging results.


Assuntos
Infecções por Helicobacter , Helicobacter pylori , Adulto , Humanos , Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/microbiologia , Metronidazol/uso terapêutico , Claritromicina/uso terapêutico , Levofloxacino/uso terapêutico , Bismuto/uso terapêutico , Amoxicilina/uso terapêutico , Tinidazol , Estudos Prospectivos , Quimioterapia Combinada , Antibacterianos/uso terapêutico , Resistência Microbiana a Medicamentos
2.
Wiad Lek ; 75(3): 611-618, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35522866

RESUMO

OBJECTIVE: The aim: To study the state of the intestinal microbiota (ІМ) in patients with Nonalcoholic fatty liver disease (NAFLD) and to determine changes in its composition at the level of basic phylotypes. PATIENTS AND METHODS: Materials and methods: The study included 114 patients with NAFLD with metabolic disorders and 64 patients of control group. Determination of the composition of the ІМ at the level of major phylotypes was performed by identifying total bacterial DNA and DNA of Bacteroidetes, Firmicutes and Actinobacteria by quantitative polymerase chain reaction (PCR) in real time (qRT-PCR) using universal primers for the 16S rRNA gene and taxon-specific primers of production (Thermo Fisher Scientific). RESULTS: Results: It was defined the weak correlation between the content of Firmicutes and proinflammatory markers (C-reactive protein (CRP) and Tumor necrosis factor (TNF) alpha) (p <0.05) and inverse correlation of CRP with the content of Bacteroidetes (p <0.001). Also have been observed significant changes in the main intestinal phyla in the direction of increasing the content of Firmicutes in patients with NAFLD with a high degree of steatosis and elevated levels of proinflammatory cytokines (p <0.05). CONCLUSION: Conclusions: IM imbalance leads to excessive synthesis of pro-inflammatory cytokines, promotes the activation of cellular mechanisms, which increases the flow of fatty acids into hepatocytes and increases the degree of hepatic steatosis.


Assuntos
Microbioma Gastrointestinal , Hepatopatia Gordurosa não Alcoólica , Biomarcadores , Citocinas , Microbioma Gastrointestinal/genética , Humanos , Inflamação , Hepatopatia Gordurosa não Alcoólica/metabolismo , RNA Ribossômico 16S
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