RESUMEN
The increase of H. pylori resistance to clarithromycin is a concern. This study evaluated the prevalence of H. pylori's primary resistance to clarithromycin and its association with virulence factors in adult dyspeptic patients and asymptomatic children. The gastric mucosa from patients (153 gastritis, 24 gastric cancer, 21 peptic ulcer) and gastric juice obtained by string test from 24 H. pylori and 23S rRNA positive asymptomatic children were included. The clarithromycin resistance was assessed by TaqMan RT-PCR 23S rRNA point mutations, A2142G and/or A2143G, and H. pylori virulence markers by PCR. Overall, the clarithromycin resistance was 14.4% (32/222), 14.2% in adults, and 12% in children, whereas origin, gender, and disease were not distinctive factors. The most prevalent point mutation was A2143G (62.5%). The point mutation was significantly less frequent in cagA-positive (11.4%) than in cagA-negative (23.6%) strains (p=0.03 OR = 0.4 95%CI = 0.19 - 0.91) as well as in cagE-positive (10.2%), cagE-negative (21.2%) (p=0.03 OR: 0.4 I.C:0.20-0.91). No difference was found in iceA or vacA alleles genotypes. Primary resistance to clarithromycin was lower than that reported in Southeast Brazil. The cagA and cagE positive H. pylori samples have few point mutations suggesting that individuals infected with virulent strains may be more susceptible to anti-H. pylori treatment.
Asunto(s)
Infecciones por Helicobacter , Helicobacter pylori , Adulto , Antibacterianos/farmacología , Brasil , Niño , Claritromicina/farmacología , Farmacorresistencia Bacteriana/genética , Genotipo , Infecciones por Helicobacter/complicaciones , Helicobacter pylori/genética , Humanos , Pruebas de Sensibilidad Microbiana , ARN Ribosómico 23S/genética , Virulencia/genéticaRESUMEN
ABSTRACT The increase of H. pylori resistance to clarithromycin is a concern. This study evaluated the prevalence of H. pylori's primary resistance to clarithromycin and its association with virulence factors in adult dyspeptic patients and asymptomatic children. The gastric mucosa from patients (153 gastritis, 24 gastric cancer, 21 peptic ulcer) and gastric juice obtained by string test from 24 H. pylori and 23S rRNA positive asymptomatic children were included. The clarithromycin resistance was assessed by TaqMan RT-PCR 23S rRNA point mutations, A2142G and/or A2143G, and H. pylori virulence markers by PCR. Overall, the clarithromycin resistance was 14.4% (32/222), 14.2% in adults, and 12% in children, whereas origin, gender, and disease were not distinctive factors. The most prevalent point mutation was A2143G (62.5%). The point mutation was significantly less frequent in cagA-positive (11.4%) than in cagA-negative (23.6%) strains (p=0.03 OR = 0.4 95%CI = 0.19 - 0.91) as well as in cagE-positive (10.2%), cagE-negative (21.2%) (p=0.03 OR: 0.4 I.C:0.20-0.91). No difference was found in iceA or vacA alleles genotypes. Primary resistance to clarithromycin was lower than that reported in Southeast Brazil. The cagA and cagE positive H. pylori samples have few point mutations suggesting that individuals infected with virulent strains may be more susceptible to anti-H. pylori treatment.
RESUMEN
PURPOSE: To evaluate the effect of propranolol on capsular architecture around silicone implants by measuring the inflammation, capsular thickness, and collagen fiber density, using a guinea pig experimental model. METHODS: Thirty six adult male guinea pigs randomly divided into two groups (n=18) were used. Each one received a silicone implant with textured-surface. The capsular tissue around implants from untreated or treated animals with the beta-adrenoceptor antagonist propranolol (10 mg/kg, dissolved in daily water) were analyzed for inflammation by histological scoring, capsular thickness by computerized histometry, and collagen fibers type I and Type III density by picrosirius polarization at different time points (7, 14 or 21 days after silicone implantation). RESULTS: Propranolol treatment reduced inflammation and impaired capsular thickness and delayed collagen maturation around the textured implant. CONCLUSION: Propranolol reduces the risk of developing capsular contracture around silicone implants with textured surface.
Asunto(s)
Antagonistas Adrenérgicos beta/farmacología , Contractura Capsular en Implantes/prevención & control , Propranolol/farmacología , Geles de Silicona/efectos adversos , Antagonistas Adrenérgicos beta/uso terapéutico , Animales , Implantes de Mama/efectos adversos , Colágeno Tipo I/análisis , Colágeno Tipo I/efectos de los fármacos , Colágeno Tipo III/análisis , Colágeno Tipo III/efectos de los fármacos , Modelos Animales de Enfermedad , Cobayas , Humanos , Contractura Capsular en Implantes/patología , Implantes Experimentales/efectos adversos , Masculino , Propranolol/uso terapéutico , Distribución Aleatoria , Reproducibilidad de los Resultados , Tejido Subcutáneo/efectos de los fármacos , Tejido Subcutáneo/patología , Factores de Tiempo , Resultado del TratamientoRESUMEN
PURPOSE: To evaluate the effect of propranolol on capsular architecture around silicone implants by measuring the inflammation, capsular thickness, and collagen fiber density, using a guinea pig experimental model. METHODS: Thirty six adult male guinea pigs randomly divided into two groups (n=18) were used. Each one received a silicone implant with textured-surface. The capsular tissue around implants from untreated or treated animals with the beta-adrenoceptor antagonist propranolol (10 mg/kg, dissolved in daily water) were analyzed for inflammation by histological scoring, capsular thickness by computerized histometry, and collagen fibers type I and Type III density by picrosirius polarization at different time points (7, 14 or 21 days after silicone implantation). RESULTS: Propranolol treatment reduced inflammation and impaired capsular thickness and delayed collagen maturation around the textured implant. CONCLUSION: Propranolol reduces the risk of developing capsular contracture around silicone implants with textured surface. .
Asunto(s)
Animales , Cobayas , Humanos , Masculino , Antagonistas Adrenérgicos beta/farmacología , Contractura Capsular en Implantes/prevención & control , Propranolol/farmacología , Geles de Silicona/efectos adversos , Antagonistas Adrenérgicos beta/uso terapéutico , Implantes de Mama/efectos adversos , Colágeno Tipo I/análisis , Colágeno Tipo I/efectos de los fármacos , Colágeno Tipo III/análisis , Colágeno Tipo III/efectos de los fármacos , Modelos Animales de Enfermedad , Contractura Capsular en Implantes/patología , Implantes Experimentales/efectos adversos , Propranolol/uso terapéutico , Distribución Aleatoria , Reproducibilidad de los Resultados , Tejido Subcutáneo/efectos de los fármacos , Tejido Subcutáneo/patología , Factores de Tiempo , Resultado del TratamientoRESUMEN
PURPOSE: To evaluate the effect of propranolol on capsular architecture around silicone implants by measuring the inflammation, capsular thickness, and collagen fiber density, using a guinea pig experimental model. METHODS: Thirty six adult male guinea pigs randomly divided into two groups (n=18) were used. Each one received a silicone implant with textured-surface. The capsular tissue around implants from untreated or treated animals with the beta-adrenoceptor antagonist propranolol (10 mg/kg, dissolved in daily water) were analyzed for inflammation by histological scoring, capsular thickness by computerized histometry, and collagen fibers type I and Type III density by picrosirius polarization at different time points (7, 14 or 21 days after silicone implantation).RESULTS: Propranolol treatment reduced inflammation and impaired capsular thickness and delayed collagen maturation around the textured implant. CONCLUSION: Propranolol reduces the risk of developing capsular contracture around silicone implants with textured surface.(AU)