RESUMO
BACKGROUND & AIMS: Non-alcoholic steatohepatitis (NASH) in children is a significant public health concern. Oxidative stress is an important component in the pathophysiology of NASH. Several enzymatic antioxidant mechanisms protect the liver from oxidative injury. Examination of the expression of these enzymes in NASH livers may provide insight on the roles for these antioxidant mechanisms in the pathophysiology of NASH. METHODS: The mRNA expression of catalase, glutathione peroxidase 1 (GPX1), glutathione reductase (GSR), paraoxonase 1 (PON1) and other reactive oxygen species-related genes was evaluated by microarray and quantitative real-time PCR analyses. The PON1 protein levels were evaluated in liver and serum by Western blot analyses. Serum enzymatic activities of GPX, GSR and PON1 (paraoxonase and arylesterase activities) were examined. RESULTS: NASH livers exhibited elevated mRNA expression of catalase and PON1, but not GPX1 or GSR. No difference in serum GPX or GSR activity was detected between NASH patients and controls. Elevated expression of PON1 mRNA and protein was detected in NASH livers, but serum PON1 protein and activities were not elevated. CONCLUSIONS: Elevated expression of catalase and PON1 suggests protective roles for these antioxidants in NASH livers. Given the importance of oxidative stress in the pathophysiology of NASH, future studies focusing on these enzymes could identify important targets for therapeutic or preventive interventions for NASH patients.
Assuntos
Arildialquilfosfatase/sangue , Fígado Gorduroso/enzimologia , Fígado/enzimologia , Estresse Oxidativo , Adolescente , Fatores Etários , Arildialquilfosfatase/genética , Biomarcadores/sangue , Western Blotting , Catalase/sangue , Catalase/genética , Criança , Pré-Escolar , Estudos Transversais , Fígado Gorduroso/sangue , Fígado Gorduroso/genética , Feminino , Perfilação da Expressão Gênica/métodos , Glutationa Peroxidase/sangue , Glutationa Peroxidase/genética , Glutationa Redutase/sangue , Glutationa Redutase/genética , Humanos , Masculino , Hepatopatia Gordurosa não Alcoólica , Análise de Sequência com Séries de Oligonucleotídeos , RNA Mensageiro/sangue , Reação em Cadeia da Polimerase em Tempo Real , Regulação para Cima , Adulto Jovem , Glutationa Peroxidase GPX1RESUMO
Helicobacter pylori is a worldwide infection that causes chronic gastritis, duodenal ulcers, and malignancy. Transmission of Helicobacter pylori within a family appears to be the predominant mode of contamination. Recurrence of the infection is frequently seen following treatment. Lack of eradication due to either inadequate treatment or resistant bacteria vs. reinfection have been explanations for detection of H. pylori following treatment. In this article we will discuss the concepts of inadequate treatment vs. resistant infection and reinfection as causes of persistent H. pylori infection.
Assuntos
Farmacorresistência Bacteriana , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori/isolamento & purificação , Antibacterianos/uso terapêutico , Quimioterapia Combinada , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/transmissão , Helicobacter pylori/efeitos dos fármacos , Humanos , Recidiva , Fatores de RiscoRESUMO
Introduction. Celiac disease, an autoimmune enteropathy, occurs in susceptible individuals and is treatable with a gluten-free diet. These may not be supplemented with vitamins. Objective. To assess the nutritional health of children who have biopsy-proven celiac disease. Methods. Charts were reviewed between July 1, 2007, and June 30, 2017. Results. A total of 252 children ages 0 to 21 years had biopsy-proven celiac disease, mean age 11 ± 4.1 years. Body mass index Z-score was 0.2 ± 1.2 at diagnosis. Except for vitamin D, few had deficiencies at diagnosis. At 1-year follow-up, there was no significant change in anthropomorphics or vitamin status. Adherence to follow-up was poor; at 5 years after diagnosis, 39% adhered to follow-up. Conclusion. Despite a rigorous, proactive protocol for contacting and following children with celiac disease, adherence to follow-up was poor. New strategies, such as follow-up through the primary care provider, are needed.