RESUMO
Intestinal dysbiosis in inflammatory bowel disease (IBD) patients depend on disease activity. We aimed to characterize the microbiota after 7 years of follow-up in an unselected cohort of IBD patients according to disease activity and disease severity. Fifty eight Crohn's disease (CD) and 82 ulcerative colitis (UC) patients were included. Disease activity was assessed by the Harvey-Bradshaw Index for CD and Simple Clinical Colitis Activity Index for UC. Microbiota diversity was assessed by 16S rDNA MiSeq sequencing. In UC patients with active disease and in CD patients with aggressive disease the richness (number of OTUs, p = 0.018 and p = 0.013, respectively) and diversity (Shannons index, p = 0.017 and p = 0.023, respectively) were significantly decreased. In the active UC group there was a significant decrease in abundance of the phylum Firmicutes (p = 0.018). The same was found in CD patients with aggressive disease (p = 0.05) while the abundance of Proteobacteria phylum showed a significant increase (p = 0.03) in CD patients. We found a change in the microbial abundance in UC patients with active disease and in CD patients with aggressive disease. These results suggest that dysbiosis of the gut in IBD patients is not only related to current activity but also to the course of the disease.
Assuntos
Doença de Crohn/etiologia , Doença de Crohn/patologia , Disbiose , Microbioma Gastrointestinal , Proteobactérias , Biodiversidade , Estudos de Casos e Controles , Doença de Crohn/diagnóstico , Progressão da Doença , Suscetibilidade a Doenças , Fezes/microbiologia , Humanos , Doenças Inflamatórias Intestinais/etiologia , Doenças Inflamatórias Intestinais/patologia , Metagenômica/métodos , RNA Ribossômico 16S/genética , Índice de Gravidade de DoençaRESUMO
BACKGROUND: Acute pancreatitis after ERCP is a severe side effect. AIM: To evaluate the preventive effect of nitroglycerin on post-ERCP pancreatitis by a meta-analysis of randomized clinical studies. METHODS: We searched on Pubmed, Embase, Cochrane Library and all abstracts presented at Digestive Disease Week and United European Gastrointestinal Week from 2004 to 2008. We used the MeSH terms 'pancreatitis' together (AND) with the terms: 'glyceryl trinitrate', 'glyceryl dinitrate', 'isosorbide dinitrate' or 'nitroglycerin'. RESULTS: Five clinical studies evaluating the incidence of post-ERCP pancreatitis after administration of nitroglycerin were identified. Meta-analysis including all five studies showed a relative risk (RR) of 0.61 (95% CI; 0.44, 0.86) with the number needed to treat (NNT) of 26 (95% CI: 16, 82). Three studies evaluated nitroglycerin administered by a dermal patch reaching together an RR of 0.66 (95% CI; 0.43, 1.01). The use of nitroglycerin is associated with a significantly increased risk of hypotension (RR 2.25) and headache (RR 3.64). No difference in mortality was observed. CONCLUSIONS: Overall, our meta-analysis supports the use of nitroglycerin in the prevention of post-ERCP pancreatitis, but administration of nitroglycerin by the dermal route, which is the preferred route of administration, did not reach statistical significance.
Assuntos
Anti-Inflamatórios/uso terapêutico , Colangiopancreatografia Retrógrada Endoscópica/efeitos adversos , Nitroglicerina/uso terapêutico , Pancreatite/prevenção & controle , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Fatores de Risco , Resultado do TratamentoRESUMO
BACKGROUND: The possible markers of liver fibrosis (plasma YKL-40, PIIINP, MMP-2 and TIMP-1) were measured at the start (t0) and end of treatment (t12) with alpha-interferon and ribavirin and repeated at 6-months follow-up (t18) in 51 patients with chronic hepatitis C. METHODS: We evaluated 1) whether treatment response is reflected by a decrease in these markers during antiviral therapy; 2) whether these markers reflect the activity of the disease; and 3) whether these markers could be used as predictors of the treatment response. RESULTS: Baseline plasma YKL-40, MMP-2, PIIINP and TIMP-1 were significantly increased in patients compared to normal controls. In responders (n = 30), plasma YKL-40 (P < 0.05), MMP-2 (P < 0.05) and TIMP-1 (P < 0.001) decreased significantly at t18, and no changes were observed at t12. Plasma PIIINP was unchanged in responders. In non-responders (n = 19), plasma MMP-2 (P < 0.01) and TIMP-1 (P < 0.01) decreased significantly at t18, whereas plasma YKL-40 and PIIINP were unchanged. The markers were significantly correlated at baseline (P < 0.001). Plasma PIIINP at baseline could predict treatment response (P = 0.01). CONCLUSIONS: Response to antiviral treatment is associated with a decrease in the fibrogenetic markers, but the markers do not reflect the biochemical disease activity during treatment. Baseline plasma PIIINP was the only marker predicting treatment response.