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1.
Gastroenterol Hepatol ; 46(4): 282-287, 2023 Apr.
Article in English, Spanish | MEDLINE | ID: mdl-35964809

ABSTRACT

BACKGROUND AND AIMS: The diagnostic and therapeutic strategy in severe lower gastrointestinal bleeding (LGIB) varies depending on the patient's clinical situation. Actual clinical practice guidelines propose different management strategies. We aim to know the attitude of the gastroenterologists from different hospitalary centers in the management of this entity. METHODS: Descriptive and observational study using an on-line questionnaire, addressed to gastroenterologists in Spain and Latin America, in December 2021. RESULTS: We included 281 anonymous questionnaires of gastroenterologists from Spain and Latin America. Diagnostic and therapeutic management of severe LGIB was heterogeneous among the participants. Regarding to the first diagnostic modalities they showed variability between performing computed tomography angiography (CTA) (44.5%), gastroscopy (33.1%), colonoscopy (20.6%) and arteriography (1.1%). The therapeutic attitude after a positive CTA mostly varied between performing arteriography (38.1%) and colonoscopy (44.1%). If negative CTA, in the majority of cases a gastroscopy was performed. If the patient needed intensive critical unit (ICU) care and to undergo colonoscopy, most participants performed an urgent colonoscopy (<24h) (31% always, 43.4% in most cases); while if the patient did not require ICU admission this percentage was lower (10% always, 33.8% in most cases). The 40.9% of the participants admitted having doubts about the management of this patients and the 98.2% considered the need for a creation of an action protocol. CONCLUSIONS: There is a high interhospitalary variability on the management of severe lower gastrointestinal bleeding among gastroenterologists. It is necessary to unify the diagnostic and therapeutic management of this pathology.


Subject(s)
Colonoscopy , Hospitalization , Humans , Colonoscopy/methods , Computed Tomography Angiography , Tomography, X-Ray Computed , Gastrointestinal Hemorrhage/diagnosis , Gastrointestinal Hemorrhage/etiology , Gastrointestinal Hemorrhage/therapy
2.
United European Gastroenterol J ; 6(10): 1508-1518, 2018 Dec.
Article in English | MEDLINE | ID: mdl-30574321

ABSTRACT

BACKGROUND: There are few large prospective cohort studies evaluating predictors of outcomes in acute pancreatitis. OBJECTIVES: The purpose of this study was to determine the role of age and co-morbid disease in predicting major outcomes in acute pancreatitis. METHODS: Data points were collected according to a predefined electronic data collection form. Acute pancreatitis and its complications were defined according to the revised Atlanta classification. Univariable and multivariable analyses were conducted using Cox proportional hazard regression and multiple logistic regression. RESULTS: From June 2013-February 2015, 1655 adult patients were recruited from 23 centres across Spain. Co-morbid disease, obesity, open surgical necrosectomy within 30 days, and pancreatic necrosis were independently associated with both 30-day mortality and persistent organ failure (p < 0.05 for all). Age was not associated with persistent organ failure, however the extreme of age (>85 years) was associated with mortality (p < 0.05). Co-morbid disease and obesity were not independently associated with a prolonged length of stay or other markers of morbidity on adjusted analysis (p > 0.05). CONCLUSION: Comorbidity and obesity are important determinates of mortality and persistent organ failure in acute pancreatitis, but in the absence of organ failure they do not appear to independently contribute to morbidity. This has important implications for severity classification and predictive models of severity in acute pancreatitis.

3.
Nutrients ; 9(9)2017 Aug 30.
Article in English | MEDLINE | ID: mdl-28867793

ABSTRACT

Inflammatory bowel diseases (IBD) represent a growing public health concern due to increasing incidence worldwide. The current notion on the pathogenesis of IBD is that genetically susceptible individuals develop intolerance to dysregulated gut microflora (dysbiosis) and chronic inflammation develops as a result of environmental triggers. Among the environmental factors associated with IBD, diet plays an important role in modulating the gut microbiome, influencing epigenetic changes, and, therefore, could be applied as a therapeutic tool to improve the disease course. Nevertheless, the current dietary recommendations for disease prevention and management are scarce and have weak evidence. This review summarises the current knowledge on the complex interactions between diet, microbiome and epigenetics in IBD. Whereas an overabundance of calories and some macronutrients increase gut inflammation, several micronutrients have the potential to modulate it. Immunonutrition has emerged as a new concept putting forward the importance of vitamins such as vitamins A, C, E, and D, folic acid, beta carotene and trace elements such as zinc, selenium, manganese and iron. However, when assessed in clinical trials, specific micronutrients exerted a limited benefit. Beyond nutrients, an anti-inflammatory dietary pattern as a complex intervention approach has become popular in recent years. Hence, exclusive enteral nutrition in paediatric Crohn's disease is the only nutritional intervention currently recommended as a first-line therapy. Other nutritional interventions or specific diets including the Specific Carbohydrate Diet (SCD), the low fermentable oligosaccharides, disaccharides, monosaccharides, and polyol (FODMAP) diet and, most recently, the Mediterranean diet have shown strong anti-inflammatory properties and show promise for improving disease symptoms. More work is required to evaluate the role of individual food compounds and complex nutritional interventions with the potential to decrease inflammation as a means of prevention and management of IBD.


Subject(s)
Diet , Epigenomics , Gastrointestinal Microbiome , Inflammatory Bowel Diseases/genetics , Inflammatory Bowel Diseases/microbiology , Genetic Predisposition to Disease , Humans
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