No abstract

Artificial nutrition is an inherent part of management in acute pancreatitis. However, there is no consensus regarding the optimal time of the commencement of feeding in these patients. Our aim was to compare the effect of enteral v. parenteral nutrition with regard to the time points when they were administered in the randomised controlled trials. The search was undertaken in the Cochrane Central Register of Controlled Trials, MEDLINE and Science Citation Index as well as in the proceedings of major gastroenterology meetings. The summary estimate of the effect associated with artificial nutrition was calculated using a random-effects model and presented as a risk ratio (RR) and 95 % CI. A total of eleven randomised controlled trials were included. When started within 48 h of admission, enteral nutrition, in comparison with parenteral nutrition, resulted in a statistically significant reduction in the risks of multiple organ failure (RR 0·44; 95 % CI 0·23, 0·84), pancreatic infectious complications (RR 0·46; 95 % CI 0·27, 0·77) and mortality (RR 0·46; 95 % CI 0·20, 0·99). After 48 h of admission, enteral nutrition, in comparison with parenteral nutrition, did not result in a statistically significant reduction in the risks of multiple organ failure (RR 0·73; 95 % CI 0·33, 1·63), pancreatic infectious complications (RR 0·31; 95 % CI 0·07, 1·34) and mortality (RR 0·67; 95 % CI 0·22, 2·10). Enteral nutrition is more effective than parenteral nutrition in reducing the risk of multiple organ failure, pancreatic infectious complications and mortality in patients with acute pancreatitis. The magnitude of these benefits may depend on the timing of the commencement of nutrition.

No abstract

The use of polymeric, compared with (semi)elemental, formulation does not lead to a significantly higher risk of feeding intolerance, infectious complications or death in patients with acute pancreatitis. Neither the supplementation of enteral nutrition with probiotics nor the use of immunonutrition significantly improves the clinical outcomes.

The association among body mass index (BMI), height, and the risk of lymphatic malignancies was investigated in the Netherlands Cohort Study. The participants (n = 120,852), Dutch men and women aged 55-69 years, completed a self-administered questionnaire at baseline in 1986. After 13.3 years of follow-up, data on 1,042 lymphatic malignancy cases (including diffuse large-cell lymphoma, chronic lymphocytic leukemia, multiple myeloma, and other subtypes) and 4,588 subcohort members were available. Incidence rate ratios were estimated by using Cox regression models. BMI at baseline and BMI change since the age of 20 years were not associated with lymphatic malignancy risk. However, the rate ratio of lymphatic malignancies per 4-unit increase in BMI at 20 years of age was 1.13 (95% confidence interval (CI): 1.01, 1.25). The rate ratio of lymphatic malignancies per 5-cm increase in height was 1.08 (95% CI: 1.02, 1.15). For diffuse large-cell lymphoma, follicular lymphoma, and chronic lymphocytic leukemia, the relative risks were 1.19 (95% CI: 1.07, 1.33), 1.15 (95% CI: 0.95, 1.40), and 1.09 (95% CI: 0.95, 1.26), respectively, for each 5-cm increase in height. The positive associations among BMI at 20 years of age, height, and the risk of lymphatic malignancies suggest that exposures during early life play a role in the etiology of lymphatic malignancies.

SUMMARY BackgroundThere has been controversy concerning the merits of enteral and parenteral nutrition compared with no supplementary nutrition in the management of patients with acute pancreatitis.

Robust policy-focused CVD risk equations can be developed solely from administrative health data to inform population health planning, and will complement CVD primary prevention at the individual level using clinical risk tools. Similar policy-focused equations could be replicated in countries and regions with linked administrative health datasets.

INTRODUCTION: New Zealand (NZ) guidelines recommend treating people for cardiovascular disease (CVD) risk on the basis of five-year absolute risk using a NZ adaptation of the Framingham risk equation. A diabetes-specific Diabetes Cohort Study (DCS) CVD predictive risk model has been developed and validated using NZ Get Checked data. AIM: To revalidate the DCS model with an independent cohort of people routinely assessed using PREDICT, a web-based CVD risk assessment and management programme. METHODS: People with Type 2 diabetes without pre-existing CVD were identified amongst people who had a PREDICT risk assessment between 2002 and 2005. From this group we identified those with sufficient data to allow estimation of CVD risk with the DCS models. We compared the DCS models with the NZ Framingham risk equation in terms of discrimination, calibration, and reclassification implications. RESULTS: Of 3044 people in our study cohort, 1829 people had complete data and therefore had CVD risks calculated. Of this group, 12.8% (235) had a cardiovascular event during the five-year follow-up. The DCS models had better discrimination than the currently used equation, with C-statistics being 0.68 for the two DCS models and 0.65 for the NZ Framingham model. DISCUSSION: The DCS models were superior to the NZ Framingham equation at discriminating people with diabetes who will have a cardiovascular event. The adoption of a DCS model would lead to a small increase in the number of people with diabetes who are treated with medication, but potentially more CVD events would be avoided. KEYWORDS: Cardiovascular disease; diabetes; prevention; risk assessment; reliability and validity