Assessing the appropriateness of parenteral nutrition use in hospitalized patients. A comparison on parenteral nutrition bag prescription in different wards and nutritional outcomes.

PURPOSE: Our aim is to assess parenteral nutrition (PN) bag prescription in hospitalized patients and evaluate clinical outcomes linked to PN therapy. METHODS: We performed an observational longitudinal retrospective study on PN prescription in a General Public Hospital in Turin, Italy, on ninety-five patients receiving PN prescribed by the Nutrition Support Team (NST). We described patients' demography and assessed nutritional outcomes, as well as PN bag prescription in different wards. Medians were calculated for several clinical parameters before and after PN therapy. A z-test for proportions has been performed to better understand the impact of various conditions on clinical outcomes and to compare differences between administered nutrients and required amounts. RESULTS: The NST resulted responsible for only 18% of bags prescribed in the geriatrics ward and for 48% in the surgery wards. PN was not able to fulfill nutritional requirements resulting in a median lack of 3.1 calories and 0.23 g of proteins per kilogram of reference body weight per day. Despite this, PN therapy was able to improve total blood proteins and calcium blood levels in our cohort. The NST changed the prescription in 55.8% of the pre-existing PN regimens. CONCLUSIONS: More strict adherence to guidelines is needed in order to maximize effectiveness of PN and observe a positive impact on clinical parameters.

Adipokines in NASH: postprandial lipid metabolism as a link between adiponectin and liver disease.

Circulating levels of four adipokines (adiponectin, TNF-alpha, leptin, and resistin) and the postprandial lipid and adiponectin responses to an oral fat load were assessed in 25 non-obese, non-diabetic patients with biopsy-proven nonalcoholic steatohepatitis (NASH) and correlated with metabolic indices and liver histology. Circulating adiponectin was lower in NASH compared with controls (5,476 +/- 344 vs. 11,548 +/- 836 ng/mL; P = .00001) and on multiple regression analysis correlated negatively with liver steatosis, necroinflammation (OR = 5.0; P = .009), and fibrosis (OR = 8.0; P = .003). The magnitude of postprandial lipemia was significantly higher in NASH than in controls and was related to fasting adiponectin (beta = -0.78; P = .00003). Controls showed a significant increase in serum adiponectin in response to the fat load, whereas patients with NASH showed a slight decrease. Postprandial free fatty acids response correlated inversely with adiponectin response in both groups and independently predicted the severity of liver steatosis in NASH (beta = 0.51; P = .031). In conclusion, hypoadiponectinemia is present before overt diabetes and obesity appear and correlates with the severity of liver histology in NASH. Impaired postprandial lipid metabolism may be an additional mechanism linking hypoadiponectinemia and NASH and posing a higher cardiovascular risk to these subjects. The mechanism(s) underlying these differences are unknown, but the type of dietary fat seems to play a role. These findings may have important pathogenetic and therapeutic implications in both liver and metabolic disease.