scholarly journals Increased procalcitonin serum levels as predictive parameter of multiple organ failure and outcome in acute pancreatitis patients

Critical Care ◽  
10.1186/cc467 ◽  
2000 ◽  
Vol 3 (S1) ◽  
Author(s):  
SMA Lobo ◽  
RF Meirelles ◽  
P Lupino ◽  
MD Pires ◽  
ML Kuga ◽  
...  
2008 ◽  
Vol 101 (6) ◽  
pp. 787-793 ◽  
Author(s):  
Maxim S. Petrov ◽  
Romana D. Pylypchuk ◽  
Antonina F. Uchugina

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.


2009 ◽  
Vol 33 (11) ◽  
pp. 2427-2432 ◽  
Author(s):  
Damian J. Mole ◽  
Katie L. McClymont ◽  
Sarah Lau ◽  
Rosamund Mills ◽  
Christopher Stamp-Vincent ◽  
...  

2016 ◽  
Vol 22 (2) ◽  
pp. 202-209 ◽  
Author(s):  
Damian J Mole ◽  
Scott P Webster ◽  
Iain Uings ◽  
Xiaozhong Zheng ◽  
Margaret Binnie ◽  
...  

Shock ◽  
1997 ◽  
Vol 7 (Supplement) ◽  
pp. 108
Author(s):  
Yong-Ming Yao ◽  
Yu Yan ◽  
Lian-Rong Lu ◽  
Zhi-Yong Sheng

Pancreas ◽  
2000 ◽  
Vol 21 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Masahiko Hirota ◽  
Fumiaki Nozawa ◽  
Akihiro Okabe ◽  
Muneyuki Shibata ◽  
Toru Beppu ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Reiko Seki

Administration of Toll-like receptor ligands (TLRLs) is known to cause liver injury in D-galN-sensitized mice. In the present study, we aimed to complement preceding reports on the TLRL/D-galN system by analyzing comparisons among TLRLs, mouse strain dependence, effects on serum levels of cytokines, and effects of sequential administrations of different TLRLs. In a preliminary set of analyses, we first confirmed that liver failure can be induced by diverse TLRLs, including LTA and R848 in combination with D-galN. Analysis using TLR4-deficient mice excluded potential confounding effects of endogenous TLR4Ls that include those referred to as DAMPs in CpG DNA/D-galN hepatotoxicity. Subsequently, we showed that LTA pretreatment could prevent mortality in both CpG DNA/D-galN- and R848/D-galN-treated mice compared to without pretreatment. Incidentally, we observed that without the LTA pretreatment, CpG DNA/D-galN showed relatively higher liver-specific toxicity whereas R848/D-galN showed more symptoms of multiple organ failure. These findings suggest that, in D-galN-sensitized mice, different TLRLs not only show similarity in the ability to induce hepatic injury but also exhibit distinctive abilities in inducing systemic inflammation and multiple organ failure. These findings also suggest the potential usefulness of cross-tolerance induction using LTA in the prevention of organ failure in TLRL-mediated acute inflammation.


Sign in / Sign up

Export Citation Format

Share Document