Search

Background Pancreaticopleural fistula (PPF) is a rare complication associated with pancreatitis, caused by disruption of the pancreatic duct, either directly or through rupture of a peripancreatic fluid collection, resulting in leakage of pancreatic juice into the pleural space. It commonly presents as massive, relapsing pleural effusions, often on the left side with high amylase content. Nonspecific chest symptoms often predominate, making it a diagnostic challenge. There is a lack of clarity regarding the management of this rare entity. Objectives This study aimed to review the typical presentations, pathophysiology, and current role of endoscopic therapy in patients with PPF. Materials and Methods A retrospective analysis of the results of endoscopic treatment of patients with symptomatic PPF due to pancreatitis was done. Results Ten patients with pancreatitis (6 males; mean age 33.6 ± 15.4 years: 6 chronic, 4 acute) with symptomatic PPF were analyzed. Endoscopic retrograde cholangiopancreatography was performed in all, with pancreatic sphincterotomy and stenting of the main pancreatic duct (passive transpapillary drainage). Technical and clinical success was achieved in 7/10(70%) and 10/10(100%) patients, respectively. Though the leak was bridged in three patients, pancreatic sphincterotomy and downstream stenting (when bridging was not possible) were successful in closing PPF. One (10%) patient needed surgery for gastric outlet obstruction. The mean duration of endotherapy was 12.1 ± 9.4 months and the time taken for leak closure was 15.3 ± 10.4 weeks. Long-term success of endoscopic treatment (median follow-up period of 48.9 ± 28.7 months) was achieved in all patients. Conclusions Endoscopic treatment (passive trans-papillary drainage) is a safe and effective procedure for managing postinflammatory PPFs, and should be attempted in cases of failure of medical treatment. [ABSTRACT FROM AUTHOR]

The article presents a simplified NMR-based protocol for urinary profiling of lactulose/mannitol ratio (LMR) and demonstrates here its utility to assess increased intestinal permeability (IP) in patients with acute on chronic liver failure (ACLF). ACLF is a serious clinical complication associated with chronic liver disease (cirrhosis). The major risk factor in its development is increased IP ('leaky gut'), which has been linked to disease progression and to infectious complications. However, IP has seldom been investigated in patients with ACLF, even though patients frequently report gastrointestinal disorders and associated complications. To this end, we first optimized the NMR-based targeted profiling of urinary metabolites (i.e. actulose, mannitol, and creatinine) and subsequently used this resulted protocol (a) first to evaluate the altered IP in ACLF patients and then (b) to explore its utility for monitoring the treatment response in these patients. The normal profiles were obtained for 7 age and sex matched healthy volunteers. The results revealed that the urinary LMR excretion was significantly higher in ACLF patients compared to normal controls (median ~0.7, range (0.12-2.84), vs median ~0.11, range (0.02-0.28), p < 0.001) suggesting that the ACLF patients' exhibit altered IP. However, the LMR excretion in six clinically improved follow-up ACLF patients was comparable to normal controls indicating restored IP after the treatment. The protocol-as demonstrated here with ACLF-is equally applicable for evaluating IP or mucosal barrier function in other intestinal disorders with reasonable sensitivity and specificity, highlighting its general utility. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background and Aims: Acute-on-chronic liver failure (ACLF), acute liver failure (ALF) and chronic liver disease (CLD) are common forms of liver failure and present with similar clinical profiles. The aim of this study was to compare brain metabolite alterations in all the three groups of patients with controls, using in vivo proton magnetic resonance spectroscopy (MRS), and to look for any significant differences in metabolites that may help in differentiating between these three conditions. Methods: Nine patients with ACLF, 10 with ALF, 10 patients with CLD and 10 age-matched controls were studied. The relative concentrations of N-acetylaspartate (NAA), choline (Cho), glutamine/glutamate (Glx) and myoinositol (mI) with respect to creatine (Cr) were measured. Results: ACLF (3.07±0.72), ALF (4.39±1.25) and CLD (3.15±0.69) patients exhibited significantly increased Glx/Cr ratios compared with controls (2.14±0.42). The NAA/Cr ratio was significantly decreased in both ACLF (mean=0.84±0.28) and CLD (mean=0.97±0.21) patients as compared with that in controls (mean=1.24±0.20). No significant difference among ALF, ACLF and CLD patients was noted in the Cho/Cr ratios. ACLF patients showed significantly lower mI/Cr and Glx/Cr ratios compared with the ALF group. Conclusion: In vivo proton MRS-derived cerebral metabolite alterations in hepatic encephalopathy owing to ALF are significantly different from the one owing to ACLF and CLD; these may be due to the differences in the pathogenesis of these two overlapping clinical conditions. [ABSTRACT FROM AUTHOR]

Background and Aims: Acute-on-chronic liver failure (ACLF), acute liver failure (ALF) and chronic liver disease (CLD) are common forms of liver failure and present with similar clinical profiles. The aim of this study was to compare brain metabolite alterations in all the three groups of patients with controls, using in vivo proton magnetic resonance spectroscopy (MRS), and to look for any significant differences in metabolites that may help in differentiating between these three conditions., Methods: Nine patients with ACLF, 10 with ALF, 10 patients with CLD and 10 age-matched controls were studied. The relative concentrations of N-acetylaspartate (NAA), choline (Cho), glutamine/glutamate (Glx) and myoinositol (mI) with respect to creatine (Cr) were measured., Results: ACLF (3.07+/-0.72), ALF (4.39+/-1.25) and CLD (3.15+/-0.69) patients exhibited significantly increased Glx/Cr ratios compared with controls (2.14+/-0.42). The NAA/Cr ratio was significantly decreased in both ACLF (mean=0.84+/-0.28) and CLD (mean=0.97+/-0.21) patients as compared with that in controls (mean=1.24+/-0.20). No significant difference among ALF, ACLF and CLD patients was noted in the Cho/Cr ratios. ACLF patients showed significantly lower mI/Cr and Glx/Cr ratios compared with the ALF group., Conclusion: In vivo proton MRS-derived cerebral metabolite alterations in hepatic encephalopathy owing to ALF are significantly different from the one owing to ACLF and CLD; these may be due to the differences in the pathogenesis of these two overlapping clinical conditions.