Investigation and prediction of enteral nutrition problems after percutaneous endoscopic gastrostomy

AIM： To investigate and predict enteral nutrition problems after percutaneous endoscopic gastrostomy （PEG）. METHODS： We retrospectively analyzed data for 252 out of 285 patients who underwent PEG at our hospital from 1999 to 2008 after PEG were defined as： Enteral nutrition problems （1） patients who required ≥ 1 mo after surgery to switch to complete enteral nutrition, or who required additional parenteral alimentation continuously; or （2） patients who abandoned switching to enteral nutrition using the gastrostoma and employed other nutritional methods. We attempted to identify the predictors of problem cases by using a logistic regression analysis that examined the patients＇ backgrounds and the specific causes that led to their problems. RESULTS： Mean age of the patients was 75 years, and in general, their body weight was low and their overall condition was markedly poor. Blood testing revealed that patients tended to be anemic and malnourished. A total of 44 patients （17.5%） were diagnosed as having enteral nutrition problems after PEG. Major causes of the problems included pneumonia, acute enterocolitis （often Clostridium difficile-related）, paralytic ileus and biliary tract infection. A multivariate analysis identified the following independent predictors for problem cases： （1） enteral nutrition before gastrectomy （a risk reduction factor）; （2） presence of esophageal hiatal hernia; （3） past history of paralytic ileus; and （4） presence of chronic renal dysfunction. CONCLUSION： Enteral nutrition problems after PEG occurred at a comparatively high rate. Patient background analysis elucidated four predictive factors for the problem cases.

Inhibitory effect of angiotensinⅡreceptor antagonist on hepatic stellate cell activation in non-alcoholic steatohepatitis

AIM： To investigate the efficacy of angiotensin Ⅱ receptor antagonist on hepatic stellate cells （HSCs） activation in the patients with non-alcoholic steatohepatitis （NASH）. METHODS： Seven patients with NASH were prescribed Iosartan, a selective angiotensin Ⅱ type 1 receptor antagonist （50 mg/d） for 48 wk. Liver biopsies were performed both at the entry and end of the study in all patients. Quiescent and activated HSCs were identified by double immunostaining using anti-p75 and α-smooth muscle actin antibodies, and the number of each phenotype was counted. Similarly, the liver specimens obtained from the eight patients with non-alcoholic fatty liver （NAFL） were also examined as controls. RESULTS： In NASH hepatic tissues, activated HSCs were dominantly distributed as compared with those in NAFL. The 48-wk Iosartan treatment induced a remarkable decrease in activated HSCs and a mild increase in quiescent phenotypes. CONCLUSION： Our data suggest the crucial involvement of HSCs in anti-fibrotic effect of angiotensin Ⅱ receptor antagonist on patients with NASH.