Can Lactobacillus acidophilus improve minimal hepatic encephalopathy? A neurometabolite study using magnetic resonance spectroscopy

Minimal hepatic encephalopathy [MHE] is diagnosed when hepatic patients perform worse on psychometric tests compared to healthy controls. This study aimed to evaluate probi-otics as alternative therapy in MHE. This is an open-label randomised controlled trial, performed in the Department of Tropical Medicine and Infectious Diseases, Tanta University Hospitals, from March 2010 to January 2012. A total of 90 patients with MHE were allocated by simple randomisation to three parallel equal groups. Group A received lactulose, group B a probiotic [Lactobacillus acidophilus] and group C served as the control. After informed consent, patients were tested for gut micrecology, fasting blood ammonia, liver functions and magnetic resonance spectroscopy [MRS] examination to study brain metabolites, mainly choline [Cho], myoinositol [ml], glutamine + glutamate [Glx] and creatinin [Cre]. Patients who developed overt encephalopathy were excluded from analysis. The whole battery of investigations was repeated in the same order after 4 weeks. The probiotic was better tolerated than lactulose. The relative risk reduction [RRR] of developing overt encephalopathy was 60% in the case of lactulose and 80% in the case of probiotic, with a number needed to treat [NNT] of 2.4 and 2.3, respectively. The differential but not total microecology count was significantly shifted towards saccharolytic rather than proteolytic bacteria. The ml/Cre and [Cho + mI]/Glx ratios were significantly increased and the Glx/Cre ratio was significantly reduced after 1 month-follow-up in the probiotic group compared to the lactulose group and in both treatment groups compared to the control group. Both probiotic and lactulose therapy can improve blood ammonia and psychometric tests in MHE and reduce the risk of developing overt encephalopathy. MRS showed more improvement in the levels of brain neurometabolites in the probiotic group

Expression of the signal transducer and activator of transcription factor 3 in colorectal carcinomas, colonic adenomas and ulcerative colitis

Despite the growing understanding of the involvement of protooncogenes and tumour suppressor genes in the oncogenesis of CRC, the exact biological and molecular mechanisms underpinning this process remain poorly understood. The signal transducer and activator of transcription [STAT3] has been implicated in the regulation of growth and malignant transformation. Accumulating evidences have come to indicate that abnormalities in the Janus kinase [JAK]/STAT pathway are involved in oncogenesis of several cancers. The aim of this study was to investigate the expression of JAK3 and STAT3 in both normal and activated forms by immunohistochemistry in adenomas of the colon, ulcerative colitis and CRC compared to normal colonic mucosa. Tissues from 30 cases with primary CRC and seven cases with ulcerative colitis [UC], removed by colectomy, were included. In addition, tissues from 10 colonic adenomas, 15 CRC and eight cases with UC, obtained by endoscopic biopsies, were examined histopathologically. Immuno-histochemical evaluation of STAT3, p-STAT3, JAK3 and p-JAK3 expression in tissue sections was completed. Statistical analysis and correlation of data were then performed. Normal colonic mucosa showed expression of STAT3 only. Immunoreactivity of p-JAK3 increased significantly [p < 0.05] and correlated with the degree of dysplasia in colonic adenomas. Immunoreactivity of p-STAT3 increased significantly [p < 0.05] and correlated with the degree of dysplasia in cases with UC. In CRC a significant positive correlation was found between p-STAT3 expression and grading, STAT3, JAK3 and p-JAI<3 and TNM or Dukes' staging, and p-STAT3 and nodal status excluding distant metastasis [p<0.05]. JAK3 and STAT3, and particularly their activated forms, were found to correlate significantly with the degree of dysplasia in adenomas and UC, indicating their potential role in colorectal carcinogenesis. They also correlate with anaplasia and invasion, suggesting a definitive role in progression of CRC

Assessment of serum and ascitic fluid leptin in spontaneous bacterial peritonitis

This study was designed to assess leptin changes in serum and ascitic fluid of patients with decompensated cirrhosis and clarify if it plays a role in the pathogenesis of SB and relation of this role- if any-to TNF alpha in those patients 30 subjects were included in the study; 10 healthy control, 10 cirrhotic patients with sterile ascites, and 10 with spontaneous bacterial peritonitis [SBP]. All participants were subjected to full clinical examination, and a range of laboratory test. ELISA test was used to assess levels of leptin and TNF alpha both in serum and ascitic fluid. The results show elevation of serum and ascitic fluid leptin and TNF alpha in cirrhotic cases versus control, with ascitic/serum ratio > 1 suggesting intra abdominal production of both cytokines. Both serum and ascitic fluid leptin and TNF alpha were significantly higher in patients with SBP than those with sterile ascites and were positively correlated. Our results suggest elevation of serum and ascitic fluid leptin to play an immunological role in pathogenesis of SBP, and TNF alpha to be a putative candidate involved in this mechanism