Assessment of the relation between serum-ascites albumin concentration gradient with esophageal varices and its complication

We aimed to evaluate the correlation between serumascites albumin concentration gradient [SAAG] with esophageal varices [EV] presence and grading, and to assess the relationship between SAAG measurements and the occurrence of gastrointestinal hemorrhage in cirrhotic patients with ascites. Our study included 45 nonalcoholic cirrhotic cases with ascites. They had routine clinical, ultrasonographic and laboratory investigations including ascitic fluid analysis. They had measurement of SAAG computed. An upper gastrointestinal endoscopy was done in all cases to assess the presence and size of EV. 36 of our patients [80%] had EV. The mean SAAG level was 1.46 +/- 0.27 gm/dL for all cases. No correlation was found between SAAG and any of the studied clinical or biochemical parameters. By using the ROC Curve, a SAAG value at a level of [>1.55gm/dL], was a good predictor of the presence of EV with 100% sensitivity and 71.4% specificity. The presence of EV was positively correlated with serum bilirubin, prothrombin time [PT], and spleen size. Meanwhile, it was negatively correlated with serum albumin, serum total protein, platelet count and total protein in ascetic fluid. On univariate analysis of variants associated with the presence of large esophageal varices, only the presence of splenomegaly could predict high grade varices. On comparing patients with and without bleeding varices, the EV grade, portal vein diameter [PVD], spleen size and creatinine level were significantly higher in the group of bleeding varices [p values were 0.002, 0.006, 0.01 and 0.012 respectively] A SAAG score [>/=1.55 gm/dL] is a useful predictor of the presence of EV in cirrhotic patients with ascites. This finding can assist clinicians in determining the urgency of care and referral for upper gastrointestinal endoscopy in cases with ascites. Meanwhile, SAAG was not valuable in screening and predicting complications, such as bleeding from esophageal varices

Evaluation of plasma adiponectin level in patients with nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease is an increasingly recognized condition that may progress to end stage liver disease; the aim was to study the level of plasma adiponectin in patients with nonalcoholic fatty liver with DM, and chronic hepatitis C in comparison with a control group. The study was conducted on 60 individuals, 37 males and 23 females, their age ranged from 26 to74 Ys, they were categorized into 3 groups: G 1: 20 apparently healthy individual serving as a control group, G2: 20 patients with type 2 DM and fatty liver, G 3: 20 patients with chronic hepatitis C and fatty liver. All cases underwent full clinical examination and laboratory investigaions, including [CBC], [ESR], liver and kidney- function tests ,fasting and 2hours PP blood glucose, lipograms, Polymerase chain reaction [PCR] for HCV-RNA in addition to abdominal ultrasonography and estimation of serum adiponectin level by ELISA technique. A significantly decreased plasma adiponectin levels were found in patients with fatty liver disease when compared to the control group. In addition, plasma adiponectin in group 2 [DM] show significant positive correlation with fasting blood glucose level [r =-52, p<0.05]. However plasma adiponectin levels, were significantly lower in group 3 [HCV] than in the other groups. A significant lower adiponectin levels was observed in male in all groups, further more plasma adiponectin in group 3 [HCV] show significant spositive correlation with blood urea [r =0.48, p <0.05] and HDL level [r =0.49, p <0.05]. Plasma adiponectin level is decreased in patients with NAFLD with type2 DM and chronic HCV and may suggest fat accumulation in the liver

Peripheral neuropathy in hepatitis C patients in Egypt

The overall prevalence of HCV antibodies in the general population is around 10-15% and is highly prevalent among Egyptian blood donors. The study was carried out on 30 patients, there was [21 male and 9 were female] age ranged from 27-62 ys with proved HCV infection by means of positive antibody assay for the virus and positive PCR for HCN RNA. The current study aimed to evaluate the role of HCV in peripheral neuropathy [PN] and to assess the response of PN to medical treatment PN was assessed clinically by motor and sensory examination. Beside routine clinical and laboratory tests, electrophysiological studies were also done. At presentation, sensory axonal degeneration neuropathy was the most prevalent type of neuropathy in the studied HCV subjects, in addition male HCV -patient are slightly more subjected to the development of HCV- associated peripheral neuropathy furthermore. Peroneal nerve conduction velocity was found to be impaired more than that of median nerve. Interestingly the presence of ascites had no significant effect on the degree of nerve conduction. The underlying mechanism of such peripheral neuropathy is mostly due to axonal degeneration. We therefore conclude that HCV- associated neuropathy had mainly a chronic evolution. PN manifestations can be the initial presenting manifestation of HCV infection

Role of leptin in non-alcoholic fatty liver disease [NAFLD]

Abstract: The role of steatosis in the pathogenesis of chronic liver disease [CLD] is now believed to form part of a continuum in non alcoholic fatty liver disease [NAFLD]. One of the unconventional areas in which leptin is now receiving great attention is liver disease. Several published studies indicate that circulating leptin is increased in cirrhosis, HCV and NASH. The aim of this study was to investigate the role of leptin in NAFLD, by measuring the serum leptin level and correlating it with biochemical markers of liver disease and the result of liver biopsy in chronic hepatitis C [CHC] patients

Patients and Methods: Sixty seven Saudi subjects were included. They were divided into 3 groups. Group A [n = 22, 8 males and 14 females] patients had diabetes mellitus [DM]; their mean age was 44 +/- 12.9 years. Group B [n = 20, 7 males and 13 females] patients had CHC as diagnosed by HCV Ab and HCV RNA; their mean age was 48.9 +/- 14.1 years and group C the control healthy volunteers [n = 25, 15 males and 10 females with a mean age of 40.68 +/- 12.6 years]. All the groups matched for age and sex. Serum leptin, C peptide and insulin were measured by radio immununoassay for all subjects. Liver biopsy was done for the HCV group only

Results: showed no correlation between leptin levels, C-peptide and serum insulin. There was a statistically significant difference in serum leptin level between groups A and B and B and C but no statistical difference between groups A and C. The HCV group patients had hypoleptinaemia in comparison to other studied groups. Serum leptin levels for the studied groups [for DM, HCV and control group] were respectively 55.65+/- 59.02 ng /ml, 25.62 +/- 37.2 ng/ml and 82.78 +/- 49.73 ng/ml. There was no correlation between the leptin level and the histopathology of the liver as regards the steatosis grade, inflammatory grading in HCV group and the fibrosis stage. The steatosis in the HCV group patients was related to body mass index [BMI] and hyperglycemia not to the leptin level. HCV appears to be a prediabetic condition

In Conclusion: Serum leptin can not be used as a non invasive marker for the prediction of steatosis, necrosis nor fibrosis in NAFLD

Concepts in leptin and liver disease

Leptin is a cytokine l6kd peptide hormone. Its crucial role is regulation of appetite and the body fat mass mainly through action on the hypothalamus. It is produced mainly in adipocytes of white fat, as well as from other tissues e.g. placenta, skeletal muscles, fundus of the stomach and activated hepatic stellate cell [HSC] and recently reported that leptin is produced from B cell of islands of the pancreas. The gene responsible for production is present on chromosome 7 called obse gene [ob/gene]. Leptin receptors [OB-R] were present in two forms short [OB-Ra or OB-RS] and long one [OB-Rb or OB-RI]. The main action of leptin depends on long form [OB-Rl], where very little evidence is available implicating a role for the short form in the action of leptin. One of the unconventional areas in which leptin is now receiving great attention is liver diseases as several published studies indicate that circulating leptin level are increased in cirrhosis, hepatitis C virus [HCV] and non-alcoholic steatohepatitis [NASH]