The impact of paracentesis flow rate in patients with liver cirrhosis on the development of paracentesis induced circulatory dysfunction

BACKGROUND/AIMS: Ascites is a dreadful complication of liver cirrhosis associated with short survival. Large volume paracentesis (LVP) is used to treat tense or refractory ascites. Paracentesis induced circulatory dysfunction (PICD) develops if no plasma expanders are given with ominous complications. To study the effect of ascites flow rate on PICD development. METHODS: Sixty patients with cirrhosis and tense ascites underwent LVP of 8 L were randomized into 3 equal groups of different flow rate extraction; group I (80 mL/minute), group II (180 mL/minute) and group III (270 mL/minute). Plasma renin activity (PRA) was measured baseline and on day six. PICD was defined as increase in PRA >50% of the pretreatment value. RESULTS: In group I through 3; the mean age was (52.5±9.4 vs. 56.4±8.5 vs. 55.8±7.1 years; P>0.05), mean arterial pressure (81.4±5.6 vs. 81.5±7 vs. 79.5±7.2 mmHg; P>0.05), MELD (17.6±4.1 vs. 15.8±4.1 vs. 14.7±4.5). Baseline PRA was comparable (1,366.0±1244.9 vs. 1,151.3±1,444.8 vs. 951.9±1,088 pg/mL; P>0.05). There was no statistically significant (P>0.05) flow mediated changes (Delta) of creatinine (0.23±0.27 vs. 0.38±0.33 vs. 0.26±0.18 mg/dL), MELD (1.25±5.72 vs. 1.70±2.18 vs. 1.45±2.21) or PRA (450.93±614.10 vs. 394.61±954.64 vs. 629.51±1,116.46 pg/mL). PICD was detected in a similar frequency in the three groups (P>0.05). On univariate logistic analysis only female sex was a fairly significant PICD predictor (Wald 3.85, odds ratio 3.14; P=0.05). CONCLUSIONS: The ascites flow rate does not correlate with PICD development.

Value of serum lentil affinity of alpha-fetoprotein in the diagnosis of hepatocellular carcinoma on top of liver cirrhosis

Hepatocellular carcinoma [HCC] is a common complication in patients with liver cirrhosis [LC]. Detection of HCC at an early stage is critical for a favorable clinical outcome. AFP-L3% is an isoform of AFP which is very specific for HCC. The AFP-L3% is the percentage of AFP-L3 over the total AFP level. The study aimed to evaluate the utility of AFPL-3% in detection of HCC developing on top of liver cirrhosis, to compare the levels of both alpha- fetoprotein [AFP] and AFP-L3% in HCC versus LC patients without HCC and to define the cut-off level of each tumor marker with the best sensitivity and specificity for HCC detection. The study was conducted on 25 cases of HCC that developed on top of LC and 25 LC cases with no evidence of HCC, as well as 25 apparently healthy controls. The levels of AFP and AFP-L3% were measured for all cases. Biochemical parameters and viral markers were also tested. Imaging and histopathological evidence of HCC were a prerequisite for inclusion in HCC group. Patients included in the HCC group had total AFP value < 200 ng/ml, which is not a diagnostic level for HCC. Levels of AFP and AFP L-3% were significantly higher in patients with HCC compared to those without HCC [P < 0.01]. Receiver-operating characteristic [ROC] curve analysis indicated that the best cut-off value was 15.4% for AFP-L3% to detect HCC as the sensitivity, specificity, positive predictive value [PPV], negative predictive value [NPV] and accuracy were 79.2%, 100%, 100%, 83.3% and 96.2% respectively. For AFP, the best cut-off in the non diagnostic range was 77.8 ng/ ml as the sensitivity, specificity, PPV, NPV, and accuracy were 75%, 68%, 69.2%, 73.9% and 70.4% respectively, The mean serum level of AFP showed no significant difference [P>0.05] regarding Child Pugh classification, numbers of tumor foci nor rumor size, however, it showed a significant difference [P<0.05] regarding lymph nodes invasion and TNM classification in HCC patients. Meanwhile, AFP-L3% showed no significant difference [P>0.05] regarding all these parameters. There was a positive significant correlation [P<0.05] between AFP and both AST and ALT, while AFP-L3% showed inverse significant correlation [P<0.05] with PC%. No significant correlation [P>0.05] was observed between serum AFP and serum AFP-L3% in HCC patients. In patients with total AFP values <200 ng/ml who present a diagnostic dilemma, AFP-L3% had higher sensitivity, specificity, PPV, NPV and accuracy for HCC detection, and was not elevated in any of the patients without HCC with specificity of 100%

Evaluation of liver hepcidin mRNA expression in patients with chronic hepatitis C virus infection [HCV] and liver cirrhosis

Elevated serum ferritin and iron accumulation in the liver are common in patients with chronic hepatitis C virus infection and have been associated with more aggressive disease and decreased response to interferon therapy, but the mechanism is unknown. Recently identified hepcidin, which is a small cysteine-rich cationic peptide produced by hepatocytes, secreted into plasma and excreted in urine, acts as regulator of intestinal iron absorption and iron recycling by the macrophage. This study was conducted to evaluate hepatic hepcidin mRNA expression in patients with chronic HCV infection and correlate its expression level with serum iron, serum ferritin and the grading and staging of liver disease. Fifty patients [40 males and 10 females] with chronic HCV infection were classified into two groups, chronic hepatitis [CH, n = 35, 28 males and 7 females] and liver cirrhosis [LC, n = 15, 12 males and 3 females]. In addition, 18 apparently healthy subjects [donors for partial liver transplantation] served as the control group. All patients were both anti-HCV and HCV RNA positive. Serum iron and serum ferritin were measured for all studied groups. Hepatic hepcidin mRNA expression level was determined by SYBR-green real-time PCR. Serum iron and ferritin were significantly higher in the patient groups compared to control group [p <0.001]. Hepatic hepcidin mRNA expression was significantly decreased in the patient groups than in the control group [p <0.001]. Also its expression was decreased in patients with liver cirrhosis than in patients with chronic hepatitis. There was a negative correlation between hepatic hepcidin mRNA and serum iron and ferritin in the patient groups. On the other hand no correlation was detected between it and histological grading of activity [r = -0.001, p >0.05]. Meanwhile there was a strong negative correlation between hepatic hepcidin mRNA and the histological stage of fibrosis [r = -0.51, p <0.001]. In conclusion failure of homeostatic regulation of hepatic hepcidin expression may be induced by HCV infection and this may cause elevation of serum iron and ferritin levels in patients with HCV infection. Therefore, understanding the role of the liver in hepcidin regulation and iron homeostasis may be helpful in the management of HCV hepatitis

Epstein barr virus DNA in hepatocelullar carcinoma tissues from hepatitis C positive Egyptian patients

Hepatocellular carcinoma [HCC] is one of the most frequent malignant tumors. It possesses the characteristics of high malignancy, rapid progress and poor prognosis. In recent years, studies have suggested that Epstein-Barr virus [EBV] is associated with HCC although opposite results have been subsequently reported. The present study was to determine the prevalence of EBV in HCC Egyptian patients, and whether EBV acts synergistically with hepatitis viruses in HCC carcinogenesis. The study included 61 patients, 20 HCV positive patients without HCC [16 males and 4 females] and 41 patients with proved HCC. They were subclassified into 3 groups [21 HCV positive [18 males and 3 female], 10 HBV positive [8 males and 2 females] and 10 HCC patients negative for both HCV and HBV [7 males and 3 females]]. Thorough clinical examination, abdominal ultrasonography and liver spiral CT were done. Liver function tests and serum alpha-fetoprotein [AFP], viral hepatitis markers for B and C, anti-EBV early antigen [EA-IgM], virus capsular antigen [VCA-IgMl and HCV RNA by reverse transcription PCR [RT-PCR] were measured. EBV-BamHI W DNA, and EBV-LMP1 DNA were performed by conventional PCR in the tumorus liver tissue of 41 HCC patients and the 20 noncarcinoma patients [HCV without HCC]. The positive ratios were compared between HCC subgroups and non tumorus HCV group. Our results revealed that, EBV-BamHI W DNA and/or EBV-LMP1 DNA were positive in 25 [40.9%] among overall 61 studied cases. In HCC patients, EBV-BamHI W DNA and/or EBV-LMP1 DNA were positive in 13 [61.9%] out of 21 HCV positive, 2 [20%] out of 10 HBV positive cases, 3 [30%] out of 10 cases negative for both HCV and HBV. However, it was positive in 7 [3 5%] out of 20 HCV cases without HCC [non tumotus cases]. The rate of EBV infection in HCC with HCV positive cases was significantly higher [Fisher exact=4.6 1; p<0.05] than HCC with HBV positive ones, HCC cases negative for both B and C virus [Fisher exact-4.28; p<0.05] and chronic HCV [non tumours] cases [Fisher exact=4. 19; p<0.05]. In addition, HCC in EBV DNA positive cases was associated with high HCV viral load, AST, ALT, low serum albumin, while there was no relation to AFP serum levels. In conclusion: the existence of EBV infection in HCC tissues suggests that EBV may be involved in the hepatocellular carcinogenesis in Egypt