The multiple functions of heme oxygenase-1 in the liver.

Heme oxygenases (HO) are essential enzymes which degrade heme into carbon monoxide (CO), biliverdin and free iron. Due to its anti-inflammatory, anti-apoptotic and, as recently described, anti-viral properties the inducible HO isoform HO-1 is an important molecule which could find its way into therapy of gastrointestinal diseases. Acute and chronic liver injuries including acute liver failure, alcoholic or viral hepatitis, chronic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma are life threatening diseases and as a consequence might result in the necessity of liver transplantation. HO-1 as well as its reaction products of heme degradation has been linked to cytoprotection. HO-1 induction in rodent models of acute and chronic hepatic inflammation resulted in improvement of liver damage and down-regulation of pro-inflammatory cytokine levels. Furthermore HO-1 induction interfered with fibrosis progression in mice and partially resolved existing fibrosis. Likewise, HO-1 induction interfered with replication of hepatitis viruses B and C, which frequently are the reason for chronic hepatitis and subsequent tumor growth. Liver transplantation is limited by ischemia/reperfusion (I/R) injury, which is characterized by hypoxia and nutrient deficiency resulting in oxidative stress, apoptosis and immune activation. Induction of HO-1 and application predominantly of CO have been shown to interfere with I/R liver injury and to improve recipient and graft survival. On the other hand HO-1 has been shown to be over-expressed in various tumors, including hepatocellular carcinoma (HCC). Due to its anti-apoptotic properties this bears the risk to promote tumor growth. Anti-apoptotic effects are predominantly mediated by CO. This review aims to summarize beneficial as well as detrimental effects of HO-1 and its products within the liver.

Prediction severity of esophageal varices: a new cutoff point for Platelet count/ spleen diameter ratio.

AIM: It is currently recommended that all patients with liver cirrhosis undergo upper gastrointestinal endoscopy (UGIE) to identify those who have esophageal varices (EV) that carry a high risk of bleeding and may benefit from prophylactic measures. In the future, this social and medical burden will increase due to the greater number of patients with chronic liver disease and their improved survival. The aim of this paper was assess value of platelet count/spleen diameter ratio (PC/SD ratio) for the prediction or screening of EV in cirrhotic patients. METHODS: In this two years prospective study, patients with liver cirrhosis referred to Al -Zahra hospital enrolled. Patients underwent detailed clinical examination, blood tests (hematology, liver function tests) and ultrasonography. Size of esophageal varices was assessed at UGIE; Paquet's grades 0-III were classified as group A (0-I; No or Mild EV) and group B (II-III; Moderate to severe EV). PC/SD ratio was also measured as possible noninvasive predictive/screening tools. Degree of eEV was assessed at UGIE. The relationship of the presence and degree of EVs with PC/SD ratio was evaluated. RESULTS: Fifty consecutive cirrhotic patients (mean age+/-SD) was 52.1 (+/-16.2); 41 male and 9 female) were enrolled; nineteen 19 (38%) patients were placed in group A (No or mild EV) while 31 (62%) had endoscopic evidence of moderate to severe EV (group B). PC/SD ratio cut off value of 921 had 93% negative predictive value. PC/SD ratio found to be significantly (P<0.05) different between group of A and B. CONCLUSIONS: The PC/SD ratio is independently associated with the presence of EV and can predict its severity in patients with cirrhosis. Use of this cost effective parameter may help identify patients with mild or no EV who may not need UGIE to reduce costs and discomfort for these patients and the burden on health system.