While this publication investigated the association of total serum testosterone with fibrosis scores and inflammatory activity, sex estradiol levels were not determined. The liver is a hormone-sensitive organ, and in fact both normal liver and hepatocellular carcinoma tissues from male and female mammals have been shown to express specific estrogen receptors (ERs). Experimentally, estrogens may act as liver tumor inducers or promoters in vivo.2, 3 In fact, estrogens are involved in the regulation of hepatocyte proliferation: a “feminization” of INCB024360 mouse the hepatic microenvironment occurs after partial hepatectomy in rats and humans
with an increase in estrogen levels and a concomitant reduction of testosterone levels.4, 5 The source of estrogens in men is from the aromatization of androgens and, broken down in the liver, the relationship may relate to the severity of liver disease. Therefore, serum total testosterone is not an accurate reflection of sex hormone status in cirrhosis and estradiol levels should also be determined in this patient group. WeiLin Mao X.X.*, * Department of Clinical Laboratory, First Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang, China. “
J, Thompson AJ, Ge D, Gumbs CE, Urban TJ, Shianna KV, et al. ITPA gene variants protect against anaemia in patients treated for chronic hepatitis C. Nature 2010;464:405-408. (Reprinted with permission.) http://www.selleckchem.com/products/Everolimus(RAD001).html Chronic infection with the hepatitis C
virus (HCV) affects 170 million people worldwide and is an important cause of liver-related morbidity and mortality. The standard of care therapy combines pegylated interferon (pegIFN) alpha and ribavirin (RBV), and is associated with a range of treatment-limiting adverse effects. One of the most important of these is RBV-induced haemolytic anaemia, which affects most patients and is severe enough to Amoxicillin require dose modification in up to 15% of patients. Here we show that genetic variants leading to inosine triphosphatase deficiency, a condition not thought to be clinically important, protect against haemolytic anaemia in hepatitis-C-infected patients receiving RBV. Chronic infection with hepatitis C virus (HCV) is a major health burden worldwide and is one of the main reasons for liver transplantation in Europe and the United States. A primary reason for the increased morbidity and mortality in affected patients is the development of progressive liver fibrosis and end-stage cirrhosis with complications such as hepatocellular carcinoma.1 However, it has become apparent from prospective and retrospective analyses that only about half of chronically infected patients are at risk of developing severe fibrosis and are therefore prime candidates for antiviral therapies.