[25] In the next 10 years, obesity rose by approximately 1.5 times in the patients with chronic liver disease in Japan.[14] In addition, presence of diabetes mellitus, hyperinsulinemia or obesity is currently regarded as a significant risk factor for liver carcinogenesis.[14-16] Furthermore, the relationship between obesity and liver inflammation and fibrosis, including NASH has become an important issue in recent years. Therefore, it is necessary to elucidate the

nourishment state of the present cirrhotic patients to update guidelines. Thus, we report in this paper a comprehensive survey of the nourishment state and QOL in the present patients with IWR-1 cell line liver cirrhosis. The etiology of the 294 cirrhotics was hepatitis

B virus in 11.9%, hepatitis C virus in 69.4%, alcohol in 8.5%, NASH in 2.0% and others in 8.2% in this study. In the 44th Annual Meeting of Japan Society of Hepatology in 2008 (Matsuyama), the reported etiology of 33 379 cirrhotics was hepatitis B virus in 13.9%, hepatitis C virus in 60.9%, alcohol in 13.6%, NASH in 2.1% and others in 9.5%,[26] indicating similar patient composition between two studies. Obesity is defined by BMI of 25 or higher in Japan but by 30 or higher by World Health Organization. In this study, the mean BMI excluding patients with ascites, edema or HCC was 23.6 ± 3.6 kg/m2 and the ratio of obese subjects with BMI of 25 or higher was 33.7% of these patients (Fig. 2). The proportion of obese people in the general population of Japan at matched age was 30.5% in 2009.[25] Thus, an equal or greater proportion check details of patients with liver cirrhosis has obesity than the general population of Japan at present. The increase in obesity, or excess energy nutrition status, and subsequent impaired glucose metabolism potentially bring about an unfavorable outcome Tryptophan synthase in cirrhotic patients. Actually, excess energy nutrition contributed to induce carcinogenesis in liver cirrhosis,[15, 27, 28] and the

number of obese subjects doubled in the candidates for liver transplantation in the previous 10 years in the USA.[29-31] As to PEM exactly defined by serum albumin and npRQ, Tajika et al. reported that protein malnutrition was identified in 75%, energy malnutrition in 62% and PEM in 50% of 109 patients with liver cirrhosis in 1995.[4] In our study, 87 patients without HCC composed a group to show comparable backgrounds to those by Tajika et al.[4] Among them, 67% had protein malnutrition, 48% had energy malnutrition and 30% had PEM (Table 3). Taken together, the protein malnutrition remains almost similar in liver cirrhosis, but the patients with energy malnutrition, particularly PEM, substantially decreased. The above-mentioned results urge that two concerns are addressed. The first is the effect of altered nutritional state of cirrhotics on their QOL, and the second is a question if exercise should be prescribed for obese cirrhotics.