Background/Aim. Malnutrition, a common problem in liver cirrhosis and HCC, may readily deteriorate the clinical functions with resultant poor prognosis. Beside the hyper catabolic state frequently encountered in chronic liver disease and HCC, anorexia and reduced food intake also worsen the malnutrition. The recently discovered peptide hormone ghrelin acts as a counterpart of leptin in regulation of food intake and fat utilization. The aim of the present study was to investigate the ghrelin and leptin levels in cirrhosis and HCC due to hepatitis B and D viruses, and the association of ghrelin and leptin with TNF-α, IL-6 and the severity of the disease. Materials and methods. We measured serum ghrelin, leptin, TNF-α, and IL-6 levels using specific immunoassay in 45 patients (23 cirrhosis, 22 HCC) with HBV and/or HDV and in 25 control subjects. Results. In comparison to controls, serum ghrelin, TNF-α, and IL-6 levels were significantly higher in cirrhosis and HCC (P < .05), whereas serum leptin levels were found decreased (P < .05). There was a positive correlation between ghrelin and TNF-α, and a negative correlation between leptin and TNF-α (P < .05). Conclusion. In cirrhosis and HCC due to HBV or HDV, serum ghrelin levels were increased with a corresponding decrease in serum leptin concentrations, acting as a physiological counterpart of ghrelin. The increasing of ghrelin is more prominent in Child C cirrhosis and the level was correlated with TNF-α. The presence of nutritional and metabolic abnormalities, including malnutrition, in cirrhosis and HCC may, at least partly, elucidate high ghrelin and low leptin levels.

Although IBS is widely present in Turkey, its prevalence is lower than that reported in Western communities. In the region where this study was carried out, IBS was more prevalent in females and in individuals with low educational and economical status.

Genistein, a strong antioxidant agent, significantly decreased the plasma TNF-alpha level and remarkably prevented the emergence of NASH by improving the biochemical and histopathological abnormalities via attenuating oxidative stress.

We sought to evaluate the effects of pentoxifylline (PTX) on steatohepatitis in a novel experimental nonalcoholic steatohepatitis (NASH) model induced by a high-fat diet (HFD). Thirty-three male Sprague-Dawley rats were randomly divided into 3 groups. The first group received only standard rat diet (control group); groups 2 (placebo group) and 3 were given HFD, ad libitum. After week 4, 0.5 mL of physiologic serum was injected subcutaneously to the placebo group and 50 mg/kg/d PTX was given intraperitoneally to the third group (group PTX). After 6 weeks all rats were humanely killed. Serum biochemistry, tumor necrosis factor-alpha (TNF-alpha), plasma, and liver tissue malondialdehyde (MDA) were analyzed. Histopathologically, steatosis, ballooning degeneration, inflammation, and fibrosis were determined. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, plasma and liver tissue MDA, and plasma TNF-alpha levels were significantly higher in placebo group than in the control group. Tumor growth factor-beta levels, however, were comparable in the placebo and control groups. On histopathologic examination, steatosis, inflammatory cells per square millimeter, and ballooning degeneration were significantly higher in the placebo group than in the control group. No fibrosis or Mallory bodies were found in the placebo group. AST, ALT, plasma and liver tissue MDA, and plasma TNF-alpha levels were significantly lower in PTX group compared to the placebo group. Histopathologically, steatosis, mean number of inflammatory cells/mm(2) and ballooning degeneration in PTX group were also significantly lower than in the placebo group. In conclusion, PTX strikingly ameliorates steatohepatitis in this novel NASH model not only by inhibiting the TNF-alpha but also suppressing the oxidative stress markers.

Background and Aim: Although rectal bleeding is a common gastrointestinal symptom, there are very few community-based studies, and all of these studies were conducted in the West. So far the epidemiologic characteristics of rectal bleeding have not been defined in an Asian country. We aimed to characterize self-reported rectal bleeding and its association with functional bowel disorders in Turkey. Factors affecting healthcare-seeking behavior were reviewed as well. Subjects and Methods: In this study, 760 subjects were chosen randomly. Questionnaires were completed by nurses during face-to-face interviews with each participant. Results: Of the 707 (93%) subjects included in this study, 9.5% had functional dyspepsia, 8.6% had irritable bowel syndrome (IBS), 24.5% had functional constipation, and 13.8% had functional abdominal bloating. The prevalence of rectal bleeding in the previous year was 14.7%. The recent onset of rectal bleeding was 2.7%. Rectal bleeding was more common among subjects younger than 45 years. Subjects who had functional constipation or constipation-dominant IBS reported rectal bleeding more frequently than others. The rate of consultation was only 41.3% among the subjects with rectal bleeding. Subjects aged ≧45 years and who had marked bleeding or bleeding more than twice a day or fear of cancer sought healthcare more frequently than others. Conclusion: Rectal bleeding is as common a symptom in Turkey as in Western countries. Advanced age and fear of cancer were independent predictors of consultation behavior in this group.

Ghrelin (G-HH) synthesized in several tissues including salivary and stomach glands stimulates appetite in humans by modulating neuropeptide Y neurons in the hypothalamic arcuate nucleus. Loss of appetite is one of the most important symptoms of stomach cancer. We conducted a study using immunohistochemistry to determine whether salivary glands and stomach cancer tissues produce ghrelin. We determined that negative ghrelin immunohistochemistry discriminates tumors from normal tissues and may therefore further our understanding of the clinically important problem of reduced food intake and anorexia in cancer patients. Radioimmunoassay analyses confirmed that cancer cells do not produce a G-HH peptide, whereas normal cells yield this peptide.

Abstract

Fulminant hepatitis is a rare complication of acute hepatitis A infection. Nevertheless, the seroepidemiology of the infection is rapidly changing with the developing world, rendering more adults susceptible to the infection, in particular with more severe course. We report here fulminant hepatitis A infection with a mortal course during an epidemic period in two siblings. Although it causes a self-limited mild disease, hepatitis A virus may have a severe course including fulminant hepatitis and may lead to mortality, especially in older ages. Hence, the risk of hepatitis A virus infection and its complications should be reduced with measures of immunization and sanitation.