Relationship between the Severity of Liver Damage and the Serum Leptin Level for Nonalcoholic Fatty Liver Disease / 대한간학회지

BACKGROUND/AIMS: Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of conditions that are mainly characterized histologically by macrovesicular hepatic steatosis. There are two histologic patterns of NAFLD: simple steatosis alone and steatohepatitis. The factors leading from simple steatosis to nonalcoholic steatohepatitis (NASH) are still obscure. The datas from several studies have suggested that leptin could be involved in the progression from hepatic steatosis to steatohepatitis including the fibrosis. We evaluated serum leptin levels in patients with NAFLD to determine whether any relationships existed between the leptin levels and the severity of hepatic inflammation or fibrosis. METHODS: We studied 62 patients with NAFLD who were diagnosed at the Hallym University Sacred Heart Hospital from July 2001 to May 2004. We measured the serum leptin level in all cases and liver biopsy samples were obtained from 31 cases. The liver biopsy specimens were graded according to methods described by Brunt. Spearman rank correlations were used to detect the associations between the serum leptin and the various anthropometric and biochemical variables. The relationship between the histologic severity and the serum leptin level was evaluated with logistic regression analysis. RESULTS: Serum leptin levels correlated with insulin, c-peptide, ALT and homeostasis model assessment insulin resistance, but not with BMI, age and gender. Serum leptin level also correlated with hepatic fibrosis, but not with hepatic steatosis or inflammation. However, the serum leptin level was not a significant independent predictor of the grade of hepatic steatosis, inflammation and fibrosis on the univariate analysis. CONCLUSIONS: The serum leptin level was not an independent predictor of the severity of liver damage in NAFLD.

24 hour esophageal pH changes in patients with peptic ulcer disease before and after Helicobacter pylori eradication / 대한내과학회지

BACKGROUND: There are many arguments that Helicobacter pylori is a protective factor or a risk factor for GERD. Some authors reported a high incidence of reflux esophagitis in patients who had received Helicobacter pylori eradication therapy. We studied the prevalence of pathologic gastroesophageal reflux in Helicobacter pylori positive peptic ulcer patients and the effects of Helicobacter pylori eradication therapy on development of pathologic gastroesophageal reflux. METHODS: A total of 44 patients with endoscopically documented peptic ulcer disease and Helicobacter pylori infection underwent 24-hour esophageal pH monitoring and received a week of triple therapy. After three months of cessation of triple therapy, patients underwent 24-hour esophageal pH monitoring again. 24-hour esophageal pH monitoring of 44 patients were compared before and after the triple therapy. Helicobacter pylori status was evaluated by Giemsa stain, rapid urease test and urea breath test at each examination. RESULTS: The patients were classified into cured and ongoing Helicobacter pylori infection group. In cured patients group, there was no significant difference in the prevalence of pathologic gastroesophageal reflux before and after Helicobacter pylori eradication (p=0.8). In 44 patients, 30 patients had pathologic gastroesophageal reflux before eradication. In these patients, 27 patients cured Helicobacter pylori infection and 3 patients were ongoing Helicobacter pylori infection. Among 27 patients who cured Helicobacter pylori infection, 5 patients recovered from pathologic gastroesophageal reflux after eradication. In patients without pathologic gastroesophageal reflux before eradication, the prevalence of pathologic gastroesophageal reflux was not associated with Helicobacter pylori eradication (p=1). CONCLUSION: We find that the prevalence of pathologic gastroesophageal reflux in patients with peptic ulcer is high before Helicobacter pylori eradication. We suggest that Helicobacter pylori eradication in patients with peptic ulcer disease is not associated with development of pathologic gastroesophageal reflux.