During the period 1986-1988, the expression of anti-HDV in different high-risk groups and its clinical impact on patients with HBV-related chronic liver disease and hepatocellular carcinoma was investigated in Iran. Using the ELISA technique, we observed a 2.5% anti-HDV positivity in asymptomatic chronic HBsAg carriers (3 of 120); in hemophiliacs, two of six HBsAg carriers were positive for anti-HDV and zero of 50 anti-HBs positives. Anti-HBs positive dialysis patients were positive for anti-HDV in 2.0% of the cases (1 of 50), whereas the rate of anti-HDV positivity was 44.5% in hemodialysis patients positive for HBsAg (16 of 36). The figures were comparable in HBsAg positive patients with chronic active hepatitis and cirrhosis (49.2%; 31 of 63). Moreover, anti-HDV was detected in five of eight patients with hepatocellular carcinoma. These data indicate the endemicity of delta infection in Iran. The increased incidence among hepatocellular carcinoma patients is an interesting finding to be further investigated with larger groups of patients in this region.

Ascites is a common complication of cirrhosis and has a major clinical impact on the patient's general well-being. Approximately 10% of patients with cirrhosis can develop diuretic-resistant, tense ascites that requires other therapeutic interventions. In recent years, there has been a renewed interest in large-volume paracentesis (LVP) as a safe, simple, and inexpensive method to substitute for other more complicated and costly therapeutic interventions for refractory ascites. In this article, we review the latest literature supporting the use of LVP for the treatment of refractory, tense ascites. We also address the role of intravascular volume expansion after LVP, note that usually no postparacentesis volume expansion is necessary, and compare, when used, the different plasma volume expanders in terms of efficacy, safety, and cost.

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A competent lower esophageal sphincter (LES) prevents gastroesophageal reflux disease (GERD) in the setting of increased abdominal pressure. Therefore, we have assessed whether a back support belt causes gastroesophageal reflux (GER). Ten healthy volunteers underwent esophageal manometric studies to locate the LES. Subsequently, each subject underwent two separate 8-hour intra-esophageal pH monitor studies on different days, the first without wearing a back support belt, and the subsequent one wearing a back support belt. A symptom diary and continuous intra-esophageal pH data were obtained during both study periods. The mean LES pressure (LESP) was 14 +/- 3.6 mm Hg without a back support belt and 15.8 +/- 4.3 mm Hg with a back support belt which was not significantly different. There were no significant differences in total episodes of GER, esophageal acid exposure, or any other parameters monitored. Symptoms of GER were the same comparing the back support belt with no back support belt. We conclude that healthy people with normal LESP do not have increased GER as a result of wearing a back support belt.

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