Search

Background: Erosive esophagitis is a frequent endoscopic feature in patients with gastro-oesophageal reflux disease. However, most of patients with heartburn/regurgitation have a non-erosive reflux disease. The reason for this heterogeneous impact of gastro-oesophageal reflux disease on oesophageal mucosa is unknown to date., Aim: To evaluate the cell proliferation status of oesophageal epithelium in both healthy normal subjects and patients with gastro-oesophageal reflux disease with or without erosions., Materials and Methods: All the subjects underwent endoscopy and biopsies were taken at 5 cm from the squamo-columnar junction. Specimens were analysed both at histology and at transmission electron microscopy. Cell proliferation was evaluated by MIB1 immunostaining. Of the 85 subjects were studied, 10 were healthy controls with normal pH-testing and macroscopical, histological and ultrastructural patterns; 37 were patients with erosive esophagitis, and 38 patients with non-erosive reflux disease., Results: At histology, of the 37 patients affected by erosive esophagitis, 30 had normal mucosa and 7 showed mild oesophagitis. One patient with non-erosive reflux disease showed signs of oesophagitis at histology. At TEM, all patients with gastro-oesophageal reflux disease had ultrastructural patterns of damage i.e. dilations of intercellular spaces (DIS), and all controls had a normal ultrastructural pattern. The mean (+/-SD) MIB1-LI values of normal subjects and non-erosive reflux disease and erosive oesophagitis patients were 62.2% (+/-9.1), 29.7% (+/-7.2) and 16.2% (+/-5.2), respectively; there were significant differences among the three groups (p<0.001)., Conclusions: Oesophageal mucosa of patients with reflux symptoms presents a decrease in MIB1 immunostaining of 50% and 25% in non-erosive reflux disease and erosive esophagitis patients with respect to normal subjects.

Background: Patients with longstanding ulcerative colitis are at increased risk of colorectal cancer. In the literature, no agreement has yet been reached regarding prevention strategies. Our report sums up a prospective study started in 1980., Methods: A total of 65 patients affected by ulcerative colitis for more than seven years were admitted to a regular colonoscopic and biopsy follow-up programme., Results: Some 20 years after the beginning of the study, 23 (35.3%) patients have been operated upon, 2 patients have died but not from cancer 29 (44.66%) patients have abandoned the programme. Only 11 (16.9%) patients have remained under colonoscopic surveillance., Conclusion: These results cast some doubts on the significance of such a programme and on its long-term feasibility.

The epidemiological and clinical characteristics of peptic ulcer were studied in 324 of 368 consecutive patients with cirrhosis of the liver during a mean period of 1.2 (+/- 0.61) years. Peptic ulcer prevalence rates in patients with cirrhosis were as follows: point prevalence 11.7%, period prevalence 15.1%, and life-time prevalence 24.2%. The annual incidence rate observed in 140 patients with cirrhosis undergoing endoscopic follow up was 4.3%. Ulcers were asymptomatic in more than 70% of patients. The peptic ulcer complication rate at entry was 20% in the whole group and 40% in those who had not a previous diagnosis of peptic ulcer when admitted to the study. Peptic ulcer was more frequent among HBsAg+ cirrhotics (p = 0.05). Patients with more severely decompensated cirrhosis also had a higher frequency of asymptomatic ulcers (p = 0.04), gastric ulcers (p = 0.01) and asymptomatic gastric ulcers (p = 0.005). After diagnosis, during endoscopic follow up, gastric ulcer in patients with cirrhosis tended to heal slowly and recurred with higher frequency than in controls without cirrhosis (p = 0.04). Seventy-nine per cent of peptic ulcer recurrences were asymptomatic in patients with cirrhosis. There were no complications during the follow-up period: this could be due to the regular timing of endoscopy, which permitted early detection and treatment of the recurrences, thus preventing further complications.

The relationship of the endoscopic aspect of esophageal varices, portal quantitative Doppler ultrasound parameters and clinical and biochemical findings was assessed in 149 patients with cirrhosis stratified according to the presence of esophageal varices (n = 115) and the absence of previous bleeding (n = 96). In this series of patients the presence of esophageal varices and red signs proved to be significantly correlated with the severity of cirrhosis. However, in the group of patients with varices, no correlation was found between variceal size and the degree of liver failure. Portal blood flow velocity was significantly different in the endoscopic subgroups, but not in the clinical and biochemical subgroups. Furthermore, portal blood flow velocity was found to correlate only with the presence and size of esophageal varices. The Congestion Index of the portal vein (derived from the ratio between the cross-sectional area of the portal vein and the mean velocity of portal flow) was significantly different in most clinical, biochemical and endoscopic subgroups and was correlated with liver function, presence and size of varices, and presence and degree of red signs. We conclude that the Congestion Index of the portal vein, the clinical status and the endoscopic aspect of varices are not independent features in patients with cirrhosis. As for liver function and endoscopic findings, portal Doppler ultrasound parameters, in particular the Congestion Index, may contribute to a better clinical assessment in patients with cirrhosis.

The recent cloning of the genome of hepatitis C virus (HCV) has allowed the detection of antibodies to HCV (anti-HCV) in human serum. The presence of serum antibodies to HCV often indicates active infection with HCV. We have assessed the serological and histological features in a group of alcoholic patients with chronic liver disease and have evaluated the possible etiologic role of HCV infection in the development of liver damage. Serum samples and liver biopsy specimens were obtained from 41 consecutive patients, all having a definite history of alcohol abuse and evidence of chronic hypertransaminasemia. Fifteen patients (37%) were positive for anti-HCV by ELISA, and 13 (86.6%) of them were also positive by RIBA. Eleven of these patients had histologic features of chronic active hepatitis (CAH), a lesion which is not known to be induced by excessive alcohol intake. No other possible causes of CAH were found, and CAH was not present in any of the anti-HCV negative patients. In patients with CAH, mean AST to ALT ratio was less than 1 (0.6), a finding which is characteristic of viral rather than alcoholic chronic liver disease. In conclusion, our study suggests that sporadic hepatitis C virus infection plays an etiologic role in the development of chronic active liver disease in a subgroup of alcoholic patients.