Oxidative stress is implicated in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In the present study, hepatic and plasma oxidative stress-related parameters were measured and correlated with clinical and histological findings in 31 NAFLD patients showing increased body mass index. Liver protein carbonyl content was enhanced by 403% in patients with steatosis (n=15) compared with control values (n=12), whereas glutathione content, superoxide dismutase (SOD) activity and the ferric reducing ability of plasma (FRAP) were decreased by 57%, 48% and 21% (P<0.05) respectively. No changes in microsomal p-nitrophenol hydroxylation and the total content of cytochrome P450 (CYP) or CYP2E1 were observed. Patients with steatohepatitis (n=16) exhibited protein carbonyl content comparable with that of controls, whereas glutathione content, SOD and catalase activities were decreased by 27%, 64% and 48% (P<0.05). In addition, FRAP values in patients with steatohepatitis were reduced by 33% and 15% (P<0.05) when compared with controls and patients with steatosis respectively, whereas p-nitrophenol hydroxylation (52%) and CYP2E1 content (142%) were significantly increased (P<0.05) compared with controls. It is concluded that oxidative stress is developed in the liver of NAFLD patients with steatosis and is exacerbated further in patients with steatohepatitis, which is associated with CYP2E1 induction. Substantial protein oxidation is followed by proteolysis of the modified proteins, which may explain the co-existence of a diminished antioxidant capacity and protein oxidation in the liver of patients with steatohepatitis.

A new classification of patients with Mirizzi syndrome and cholecystobiliary fistula is presented. Type I lesions are those with external compression of the common bile duct. In type II lesions a cholecystobiliary fistula is present with erosion of less than one-third of the circumference of the bile duct. In type III lesions the fistula involves up to two-thirds of the duct circumference and in type IV lesions there is complete destruction of the bile duct. A total of 219 patients were identified with these lesions from 17,395 patients with benign biliary tract diseases undergoing surgery. The incidence of type I lesions was 11 per cent, type II 41 per cent, type III 44 per cent and type IV 4 per cent. The majority had obstructive jaundice. In type I lesions, cholecystectomy plus choledochostomy is effective. In type II lesions, suture of the fistula with absorbable material or choledochoplasty with the remnant of gallbladder can be performed. In type III lesions suture is not indicated and choledochoplasty is recommended. In type IV lesions, bilioenteric anastomosis is preferred. Operative mortality rate increases according to the severity of the lesion, as does postoperative morbidity. During cholecystectomy, partial resection is recommended in order to extract the stones, visualize the common bile duct and define the type and location of the fistula. T tubes should be placed distal to the fistula.

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Adenocarcinomas located at the gastroesophageal junction were associated with Barrett's metaplasia in nearly one half of the patients. The length of the Barrett segment tends to be short and may be missed during endoscopy. The presence of high-grade dysplasia within Barrett's mucosa supports a barrett's origin for half of the adenocarcinomas arising at this location.

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The occurrence of an anastomotic leak is nearly 2% after gastric bypass. The majority of them can be managed medically, without the need for a reoperation, due to the fact that there is no acid production in the small gastric pouch and there is no intestinal reflux due to the long Roux loop.

The transthoracic and transhiatal open approaches have similar early and late results. Minimally invasive surgery is an option for patients with esophageal carcinoma, with reported results similar to those for open surgery. This approach is indicated mainly for selected patients with early stages of the disease.

A prospective study was performed in 190 control subjects and in 236 patients with different degrees of endoscopic esophagitis in order to determine the prevalence of Helicobacter pylori infection at duodenal gastric and esophageal mucosa and its correlation with histological findings. All patients with pathologic gastroesophageal reflux had 24-h pH monitoring studies confirming the presence of acid reflux into the esophagus. Besides the endoscopic findings, biopsies were taken from the duodenal bulb, gastric antrum, gastric fundus and distal esophagus or at the specialized columnar epithelium in patients with Barrett's esophagus. Patients with pathological gastroesophageal reflux were divided into three groups: 55 with absence of endoscopic esophagitis (gastroesophageal reflux), 81 patients with erosive esophagitis and 100 patients with Barrett's esophagus. There was no H. pylori infection present at duodenal or esophageal mucosa or at the specialized columnar epithelium of the distal esophagus in any case. The prevalence of H. pylori infection at gastric antrum was similar in controls and in any group of patients with reflux disease (20-25% of H. pylori infection). No differences in age and sex distribution were seen. H. pylori infection at gastric fundus was very low (less than 5%). The presence of HP infections was correlated with the finding of chronic active superficial or athrophic gastritis while, in the absence of H. pylori infection, gastric mucosa was normal. In the presence of intestinal metaplasia, no H. pylori infection occurred. Based on these findings, it seems that there is no significant evidence for an important pathogenic role for H. pylori infection in the development of pathologic chronic gastroesophageal reflux, erosive esophagitis or Barrett's esophagus, and the presence of antral gastritis in patients with Barrett's esophagus is closely related to the presence of H. pylori infection, and probably not related to an increased duodenogastric reflux.