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.

Different ways exist to manage gastric leak, depending on the magnitude of the collection and the clinical repercussions. When treatment necessitates reintervention and is performed early, suture repair is more likely to be successful. Leakage closure time will vary.

SUMMARY Late results in 81 patients with achalasia treated in a prospective randomised study comparing forceful pneumatic dilatation with the Mosher bag and surgical anterior oesophagomyotomy by abdominal route, are reported. There were no deaths from either of the treatments.Two patients (5*6%) had a perforation of the abdominal oesophagus after pneumatic dilatation and were excluded from late follow up. In patients having surgery at radiological evaluation there was gullet diameter significantly increased at the oesophagogastric junction and decreased at the middle third of the oesophagus. One patient was lost from follow up and one died of an oesophageal carcinoma, leaving 95% of excellent results at the late follow up (median 62 months). Resting gastro-oesophageal sphincter pressure decreased significantly to approximately 10 mmHg; this was maintained five years after surgery. By contrast, in patients having pneumatic dilatation, there were good results in only 65% (follow up median 58 months), with 30% failures. One patient was lost from follow up and one developed oesophageal carcinoma. Measurement of resting gastro-oesophageal sphincter pressure after dilatation was highly predictive of the outcome. The study shows that surgical treatment offers a better final clinical result than pneumatic dilatation with the Mosher bag.The aim of treating patients with achalasia of the oesophagus is to obtain an adequate emptying of the gullet into the stomach, either by rupture or by surgical division of the circular muscle fibres of the distal oesophagus, where the hypertensive gastrooesophageal sphincter is located.'2 This can be achieved either by forceful dilatation, or by surgical oesophagomyotomy. We have previously reported the results of a prospective randomised study comparing the two treatments in 38 patients with achalasia.?The aim of this study is to report the late results of a greater number of patients included in this trial.

No abstract

When during surgery for gallstone disease a cholecystoenteric fistula is encountered, the possibility of an associated Mirizzi syndrome must be considered. The findings of this study confirm the association of Mirizzi syndrome with cholecystoenteric fistula.

Sterol receptor element-binding protein-1c (SREBP-1c) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) mRNA expression was assessed in liver as signaling mechanisms associated with steatosis in obese patients. Liver SREBP-1c and PPAR-alpha mRNA (RT-PCR), fatty acid synthase (FAS) and carnitine palmitoyltransferase-1a (CPT-1a) mRNA (real-time RT-PCR), and n-3 long-chain polyunsaturated fatty acid (LCPUFA)(GLC) contents, plasma adiponectin levels (RIA), and insulin resistance (IR) evolution (HOMA) were evaluated in 11 obese patients who underwent subtotal gastrectomy with gastro-jejunal anastomosis in Roux-en-Y and 8 non-obese subjects who underwent laparoscopic cholecystectomy (controls). Liver SREBP-1c and FAS mRNA levels were 33% and 70% higher than control values (P<0.05), respectively, whereas those of PPAR-alpha and CPT-1a were 16% and 65% lower (P<0.05), respectively, with a significant 62% enhancement in the SREBP-1c/PPAR-alpha ratio. Liver n-3 LCPUFA levels were 53% lower in obese patients who also showed IR and hipoadiponectinemia over controls (P<0.05). IR negatively correlated with both the hepatic content of n-3 LCPUFA (r=-0.55; P<0.01) and the plasma levels of adiponectin (r=-0.62; P<0.005). Liver SREBP-1c/PPAR-alpha ratio and n-3 LCPUFA showed a negative correlation (r=-0.48; P<0.02) and positive associations with either HOMA (r=0.75; P<0.0001) or serum insulin levels (r=0.69; P<0.001). In conclusion, liver up-regulation of SREBP-1c and down-regulation of PPAR-alpha occur in obese patients, with enhancement in the SREBP-1c/PPAR-alpha ratio associated with n-3 LCPUFA depletion and IR, a condition that may favor lipogenesis over FA oxidation thereby leading to steatosis.

GBP induces a significant BMD loss related with changes in body composition, although some metabolic mediators, such as adiponectin increase, may have an independent action on BMD which deserves further study.