Dynamic esophageal stents.

Esophageal stenting represents a new strategy in the treatment of resistant or recurrent stenosis that obviates the need for multiple dilations. Our custom dynamic stent (DS) improves esophageal motility unlike the widespread self-expandable plastic or metallic esophageal stents. The DS allows food and secretions to pass in the space between the esophageal wall and the stent wall. This contrasts with the other types of stent, in which food passes into the stent that presses into the esophageal wall. Until the stent patent is complete, we use slices of silicon drains overlapped with each other to fashion the stent to the desired length and diameter (7-, 9-, or 12.7-mm external diameter). It is built coaxially on a nasogastric tube that guarantees the correct position. The two ends are tailored to allow an easy introduction and food passage between stent and esophageal wall. The stent is inserted after stricture dilations (Savary-Gilliard dilators) under fluoroscopic guidance. All patients who underwent stenting were treated with dexamethasone (2 mg/kg/day) for 3 days and proton pump inhibitors (omeprazole or lansoprazole, 1-2 mg/kg/day). From 1992 to 2012, 387 patients (mean age 38.6 months; range 3-125 months) with post-surgical esophageal stricture because of esophageal atresia correction were enrolled in this study. Twenty-six of 387 patients (6.7%) underwent custom DS placement for recurrent stricture instead of a program of serial dilations. The stent was left in place for at least 40 days and was effective in 21 (80.7%) of 26 patients. There were two stent-related major complications (subclavian-esophageal fistula). Our custom stent represents an effective and safe option in the treatment of severe and recurrent post-surgical esophageal strictures. Surgery with stricture resection, and reanastomosis or jeunoplasty represents the rescue strategy.

Eosinophilic esophagitis: management and pharmacotherapy.

Eosinophilic esophagitis represents the most debated disease of the last 10 years, too often speculated or overestimated and certainly well known and examined. The aim of this study was to summarize the recent therapeutic trends in order to show persistent doubts regarding several debated therapies. The study combined the most recent international literature and the authors' daily experience to define the scope of the review, with limits caused by a lack of available randomized studies between dietetic and pharmacological treatment. It was concluded that eosinophilic esophagitis is an immunoallergic disease that is generally caused by identifiable food and environmental allergens although, in a minority of cases, the etiological trigger remains undetermined. Therapy usually fights the responsible agents, but sometimes they are not resolved. A need for more pathogenetically driven treatments is invoked.

Liver, pancreas and biliary tract enhanced lipoperoxidation products in pure pancreatic juice: evidence for organ-specific oxidative stress in chronic pancreatitis.

BACKGROUND: Oxygen-free radicalscan play a role in the development of chronic pancreatitis, altering the redox state with damage of cell constituents and decrease in antioxidant defences. AIMS: To measure levels of lipoperoxidation products, conjugated dienes and lipid hydroperoxides, in pure pancreatic juice and serum of chronic pancreatitis patients and compare them to that in controls. To investigate a possible correlation with serum indexes of pancreatic inflammation (amylase and lipase). PATIENTS: Pancreatic juice was collected during ERCP, after secretin stimulation, in 20 patients with chronic pancreatitis and 11 controls with biliary diseases. METHODS: Lipid hydroperoxide levels were determined with FOX2 method and measured as absorbance at 560 nm. Conjugated diene levels were measured using second-derivative spectroscopy. RESULTS: No substantial difference was present in serum levels of lipid hydroperoxides, conjugated dienes (in both isomeric forms) and isomer-ratio values between those of patients with chronic pancreatitis and controls. In pancreatic juice, there was a significant increase in lipid hydroperoxides and conjugated dienes levels (especially trans-trans isomers) in chronic pancreatitis patients compared with controls, with a decrease in cis-trans isomers and a significant difference in isomer-ratio values. CONCLUSIONS: Increased levels of lipid hydroperoxides and conjugated dienes in the pancreatic juice of chronic pancreatitis patients is indicative of an enhanced lipoperoxidation and antioxidants consumption in pancreatic tissue, confirmed by the decreased isomer-ratio values as an indirect index of decreased antioxidant capacity. The lack of significant difference in conjugated diene and lipid hydroperoxide levels in the serum of chronic pancreatitis patients versus that of controls suggests an oxidative stress limited to pancreatic tissue and indicative of an organ-specific pathology, confirmed by the parallel behaviour of oxidative parameters (lipid hydroperoxides and conjugated dienes) and indexes of pancreatic inflammation (amylase and lipase).

Proteases in gastrointestinal neoplastic diseases.

Cysteine and serine proteases are involved in cancer invasion and metastasis. In the past few years we investigated the tissue levels of these proteases in gastric cancer (GC), gastric precancerous changes (CAG), colorectal cancer (CRC) and the plasma and serum levels of proteases in several gastrointestinal tumours, using ELISA methods. Significantly higher antigen levels were found not only in GC tissue but also in CAG with respect to the levels found normal tissue; with respect to CAG, patients with dysplasia had higher levels than patients without dysplasia. The same findings were obtained in CRC. In general protease levels correlated with the major histomorphological parameters, such as grading and histotype in GC as well as in CRC. Tissue protease levels had a strong prognostic impact in GC, in which UPA was singled out by multivariate analysis as the major prognostic factor, and CRC. The plasma levels of urokinase-type plasminogen activator (UPA) and the serum levels of cathepsin B were significantly increased in patients with gastrointestinal tumours. In conclusions, cysteine and serine proteases may have a part not only in GC and CRC invasion and metastasis, but also in the progression of gastric precancerous changes into cancer. They are strong prognostic factors in GC and CRC. These proteases may also have a role as tumour markers in the early diagnosis of gastrointestinal tract tumours.

Helicobacter pylori and the liver: any relationship?

Helicobacter pylori infection is being correlated to a number of human diseases, among which also those of the liver. From a clinical point of view, 4 "areas of interest" for the suggested correlation can be identified: 1. Helicobacter pylori and portal hypertension-related congestive gastropathy in cirrhotics. There are, in the literature, at least 7 studies confirming that the microorganism has no role in causing or worsening the disease. 2. Helicobacter pylori and duodenal ulcer in cirrhotic patients. Apparently, in the cirrhotic patient, the microorganism has no role in causing duodenal ulcer. 3. Helicobacter pylori, ammonia production and hepatic encephalopathy. In this case, there are at least three studies showing that Helicobacter pylori infection increases the risk of developing encephalopathy in the cirrhotic patient, this being a somewhat expected finding. 4. Helicobacter pylori infection in chronic liver disease and its diagnosis. Evidence in the literature suggests: a) that hypertensive gastropathy might not represent a favourable environment for Helicobacter pylori thus making the diagnostic sensitivity of the biopsy lower than expected, and b) that even serological diagnosis might provide data of difficult interpretation, as shown in non alcoholic cirrhosis and, by our own group, in primary biliary cirrhosis. More intriguing are the data generated with respect to the potential capacity of Helicobacter pylori and Helicobacter pylori-like bacteria such as, in particular, Helicobacter hepaticus to damage the liver by producing toxins with a granulating effect on liver cell lines which, in vivo, through the portal tract, might reach the liver, thus causing hepatocellular damage. The point has been addressed by a number of investigators and autoimmune mechanisms have also been suggested. In summary, from the clinical point of view, some evidence suggests that Helicobacter pylori infection might be relevant in the pathogenesis of hepatic encephalopathy in cirrhosis. The data being generated with respect to a direct hepatotoxicity are, at present, stimulating but only speculative.