Do we really understand what the immunological disturbances in inflammatory bowel disease mean?

The gastrointestinal tract uses a system of tolerance and controlled inflammation to limit the response to dietary or bacteria-derived antigens in the gut. When this complex system breaks down, either by a chemical or pathogenic insult in a genetically predisposed individual the resulting immune response may lead to inflammatory bowel disease. Although the aetiopathogenesis of inflammatory bowel disease remains unsolved current evidence indicates that defective T-cell apoptosis and impairment of intestinal epithelial barrier function play important roles. In inflammatory bowel disease, it has been reported that activation of macrophages seems to be as important as increased production of the macrophage-derived cytokines such as TNF-α, IL-1 and IL-6. The triggering factor for this cascade is still to be elucidated as to whether it represents an auto-antigen or a hetero-antigen. It has been also demonstrated that a serologic anti-microbial response exists. This response includes antibodies against saccharomyces cerevisiae (ASCA), E. coli outer membrane porin C (Omp-C),flagelin (cBir1) and pseudomonas aeroginosa (I2). Host response to microbial pathogens includes self-defense mechanisms including defensins, pattern recognition receptors and Toll-like receptors. Neuroimmunomodulation in inflammatory bowel disease (IBD) is another interesting approach with implications on the influence of brain-gut axis on intestinal inflammation and its perpetuation. It is probable that inflammatory bowel disease represents a heterogenic group of diseases that share similar mechanisms of tissue damage but have different initiating events and immunoregulatory abnormalities. A better understanding of all these events will hopefully provide new insights into the mechanisms of epithelial responses to microorganisms and ideas for therapies.

Steatosis and steatohepatitis in postmortem material from Northwestern Greece

AIM: To determine the prevalence of steatosis and steatohepatitis in a series of autopsies in Northwestern Greece. METHODS: Liver biopsy material from a total of 600 autopsies performed over a period of 2 years (2006-2008) to def ine the cause of death was subjected to histological examination. Patient demographic data were also collected. Tissue sections were stained with different dyes for the evaluation of liver architecture, degree of fibrosis and other pathological conditions when necessary. RESULTS: Satisfactory tissue samples for histological evaluation were available in 498 cases (341 male, 157 female) with a mean age of 64.51 ± 17.78 years. In total, 144 (28.9%) had normal liver histology, 156 (31.3%) had evidence of steatosis, and 198 (39.8%) had typical histological findings of steatohepatitis. The most common causes of death were ischemic heart disease with or without myocardial infarction (43.4%), and traffic accidents (13.4%). CONCLUSION: A high prevalence of steatosis and steatohepatitis was detected in postmortem biopsies from Northwestern Greece. Since both diseases can have serious clinical consequences, they should be considered as an important threat to the health of the general population in Greece.

Diagnosis and endoscopic treatment of esophago-bronchial fistula due to gastric heterotopy

Heterotopic gastric mucosa patches are congenital gastrointestinal abnormalities and have been reported to occur anywhere along the gastrointestinal tract from mouth to anus.Complications of heterotopic gastric mucosa include dysphagia,upper gastrointestinal bleeding,upper esophageal ring stricture,adenocarcinoma and fistula formation.In this case report we describe the diagnosis and treatment of the first case of esophago-bronchial fistula due to heterotopic gastric mucosa in mid esophagus.A 40-year old former professional soccer player was referred to our department for treatment of an esophago-bronchial fistula.Microscopic examination of the biopsies taken from the esophageal fistula revealed the presence of gastric heterotopic mucosa.We decided to do a non-surgical therapeutic endoscopic procedure.A sclerotherapy catheter was inserted through which 1 mL of ready to use synthetic surgical glue was applied in the fistula and it closed the fistula opening with excellent results.