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Objective: To provide an embryological explanation for the presence of ovarian stroma in cystadenomas of the liver and pancreas., Design: Investigation of patients and embryos., Method: From 1997 to 2001 in the Academic Medical Centre, Amsterdam, the Netherlands, nine women were treated for a cystadenoma with ovarian stroma, six of which were situated in the liver and three in the tail of pancreas. In one patient with a cystadenoma in the liver, malignant changes had taken place. In embryos at 5-8 weeks development, the regional differences in the morphology of the epithelium of the peritoneal cavity and the position of the gonads in relation to the embryonic liver, pancreas and spleen were examined., Results: In the foetal period before the gonads begin to descend, they are situated directly dorsal to the liver, tail of pancreas and spleen, but are separated from these by the peritoneal cavity. The cells that cover the urogenital folds distinguish themselves from those elsewhere in the peritoneal cavity as they are bulging in shape as opposed to flattened. This activated morphology suggests that on physical contact with a neighbouring organ the cells covering the gonads may become detached and lodge in that organ., Conclusion: It is likely that cystadenomas of the liver and pancreas have their origin in the cells that cover the embryonic gonads. The anomalous morphology of these covering cells in fact suggests that they are relatively easily mobilized. They are probably comparable with inoculation metastasis in the coelomic cavity. Taking the chance of malignant transformation of a cystadenoma into account, the treatment of choice is radical resection of the abnormality.

The incidence of Barrett carcinoma has increased almost six-fold in the last 20 years. Barrett oesophagus is defined as the presence of metaplastic columnar epithelium in the oesophagus in continuity with the gastric mucosa. It is regarded as an acquired abnormality, developed as a result of chronic (duodenal) gastro-oesophageal reflux. It is especially the intestinal type of columnar epithelium that has a greatly enhanced risk of malignant degeneration. It is advisable that patients with a Barrett oesophagus should regularly be examined endoscopically, with extensive tissue biopsy. Presence of Barrett epithelium without dysplasia or with only moderate dysplasia does not in itself constitute an indication for supplementary treatment. Major dysplasia constitutes an indication for prophylactic resection. In the treatment with curative intention of Barrett carcinoma, surgery is the therapy of first choice.

The isolation of Helicobacter pylori from the human stomach has changed the insights into the mechanisms of chronic gastritis. The altered concepts are reflected in newly developed classification systems. In 1989 distinction of the types A, B and C of chronic gastritis was proposed as a working formulation. In this classification type A gastritis is an autoimmune disease with antibodies against parietal cells and intrinsic factor. It is limited to the body of the stomach and may be complicated by pernicious anaemia. Type B gastritis is related to bacterial infection by Helicobacter pylori and predominantly affects the antrum. It is associated with peptic ulcer disease. Type C gastritis is caused by chemical injury due to bile reflux and drugs. Especially NSAIDs are implicated. Each of these forms of gastritis has its histological counterpart. In 1990 the A, B, C terminology was overruled by the Sydney system, which recognises three forms of gastritis: acute, chronic and special forms and is otherwise mainly descriptive. The different classification systems are briefly discussed. It is concluded that uniformity in classification is most important since it will facilitate epidemiologic research of the natural history and long-term outcome of these diseases.