Background-Barrett's oesophagus is acquired by severe gastro-oesophageal reflux and is a premalignant condition. Acid suppression or anti-reflux surgery alone do not cause significant regression of the metaplastic mucosa nor reduce the malignant potential. Recent reports have suggested that the combination of mucosal ablation with acid suppression may result in squamous regeneration. Aims-To destroy Barrett's mucosa by thermal ablation (in the setting of acid suppression) and so induce squamous regeneration. Patients-Sixteen patients with nondysplastic Barrett's oesophagus were recruited from a surveillance programme. All had been on a proton pump inhibitor. Methods-Atintervals, non-circumferential areas of columnar mucosa were ablated using the KTP laser. Acid suppression was obtained with 40 mg omeprazole daily. Multiple biopsy specimens were obtained for histological examination from ablated areas. Results-Ablation of all areas of glandular mucosa resulted in squamous regeneration. The number of treatments required depended on the length of the Barrett's segment. In 11 patients there was evidence of squamous regeneration over remaining Barrett's glands (in some of the posttreatment biopsy specimens) whilst in nine patients squamous metaplasia was seen within Barrett's glands. Conclusion-Mucosal ablation of Barrett's oesophagus by laser, in the setting of acid suppression, results in squamous regeneration (though some burying of Barrett's glands did occur). (Gut 1997; 41: 281-284)

No abstract

A histologically benign hidradenoma, occurring in a 15-year-old female inadequately excised at first procedure, recurred locally over the course of 11 years and exhibited first local and subsequently regional metastatic spread. The insidious progression was associated with increasing cytological atypia and alteration of epithelial antigenic expression. In view of the rarity of malignant sweat-gland tumours and consequent lack of a specific treatment protocol, this case serves to emphasize the importance of adequate primary local excision, with histological confirmation of clearance, in the management of sweat-gland tumours.

Barrett's metaplasia is the only known morphological precursor to oesophageal adenocarcinoma and is characterized by replacement of stratified squamous epithelium by columnar epithelium. The cell of origin is uncertain and the molecular mechanisms responsible for the change in cellular phenotype are poorly understood. We therefore explored the role of two transcription factors, Cdx2 and HNF4α in the conversion using primary organ cultures. Biopsy samples from cases of human Barrett's metaplasia were analysed for the presence of CDX2 and HNF4α. A new organ culture system for adult murine oesophagus is described. Using this, Cdx2 and HNF4α were ectopically expressed by adenoviral infection. The phenotype following infection was determined by a combination of PCR, immunohistochemical and morphological analyses. We demonstrate the expression of CDX2 and HNF4α in human biopsy samples. Our oesophageal organ culture system expressed markers characteristic of the normal SSQE: p63, K14, K4 and loricrin. Ectopic expression of HNF4α, but not of Cdx2 induced expression of Tff3, villin, K8 and E-cadherin. HNF4α is sufficient to induce a columnar-like phenotype in adult mouse oesophageal epithelium and is present in the human condition. These data suggest that induction of HNF4α is a key early step in the formation of Barrett's metaplasia and are consistent with an origin of Barrett's metaplasia from the oesophageal epithelium.

Two elderly male patients presented with similar, widespread, papular, granulomatous eruptions and developed myelodysplastic syndromes. The first showed histological features of diffuse granuloma annulare and had mild hypergammaglobulinaemia, slightly abnormal liver function and a leucoerythroblastic anaemia. He developed acute myeloid leukaemia (AML) secondary to a background myelodysplastic syndrome and was treated with combination chemotherapy during which his eruption settled; his AML and his skin are in remission 1 year later. The second developed a myelodysplastic syndrome and a similar rash with histological features of papular cutaneous sarcoidosis but no systemic abnormalities apart from mild hypergammaglobulinaemia, cutaneous anergy to multiple recall antigens and activation of circulating monocytes. He has remained well but his rash and myelodysplastic syndrome have persisted. These cases are interesting because of the striking similarity of their granulomatous eruptions and their associated haematological abnormalities. Patients with such disseminated, granulomatous cutaneous infiltrations should be investigated to exclude associated haematological abnormalities if there is any abnormality of their peripheral blood picture.