PubMed · 9740194
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R A Lopchinsky, P I Tartter. 1998. Sentinel lymph node biopsy.. https://pubmed.ncbi.nlm.nih.gov/9740194/
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BACKGROUND: Intestinal metaplasia occurs in the esophagus as a consequence of gastroesophageal reflux disease and in the stomach secondary to H. pylori infection. The etiology of intestinal metaplasia limited to the gastroesophageal junction or cardia (CIM) is disputed. We hypothesized that CIM has dual etiologies: gastroesophageal reflux in some, H. pylori infection in others, and that cytokeratin immunostaining can help to differentiate between these two etiologies. METHODS: We defined CIM as the presence of intestinal metaplasia within cardiac mucosa on biopsy from an endoscopically normal-appearing gastroesophageal junction. Thirty patients with CIM who had multiple biopsy specimens taken from the esophagus, gastroesophageal junction, and stomach were identified. Tissue blocks from biopsy specimens taken at the gastroesophageal junction were sectioned and immunostained for cytokeratins 7 and 20. The cytokeratin 7/20 staining of the CIM in each patient was determined to be either a Barrett's or non-Barrett's pattern. H. pylori infection was assessed by Giemsa staining of antral biopsy specimens. RESULTS: H. pylori infection was present in 16 patients. A Barrett's cytokeratin 7/20 staining pattern in the CIM was present in only 46% of the H. pylori-positive patients, as compared to 86% in the 14 patients with CIM and no H. pylori (p = 0.025). Objective evidence of reflux disease was present in 71% of patients with CIM and no H. pylori, as compared to 31% of patients with H. pylori. CONCLUSIONS: The two different patterns of cytokeratin 7/20 staining found in patients with CIM support the concept of dual etiologies for CIM. A Barrett's staining pattern was associated with objective evidence of gastroesophageal reflux and the absence of H. pylori, suggesting that cytokeratin 7/20 immunostaining is useful to determine the likely etiology of CIM.
HISTORY AND CLINICAL FINDINGS: A 56-year-old man presented himself at our polyclinic with the symptoms of dyspnoea at rest and exhaustion. The case history revealed an alcoholic liver cirrhosis (Child B) and recurrent heart burn as a sign of a gastro-esophageal reflux disease. The examination showed jaundice and enlargement of the liver as pathological features. INVESTIGATIONS: At gastroscopy multiple openings of pseudodiverticula and a high-grade inflammatory reaction of the esophageal mucosa was found, indicating pseudodiverticulosis of the esophagus. After staining with lugol-solution and directed biopsy of unstained areas there was no sign of malignancy in the histopathological report. TREATMENT: The candida esophagitis and gastroesophageal reflux disease were treated with antimycotic and proton-pump-inhibiting drugs after which the patient had no more complains. Regular gastroscopic controls are planned. CONCLUSION: Pseudodiverticulosis of the esophagus is a very rare disease which arises from ductal dilatation of the mucosal glands during chronic inflammation of the esophagus. In most cases the pseudodiverticulosis is an accidental finding without symptoms. Risks can arise from the most frequent complications like development of inflammatory strictures, motility disorders and transformation to malignancy. Therefore it is necessary to perform regular inspection of the esophagus by endoscopy.
Cadherins represent a family of calcium-dependent cell adhesion molecules with an important regulatory function for maintenance of tissue architecture. Alterations of cadherin expression have been demonstrated in the development and progression of different epithelial tumors. In renal cell carcinoma (RCC), the majority of tumors express N-cadherin and cadherin-6. Screening a series of 16 RCC cell lines for the expression of different novel type II cadherins by RT-PCR revealed a complex pattern of cadherin expression: cadherins 6 and 14 were expressed in most of the RCC cell lines, whereas cadherins 11, 12 and 13 could not be detected at all. Interestingly, cadherin-8, previously shown in mice to be restricted to the CNS and thymus during development, was detected by RT-PCR, immunofluorescence and in situ hybridization in 4 of 16 RCC cell lines as well as in paraffin sections of the corresponding human RCC biopsies. In normal renal tissue, however, cadherin-8 could be detected only during the early stages of kidney development. These results suggest that alterations of type II cadherin expression may play a role in RCC development. In particular, cadherin-8 may be involved in both kidney morphogenesis as well as tumorigenesis in some types of RCC.