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  • 1
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To ascertain the progression of atrophic gastritis due to Helicobacter pylori infection, we conducted a 10-year prospective follow-up study with annual endoscopy of the stomach.〈section xml:id="abs1-2"〉〈title type="main"〉Methods:Prospective endoscopic observation was started in 53 subjects in 1989 and 1990 after informed consent was obtained. The progression of atrophic gastritis was evaluated mainly by the endoscopic pattern of atrophy. Histological assessment was performed on biopsy specimens taken from the lesser curvature of the lower corpus. By 2000, 43 patients (20 males, 23 females, mean age 56.7 years at entry) had completed at least 10 years of endoscopic follow-up.〈section xml:id="abs1-3"〉〈title type="main"〉Results:Eight H. pylori-negative patients with normal fundic mucosa showed no change endoscopically or histologically. In 35 H. pylori-positive patients, the progression of histological atrophy was observed in 46% and intestinal metaplasia was observed in 49%. Fifteen of 35 H. pylori-positive cases exhibited a cephaloid shift of the endoscopic atrophic border. The cephaloid shift of the atrophic area occured suddenly. The cumulative progression rate of atrophic patterns was 6% after 2 years, 22% after 4 years, 34% after 6 years and 43% after 10 years. These atrophic changes were related to neutrophil infiltration.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusion:The progression of atrophic gastritis is a result of chronic active gastritis caused by H. pylori infection.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  We recently proposed that certain palmoplantar epidermoid cysts may be related to eccrine ducts and that human papillomavirus (HPV) 60 may play a role in their pathomechanism. However, the origin of palmoplantar epidermoid cysts is still controversial.Objectives  To examine the contribution of eccrine ducts and HPV 60 in the development of epidermoid cysts.Methods  Five epidermoid cysts and four ridged warts that had developed on the soles of a patient were studied histologically, immunohistochemically and by DNA–DNA in situ hybridization. Using serial sections obtained from its entire body, a three-dimensional reconstruction (3DR) analysis was performed on the smallest cyst to analyse the relationship between the epidermoid cyst, eccrine duct and the overlying epidermis.Results  Histological and DNA–DNA in situ hybridization analyses demonstrated both homogeneous intracytoplasmic inclusion bodies pathognomonic for HPV 60 infection and HPV 60 DNA sequences not only in all of the epidermoid cysts and ridged warts but also in the acrosyringeal portion of an eccrine duct, with the dermal portion of which the smallest cyst had been revealed to connect by 3DR analysis. However, immunohistochemical analyses using antibodies against human carcinoembryonic antigen (CEA), involucrin and several cytokeratins (CKs) revealed that the immunoreactivity of the cyst was not identical to that of the eccrine dermal duct but was identical to that of suprabasal layers of the epidermis.Conclusions  It was clearly demonstrated that an HPV 60-associated epidermoid cyst with immunoreactivities for CEA, involucrin and CKs which were identical to those of the epidermis connected with the eccrine dermal duct, supporting the idea that certain palmoplantar epidermoid cysts may develop following the epidermoid metaplasia of eccrine ducts with HPV 60 infection.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2307
    Keywords: Pancreas ; Serous cystic tumours ; Microcystic adenoma ; Serous oligocystic ill-demarcated adenoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serous cystic tumours of the pancreas are uncommon and are usually classified as microcystic adenomas (MCA). As new types of serous cystic tumours of this organ have been reported we reviewed a series of 14 lesions and from macroscopic findings two groups were distinguished: ten tumours revealed the features of MCA, while four were clearly distinct from MCA. Grossly, the latter tumours showed only few cysts which were irregularly assembled in fibrous stroma. On the cut surface, there was neither a central stellate scar nor a circumscribed tumour border, features characterizing MCA. Microscopically, the cysts were lined by cuboidal, non-mucin-producing cells. Immunocytochemical staining for cytokeratins 7, 8, 18 and 19 revealed a ductal phenotype. All non-MCA were found in the head of the pancreas and three of them occurred in men. There were no tumour recurrences or signs of malignant transformation after resection (mean follow-up, 2.9 years). These results suggest that there are serous cystic tumours distinct from MCA which may represent another variant of the category of serous cystic adenomas of the pancreas. We propose the term serous oligocystic and ill-demarcated adenoma (SOIA) for these tumours. It is possible that the recently described macrocystic subtype of serous cystadenoma and SOIA are variants of the same tumour.
    Type of Medium: Electronic Resource
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