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Gastric pyloric gland adenoma: a multicentre clinicopathological study of 67 cases.
Choi, Won-Tak; Brown, Ian; Ushiku, Tetsuo; Yozu, Masato; Setia, Namrata; Srivastava, Amitabh; Johncilla, Melanie; Pai, Rish K; Gill, Ryan M; Fukayama, Masashi; Misdraji, Joseph; Lauwers, Gregory Y.
Afiliação
  • Choi WT; Department of Pathology, University of California at San Francisco, San Francisco, CA, USA.
  • Brown I; Envoi Pathology, Kelvin Grove, Brisbane, Qld, Australia.
  • Ushiku T; Department of Pathology, University of Tokyo, Tokyo, Japan.
  • Yozu M; Department of Pathology, Massachusetts General Hospital, Boston, MA, USA.
  • Setia N; Department of Pathology, University of Chicago, Chicago, IL, USA.
  • Srivastava A; Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA.
  • Johncilla M; Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA.
  • Pai RK; Department of Pathology, Mayo Clinic, Scottsdale, AZ, USA.
  • Gill RM; Department of Pathology, University of California at San Francisco, San Francisco, CA, USA.
  • Fukayama M; Department of Pathology, University of Tokyo, Tokyo, Japan.
  • Misdraji J; Department of Pathology, Massachusetts General Hospital, Boston, MA, USA.
  • Lauwers GY; Department of Pathology, H. Lee Moffitt Cancer Center, Tampa, FL, USA.
Histopathology ; 72(6): 1007-1014, 2018 May.
Article em En | MEDLINE | ID: mdl-29278427
AIMS: There is limited information regarding the clinicopathological and immunohistochemical characteristics of gastric pyloric gland adenomas (PGAs). METHODS AND RESULTS: Sixty-seven cases of gastric PGA from 57 patients were analysed. PGAs occurred with similar frequency in men and women (47.4 and 52.6%, respectively), with a mean age of 66 years. Most presented in the gastric body/fundus (67.2%). Fifteen cases (22.4%) developed against a background of autoimmune gastritis (AIG), whereas normal mucosa was seen in 35.8%. Only 16.4% (11 cases) developed in patients with a genetic predisposition, most commonly familial adenomatous polyposis. Low-grade lesions had a mean size of 1.5 cm, while PGAs with high-grade dysplasia (HGD) or adenocarcinoma had a mean size of 3.5 cm (P < 0.001) and more commonly showed tubulovillous architecture (50.0 versus 25.6% in low-grade dysplasia; P = 0.040). Most PGAs (61.2%) co-expressed mucin (MUC)5AC and MUC6 (mixed type), which was associated significantly with HGD or adenocarcinoma (P = 0.013). AIG was also associated with HGD (P = 0.027), but genetic predisposition did not correlate with the grade of dysplasia (P = 0.793). The recurrence rate of PGA was similar for high- (11.8%) and low-grade lesions (7.4%) (P = 0.624). CONCLUSIONS: The risk of HGD increases with the size of PGA, tubulovillous architecture and the presence of AIG as well as mixed immunophenotype. As the overall local recurrence rate is less than 10%, PGAs may be treated conservatively, but they should be excised completely if possible, particularly if they are large or show high-grade features.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias Gástricas / Adenoma / Mucosa Gástrica Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias Gástricas / Adenoma / Mucosa Gástrica Idioma: En Ano de publicação: 2018 Tipo de documento: Article