title: Pancreatic fatty degeneration and fibrosis as predisposing factors for the development of pancreatic ductal adenocarcinoma.
abstract: OBJECTIVE
  Knowledge of risk factors for development of pancreatic ductal adenocarcinoma (PDAC) is limited. To clarify the background condition of the pancreas for the development of PDAC, we analyzed pancreatic histological changes in noncancerous lesion specimens after pancreatectomy in PDAC patients.
  
  
  METHODS
  Seventy-six patients with PDAC were enrolled in this study. The PDAC was in the pancreatic head in 37 patients, in the body in 31, and in the tail in 8. No patients had a history of clinical chronic pancreatitis. As controls, 98 patients without PDAC were enrolled. The following parameters were examined: fibrosis, fatty degeneration, and inflammatory cell infiltration. More than 5% of fatty degeneration in the specimen, more than 10% of fibrosis, and more than 5% of inflammatory cell infiltration were considered positive changes.
  
  
  RESULTS
  Pancreatectomy specimens showed a higher ratio of positive change in fibrosis (86% vs 42%), fatty degeneration (72% vs 44%), and inflammatory cell infiltration (14% vs 3%) than control samples. Multivariate analyses demonstrated that each histological change was a significant, independent determinant for PDAC.
  
  
  CONCLUSIONS
  Our study demonstrated that cryptogenic pancreatic inflammation with fatty changes represents an important predisposing factor for PDAC. Screening for subclinical chronic pancreatitis in healthy populations may enable the detection of PDAC at an early stage.
authors.affiliation: From the *Department of Pathology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan; †Department of Molecular Biochemistry and Clinical Investigation, Osaka University Graduate School of Medicine, Osaka, Japan; and ‡Department of Surgery, National Hospital Organization Kure Medical Center, Hiroshima, Japan.
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Tomita
authors.forename: Kanako
authors.initials: K
authors.lastname: Azuma
authors.forename: Yuji
authors.initials: Y
authors.lastname: Nonaka
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Kamada
authors.forename: Miki
authors.initials: M
authors.lastname: Tomoeda
authors.forename: Mioka
authors.initials: M
authors.lastname: Kishida
authors.forename: Masahiro
authors.initials: M
authors.lastname: Tanemura
authors.forename: Eiji
authors.initials: E
authors.lastname: Miyoshi
mesh_terms: D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D021441:Carcinoma, Pancreatic Ductal / Q000209:etiology* / Q000473:pathology / Q000601:surgery / Q000628:therapy; D002471:Cell Transformation, Neoplastic; D059248:Chemoradiotherapy; D003131:Combined Modality Therapy; D015897:Comorbidity; D018450:Disease Progression; D042241:Early Diagnosis; D005260:Female; D005355:Fibrosis; D006801:Humans; D008297:Male; D008875:Middle Aged; D020360:Neoadjuvant Therapy; D009765:Obesity / Q000150:complications / Q000473:pathology; D010179:Pancreas / Q000473:pathology*; D010180:Pancreatectomy; D010196:Pancreatic Elastase / Q000097:blood; D010190:Pancreatic Neoplasms / Q000209:etiology* / Q000473:pathology / Q000601:surgery / Q000628:therapy; D050500:Pancreatitis, Chronic / Q000000981:diagnostic imaging / Q000473:pathology; D011230:Precancerous Conditions / Q000175:diagnosis / Q000473:pathology; D012307:Risk Factors; D016896:Treatment Outcome; D014463:Ultrasonography
chemical_list: D010196:Pancreatic Elastase