Yosuke Yagi1, Atsuhiro Masuda2, Yoh Zen3, Hideyuki Shiomi4, Hirochika Toyama5, Keitaro Sofue6, Mamoru Takenaka7, Takashi Kobayashi4, Takashi Nakagawa4, Kodai Yamanaka8, Takuya Ikegawa4, Namiko Hoshi4, Masaru Yoshida4, Yoshifumi Arisaka1, Yoshihiro Okabe9, Hiromu Kutsumi10, Takumi Fukumoto5, Yonson Ku11, Takeshi Azuma4. 1. Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan; Department of Gastroenterology, Nissay Hospital, Japan. 2. Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan. Electronic address: atmasuda@med.kobe-u.ac.jp. 3. Division of Diagnostic Pathology, Kobe University Graduate School of Medicine, Japan. 4. Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan. 5. Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, Kobe University Graduate School of Medicine, Japan. 6. Department of Radiology, Kobe University Graduate School of Medicine, Japan. 7. Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan; Department of Gastroenterology and Hepatology, Kinki University Hospital, Faculty of Medicine, Japan. 8. Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan; Department of Internal Medicine, Rokko Island Konan Hospital, Japan. 9. Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan; Department of Gastroenterology, Kakogawa Central City Hospital, Japan. 10. Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan; Center for Clinical Research and Advanced Medicine Establishment, Shiga University of Medical Science, Japan. 11. Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, Kobe University Graduate School of Medicine, Japan; Department of Surgery, Kohnan Hospital, Japan.
Abstract
BACKGROUND: Inflammation-induced carcinogenesis in pancreatic ductal adenocarcinoma (PDAC) has been reported; however, its involvement in PDAC with intraductal papillary mucinous neoplasm (IPMN) remains unclear. We herein investigated the relationship between pancreatic atrophy and inflammation and the incidence of PDAC concomitant with IPMN. METHODS: This study included 178 consecutive patients who underwent surgical resection for PDAC with IPMN (N = 21) and IPMN (N = 157) between April 2001 and October 2016. A multivariable logistic regression analysis was conducted to assess the relationship between pancreatic inflammation and atrophy and the incidence of PDAC concomitant with IPMN, with adjustments for clinical characteristics and imaging features. Pathological pancreatic inflammation and atrophy were evaluated in resected specimens. RESULTS: High degrees of pancreatic inflammation and atrophy were not associated with the incidence of PDAC with IPMN (multivariable odds ratio [OR] = 0.5, 95% confidence interval [CI] = 0.07 to 3.33, P = .52, adjusted by clinical characteristics, OR = 0.9, 95% CI = 0.10 to 5.86, P = .91, adjusted by imaging studies; OR = 0.2, 95% CI = 0.009 to 1.31, P = .10, adjusted by clinical characteristics, OR = 0.2, 95% CI = 0.01 to 1.43, P = .12, adjusted by imaging studies, respectively). CONCLUSIONS: Pancreatic inflammation and atrophy were not associated with pancreatic cancer concomitant with IPMN.
BACKGROUND:Inflammation-induced carcinogenesis in pancreatic ductal adenocarcinoma (PDAC) has been reported; however, its involvement in PDAC with intraductal papillary mucinous neoplasm (IPMN) remains unclear. We herein investigated the relationship between pancreatic atrophy and inflammation and the incidence of PDAC concomitant with IPMN. METHODS: This study included 178 consecutive patients who underwent surgical resection for PDAC with IPMN (N = 21) and IPMN (N = 157) between April 2001 and October 2016. A multivariable logistic regression analysis was conducted to assess the relationship between pancreatic inflammation and atrophy and the incidence of PDAC concomitant with IPMN, with adjustments for clinical characteristics and imaging features. Pathological pancreatic inflammation and atrophy were evaluated in resected specimens. RESULTS: High degrees of pancreatic inflammation and atrophy were not associated with the incidence of PDAC with IPMN (multivariable odds ratio [OR] = 0.5, 95% confidence interval [CI] = 0.07 to 3.33, P = .52, adjusted by clinical characteristics, OR = 0.9, 95% CI = 0.10 to 5.86, P = .91, adjusted by imaging studies; OR = 0.2, 95% CI = 0.009 to 1.31, P = .10, adjusted by clinical characteristics, OR = 0.2, 95% CI = 0.01 to 1.43, P = .12, adjusted by imaging studies, respectively). CONCLUSIONS:Pancreatic inflammation and atrophy were not associated with pancreatic cancer concomitant with IPMN.