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Retrospective Study
©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Aug 15, 2017; 9(8): 314-318
Published online Aug 15, 2017. doi: 10.4251/wjgo.v9.i8.314
S-1 induced hepatic steatosis in patients with pancreatic cancer: Retrospective analysis
Kunihiro Tsuji, Hisashi Doyama
Kunihiro Tsuji, Hisashi Doyama, Department of Gastroenterology, Ishikawa Prefectural Central Hospital, Ishikawa 920-8530, Japan
Author contributions: Tsuji K designed this study and wrote the paper; Doyama H contributed to revision of the manuscript for important content.
Institutional review board statement: This study was reviewed and approved by the Institutional Review Board of Ishikawa Prefectural Central Hospital.
Informed consent statement: All study participants provided informed consent to study enrollment.
Conflict-of-interest statement: The authors declare that they have no financial considerations or relationships that may pose a conflict of interest.
Correspondence to: Dr. Kunihiro Tsuji, Department of Gastroenterology, Ishikawa Prefectural Central Hospital, 2-1 Kuratsukihigashi, Kanazawa, Ishikawa 920-8530, Japan. m92162g@ipch.jp
Telephone: +81-76-2378211 Fax: +81-76-2385366
Received: December 13, 2016
Peer-review started: December 14, 2016
First decision: March 6, 2017
Revised: March 20, 2017
Accepted: June 12, 2017
Article in press: June 16, 2017
Published online: August 15, 2017
Processing time: 240 Days and 1.9 Hours
Abstract
AIM

To determine whether S-1 induces hepatic steatosis in patients being treated for pancreatic cancer.

METHODS

This retrospective study evaluated 22 patients who received oral S-1 as a first-line treatment for pancreatic cancer between January 2008 and July 2015 at the Ishikawa Prefectural Central Hospital. Patients underwent abdominal computed tomography (CT) scans before chemotherapy and within 3 mo from the start of treatment. CT numbers of the liver and spleen were measured before and after S-1 administration. Steatosis was diagnosed when the ratio of the CT number of the liver to that of the spleen (liver/spleen ratio) was < 0.9.

RESULTS

Median patient age was 68 years (range, 48-85 years), and median body mass index was 21 kg/m2 (range, 18-27 kg/m2). Of the 22 patients, six (27%) regularly consumed alcohol, and five (23%) had liver metastases. The mean ratio of CT number of the liver to the spleen was significantly higher before administration of S-1 (1.27 vs 1.09, P = 0.012) compared with after. Of the 22 patients, five (23%) had hepatic steatosis and 17 (77%) did not. The pretreatment demographic and clinical characteristics of these two groups showed no significant differences. The relationship between liver/spleen ratio and alanine transaminase activity in these patients. A statistically significant inverse correlation was observed (r = -0.417, P < 0.027).

CONCLUSION

Of the 22 patients with pancreatic cancer, five (23%) experienced S-1 induced hepatic steatosis. Care should be taken during S-1 treatment of patients with pancreatic cancer.

Keywords: S-1; Hepatic steatosis; Pancreatic cancer; Drug induced hepatitis; 5-fluorouracil

Core tip: Drug induced hepatic steatosis is a rare form of liver injury. Although hepatic steatosis has been observed in some patients with pancreatic cancer who were administered S-1, the ability of 5-fluorouracil alone to induce hepatic steatosis has not been evaluated systematically. The purpose of our study was to determine whether S-1 induces hepatic steatosis in patients being treated for pancreatic cancer. After analyzing a total of 22 patients, we found that S-1 chemotherapy induced hepatic steatosis in some patients with pancreatic cancer within three months and the correlation between the development of hepatic steatosis and liver function was weak in these patients.

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