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Unexpectedly frequent hepatitis B reactivation by chemoradiation in postgastrectomy patients†

  1. Jason Chia-Hsien Cheng M.D., M.S.1,2,3,‡,*,
  2. Mei-Ching Liu M.D.4,
  3. Stella Y. Tsai M.D.1,
  4. Wei-Tse Fang M.D.4,
  5. James Jer-Min Jian M.D.1,
  6. Juei-Low Sung M.D.5

Article first published online: 23 SEP 2004

DOI: 10.1002/cncr.20591

Issue

Cancer

Cancer

Volume 101, Issue 9, pages 2126–2133, 1 November 2004

Additional Information

How to Cite

Cheng, J. C.-H., Liu, M.-C., Tsai, S. Y., Fang, W.-T., Jer-Min Jian, J. and Sung, J.-L. (2004), Unexpectedly frequent hepatitis B reactivation by chemoradiation in postgastrectomy patients. Cancer, 101: 2126–2133. doi: 10.1002/cncr.20591

Author Information

  1. 1

    Department of Radiation Oncology, Koo Foundation Sun Yat-Sen Cancer Center, Taipei, Taiwan

  2. 2

    Cancer Research Center, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan

  3. 3

    Department of Oncology, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan

  4. 4

    Department of Medical Oncology, Koo Foundation Sun Yat-Sen Cancer Center, Taipei, Taiwan

  5. 5

    Department of Internal Medicine, Koo Foundation Sun Yat-Sen Cancer Center, Taipei, Taiwan

  1. ‡

    Fax: (011) 886 223711174

*Division of Radiation Oncology, Department of Oncology, National Taiwan University Hospital, No. 7 Chung-Shan South Road, Taipei 100, Taiwan

  1. †

    Presented in part at the 44th Annual Meeting of the American Society for Therapeutic Radiology and Oncology, New Orleans, Louisiana, October 6–9, 2002.

Publication History

  1. Issue published online: 18 OCT 2004
  2. Article first published online: 23 SEP 2004
  3. Manuscript Accepted: 13 JUL 2004
  4. Manuscript Revised: 22 JUN 2004
  5. Manuscript Received: 12 APR 2004

Funded by

  • National Science Council, Executive Yuan, Taiwan, ROC. Grant Number: NSC 92-2314-B-002-204
  • National Taiwan University Hospital. Grant Numbers: NTUH 92A04-4, NTUH 93N002

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Keywords:

  • gastric carcinoma;
  • adjuvant chemoradiotherapy;
  • hepatic toxicity;
  • hepatitis B viral reactivation

Hepatitis B virus (HBV) carriers had a higher incidence of chemoradiation-induced liver disease (CRILD) after postgastrectomy adjuvant, concomitant chemoradiotherapy, probably related to HBV reactivation. Dosimetric parameters modulated the risk of CRILD in noncarriers, but not in carriers.

Abstract

BACKGROUND

Postgastrectomy patients undergoing chemoradiation risk chemoradiation-induced liver disease (CRILD). The objectives of this study were to investigate dosimetric implications and assess biologic susceptibility to CRILD in these patients.

METHODS

Sixty-two patients with Stage IB–IV gastric/gastroesophageal adenocarcinoma without metastases underwent radical total/subtotal gastrectomy; regional lymph node dissection; and postoperative, adjuvant, concomitant chemoradiotherapy (CCRT). Among these, 8 patients developed CRILD (defined as Grade 3–4 liver toxicity), and 11 patients were chronic hepatitis B virus (HBV) carriers (HBV+). Chemotherapy consisted of 1 cycle of etoposide, leucovorin, and 5-fluorouracil (ELF); followed by 5 weekly high doses of 5-fluorouracil (2000–2600 mg/m2) and leucovorin concurrent with radiotherapy (median dose, 45 grays [Gy] to the tumor bed/regional lymphatics); followed by 3 cycles of ELF separated by a 21-day interval. Patients were followed for ≥ 4 months after CCRT. Patient-related and dosimetric factors were correlated with CRILD.

RESULTS

HBV+ status was the only independent factor associated with CRILD. HBV+ patients had a higher CRILD incidence (6 of 11 patients vs. 2 of 51 patients; P < 0.001). HBV-negative patients with CRILD were recipients of a higher mean liver dose (MLD) (23.8 Gy vs. 15.2 Gy; P = 0.009) and a higher volume fraction of liver that received > 30 Gy (36.5% vs. 19.7%; P = 0.009) compared with noncarriers without CRILD, but no MLD difference was found between HBV+ patients with or without CRILD. Moreover, in four of six carriers with CRILD, HBV infection was reactivated during CRILD. Two of the toxicities were fatal.

CONCLUSIONS

HBV carriers had a higher incidence of CRILD after postgastrectomy CCRT, probably related to HBV reactivation. Dosimetric parameters modulated the risk of CRILD in noncarriers, but not in carriers. These factors deserve attention in CRILD/HBV+ patients, and the underlying pathogenesis warrants investigation. Cancer 2004. © 2004 American Cancer Society.

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