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<p>Epstein–Barr virus (EBV)–associated lymphoproliferative disorders have been reported in patients receiving immunosuppressive therapy for inflammatory bowel disease; however, the onset of classic Hodgkin lymphoma (cHL) during vedolizumab therapy is extremely rare. A 73 year-old woman with ulcerative colitis (UC) was steroid-dependent, showing disease exacerbation when prednisolone was tapered or discontinued. Azathioprine was administered eight years prior but was discontinued after a short period due to liver dysfunction. Vedolizumab was initiated 31&#xa0;months before presentation. Despite initial improvements in UC with vedolizumab, hematochezia subsequently persisted. Other biologics or immunomodulators that could cause systemic immunosuppression were avoided because she was receiving treatment for breast cancer. Colonoscopy showed erosions in the transverse colon and an ulcerative lesion in the sigmoid colon. A biopsy revealed high-grade dysplasia in the transverse colon and inflammatory granulation tissue without malignancy in the sigmoid lesion; therefore, surgery was indicated. Laparoscopic total proctocolectomy was performed, and the surgical specimen contained Reed–Sternberg cells positive for CD20, CD30, PD-L1, and EBV-encoded RNA, establishing EBV-associated cHL. Although the development of cHL is likely multifactorial, clinicians should be aware that EBV-associated intestinal cHL may develop in patients with UC receiving vedolizumab when tumor-like ulcers or mural thickening are encountered.</p>

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Classic hodgkin lymphoma associated with Epstein–Barr virus reactivation during vedolizumab therapy for ulcerative colitis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月28日

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  • Tatsuya Hasegawa,
  • Masatsugu Kojima,
  • Toru Miyake,
  • Mai Noujima,
  • Takayuki Imai,
  • Soichiro Tani,
  • Keiji Muramoto,
  • Tomoharu Shimizu,
  • Takuji Iwashita,
  • Masaji Tani

摘要

Epstein–Barr virus (EBV)–associated lymphoproliferative disorders have been reported in patients receiving immunosuppressive therapy for inflammatory bowel disease; however, the onset of classic Hodgkin lymphoma (cHL) during vedolizumab therapy is extremely rare. A 73 year-old woman with ulcerative colitis (UC) was steroid-dependent, showing disease exacerbation when prednisolone was tapered or discontinued. Azathioprine was administered eight years prior but was discontinued after a short period due to liver dysfunction. Vedolizumab was initiated 31 months before presentation. Despite initial improvements in UC with vedolizumab, hematochezia subsequently persisted. Other biologics or immunomodulators that could cause systemic immunosuppression were avoided because she was receiving treatment for breast cancer. Colonoscopy showed erosions in the transverse colon and an ulcerative lesion in the sigmoid colon. A biopsy revealed high-grade dysplasia in the transverse colon and inflammatory granulation tissue without malignancy in the sigmoid lesion; therefore, surgery was indicated. Laparoscopic total proctocolectomy was performed, and the surgical specimen contained Reed–Sternberg cells positive for CD20, CD30, PD-L1, and EBV-encoded RNA, establishing EBV-associated cHL. Although the development of cHL is likely multifactorial, clinicians should be aware that EBV-associated intestinal cHL may develop in patients with UC receiving vedolizumab when tumor-like ulcers or mural thickening are encountered.