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<p>ALK-positive large B-cell lymphoma (ALK + LBCL) is a rare subtype of large B-cell lymphoma characterized by plasmablastic morphology, intra-sinusoidal or sheet-like proliferation, loss of pan–B-cell markers, and expression of plasmacytic markers. According to WHO classification, CD30 expression is generally absent and Epstein–Barr virus (EBV) infection is not detected [1,2,5]. We aim to report the first case of ALK-positive, EBV-positive large B-cell lymphoma (ALK + EBV + LBCL) in an HIV-infected patient. A 60-year-old Thai male with HIV infection and severe immunosuppression (CD4 count: 93 cells/mm<sup>3</sup>) presented with generalized lymphadenopathy and an epiglottic mass. Biopsy showed a plasmablastic neoplasm proliferating in loose sheets, negative for pan–B-cell markers except OCT2, and positive for plasmacytic markers and CD30. The tumor also expressed EBER, ALK1 (paranuclear dot pattern), and ALK D5F3; HHV8 was negative. FISH confirmed ALK gene rearrangement, and targeted sequencing revealed a <i>GORASP2::ALK</i> fusion gene. The diagnosis of ALK + EBV + LBCL in the setting of HIV-related immunodeficiency was established. The patient developed pneumonia with septic shock and died during admission. EBV-positive plasmablastic B-cell neoplasms in HIV-infected patients are not always plasmablastic lymphoma. Immunohistochemistry for ALK and HHV8 should be included in the diagnostic panel. Importantly, CD30 and EBER positivity do not exclude ALK + LBCL.</p>

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ALK-positive, EBV-positive Large B-cell lymphoma in an HIV patient: a diagnostic pitfall mimicking plasmablastic lymphoma

  • 期刊论文

  • 发表日期：

    2026年3月10日

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  • Chutima Pinnark Surintrspanont,
  • Benjamaporn Buasatit,
  • Narittee Sukswai,
  • Suphakit Hemla,
  • Chinachote Teerapakpinyo,
  • Shanop Shuangshoti

摘要

ALK-positive large B-cell lymphoma (ALK + LBCL) is a rare subtype of large B-cell lymphoma characterized by plasmablastic morphology, intra-sinusoidal or sheet-like proliferation, loss of pan–B-cell markers, and expression of plasmacytic markers. According to WHO classification, CD30 expression is generally absent and Epstein–Barr virus (EBV) infection is not detected [1,2,5]. We aim to report the first case of ALK-positive, EBV-positive large B-cell lymphoma (ALK + EBV + LBCL) in an HIV-infected patient. A 60-year-old Thai male with HIV infection and severe immunosuppression (CD4 count: 93 cells/mm3) presented with generalized lymphadenopathy and an epiglottic mass. Biopsy showed a plasmablastic neoplasm proliferating in loose sheets, negative for pan–B-cell markers except OCT2, and positive for plasmacytic markers and CD30. The tumor also expressed EBER, ALK1 (paranuclear dot pattern), and ALK D5F3; HHV8 was negative. FISH confirmed ALK gene rearrangement, and targeted sequencing revealed a GORASP2::ALK fusion gene. The diagnosis of ALK + EBV + LBCL in the setting of HIV-related immunodeficiency was established. The patient developed pneumonia with septic shock and died during admission. EBV-positive plasmablastic B-cell neoplasms in HIV-infected patients are not always plasmablastic lymphoma. Immunohistochemistry for ALK and HHV8 should be included in the diagnostic panel. Importantly, CD30 and EBER positivity do not exclude ALK + LBCL.