ArticleFrontiers in immunology2026
Case Report: Hemophagocytic lymphohistiocytosis after SARS-CoV-2 infection revealing clinically diagnosed stage IVB diffuse large B-cell lymphoma in quiescent adult-onset Still's disease.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Adult hemophagocytic lymphohistiocytosis (HLH) may be triggered by infection, malignancy, or systemic inflammatory disease. Attribution is challenging when recent SARS-CoV-2 infection, quiescent adult-onset Still's disease (AOSD), and an occult B-cell clonal disorder coexist. Case report: A 71-year-old man with AOSD controlled for 14 years on low-dose methotrexate developed persistent fever and fatigue after mild SARS-CoV-2 infection. He subsequently developed cytopenias, hyperferritinemia, markedly elevated lactate dehydrogenase, diffuse FDG-avid lymphadenopathy, hepatosplenomegaly, elevated soluble interleukin-2 receptor, reduced natural killer-cell activity, and bone marrow hemophagocytosis, fulfilling HLH criteria. Broad pathogen evaluation, including blood and bone marrow metagenomic next-generation sequencing, did not identify an alternative infectious trigger. Bone marrow histopathology did not show definite tumor cells; however, flow cytometry identified monoclonal mature B cells, and peripheral-blood smear high-throughput sequencing detected lymphoma-associated mutations including MYD88, CD79B, IGLL5, PRDM1, DTX1, DUSP2, and BTG1. Multidisciplinary consultation favored probable lymphoma-associated HLH with clinically diagnosed stage IVB diffuse large B-cell lymphoma. HLH-directed therapy followed by rituximab-based lymphoma-directed chemotherapy led to transient clinical improvement, but the patient later died from infectious complications. Conclusion: Mild SARS-CoV-2 infection may act as a co-trigger or unmasking event rather than the sole cause of HLH. Persistent high lactate dehydrogenase and soluble interleukin-2 receptor, diffuse lymphadenopathy, clonal mature B cells, lymphoma-associated mutations, and negative broad pathogen testing should prompt evaluation for occult lymphoma-associated HLH.
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