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Aggressive large B-cell lymphoma triggered by a parvovirus B19 infection in a previously healthy child
Laura Olivier-Gougenheim1, Frederique Dijoud2, Alexandra Traverse-Glehen3
1Institute of Pediatric Hematology and Oncology, Hospices Civils de Lyon, Claude Bernard Lyon I University, Lyon, France.
Insights
Parvovirus B19 infection, typically benign, presented unusually in a child with bicytopenia and adenopathy. This case suggests a potential link between parvovirus B19 and the development of childhood lymphoma.
Area of Science:
- Pediatric Hematology
- Viral Infections
- Oncology
Background:
- Parvovirus B19 (PVB-19) is generally considered a benign viral infection in individuals without underlying red blood cell disorders or immune deficiencies.
- PVB-19 infections typically manifest with symptoms like erythema infectiosum (fifth disease) or transient aplastic crisis.
Observation:
- A previously healthy 10-year-old boy presented with a PVB-19 infection.
- Clinical presentation included bicytopenia and significant axillary adenopathy.
- Initial lymph node biopsy revealed a reactive lymphoid population.
Findings:
- The patient did not achieve remission.
- A subsequent biopsy of the axillary adenopathy, nine months later, diagnosed Hodgkin lymphoma with areas of T-cell rich aggressive large B-cell lymphoma.
- This progression occurred in the absence of any identified red blood cell disease or immune defect.
Implications:
- This case raises the possibility of parvovirus B19 acting as a potential trigger for malignant childhood hemopathies.
- The findings prompt further investigation into the role of PVB-19 in lymphomagenesis.
- Further research is warranted to explore the potential oncogenic mechanisms of PVB-19 in pediatric lymphoma development.
Abstract:
In absence of red blood cells disease or immune defect, parvovirus B19 (PVB-19) is usually considered as a benign condition. Here, we report the case of a 10-year-old boy, previously healthy, presenting with a PVB-19 infection revealed by a bicytopenia and a voluminous axillary adenopathy. Pathophysiology examination showed reactional lymphoid population. Nine months later and in the absence of remission, a new biopsy of the same adenopathy revealed a Hodgkin lymphoma with area of T-cell rich aggressive large B-cell lymphoma. This case suggests PVB-19 as potential trigger of this malignant childhood hemopathy. Although no definitive conclusion can be drawn, our clinical case questions the role of PVB-19 in lymphomagenesis.
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