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Published on: October 19, 2014
[Lymphocytosis with large granular lymphocytes: case report]
Y Brychtová1, M Doubek, J Mayer
1Interní hematoonkologická klinika FN Brno.
Insights
Large granular lymphocyte (LGL) lymphoproliferative disorders involve T cells or natural killer cells. A case study highlights spontaneous regression in a young woman with T-cell LGL disorder, bacterial infection, and lymphadenopathy.
Area of Science:
- Hematology
- Immunology
- Oncology
Background:
- Large granular lymphocyte (LGL) lymphoproliferative disorders originate from T cells or natural killer cells.
- These conditions, including LGL lymphocytosis and LGL leukemia, present with infections, splenomegaly, and autoimmune associations.
- Key hematologic findings include lymphocytosis and neutropenia.
Observation:
- The study details a young woman diagnosed with a T-cell LGL lymphoproliferative disorder.
- Her presentation included significant bacterial infection and reactive lymphadenopathy.
- Notably, her lymphocytosis exhibited spontaneous regression over a six-month period.
Findings:
- Distinguishing T-cell LGL lymphocytosis from T-cell LGL leukemia requires T cell receptor gene rearrangement analysis.
- The case demonstrated a T-cell LGL lymphoproliferative disorder with concurrent bacterial infection and reactive lymphadenopathy.
- Spontaneous resolution of lymphocytosis was observed within six months.
Implications:
- This case underscores the potential for spontaneous regression in certain T-cell LGL lymphoproliferative disorders.
- Understanding the distinct pathways of T-cell receptor rearrangement is crucial for accurate diagnosis.
- Further research may elucidate mechanisms driving regression in LGL lymphoproliferative disorders.
Abstract:
Lymphoproliferative disorders of large granular lymphocytes (LGL) can arise from either CD3+ T cells or CD3- natural killer cells. Polyclonal proliferation of LG lymphocytes is called LGL lymphocytosis, monoclonal proliferation of LG lymphocytes is LGL leukaemia. Prominent clinical manifestations of LGL lymphocytosis and leukaemia are bacterial infections, splenomegaly, and may be connected with rheumatic or autoimmune disorders. Hematologic findings reveal particularly lymphocytosis, and severe neutropenia. The beta chain gene of T cell receptor rearrangement analysis is necessary for distinguishing of T LGL lymphocytosis from T LGL leukaemia. The authors report a case of young woman with T cells LGL lymphroproliferative disorder, bacterial infection, reactive lymphadenopathy, and spontaneous regression of the lymphocytosis within 6 months.
