HTLV-I associated myelopathy (HAM) after blood transfusion in a patient with CD2+ hairy cell leukemia
M Kurosawa1, T Machii, T Kitani
1Department of Internal Medicine, Asahikawa Kosei Hospital, Japan.
Insights
A patient with hairy cell leukemia and hemolytic anemia experienced remission after a blood transfusion. This transfusion may have also transmitted Human T-lymphotropic virus type I (HTLV-I), leading to myelopathy.
Area of Science:
- Hematology
- Immunology
- Neurology
Background:
- Hairy cell leukemia (HCL) is a rare B-cell malignancy.
- Hemolytic anemia can complicate various hematologic disorders.
- Human T-lymphotropic virus type I (HTLV-I) is associated with neurological diseases.
Observation:
- A 46-year-old woman presented with HCL and hemolytic anemia.
- Hairy cells expressed CD20, CD2, and surface IgG (kappa).
- The patient improved after a blood transfusion, with resolution of hemolysis and HCL.
Findings:
- The patient subsequently developed HTLV-I-associated myelopathy (HAM) seven months post-transfusion.
- HTLV-I antibodies were detected in serum and cerebrospinal fluid.
- Autopsy revealed spinal cord white matter demyelination and gliosis, without leukemic infiltration.
Implications:
- Blood transfusion may have facilitated hematologic improvement in HCL, potentially via HTLV-I transmission.
- This case highlights a potential link between HTLV-I infection and unexpected therapeutic effects in hematologic malignancies.
- The study underscores the importance of considering viral etiologies in complex clinical presentations involving hematologic and neurologic symptoms.
Abstract:
Hairy cell leukemia complicating hemolytic anemia developed in a 46-year-old woman. Morphologically and cytochemically typical hairy cells were found to express both CD20 and CD2 antigens. Expression of surface IgG of kappa-chain type and the rearrangement of Ig but not T-cell receptor beta genes confirmed a B-cell origin of the leukemia. Blood transfusion was followed by disappearance of the hemolysis and a marked improvement of the leukemia. However, the patient developed progressive spastic spinal paraplegia about seven months after transfusion and was diagnosed as having HTLV-I associated myelopathy (HAM) by the demonstration of HTLV-I antibodies in serum and cerebrospinal fluid. HTLV-I infection via the transfusion may have been involved in the hematologic improvement seen in this patient. Autopsy showed demyelination, vacuolar degeneration, gliosis, and perivascular cuffing in the white matter of spinal cord without evidence of leukemic infiltration.
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