Miliary tuberculosis in a patient with Epstein-Barr virus-associated angioimmunoblastic lymphadenopathy
- Cite this article as:
- Rho, R., Laddis, T., McQuain, C. et al. Ann Hematol (1996) 72: 333. doi:10.1007/s002770050182
- 38 Downloads
A 74-year-old woman developed angioimmunoblastic lymphadenopathy (AILD) with involvement of intra-abdominal and retroperitoneal lymph nodes. Southern blot analysis showed germline configuration of the JH genes and an oligoclonal pattern of the TcRβ genes. The immunoblasts were of B-cell phenotype and often expressed the CD30 antigen and the latent membrane protein 1 (LMP1) oncogene. Six nonsilent point mutations were identified near the 3′ end of the LMP1 gene, leading to a cluster of six amino acid changes within a protein domain needed for maximal NF-κB stimulation. After a clinical remission of 8 months the patient relapsed with generalized lymphadenopathy and died secondary to tuberculosis. The oligoclonal rearrangements of the TcRβ genes may reflect an unsuccessful cellular immune response to Mycobacterium tuberculosis or an HLA-restricted T-cell response to B-immunoblasts expressing mutated viral antigens. A positive percutaneous tuberculin test observed 6 months prior to the onset of AILD is in favor of the first possibility.