A 67-year-old severely mentally retarded woman presented with recent onset of haematuria. She had past history of rheumatic heart disease, status post bioprosthetic aortic replacement as well as mitral valve replacement and tricuspid valve repair. She had a history of pulmonary hypertension related to right heart failure and was status post aortic artial septal defect repair. She was on multiple medications for medical problems. Physical examination showed no fever or lymphadenopathy. The white blood cell count was 5,500/ul with mild lymphopenia (1% lymphocytes) and mild anemia with Hb at 10.5mg/dl. The imaging  and cystoscopic examination revealed a localized 2.5 cm plaque-like mucosal mass on the right posterior and lateral wall of the bladder and a biopsy sample was obtained from the lesion.
Imaging picture showing a plaque-like lesion in the bladder
The biopsy sample was fixed in 10% buffered formaldehyde and routine H&E preparation was done for histological examination. Immunohistochemistry was performed on the formalin fixed paraffin embedded tissue sections using the avidin biotin peroxidase complex method in a Dako autostainer.[5
] The following antibodies from Dako were used: CD20, CD79a, CD3, CD5, CD7, CD4, CD8, CD30, CD15, MIB-1, Tdt, CD-56 CD68, S100, myeloperoxidase, ALK-1, CD117, CD35, CD1a, CD43, CD23, CD31, CD34, CK7, CK20, cytokeratin -AE1/AE3 and alpha smooth muscles actin. In situ hyvridization (ISH) for EBV was performed using anti-EBER-1 probe (Dako) according to a previously described method. Polymerase chain reaction (PCR) for B cell gene rearrangement was done using the standard method (Quest Diagnostics Incorporated) to detect the clonality of the immunoglobin heavy chain on chromosome 14.[5
H&E sections showed a diffuse and densely atypical polymorphous mixed small and large lymphoid infiltrate involving mucosa and deep muscles of the bladder . The atypical cells showed a spectrum of cell sizes and shapes, and many large atypical lymphoid cells formed small clusters and/or sheets, and some atypical cells showed plasmacytic differentiation. The background cells were composed of numerous small lymphocytes, histiocytes, occasional plasma cells and neutrophils. The large atypical cells were CD20+ , CD79a+, CD30+9 , CD43+, EMA+ (focally); but negative for CD2, CD5, CD8, CD4, CD7 and myelomonocytic markers including (myeloperoxidase) MPO, CD117, CD68 (PGM-1), as well as CD10, terminal deoxynucleotidyl transferase (Tdt) and ALK-1. The majority of atypical large lymphoid cells were strongly positive for EBV by ISH using anti-EBER-1 probe . PCR for immunoglobulin heavy chain gene rearrangement study was positive.
Tumour shows diffuse, large, atypical polymorphic lymphoid infiltrates (H&E, ×400)
Most large, atypical lymphoid cells are CD20 positive. ×400
Many cells also show CD30 positivity. ×200
Most cells are EBV positive (anti -EBER probe), × 200