We describe a 66-year-old woman with Epstein-Barr virus-associated lymphoproliferative disorder with lung and gastric tumors. We identified two lung tumors measuring 13 and 20 mm in diameter that consisted of CD30-, CD15-, and CD20-positive Hodgkin- and Reed-Sternberg-like cells and heterogeneous cellular infiltrates in a pronounced nodular pattern, with necrosis and vasculitis, diagnosed as nodular sclerosis classical Hodgkin lymphoma. A gastric tumor showed low-grade extranodal marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue type. Neoplastic cells in all tumors expressed Epstein-Barr virus-encoded RNA based on in situ hybridization. The present case is a rare composite lymphoma arising from different extranodal organs, associated with EBV infection. Her medical history included gamma-knife therapy for clinical diagnosis with a suspicion of cerebral lymphoma.

We demonstrated an 83-year-old male case of composite lymphoma. Before 18 years, he was diagnosed with nodal marginal zone B-cell lymphoma in the cervical lymph node. Peripheral blood showed anemia and IgA (kappa)-type monoclonal gammopathy (IgA; 3,625 mg/dL). Bone marrow aspiration biopsy exhibited plasma cell myeloma, in which atypical plasma cells were positive for cytoplasmic IgA (kappa) and atypical lymphoid cells intermingled were positive for CD20. In contrast, cervical lymph node biopsy revealed nodal marginal zone B-cell lymphoma, in which lymphoma cells were positive for cytoplasmic IgG (lambda). Southern blotting analysis of the IgH gene showed same clonal rearrangement band in both lymph node and bone marrow samples and additional band in the bone marrow. Sequence analyses of the IgH gene showed an identical sequence of CDR3 in both samples. Thus, we demonstrated a common clonal origin of composite lymphoma comprising nodal marginal zone B-cell lymphoma and plasma cell myeloma. Nodal marginal zone B-cell lymphoma recurred in cervical lymph node and involved into the bone marrow, differentiating into plasma cell myeloma in which Ig isotype switched and monoclonal gammopathy developed. Sequence analysis of the IgH gene was a powerful tool for determination of clonal origin.

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We present a patient with myelodysplastic syndromes (MDS) whose neutrophils exhibited defective expression of complement receptor type 1 (CR1). A 73-year-old man was admitted with an evolution of MDS from RA into RAEBT according to the FAB classification of MDS. The neutrophil alkaline phosphatase (NAP) score was zero. The surface expression of membrane effector molecules on neutrophils was determined by indirect immunofluorescence using flow cytometry and monoclonal antibodies. The expression of CR1 on neutrophils as identified by staining with CD35 was defective in the patient, and the expression of other complement receptors (CR3 and CR4), Fc receptors and adhesion molecules was normal. CR1 deficiency and defective NAP score on neutrophils in the patient might account for impairment of common storage pool, presumably novel intracellular secretory vesicles.

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