Kazuhiro Yago

Primary low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT)-type of the liver in a patient with hepatitis C virus infection.

We report a case of primary low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT)-type of the liver presenting as a solitary mass in a patient with hepatitis C virus infection. A 73-year-old male was referred to our hospital because of a solitary mass in the liver, which was identified by ultrasonography during a routine follow-up study for his hepatitis C virus carrier status. A fine-needle biopsy was performed and the mass was diagnosed as non-Hodgkins lymphoma. A detailed investigation showed no evidence of lymphoma in other sites. Left lateral segmentectomy was performed. Histologic examination showed diffuse, monotonous infiltration of centrocyte-like cells that are CD 19(+), CD 20(+), sIgM-   (+), CD 3 (m ), CD 5 (m ), CD 10 (m ). The patient received no adjuvant chemotherapy and is alive and disease free 34 months after surgery.

IgM-producing renal plasmacytoma

A seventy-six-year-old woman with plasmacytoma presenting as a renal mass died three months after diagnosis. Bone surveys disclosed no lytic lesions. Gallium-67 scan showed an avid uptake of the radionuclide in the renal mass. Histologic and immunofluorescence studies of resected specimens demonstrated that the renal parenchyma was destroyed by sheets of immature plasma cells producing IgM-lambda and by massive deposits of amorphous, eosinophilic substance stained with anti-mu and anti-lambda antisera. The literature is reviewed. We believe this case is the first one of well-documented IgM-producing renal plasmacytoma.

Reversible Acceleration of Disease Progression Following Cyclosporin A Treatment in a Patient With Myelodysplastic Syndrome

A 38-year-old Japanese man with myelodysplastic syndrome (MDS), whose bone marrow smears demonstrated hypercellularity, was treated with oral cyclosporin A (CsA) therapy. During the course of this therapy, the numbers of peripheral blood and bone marrow blasts increased and the level of serum lactate dehydrogenase increased.After discontinuation of CsA treatment, all of these levels rapidly decreased. We consider that CsA might accelerate disease progression in certain MDS cases.