Type B lactic acidosis is a rare complication of hematologic malignancies. The exact mechanism of this process is not well understood. Because caregivers may not be aware of the association of type B lactic acidosis with hematologic malignancies, it may go unrecognized as a cause of acidosis in these patients. We report the cases of 7 patients with type B lactic acidosis who were cared for by members of the Brown Medical School Hematology/Oncology Division. Of the 7 patients reported, 5 had lymphomas and 2 had chronic lymphocytic leukemia. One of the lymphomas was a T-cell lymphoma. Of the patients we were able to evaluate, there did not seem to be a unique cluster of differentiation marker in association with type B lactic acidosis. We also review 14 additional cases, most reported since 2001. From our review of the literature, we suggest that a deficiency of thiamine or riboflavin may play a more pivotal role than previously recognized in the development of type B lactic acidosis associated with malignancy. Further investigation should be undertaken to learn if thiamine or riboflavin replacement might be useful in treating this disorder.

Systematic and effective procedures for developing standardized-patient-based test materials and for training standardized patients have been developed. This technique is best used for measuring data gathering and interviewing skills. Correlations with commonly used evaluation methods were generally low; this may be because standardized patients measure different skills. Local use of this technique by residency programs and the development of regional consortia sharing resources, costs, and expertise are advocated.

Human herpesvirus-8 (HHV-8) is associated with several distinct lymphoproliferative disorders: primary effusion lymphoma, multicentric Castleman disease (MCD), MCD-associated plasmablastic lymphoma and HHV-8+, Epstein-Barr virus (EBV)+ germinotropic lymphoproliferative disorder. We report the case of a human immunodeficiency virus (HIV)+ male with fever, generalized lymphadenopathy, and splenomegaly. Two peripheral lymph nodes were excised and showed features of MCD and a prominent proliferation of HHV-8+, EBV+, CD20, CD138, MUM1+, lambda dim+, Ig heavy chain plasmablasts and immunoblasts replacing some follicles. Subsequently, a splenectomy and biopsy of retroperitoneal lymph nodes were performed; the retroperitoneal and splenic hilar lymph nodes showed changes similar to those in the peripheral lymph nodes while the markedly enlarged spleen showed replacement of occasional white pulp by the HHV-8+, EBV+ large cells. The histologic features and coinfection by EBV and HHV-8 suggested a diagnosis of HHV-8+ germinotropic lymphoproliferative disorder. However, the occurrence in an HIV+ individual, the background of MCD, the widespread anatomic distribution and the aggressive clinical course tended to exclude germinotropic lymphoproliferative disorder, and to favor multifocal plasmablastic microlymphoma. The patient died shortly after surgery; postmortem examination showed progression to overt lymphoma. The marrow showed extensive hemophagocytosis, consistent with development of a hemophagocytic syndrome. This unique case has clinical features compatible with a MCD-associated plasmablastic lymphoproliferative disorder, with pathologic features intermediate between HHV-8+ plasmablastic microlymphoma, and HHV-8+ germinotropic lymphoproliferative disorder, although in contrast to both of these, in our case, light chain expression was dim and heavy chain was not detected.

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