Leptomeningeal involvement in B-cell chronic lymphocytic leukemia: a case report and review of the literature.

BACKGROUND: Central nervous system involvement is considered a rare complication of chronic lymphocytic leukemia, and so there is the risk of being overlooked. CASE PRESENTATION: We report a case of central nervous system involvement in a 75-year-old mulatto woman with chronic lymphocytic leukemia after 5 years of follow-up and a literature review on the subject. The clinical course, treatment and outcome are described. A systematic, meticulous and comprehensive analysis of existing publications regarding chronic lymphocytic leukemia with central nervous system involvement was performed. CONCLUSION: We concluded that central nervous system involvement of chronic lymphocytic leukemia is probably not associated with any evident risk factors. Diagnostic approach differs by institutions but often includes imaging, morphology and flow cytometry. Resolution of central nervous system symptoms can usually be accomplished with intrathecal chemotherapy or irradiation followed by systemic treatment. The recognition of this entity by clinicians could lead to early detection and treatment, resulting in better outcomes in this rare complication.

A phosphoramidon-sensitive metalloprotease induces apoptosis of human endothelial cells by Group B Streptococcus.

We explored Group B Streptococcus (GBS)-induced apoptosis in human umbilical vein endothelial cells (HUVEC) and the role of phosphoramidon, a zinc metalloprotease inhibitor, in this process. GBS 90186 strain (serotype V, a blood isolate) and concentrated supernatant (CS) were used to investigate the viability and morphological alterations in HUVEC by Trypan blue uptake, electrophoresis in 2 % agarose gel and scanning electron microscopy assays. Apoptosis before and after phosphoramidon-treatment were verified by flow cytometry using annexin V-FITC labeling. Differences were considered significant when P < 0.05 using unpaired Student's t test. GBS and CS induced HUVEC death by apoptosis (76.5 and 32 %, respectively) with an increasing pro-apoptotic Bax expression and decreasing anti-apoptotic Bcl-2 expression. Caspase-3 was activated during GBS-induced endothelial apoptosis. Phosphoramidon reduced 89.3 and 100 % of GBS and CS cell death by apoptosis, respectively. Some GBS strains may induce cell death by apoptosis with involvement of metalloproteases and signaling through the intrinsic pathway of apoptosis, which may contribute to GBS survival during sepsis of adults and neonates.