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Umbilical cord blood transplantation (CBT) is widely accepted, but one critical issue for adult patients is a low engraftment rate, of which one cause is haemophagocytic syndrome (HPS). We aimed to identify the contribution of HPS to engraftment failure after CBT, following preparative regimens containing fludarabine phosphate, in 119 patients (median age, 55 years; range; 17-69 years) with haematological diseases. Graft-versus-host disease prophylaxis comprised continuous infusion of a calcineurin inhibitor with or without mycophenolate mofetil. Of the 119 patients, 20 developed HPS within a median of 15 d (cumulative incidence; 16.8%) and 17 of them did so before engraftment. Donor-dominant chimaerism was confirmed in 16 of 18 evaluable patients with HPS. Despite aggressive interventions including corticosteroid, ciclosporin, high-dose immunoglobulin and/or etoposide, engraftment failed in 14 of 18 patients. Of these 14 patients, four received second rescue transplantation and all resulted in successful engraftment. Overall survival rates significantly differed between patients with and without HPS (15.0% vs. 35.4%; P < 0.01). Univariate and multivariate analysis identified having fewer infused CD34(+) cells as a significant risk factor for the development of HPS (P = 0.01 and 0.006, respectively). We concluded that engraftment failure closely correlated with HPS in our cohort, which negatively impacted overall survival after CBT.

Background The route of Helicobacter cinaedi bacteremia has not yet been clarified. Although bacterial translocation from the intestinal tract into the circulation has been suggested, it has not been demonstrated thus far. The objective of this study was to investigate the port of entry of this bacterium. Material and methods We conducted a retrospective study on patients with H. cinaedi bacteremia between March 2009 and May 2013. Records of patients in whom H. cinaedi was detected in both blood and stool cultures were extracted. H. cinaedi was identified using gyrB-targeted PCR. Pulse-field gel electrophoresis was used to investigate the consistency of the genotypes. Results Seventy-one patients were diagnosed with H. cinaedi bacteremia during the study period. H. cinaedi was detected in both blood and stool samples of 21 patients. Pulse-field gel electrophoresis was used to investigate the consistency of the genotypes in 18 evaluable strains (from 9 patients). The pulse-field gel electrophoresis patterns of the stool- and blood-derived strains of H. cinaedi were consistent among all 9 patients. Most of the 9 patients analyzed were immunocompromised and being treated with anticancer drugs or steroids, which suggests reduced intestinal immunity. Conclusions This is the first study to demonstrate that bacterial translocation from the intestinal tract could represent one route of H. cinaedi bacteremia.

The concept that central nervous system (CNS) could be a target of graft-versus-host disease (GVHD) is controversial. There are a few case reports which support the possibility of CNS-GVHD [1,2]. Here, we describe a patient who developed unique CNS symptoms soon after cord blood transplantation with reduced-intensity conditioning (RI-CBT). On Day 7 post-transplant, a high fever, slight skin eruption, moderate diarrhea, and liver damage suddenly developed. Three days later, her white blood cell (WBC) count rapidly increased to 1,700 μl ―1 and consisted mostly of mature lymphocytes. Generalized convulsions developed on the same day. An analysis of the cerebrospinal fluid (CSF) revealed elevated proteins and pleocytosis comprising mostly mature lymphocytes. The lymphocytes found in the peripheral blood (PB) and CSF were phenotypically polyclonal T-cells that were donor derived. Extensive investigations did not detect any microorganisms or other causes for the T-cell proliferation and CNS symptoms. Considering the coexistence of CNS and systemic GVHD-like symptoms, proliferation of donor-derived polyclonal T-cells in the CSF and PB, and no microorganisms or other factors detected, CNS GVHD seems to be the most likely explanation for her clinical course.