Search

Summary: Invasive fungal diseases (IFD) are a primary cause of morbidity and mortality in patients with haematological malignancies. These infections are mostly life‐threatening and an early diagnosis and initiation of appropriate antifungal therapy are essential for the clinical outcome. Most commonly, Aspergillus and Candida species are involved. However, other Non‐Aspergillus moulds are increasingly identified in case of documented IFD. For definite diagnosis of IFD, a combination of diagnostic tools have to be applied, including conventional mycological culture and non‐conventional microbiological tests such as antibody/antigen and molecular tests, as well as histopathology and radiology. Although varying widely in cancer patients, the risk of invasive fungal infection is highest in those with allogeneic stem cell transplantation and those with acute leukaemia and markedly lower in patients with solid cancer. Since the last edition of Diagnosis of Invasive Fungal Diseases recommendations of the German Society for Hematology and Oncology in 2012, integrated care pathways have been proposed for the management and therapy of IFDs with either a diagnostic driven strategy as opposed to a clinical or empirical driven strategy. This update discusses the impact of this additional evidence and effective revisions. [ABSTRACT FROM AUTHOR]

This article discusses a study which identified the haematopoietic transcription factors PU.1 and CEBPA as transcriptional regulators of the actin-binding protein CORO1A in patients with acute promyelocytic leukemia (APL) and acute myeloid leukemia (AML). Researchers found that significantly lower CORO1A levels were found in APL and in CEBPA-mutated AML patient samples. They also learned that inhibiting CORO1A markedly impaired neutrophil differentiation of APL cells.

T. Weber, S. Theurich, M. Christopeit, T. Klapperstueck, G. Behre. Human herpesvirus-6 as an inducer of porphyria cutanea tarda: implications from a case. Transpl Infect Dis 2010: 12: 432-436. All rights reserved Here we describe a case that might deliver a link between sporadic porphyria cutanea tarda (PCT) and human-herpesvirus-6 (HHV6) hepatitis. Sporadic PCT is a rare disease of the heme synthesis pathway. The pathogenesis has not been fully determined but iron overload and viral infections - e.g., hepatitis C virus - are thought to play an important role. We present the case of a patient suffering from myelo-monocytic leukemia. He developed symptomatic sporadic PCT concomitant with HHV6-associated subclinical hepatitis after allogeneic stem cell transplantation (SCT). Although HHV6 often reactivates after SCT and HHV6-induced hepatitis can occur in immunocompromised patients, it has not been described that HHV6 might trigger PCT. A contribution of HHV6 to the pathogenesis of sporadic PCT could have dramatic implications on our current therapeutic approach. [ABSTRACT FROM AUTHOR]

Infections and adverse drug reactions both contribute substantially to mortality after allogeneic stem cell transplantation. It is therefore crucial to the transplant physician to develop an optimal anti-infective strategy, i.e. one which is highly effective and shows few side effects. Caspofungin acetate, the founding member of the echinocandins, is widely used against invasive fungal infections. We retrospectively assessed the hepatotoxicity of caspofungin acetate when administered with cyclosporine A. We reviewed the medical charts of 20 recipients of an allogeneic transplant. In detail, the median value of alanine amino transferase before, during and after administration of caspofungin acetate was 0.39 [standard error of the mean (SEM) 0.65], 0.77 (17) and 0.56 (0.77) μmol l−1. The maximal value was 4-, 104- and 3.3-fold the upper normal level. The median value of aspartate amino transferase was 0.28 (SEM 0.45), 0.71 (26.26) and 0.60 (0.84) μmol l−1. The maximal value before, during and after the administration of caspofungin acetate was 3.6-, 203- and 5.3-fold the upper normal level. The median value of gamma glutamyl transferase before, during and after administration of caspofungin acetate was 1.27 (SEM 1.78), 2.33 (3.41) and 1.77 (4.32) μmol l−1. The maximal value was 1.38-, 2.53- and 1.93-fold the upper normal level. The median value of alkaline phosphatase before, during and after administration of caspofungin acetate was 1.11 (SEM 0.4), 1.97 (2.30) and 1.66 (5.48) μmol l−1. The maximal value was 0.88-, 4.2- and 8.42-fold the upper normal level, respectively. The median value of total bilirubin before, during and after administration of caspofungin acetate was 23 (SEM 19.69), 38 (55.41) and 20 (67.23) μmol l−1. The maximal value was 4.18-, 14.18- and 17.88-fold the upper normal level. Taken together, the elevations observed fell after the discontinuation of caspofungin acetate. This report is in accordance with published data. As expected, we did not find any evidence pointing to an increase in nephrotoxicity by caspofungin acetate. [ABSTRACT FROM AUTHOR]

Objective: Toxicity related to the infusion of dimethylsulfoxide (DMSO)-cryopreserved peripheral blood stem cells (DMSO-PBSC) mainly comprises cardiovascular events. Fatal neurotoxicity has been reported in a few cases. DMSO represents the putative causative agent of such rare toxicities and elaborate strategies to replace DMSO would benefit from the identification of predisposing factors for DMSO-related toxicities. Methods: Here, we report on DMSO-related neurotoxicity in a series of patients ( n = 51) receiving DMSO-PBSC. The analyzed patient-series included eight patients with pre-existing cerebral disease, partially with a history of epileptic seizures. Results: Neurotoxicity was observed in only one patient who suffered from a generalized tonic seizure upon infusion of DMSO-PBSC and for which the clinical course is reported herein. No neurotoxicity was observed in the group of patients with pre-existing neurological disease. Furthermore, no neurotoxicity was observed in patients who received particularly large volumes of DMSO. In all patients, mild non-neurological side effects occurred but besides the reported seizure no other severe adverse events were observed upon PBSC-infusion. Conclusions: To our knowledge, this is the first report addressing the identification of predisposing factors for DMSO-related neurotoxicty. We conclude that infusion of DMSO-PBSC can be performed safely in patients with pre-existing cerebral disease despite the rare occurrence of severe neurotoxicity. Retrospective multicenter studies are warranted to identify patients who would benefit from elaborate methods of DMSO-replacement. [ABSTRACT FROM AUTHOR]

The article reports data of five patients with severe progressive systemic sclerosis (SSc) who underwent mesenchymal stromal cells (MSC) transplantation from allogeneic related donors. Details related to the characteristics of the patients in are provided along with factors monitored after the transplant. It was concluded that while MSC transplantation seems promising for patients with refractory autoimmune disease, the phase II trials for patients with severe SSc are necessary.

A letter to the editor is presented in response to the article about parvovirus B19 infection as trigger of graft vs. host disease published in the previous issue.