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PubMed2006

Sinopulmonary aspergillosis in children with hematological malignancy.

Invasive pulmonary aspergillosis is a serious infectious complication in immunocompromised especially neutropenic patients. Despite improvements in early diagnosis and effective treatment, invasive pulmonary aspergillosis is still a devastating opportunistic infection. These infections also interfere with the anticancer treatment. We report our experience in the diagnosis and therapeutic management of sinopulmonary aspergillosis in 4 children with hematologic malignancy. All patients except the first were neutropenic when sinopulmonary aspergillosis was diagnosed. Clinical signs included fever, cough, respiratory distress, swallowing difficulty, headache, facial pain-edema and hard palate necrosis. Radiodiagnostic methods showed bilateral multiple nodular infiltrations, soft tissue densities filling all the paranasal sinuses, and bronchiectasis. Diagnosis of aspergillosis was established by bronchoalveolar lavage in one case, tissue biopsy, positive sputum and positive cytology, respectively, in the other 3 cases. One patient was treated with liposomal amphotericin B and other 3 cases were treated with liposomal amphotericin B + itraconozole. Outcome was favorable in all cases except the one who died due to respiratory failure. Early diagnosis, appropriate treatment and primary disease status are important factors on prognosis of Aspergillus infections in children with hematological malignancy.

Acute Disease↗

PubMed2000

Acquired hemophilia in patients with hematologic malignancies.

OBJECTIVES: To evaluate the occurrence of acquired hemophilia in patients with hematologic malignancies and to assess their response to treatment. DESIGN: Data on 8 patients with hematologic neoplastic disorders and inhibitor against factor VIII were analyzed retrospectively. SETTING: Three large tertiary-care centers. RESULTS: All 8 patients presented with spontaneous or posttraumatic hemorrhages. The mean inhibitor titer at the time of diagnosis was 79 Bethesda units (BU), and residual factor VIII activity was detectable in 3 patients. The inhibitor disappeared in 5 patients after a mean of 92 days, but persisted in the 3 other patients. The patients who achieved complete resolution of their circulating anticoagulant had lower mean inhibitor titers at the time of diagnosis than those who had persistent inhibitor (27 BU vs. 167 BU, respectively). Two patients died as a result of major hemorrhages that did not respond to treatment. CONCLUSIONS: Antibodies against factor VIII may be responsible for some bleeding episodes in patients with lymphoid or myeloid malignancies. Acquired hemophilia in this setting should be differentiated from other causes of bleeding because the approach to treatment is different. No conclusion can be drawn regarding the association between the activity of the underlying illness and the inhibitor titer, although it appears that at least in some patients such a relationship may exist. The underlying pathogenetic mechanisms responsible for the production of autoantibodies against factor VIII remain unclear, but we provide a few explanations in this article.

Aged↗

PubMed2004

Constitutional chromosome aberrations as pathogenetic events in hematologic malignancies.

A predisposition to tumor development is associated with some constitutional chromosomal abnormalities. Investigations of families with an apparent hereditary cancer and constitutional chromosome rearrangements have led to the molecular identification of tumor suppressor genes. Under the somatic mutation theory for the development of cancer, two mutational events are required. The first step may be a constitutional event and the second an acquired genetic mutation. Cytogenetic studies were performed on 5633 bone marrow specimens from patients with hematologic malignancies from a single institution. Fifty cases of constitutional chromosome aberrations were detected. Data collected from the literature and from our series are reviewed and compared with the incidence of specific constitutional chromosome aberrations in the newborn population. Possible mechanisms that may predispose individuals with constitutional chromosome aberrations to the development of a hematologic malignancy are reviewed.

Adolescent↗

PubMed1999

Rituximab therapy in hematologic malignancy patients with circulating blood tumor cells: association with increased infusion-related side effects and rapid blood tumor clearance.

PURPOSE: Rituximab was recently approved for use in relapsed, low-grade non-Hodgkin's lymphoma; however, few data exist regarding the safety of this agent in patients with a high number of tumor cells in the blood. METHODS AND RESULTS: After the observation at our institution of a rapid reduction of peripheral-blood tumor cells with associated severe pulmonary infusion-related toxicity in two patients with refractory hematologic malignancies, data on three additional cases were collected from physician-submitted reports of adverse events related to rituximab treatment. Five patients with hematologic malignancies possessing a high number of blood tumor cells were treated with rituximab and developed rapid tumor clearance. The median age was 68 years (range, 26 to 78 years). Patients were diagnosed with B-cell prolymphocytic leukemia (n = 2), chronic lymphocytic leukemia (n = 2), or transformed non-Hodgkin's lymphoma (n = 1). All of these patients had bulky adenopathy or organomegaly. All five patients developed a unique syndrome of severe infusion-related reactions, thrombocytopenia, rapid decrement in circulating tumor cell load, and mild electrolyte evidence of tumor lysis, and all required hospitalization. In addition, one patient developed ascites. These events resolved, and four patients were subsequently treated with rituximab without significant complications. CONCLUSION: Rituximab administration in patients who have a high number of tumor cells in the blood may have an increased likelihood of severe initial infusion-related reactions. These data also suggest that rituximab may have activity in a variety of other lymphoid neoplasms, such as chronic lymphocytic leukemia and B-cell prolymphocytic leukemia.

Adult↗

PubMed2003

Non-myeloablative hematopoietic cell transplantation as immunotherapy for hematologic malignancies.

Conventional approaches to hematopoietic stem cell transplantation (HSCT) carry risks of morbidity and mortality from regimen-related toxicities, which have restricted the procedure to relatively young patients in good medical condition. This age restriction is unfortunate because the median age of patients with most candidate diseases (e.g., acute and chronic leukemias, myelodysplasia, myeloproliferative diseases, myeloma, and non-Hodgkin lymphoma) for HSCT is greater than 60 years. In non-myeloablative allogeneic HSCT, high-dose cytotoxic therapy as the conceptual basis for treating hematopoietic malignancies has been replaced by graft-versus-tumor effects. The use of potent pre- and postgrafting immunosuppression derived from preclinical studies has allowed omission of myeloablative cytotoxic therapy without compromising hematopoietic donor cell engraftment. This results in a marked reduction in transplant-related toxicities which makes older or medically infirm patients candidates for this treatment option. Initial results in patients with a variety of hematologic malignancies have been encouraging, with documented sustained cytogenetic and molecular remissions in a substantial number of sometimes heavily pretreated and previously refractory patients. While patients with hematologic malignancies will likely require conversion to full donor hematopoiesis for long-term disease control, a state of mixed donor/host hematopoietic chimerism might suffice to 'cure' the disease phenotypes in various non-malignant diseases. Strategies aimed at inducing donor-specific tolerance and optimizing post-transplant immunosuppression may eventually eliminate the need for pre-transplant total body irradiation which is relevant for minimizing late toxicities.

Animals↗

PubMed2001

Vascular endothelial growth factor signaling pathway as an emerging target in hematologic malignancies.

Angiogenesis is important in a variety of physiologic and pathologic disorders. It is a central element in embryogenesis, ovulation, wound healing, diabetic retinopathy, and rheumatoid arthritis and in the establishment and spread of malignant tumors. Angiogenic factors include direct angiogens, indirect angiogens, and integrins. Direct angiogens stimulate the formation of new blood vessels directly. Indirect angiogens promote neovascular formation by paracrine stimulation of direct angiogens. Integrins mediate interactions between the developing vessels and components of the extracellular matrix. Vascular endothelial growth factor (VEGF) is a principal direct angiogen. By binding to 1 of 3 receptors (VEGFR-1, -2, or -3), it influences vasculogenesis during embryogenesis, physiologic and neoplastic angiogenesis, and lymphangiogenesis. Although the importance of angiogenesis in solid tumors has been recognized for some time, its exact significance in hematologic malignancies is less clear. Evidence now suggests that VEGF has a major role in the development and progression of hematologic malignancies such as acute leukemia, chronic leukemia, myelodysplasia, non-Hodgkin's lymphoma, and multiple myeloma. Potential therapeutic interventions to interrupt the VEGF signaling pathway of malignancy include antibodies that neutralize the growth factor and small molecules that inhibit the receptor tyrosine kinase activity of VEGF receptors.

Endothelial Growth Factors↗

PubMed1995

Loss of expression of the human MSH3 gene in hematological malignancies.

Human MSH3 (hMSH3), previously named human mismatch repair protein 1 (MRP1), is one of the human homologs of the bacterial DNA mismatch repair protein MutS. The hMSH3 gene is expressed at low level in most types of cells. Using the RT-PCR technique, we examined the expression of the hMSH3 gene in bone marrow cells from 40 patients with various hematological malignancies. The hMSH3 mRNA was not detectable in 7 cases including 3 of chronic myelogenous leukemia, 2 of acute myelogenous leukemia, and 1 of acute lymphocytic leukemia, and 1 of myelodysplastic syndrome. In addition, 17 cases showed significantly reduced expression of the hMSH3 gene. Southern blot analysis of genomic DNA demonstrated no remarkable changes in the structure and the copy number of the hMSH3 gene in all cases. These results suggest that inactivation of the hMSH3 gene may be involved in the development of hematological malignancies.

Base Sequence↗

PubMed2006

A study of a reduced-intensity conditioning regimen followed by allogeneic stem cell transplantation for patients with hematologic malignancies using Campath-1H as part of a graft-versus-host disease strategy.

Nonmyeloablative transplantation (NMT) is intended to be less toxic than traditional allografts, but such regimens as fludarabine/melphalan still pose a significant risk of graft-versus-host disease (GVHD). We used Campath-1H in an attempt to reduce the risk of GVHD in NMT. Patients with hematologic malignancies suitable for allogeneic transplantation underwent transplantation using a regimen of fludarabine 30 mg/m(2) on days -5 to -2 (total, 120 mg/m(2)), total body irradiation of 200 cGy on day -1, and Campath-1H 20 mg/day on days -7 to -3 (total dose, 100 mg). After loss of graft in 5 of the first 6 patients, the protocol was amended by decreasing the Campath-1H dose to 20 mg on days -4 and -3 and 10 mg on day -2 (total dose, 50 mg) for all subsequent patients. GVHD prophylaxis consisted of only cyclosporine, due to the immunosuppressive effect of Campath-1H. Patients received prophylactic acyclovir, fluconazole, and a quinolone. Other requirements included creatinine clearance > or = 25 mL/min, diffusing capacity > or = 45% of predicted, and cardiac ejection fraction > or = 40%. Twenty-five patients with hematologic malignancies entered the study. The median age was 40 years (range, 26-71 years). Median time to engraftment (defined as a neutrophil count of 500 mm(3) and a platelet count of 20,000 mm(3) without platelet support on at least 2 days) was 19 days (range, 9-32 days). All patients who were treated after the amendment engrafted with 90%-100% donor cells by day 100 except for 2 early deaths. Acute GVHD developed in 40% of the patients. Patients who underwent related transplants developed GVHD after donor lymphocyte infusions for poor engraftment or relapse whereas those undergoing unrelated transplants developed GVHD de novo. Two patients (8%) developed chronic GVHD, and 48% had cytomegalovirus reactivation, which was easily managed medically. Nonrelapse mortality within the first 12 months was 12%; 32% of the patients survived at a median of 269 days. We conclude that Campath-1H, fludarabine, and melphalan is a reasonable preparative regimen for reduced-intensity transplantation with a low nonrelapse mortality, but that issues of GVHD remain problematic, due to either the use of donor lymphocyte infusions or the use of volunteer unrelated donors.

Adult↗

PubMed1998

Liver dysfunction in patients infected with hepatitis C virus undergoing chemotherapy for hematologic malignancies.

BACKGROUND: Reactivation of chronic hepatitis B virus (HBV) infection with the development of fulminant hepatitis induced by withdrawal of chemotherapy and/or corticosteroids (CS) is well known. However, less is known about liver dysfunction in patients with hepatitis C virus (HCV) who are undergoing chemotherapy. Thus, the authors conducted this study to determine whether chemotherapy for HCV positive patients with hematologic malignancies is associated with hepatic injury. METHODS: Thirty-three consecutive HCV positive patients were studied. Twenty-six had B-cell lymphoma, two had Hodgkin's disease, two had acute myeloblastic leukemia (AML), two had chronic myelocytic leukemia, and one had multiple myeloma. HCV infection was detected by anti-HCV antibodies (enzyme immunoassay) and HCV RNA (reverse transcription polymerase chain reaction). In 28 of 33 patients, CS were used as part of the chemotherapy regimens. Liver function tests (LFTs) were evaluated prior to chemotherapy, a mean of 19 days after each cycle of chemotherapy, and during the follow-up period after the completion of chemotherapy. Mean follow-up was 14 months (range, 7-26 months). RESULTS: Twenty-seven of 33 patients (82%) were positive for both anti-HCV and HCV RNA, 5 for HCV RNA only, and 1 for anti-HCV antibodies only. Fourteen patients (42%) had normal pretreatment LFTs. During treatment, 18 patients (55%) (7 with normal and 11 with abnormal pretreatment transaminase levels) had mild-to-moderate increases of alanine aminotransferase (ALT) (median, 156 U/L; range, 59-491) and aspartate aminotransferase (AST) (median, 121; range, 45-243), which occurred 2-3 weeks after the withdrawal of chemotherapy without associated hyperbilirubinemia. Only one patient with baseline ALT and AST of 182 IU/L and 117 IU/L had a severe "flare" of hepatitis C, with peak ALT and AST of 491 IU/L and 243 IU/L. No patient developed fulminant hepatitis or died of liver-related causes. Posttreatment levels of transaminases were not significantly different from pretreatment levels. Abnormal pretreatment transaminase levels did not predict further increase during treatment. CONCLUSIONS: Significant hepatic dysfunction is uncommon among HCV infected patients treated with chemotherapy for hematologic malignancies.

Acute Disease↗

PubMed2002

Allele-specific replication associated with aneuploidy in blood cells of patients with hematologic malignancies.

We hypothesize that coordination between the two DNA parental sets in somatic cells is essential for the stability of the diploid genome, and that its disruption is associated with the many alterations observed in the various cancerous phenotypes. As coordination between two allelic counterparts is well exemplified by synchrony in replication timing, we examined, in blood cells of patients suffering from various hematologic malignancies, replication patterns of five loci. These loci were three cancer-implicated genes (TP53, AML1, and RB1) and two nontranscribed sequences engaged in chromosome segregation. All five loci normally display synchrony in allelic replication timing. In addition, in order to exemplify an asynchronous mode of allelic replication, we followed the replication of allelic counterparts of an imprinted gene (SNRPN), which is distinguished by its asynchronous mode of allelic replication (allele-specific replication). Allelic replication patterns were studied by fluorescence in situ hybridization (FISH), which has been shown to distinguish between nonreplicated and replicated regions of the genome in interphase cells, based on the structure of the specific hybridization signals that are being detected. Using the FISH replication assay we observed, for all loci which normally exhibit synchrony in allelic replication, loss of synchrony when present in blood cells of patients with hematologic malignancies. The loss of synchrony in allelic replication in patients' cells was accompanied by aneuploidy (chromosome losses and gains), the hallmark of cancer. We were able to reinstate the normal pattern of replication in the patients' cells by introducing an inhibitor of DNA methylation. It thus appears loss of allelic coordination is an epigenetic alteration characterizing cancer, which is easily identified by simple cytogenetic means and has a potential use in both cancer investigation and detection.

Adolescent↗

PubMed2006

Inhibition of the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway in hematologic malignancies.

The phosphatidylinositol 3-kinase (PI3-K)/mammalian target of rapamycin (mTOR) signal transduction pathway integrates signals from multiple receptor tyrosine kinases to control cell proliferation and survival. Key components of the pathway are the lipid kinase PI3-K, the small guanosine triphosphate-binding protein Rheb, and the protein kinases Akt and mTOR. Important natural inhibitors of the pathway include the lipid phosphatase PTEN and the tuberous sclerosis complex. Several components of this pathway are targeted by investigational antineoplastic agents. Rapamycin (sirolimus), the prototypic mTOR inhibitor, exhibits activity in acute myeloid leukemia. Three rapamycin analogs, temsirolimus, everolimus, and AP23573, are in clinical trials for various hematologic malignancies. Temsirolimus has produced a 38% overall response rate in relapsed mantle cell lymphoma, and AP23573 has demonstrated activity in acute leukemia. Everolimus is undergoing clinical testing in lymphoma (Hodgkin and non-Hodgkin) and multiple myeloma. In addition, perifosine, an inhibitor of Akt activation that exhibits substantial antimyeloma activity in preclinical models, is being examined in relapsed multiple myeloma. Based on results obtained to date, it appears that inhibitors of the PI3-K/mTOR pathway hold promise as single agents and in combination for hematologic malignancies.

Antibiotics, Antineoplastic↗

PubMed2003

Itraconazole prevents invasive fungal infections in neutropenic patients treated for hematologic malignancies: evidence from a meta-analysis of 3,597 patients.

PURPOSE: Efficacy of antifungal prophylaxis has not yet been convincingly proven in numerous trials of various antifungals. New evidence and the anti-Aspergillus efficacy of itraconazole prompted a new look at the data for the prevention of invasive fungal infections. PATIENTS AND METHODS: Randomized, controlled studies with itraconazole for antifungal prophylaxis in neutropenic patients with hematologic malignancies were identified from electronic databases and hand searching. RESULTS: Thirteen randomized trials included 3,597 patients who were assessable for invasive fungal infections. Itraconazole reduced the incidence of invasive fungal infection (mean relative risk reduction, 40% +/- 13%; P =.002), the incidence of invasive yeast infections (mean, 53% +/- 19%; P =.004) and the mortality from invasive fungal infections (mean, 35% +/- 17%; P =.04) significantly. The incidence of invasive Aspergillus infections was only reduced in trials using the itraconazole cyclodextrine solution (mean, 48% +/- 21%; P =.02) and not itraconazole capsules (mean, 75% +/- 73% increase; P =.3). The overall mortality was not changed. Adverse effects were rare, hypokalemia was noted in three studies, and a higher rate of drug discontinuation was found in trials that compared itraconazole cyclodextrine solution to a control without cyclodextrine. The effect of prophylaxis was clearly associated with a higher bioavailable dose of itraconazole. CONCLUSION: Antifungal prophylaxis with itraconazole effectively prevents proven invasive fungal infections and-shown for the first time for antifungal prophylaxis-reduces mortality from these infections and the rate of invasive Aspergillus infections in neutropenic patients with hematologic malignancies. Adequate doses of the oral cyclodextrine solution (at least 400 mg/d) or i.v. formulations (200 mg/d) of itraconazole are necessary for these effects.

Antifungal Agents↗

PubMed2004

Microarray-based gene expression profiling of hematologic malignancies: basic concepts and clinical applications.

Each cell in our body contains a set of tens of thousands of genes, out of which a set of several thousands determines the cell's characteristics. The deciphering of the sequence of the human genome combined with the technical feasibility to simultaneously measure the gene expression levels of thousands of genes had revolutionized our understanding of cellular processes. This ability has great significance in our comprehension of the mechanisms that bring about diseases in general and hematologic malignancies in particular. Several new high-throughput technologies, commonly referred as microarrays, enable us to perform such measurements and concurrently, bioinformatic and statistical tools were developed to analyze the data obtained by using microarrays. In this review we present examples of analyses of hematologic malignancies using microarrays which contribute to refinement of diagnosis, identification of novel disease subtypes and of relationships between diseases that were previously considered to be unrelated, prediction of response to treatment and identification of genes and pathways linked to pathogenesis, thus defining targets to rational therapy.

Databases as Topic↗

PubMed1997

Abdominal ultrasound findings mimicking hematological malignancies in a study of 218 Gaucher patients.

Gaucher disease, the most prevalent sphingolipidosis, generally presents with splenomegaly, anemia, and thrombocytopenia. Hence, hematologists are often the specialists involved in diagnosis and management of these patients. We present ultrasonographic characteristics in a cohort of 218 consecutive Gaucher patients evaluated in our clinic during the past 5 years. Our data emphasize the high prevalence of lesions mimicking hematological malignancies in Gaucher disease. One fifth of 184 non-splenectomized patients had intra-splenic lesions, 6% of all patients had similar lesions in the liver, and 32% of 34 splenectomized patients (but none of the other patients) had marked retroperitoneal or peri-portal lymphadenopathy. The presence of splenic lesions correlated with age and splenic size, but not with extent of bone involvement or genotype. Interestingly, they were not affected by reduction in splenomegaly following enzyme replacement therapy. The importance of these findings is to include Gaucher disease in the differential diagnosis of splenic or hepatic lesions, especially in Ashkenazi Jews. Conversely, they are relevant for follow-up of all Gaucher patients, including asymptomatic individuals, because of the reported increased incidence of hematological malignancies in Gaucher disease.

Adolescent↗

PubMed2025

Mutagenic Impact and Evolutionary Influence of Chemoradiotherapy in Hematologic Malignancies.

UNLABELLED: Ionizing radiotherapy (RT) is a widely used treatment strategy for malignancies. In solid tumors, RT-induced double-strand breaks lead to the accumulation of insertion-deletions (indels; ID), and their repair by nonhomologous end joining has been linked to the ID8 mutational signature in surviving cells. However, the extent of RT-induced mutagenesis in hematologic malignancies and its impact on their mutational profiles and interplay with commonly used chemotherapies has not yet been explored. In this study, we interrogated 580 whole-genome sequence (WGS) samples from patients with large B-cell lymphoma, multiple myeloma, and myeloid neoplasms and identified ID8 only in relapsed disease. Yet ID8 was detected after exposure to both RT and mutagenic chemotherapy (i.e., platinum and melphalan). Using WGS of single-cell colonies derived from treated lymphoma cells, we revealed a dose-response relationship between RT and platinum and ID8. Finally, using ID8 as a genomic barcode, we demonstrate that a single RT-surviving cell may seed distant relapse. SIGNIFICANCE: RT and the ID8 indel signature are related, but their genomic impact on hematologic malignancies is unclear. Leveraging WGS, we linked ID8 to both RT and mutagenic chemotherapy and validated that platinum can induce ID8. We used ID8 as a genomic barcode to reveal that RT-resistant cells may seed systemic relapse.

Humans↗

PubMed2002

Apoptosis: molecular regulation of cell death and hematologic malignancies.

We describe the molecular mechanisms of apoptosis and its relationships with hematologic malignancies, stressing the concept that, both positive and negative deregulation of apoptosis, may be involved in hematologic human diseases. So, this fundamental process must be balanced by so far unknown mechanisms, involving caspases (cysteine proteases, cleaving the protein substrate after an aspartate residue). These, so far known, ten proteases, are interconnected in a molecular cascade, initiated by the release of cytochrome C from mitochondrial membranes and its interaction with APAF-1 (the homolog of the Caenorhabditis e. CED-4) and with caspase 9, that initiates the proteolitic cascade (1,2). The conclusion is that apoptosis is a very important process, but yet poorly known in molecular details, in spite of the efforts of many scientists. Even the role of bcl-2, the main gene protecting from apoptosis, is still unknown. We close this chapter with a list of ten different technical approaches that can be useful tools to study apoptosis, and tracing the molecular principles on which they are based.

Animals↗

PubMed2006

Tissue factor as an effector of angiogenesis and tumor progression in hematological malignancies.

In the last few years, it has become clear that the processes of tumor angiogenesis, metastasis and invasiveness are highly dependent on components of the blood coagulation cascade. One of the key proteins in coagulation is tissue factor (TF). In addition, TF is also known as a mediator of intracellular signaling events that can alter gene expression patterns and cell behavior. TF significantly participates in tumor-associated angiogenesis and its expression levels have been correlated with the metastatic potential of many types of hematological malignancies. Signaling pathways initiated by both, tissue factor-activated factor VII (TF-FVIIa) protease activation of protein-activated receptors (PARs), and phosphorylation of the TF-cytoplasmic domain, appear to regulate these tumoral functions. Advances in antiangiogenic therapies and preclinical studies with TF-targeted therapeutics are hopeful in the control of tumor growth and metastasis, but continued studies on the regulation of TF are still needed. In the last few years, the use of approaches of functional genomics and proteomics has allowed the discovery of new proteins involved in the origin of the neoplasia and their participation in the development of the disease. This review attempts to establish a cellular and molecular causal link between cancer coagulopathy, angiogenesis and tumor progression in hematological malignancies.

Animals↗

PubMed2004

Methicillin-resistant staphylococcal bacteremia in patients with hematologic malignancies: clinical and microbiological retrospective comparative analysis of S. haemolyticus, S. epidermidis and S. aureus.

Although Staphylococcus haemolyticus (SH) represents an emerging etiology of methicillin-resistant (MR) coagulase-negative staphylococcal nosocomial bacteremia, little is known of clinical significance of this infection. Thus, we performed case-control retrospective comparative analysis of MRSH bacteremias (MRSHB), methicillin-resistant S. epidermidis bacteremias (MRSEB), and methicillin-resistant S. aureus bacteremias (MRSAB) in patients with hematologic malignancies. Most patients in the three groups were neutropenic and had a central venous catheter (CVC) in place at the onset of bacteremia. However, MRSHB patients had a CVC in place prior to bacteremia for a time significantly more prolonged than MRSEB and MRSAB ones (p<0.05). Severe sepsis or septic shock were more common in patients with MRSAB as compared with MRSHB (p=0.02). Nosocomial attributable mortality rate was very low in the 3 study groups (0 to 5.4%) and only two patients developed metastatic infections. Overall, reduced susceptibility to teicoplanin was observed in 19 (47.5%) MRSH and in 4 (10%) MRSE isolates. Resistance to teicoplanin was observed in 6 isolates, all MRSH. Reduced susceptibility or resistance to vancomycin was observed in 2 isolates, both MRSH. All MRSA isolates were susceptible to the glycopeptides. Comparison between cases of bacteremia in patients with MRSH isolates with reduced susceptibility to teicoplanin and those with susceptible MRSH did not reveal significant differences in the clinical-microbiological response to teicoplanin therapy and outcome. Our results seem to suggest that MRSHB in hematologic patients is associated with low morbidity and mortality rates. MRSH frequently shows a reduced susceptibility to teicoplanin; however these in vitro data do not seem associated with an unfavorable clinical response to teicoplanin therapy for MRSHB in patients with hematologic malignancies.

Adolescent↗