1,721,091 research outputs found
Anticoagulation therapy in ICU patients
Most patients admitted to an ICU have multiple risk factors for thromboembolic complications, which are very often present in the guise of deep venous thrombosis (DVT) and/or pulmonary thromboembolism (PTE). Risks factors may be present before the ICU admission (advanced age, malignancy, major surgery, major trauma), or may be related to the ICU stay (such as mechanical ventilation and central venous catheters). In such settings, there are strong indications for prolonged thromboprophylaxis and/or treatment of thrombotic complications. This is achieved by a number of pharmacological and nonpharmacological provisions, each having specific advantages and shortcomings. To date, heparin and vitamin K antagonists are the two most widely used measures for both prevention and treatment of DVT and PTE. Critically ill patients are peculiar in having altered pharmacokinetic and pharmacodynamic variability. This variability can lead to unpredictable drug effects, greater toxicity, and increased potential for adverse drug effects associated with disorders of coagulation. ICU patients can receive simultaneously several different medications throughout their stay, increasing the potential for drug interactions or a synergistic/enhanced response
OUTCOME OF CHILDREN (NON-INFANT) WITH T(4;11) POSITIVE ACUTE LYMPHOBLASTIC LEUKEMIA TREATED WITH AIEOP-LLA 2000-R2006 PROTOCOLS
A single amino acid change A19V in perforin: a novel, frequent predisposing factor to childhood acute lymphoblastic leukemia?
We screened 100 children with acute lymphoblastic leukemia (ALL) to assess the incidence of single amino acid change A91V in perform. Heterozygous A91V was found in 12/100 patients and 5/127 controls (OR, 3.4; 95%CI: 1.15-9.95; p=0.014). A91V is a novel and frequent predisposing factor for childhood ALL
Comparative sequence analysis of incomplete DJH and TCR gene rearrangements in children with relapses of T-ALL
The detection of minimal residual disease (MRD) during the first
phase of treatment can predict outcome in childhood acute
lymphoblastic leukemia (ALL).1 Currently MRD detection in ALL
patients provides important information in order to assign a
tailored-treatment and the risk of an impending relapse. Nevertheless,
the major treatment failure in ALL occurs predominantly
in patients with T-cell ALL. This reflects especially a more
therapy-resistance and a slower clearance of blasts of T-ALL in
comparison with precursor-B-ALL.2 Therefore, the quantification
of early response to therapy and the monitoring of MRD
during and after treatment can greatly improve the outcome and
long-term quality of life of these patients. In childhood ALL,
detection of MRD with high sensitivity (ie 104, 105) can be
achieved by quantitative PCR methods (RQ-PCR) of rearranged
immunoglobulin (Ig) and T-cell receptor (TCR) genes.1,3 The
usefulness of these specific PCR targets should give attention to
the possible modification of Ig and TCR gene rearrangements that
could occur during the course of disease, due to continue activity
of the V(D)J recombinase enzymes in leukemic blast
Comparative analysis of bone marrow response kinetics in disseminated burkitt's lymphoma and B-cell acute leukemias
ASSOCIATION OF CYTOGENETIC ABNORMALITIES WITH DETECTION OF BCR-ABL FUSION TRANSCRIPTS IN CHILDREN WITH T-LINEAGE LYMPHOPROLIFERATIVE DISEASES
Detection of Philadelphia chromosome (Ph) in childhood T-lineage acute lymphoproliferative disorders is a rare event. Additional cytogenetic abnormalities are particularly uncommon in ALL. We here report two cases with T lineage acute lymphoproliferative disorders (T-ALL and T-NHL) presenting with both cytogenetic alterations and BCR-ABL fusion transcripts, associated with an aggressive presentation and a poor outcome. We point out firstly on the cytogenetic aberrations, supporting the hypothesis of multi-lineage involvement of ALL expressing Ph chromosome; secondly, on the persistence of T-cell leukemic clone detected by minimal residual disease (MRD) analysis, despite of the early disappearance of BCR-ABL fusion transcrip
A specific proteomic profile is differentially expressed in childhood leukaemias with MLL translocations
LATE PROGRESSION OF A NEUROBLASTOMA AS A MALIGNANT SCHWANNOMA
Med.Pediatr Oncol - XXXII SIOP Meetin
ArgBP2, encoding a negative regulator of ABL, is fused to MLL in a case of infant M5 acute myeloid leukemia involving 4q35 and 11q23.
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