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  • 1
    Electronic Resource
    Electronic Resource
    C1 esterase inhibitor concentrate for capillary leakage syndrome following bone marrow transplantation (1997)
    Springer
    Annals of hematology 75 (1997), S. 95-101 
    Details
    ISSN: 1432-0584
    Keywords: Key words Capillary leakage syndrome ; Bone marrow transplantation ; C1 esterase inhibitor ; Autologous stem cell transplantation ; Complement activation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The prognosis of patients with severe capillary leakage syndrome (CLS) after bone marrow transplantation (BMT) is dismal despite aggressive use of intensive care therapy. Because the activated classical pathway of complement and relatively low levels of C1 esterase inhibitor (C1 INH) acitivity are known features in these patients, we evaluated the efficacy of a therapy using purified, human C1 INH concentrate. Severe CLS was defined as increase in body weight by more than 3% within 24 h combined with generalized edema, impaired hemodynamic system (tachycardia and/or decreased blood pressure), and non-responsiveness to furosemide. Of 142 patients, 22 developed severe CLS. The first seven patients whom we diagnosed with this complication were assessed as control patients. Fifteen patients with severe CLS were treated with C1 INH concentrate using a cumulative dose of 180 units/kg body wt. (initial dose: 60 units/kg, followed by two doses at 30 units/kg and four doses at 15 units/kg, every 12 h). The survival rate of patients with CLS was 57% at 1 year after BMT in the C1 INH treatment group, compared with 14% in the control group (p=0.008). Eight of 15 treated patients are alive at a median of 9 months (range: 4–55) after BMT. The plasma levels of the complement activation parameters C4d and C5a were 3±1.1 mg/dl (mean±S.D.) and 0.3±0.1 μg/l, respectively, prior to BMT, increasing to 8.2±2.1 mg/dl and 1.3±0.4 μg/l, respectively, at diagnosis of CLS. After infusion of C1 INH concentrate the plasma levels of C5a and C4d normalized. The activity of C1 INH rose to 139±10% of normal human plasma NHP pool (mean±S.D.) after infusion. The CH50 values were not significantly altered. The fluid status normalized within 11 days in 14 of 15 treated patients. The results of this study suggest that therapy with C1 INH concentrate improves the prognosis of patients with CLS after BMT. This has to be confirmed in a randomized, controlled trial.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050321
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  • 2
    Electronic Resource
    Electronic Resource
    Activity of C1 esterase inhibitor in patients with vascular leak syndrome after bone marrow transplantation (1993)
    Springer
    Annals of hematology 67 (1993), S. 17-21 
    Details
    ISSN: 1432-0584
    Keywords: Vascular leak syndrome ; Bone marrow transplantation ; Complement activation ; Contact system activation ; C1 esterase inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vascular-leak syndrome (VLS) is a common complication in the first 3 weeks after bone marrow transplantation (BMT). The patients present with weight gain, generalized edema, ascites, pericardial or pleural effusions, tachycardia, arterial hypotonia, and/ or pre-renal failure. The aim of our study was to investigate the role of the complement system in VLS. The protein concentrations of C3 and C4 were studied by immunodiffusion, and total hemolytic complement activity was studied by assessment of CH50. C1 esterase inhibitor (C1 Inh), the major inhibitor of the classical pathway of complement, was assessed by a functional test. Activation of complement was assessed by C4d (a C4 activation product). Twelve patients were followed prospectively from start of conditioning therapy to day +21 after bone marrow transplantation. Eight of 12 patients did not develop VLS. These patients had an increase of C3 between day +9 and day +13 (range: 1.3- to 1.5-fold, median: 1.4-fold), C4 (range: 1.3- to 1.9-fold, median: 1.4-fold), CH50 (range: 1.3- to 1.6-fold, median: 1.4-fold), and C1 Inh (range: 1.2- to 1.5-fold, median: 1.3-fold). Four of 12 patients developed VLS. C1 Inh activity was decreased to 0.60- to 0.80-fold. This decrease began 2–6 days prior to clinical diagnosis of VLS (n=3), or at onset of VLS (n=1). Patients with VLS showed elevated C4d concentrations (up to 2.4 mg/dl, upper normal treshold value: 0.9 mg/dl). Patients with VLS reveal an activated state of the complement system which is accompanied by a reduced activity of C1 Inh. Insufficient control of complement activation may contribute to VLS in patients after BMT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01709661
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  • 3
    Electronic Resource
    Electronic Resource
    Definition of a new score for severity of generalizedNeisseria meningitidis infection (1995)
    Springer
    European journal of pediatrics 154 (1995), S. 896-900 
    Details
    ISSN: 1432-1076
    Keywords: Complement activation ; Sepsis score ; TNF-α ; Waterhouse-Friderichsen-syndrome ; Neisseria meningitidis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neisseria meningititidis infection may present as meningitis or as severe, fulminant sepsis. In order to classify individual patients early according to the expected course of the disease, we developed a score named Neisseria sepsis index [NESI]. The NESI was defined using the parameters heart rate, mean arterial blood pressure, base excess and presence of acute subcutaneous bleeding and/or skin necroses (minimal value [=no evidence for sepsis] NESI 0; maximum value [=most severe sepsis] NESI 8). Seventeen patients with documented, systemicN. meningitidis infection were prospectively assessed for the terminal complement complex (TCC), serum tumour necrosis factorα (TNFα) levels (as laboratory parameters for severity of sepsis) and NESI score. The evaluation was immediately performed when the patients were admitted to the hospital. The 17 patients showed the following distribution of data: NESI 0 (n=4), NESI 1 (n=6), NESI 2 (n=0), NESI 3 (n=1), NESI 4 (n=2), NESI 5 (n=1), NESI 6 (n=0), NES( 7 (n=1), NESI 8 (n=1). Mortality was 4/17 patients, all had NESI ≧5. TCC values ranged from 647–6461 ng/ml (normal range: 130–360 ng/ml); and was not correlated to NESI. TNFα values ranged from 10–910 pg/ml and were correlated to NESI (r 2=0.71,n=17,P〈0.001). In patients with fatal outcome, TNFα was 600±160 pg/ml (mean±SEM) and in surviving patients 130±50 pg/ml (mean ± SEM). TNFα was increased in 15/17 patients when compared to normal controls (〈27 pg/ml). Conclusion The NESI is based on few clinical, objective data, that are available in every hospital. NESI appears to offer an instrument: (1) for making decisions in regard to appropriate monitoring and treatment of vital organ function; and (2) for assessing the quality of care for this life-threatening infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01957501
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