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1.
Eur J Clin Microbiol Infect Dis ; 36(3): 523-528, 2017 Mar.
Article in English | MEDLINE | ID: mdl-27815777

ABSTRACT

Early-onset pneumonia (EOP) is frequent after burn trauma, increasing morbidity in the critical resuscitation phase, which may preclude early aggressive management of burn wounds. Currently, however, preemptive treatment is not recommended. The aim of this study was to identify predictive factors for EOP that may justify early empirical antibiotic treatment. Data for all burn patients requiring ≥4 h mechanical ventilation (MV) who were admitted between January 2001 and October 2012 were extracted from the hospital's computerized information system. We reviewed EOP episodes (≤7 days) among patients who underwent endotracheal aspiration (ETA) within 5 days after admission. Univariate and multivariate analyses were performed to identify independent factors associated with EOP. Logistic regression was used to identify factors predicting EOP development. During the study period, 396 burn patients were admitted. ETA was performed within 5 days in 204/290 patients receiving ≥4 h MV. One hundred and eight patients developed EOP; 47 cases were caused by Staphylococcus aureus, 37 by Haemophilus influenzae, and 23 by Streptococcus pneumoniae. Among the 33 patients showing S. aureus positivity on ETA samples, 16 (48.5 %) developed S. aureus EOP. Among the 156 S. aureus non-carriers, 16 (10.2 %) developed EOP. Staphylococcus aureus carriage independently predicted EOP (p < 0.0001). We identified S. aureus carriage as an independent and strong predictor of EOP. As rapid point-of-care testing for S. aureus is readily available, we recommend testing of all patients at admission for burn trauma and the consideration of early preemptive treatment in all positive patients. Further studies are needed to evaluate this new strategy.


Subject(s)
Burns/complications , Carrier State/microbiology , Pneumonia, Staphylococcal/epidemiology , Staphylococcus aureus/isolation & purification , Wounds and Injuries/complications , Adult , Female , Humans , Male , Middle Aged , Pneumonia, Staphylococcal/microbiology , Pneumonia, Staphylococcal/therapy , Respiration, Artificial/statistics & numerical data , Retrospective Studies , Risk Assessment
2.
Nat Med ; 5(9): 1044-7, 1999 Sep.
Article in English | MEDLINE | ID: mdl-10470082

ABSTRACT

Hemophilia A is an X chromosome-linked recessive disorder resulting in defective or deficient factor VIII (FVIII) molecules, which, in its severe form, is a life-threatening and crippling hemorrhagic disease. Infusion of homologous FVIII to patients with severe hemophilia A results, in 25% of patients, in the emergence of alloantibodies against FVIII (inhibitors)( ref. 1) that inhibit FVIII procoagulant activity by steric hindrance of the interaction of FVIII either with stabilizing molecules, with molecules essential for its activity or with activating molecules. Here, we report on the proteolysis of FVIII by alloantibodies of two patients with severe hemophilia A, demonstrating a previously unknown mechanism by which FVIII inhibitors may prevent the pro-coagulant function of FVIII. The kinetic parameters of FVIII hydrolysis indicate a functional role for the catalytic immune response in the inactivation of FVIII in vivo. The characterization of alloantibodies against FVIII as site-specific proteases may provide new approaches to the treatment of FVIII inhibitors.


Subject(s)
Antibodies, Catalytic/metabolism , Endopeptidases/metabolism , Factor VIII/immunology , Hemophilia A/immunology , Isoantibodies/metabolism , Antibodies, Catalytic/immunology , Antibodies, Catalytic/isolation & purification , Binding, Competitive , Endopeptidases/immunology , Endopeptidases/isolation & purification , Factor VIII/antagonists & inhibitors , Factor VIII/metabolism , Hemophilia A/enzymology , Humans , Hydrolysis , Immunoglobulin G/immunology , Immunoglobulin G/isolation & purification , Immunoglobulin G/metabolism , Isoantibodies/immunology , Isoantibodies/isolation & purification , Kinetics , von Willebrand Factor/metabolism
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