Chagas' disease (American trypanosomiasis) is a very uncommon disease in non-endemic areas. A few cases in immunosuppressed patients have been reported in America. This report describes, to our knowledge, the first fatal case of acute Chagas' disease in Europe following bone marrow transplantation.
In septic shock, hypotension, disseminated intravascular coagulation, and neutrophil activation are related to the activation of the blood coagulation contact system. This study evaluates in dogs the effect of the Cl-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associated with endotoxic shock. Two groups were included: controls, which received Escherichia coli endotoxin, and a C1-INH group in which Cl-INH was infused before E. coli endotoxin administration.In both groups, endotoxin produced hypodynamic shock; however, the decrease in the systolic index and the ventricular systolic work indexes were greater in controls than the C1-INH group. In controls, the arterial 02 partial pressure decreased by 30% and the alveolo-arterial 02 difference increased by 625%, these parameters remained unchanged in the C1-INH group. Hypoxemia was associated with increased intrapulmonary shunt, decreased blood coagulation contact factors, and decreased C3c. In contrast, C1-INH administration prevented endotoxin-induced hypoxemia, the increase in intrapulmonary shunt, and the decrease in blood coagulation contact factors.This study shows that, in dogs with endotoxic shock, pulmonary dysfunction is associated with an activation of the blood coagulation contact phase system. An inhibition of this system by C1-INH prevented the hypoxemia induced by endotoxic shock. (J. Clin. Invest. 1993.91:2754-2760
This study evaluates the contact system, coagulation inhibitors and fibrinolysis in 23 full-term newborns with sepsis (8 with septic shock). The results were compared with a group of 20 healthy newborns. Blood samples were obtained at the time of clinical diagnosis and 3 days after the antibiotic therapy was started. The results showed that: severe infection was associated with activation of the contact system, depletion of anticoagulant proteins and elevation of C4b-binding protein levels. There was a shift in protein S to the complexed inactive form, and the thrombin-antithrombin complexes increased. These changes occurred in parallel to both activation and inhibition of fibrinolysis. These changes were more pronounced in the septic shock patients than in nonshock neonates. After therapy, this procoagulant state decreased among survivor patients while in those who died, the abnormalities in coagulation did not improve. Our study suggests that neonatal sepsis induces a hypercoagulable state that persists in nonsurvivor neonates despite a correct treatment.
The results suggest that apoptosis occurs during meniscus cryopreservation. The major findings of this study are cellular damage in meniscus cryopreservation suggesting apoptosis-mediated cell loss. The findings reported herein encourage to further investigations in preservation procedures to enhance maximum long-term clinical survival.
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