ABSTRACT
Sepsis is a systemic inflammatory response syndrome in the presence of suspected or proven infection; and it may progress to or encompass organ failure (severe sepsis) and hypotension (septic shock). Clinicians possess an arsenal of supportive measures to combat severe sepsis and septic shock; and some success; albeit controversial; has been achieved by using low doses of corticosteroids or recombinant human activated protein C. However; a truly effective mediator-directed specific treatment has not been developed yet. Treatment with low doses of corticosteroids or with recombinant human activated protein C remains controversial and its success very limited. Attempts to treat shock by blocking LPS; TNF or IL-1 were unsuccessful; as were attempts to use interferon-gamma or granulocyte colony stimulating factor. Inhibiting nitric oxide synthases held promise but met with considerable difficulties. Scavenging excess nitric oxide or targeting molecules downstream of inducible nitric oxide synthase; such as soluble guanylate cyclase or potassium channels; might offer other alternatives
Subject(s)
Adrenal Cortex Hormones , Nitric Oxide , Protein C , Sepsis/therapyABSTRACT
Sepsis is a systemic inflammatory response syndrome in the presence of suspected or proven infection; and it may progress to or encompass organ failure (severe sepsis) and hypotension (septic shock). Clinicians possess an arsenal of supportive measures to combat severe sepsis and septic shock; and some success; albeit controversial; has been achieved by using low doses of corticosteroids or recombinant human activated protein C. However; a truly effective mediator-directed specific treatment has not been developed yet. Treatment with low doses of corticosteroids or with recombinant human activated protein C remains controversial and its success very limited. Attempts to treat shock by blocking LPS; TNF or IL-1 were unsuccessful; as were attempts to use interferon-gamma or granulocyte colony stimulating factor. Inhibiting nitric oxide synthases held promise but met with considerable difficulties. Scavenging excess nitric oxide or targeting molecules downstream of inducible nitric oxide synthase; such as soluble guanylate cyclase or potassium channels; might offer other alternatives
Subject(s)
Nitric Oxide , Protein C , SepsisABSTRACT
L'objectif de cette etude est de depister le deficit en proteine C dans une population de patients noirs africains atteints de maladie thromboembolique veineuse. C'est une etude descriptive transversale qui a inclus systematiquement tous les patients hospitalises pour MTEV aigue ou suivis dans les suites de MTEV qui ont accepte d'y participer. Un dosage quantitatif de la proteine C a ete realise sur un equipement de type Minividas. Le prelevement sanguin a ete effectue en dehors de tout traitement antivitamine K. Un deuxieme prelevement est effectue pour confirmation au cas ou le premier dosage affirme un deficit. En cas de deficit la recherche d'une etiologie acquise est systema- tique. Pour les 54 patients retenus la sex-ratio etait de 1;08 et l'age moyen est de 52;7+/- 14;1 ans. Un deficit en proteine C a ete diagnostique chez 9;3des patients et 12;5des patients presentant des criteres de thrombophilie ( p=1). Aucune etiologie acquise n'a ete mise en evidence