Articles: sepsis.
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Nihon Geka Gakkai zasshi · Dec 1996
Review[Prevention and treatment of postoperative septic MOF and DIC and efficacy of blood purification].
Pathophysiologic concept of SIRS has been proposed for the better management of postoperative severe infection and septic MOF, and the concept has been found to be very useful. It is very important to identify the high risk SIRS patients of the development of septic MOF and to treat those patients aggressively to prevent the development of septic MOF. ⋯ CHDF has been claimed to be very effective to removal of causative humoral mediators from the blood stream. The concept of DIC has been changed recently and the concept of DII (disseminated intravascular inflammation) should be applied instead of DIC, since the main feature of this pathologic condition is the damage of endothelial cells due to extensive systemic inflammation.
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Blood levels of various cytokines were determined in patients with burn injury immediately after the accident, and the relationship between cytokines and morbid condition was investigated. There was almost no marked elevation of cytokines in the early stage of burn injury. Throughout the entire course, tumour necrosis factor alpha, interleukin 6 and interleukin 8, as cytokines, showed high levels in patients with burn injury associated with sepsis and those who died. These levels well reflected the severity in the phase complicated with sepsis.
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Nihon Geka Gakkai zasshi · Dec 1996
Review[Cytokine-mediated biological response to severe infections in surgical patients].
Cytokines serve to initiate the acute inflammatory response and to integrate nonspecific and specific immunological responses to infections occurring in perioperative patients. Microbial substances induce macrophages to produce pivotal cytokines (TNF-alpha and IL-1 beta). This results in an activation of other cytokine productions including IL-2, IL-3, IL-4, IL-6, chemokines, and IL-10. ⋯ This condition is termed "Cytokine Storm" by the author. In cytokine storm, not only proinflamamtory cytokines, but also anti-inflammatory cytokines appear in circulating blood, leading to septic shock, multiple organ dysfunction, and immunosuppression. With further understanding of the roles of cytokines in sepsis, modulation of cytokine responses could be a new modality of the treatment.
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Critical care medicine · Dec 1996
Comparative StudyAcute-phase gene expression correlates with intrahepatic tumor necrosis factor-alpha abundance but not with plasma tumor necrosis factor concentrations during sepsis/systemic inflammatory response syndrome in the rat.
To test the hypothesis that after cecal ligation and puncture in the rat, there is increased expression of the tumor necrosis factor (TNF)/interleukin-1-dependent, acute-phase reactant alpha 1-acid glycoprotein in the liver, and that this change correlates temporally with increased abundance of TNF-alpha in the hepatic parenchyma but not with circulating concentrations of TNF-alpha. ⋯ The changes in TNF-alpha-dependent hepatic gene expression that accompany an animal model of the systemic inflammatory response syndrome correlate with intrahepatic, and not circulating, TNF-alpha concentrations and reflect paracrine, and not endocrine, activity. Therefore, plasma concentrations of TNF-alpha do not appropriately reflect hepatocellular responses during the systemic inflammatory response syndrome.
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Exposure to endotoxin produces a state of macrophage hyporesponsiveness on subsequent stimulation. Monocytes in patients with septic shock demonstrate a similar hyporesponsiveness to endotoxin. The purpose of this study was to examine whether this state of hyporesponsiveness extends to other inflammatory stimuli and the relationship of this state to cell surface receptor expression and the release of anti-inflammatory cytokines. ⋯ TGF-beta1 levels were decreased in patients with septic shock (25 +/- 6 pg/ml) as compared with those in normal subjects (37 +/- 2 pg/ml)(p < 0.05). PGE2 levels were significantly increased in patients with septic shock and patients with sepsis. These data are consistent with a more generalized monocyte hyporesponsiveness to bacterial toxins that may be related to altered cell surface receptor expression and the release of anti-inflammatory cytokines.