Articles: sepsis.
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The production by monocytes of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF alpha) in intensive care unit (ICU) patients with sepsis syndrome (n = 23) or noninfectious shock (n = 6) is reported. Plasma cytokines, cell-associated cytokines within freshly isolated monocytes and LPS-induced in vitro cytokine production were assessed at admission and at regular intervals during ICU stay. TNF alpha and IL-6 were the most frequently detected circulating cytokines. ⋯ This reduced LPS-induced production of cytokines was most pronounced in patients with gram-negative infections. Finally, monocytes from survival patients, but not from nonsurvival ones recovered their capacity to produce normal amounts of cytokines upon LPS stimulation. In conclusion, our data indicate an in vivo activation of circulating monocytes during sepsis as well as in noninfectious shock and suggest that complex regulatory mechanisms can downregulate the production of cytokines by monocytes during severe infections.
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Because of the potential importance of interleukin 1 (IL-1) in modulating inflammation and the observations that human blood neutrophils (PMN) express IL-1 receptors (IL-1R) and synthesize IL-1 alpha and IL-1 beta, we studied the IL-1R on blood PMN from a group of patients with the sepsis syndrome. We report a marked enhancement in the sites per cell of IL-1R expressed on sepsis-PMN of 25 consecutively studied patients compared to 20 controls (patient mean = 9,329 +/- 2,212 SE; control mean = 716 +/- 42 SE, respectively). There was no demonstrable difference in the Kd of IL-1R on sepsis-PMN (approximately 1 nM) as determined by saturation curves of 125I-IL-1 alpha binding and the IL-1R on sepsis-PMN had an apparent Mr approximately 68,000, a value like that of normal PMN. ⋯ Similar increases in expression of IL-1R were not observed in various other inflammatory processes, including acute disseminated inflammation and organ failure not caused by infection, acute infection without organ failure, and immunopathologies such as active systemic lupus erythematosus and rheumatoid arthritis. Enhanced expression of IL-1R was not related simply to the state of myeloid stimulation. Increased expression of IL-1R on normal PMN was induced in vitro by incubating cells with recombinant human granulocyte-macrophage/colony-stimulating factor for 18 h and this response was inhibited by cycloheximide, suggesting the possibility that de novo synthesis of IL-1R might occur in PMN during the sepsis syndrome.
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Embolic phenomena in patients with infective endocarditis may complicate the placement of a cardiac valvular prosthesis. To evaluate the vascular consequences of these emboli, a 15-year review of 102 patients undergoing valve replacement for proven infective endocarditis was undertaken. Thirty-one patients with 36 episodes of septic embolization were identified. ⋯ The presentation of peripheral vascular emboli is that of acute extremity ischemia. The diagnosis should be confirmed by angiography to rule out the possibility of multiple emboli. When possible, valve replacement should precede peripheral vascular management, which may include operative or medical components as dictated by the extent of limb ischemia.
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A new management approach to selected febrile infants 4 to 8 weeks old evaluated for possible sepsis is outpatient ceftriaxone therapy, with subsequent re-evaluation 24 to 48 hours after presentation. This study assessed whether the temperature profile of such infants during the 24- to 48-hour period after treatment distinguished those with from those without serious bacterial infections (SBIs). ⋯ Infants 4 to 8 weeks old who remain febrile during the 24 to 48-hour period after presentation and initiation of parenteral antibiotic therapy are less likely to have SBI. This study did not have sufficient power for this difference to be statistically significant.