[Septicemia and systemic inflammatory response]. / Setticemia e risposta infiammatoria sistemica.

To determine the relation between endocarditis/septicemia and systemic inflammatory response syndrome (SIRS), septic shock, MODS, we performed a retrospective analysis in 196 HIV-negative patients, with endocarditis/septicemia. No deaths were observed between 20 patients with endocarditis without severe infective SIRS/septic shock. On the other hand among 10 patients with endocarditis with severe infective SIRS/septic shock we registered 3 deaths (P = 0.052). No deaths were registered among 93 patients with septicemia without severe infective SIRS/septic shock. Between 73 patients with septicemia and severe infective SIRS/septic shock 9 (12.3%) patients died and, precisely, 7/61 in severe infective SIRS (11.4%) and 2/.12 (16.6%) in septic shock (P = 0.003). The definition of septicemia according to Schottmüller (1914), as a generalized bacterial infection with a persistent bacteremia is still justified. The term "sepsis" has become ambiguous because it has been used as synonym of "acute response to infection", while in the past and presently, at least in Europe, it is synonym of septicemia, persistent bacteremia. The term of SIRS could avoid the misunderstanding. The words: "infective SIRS", "severe infective SIRS", may label properly the reactive events mounted by the host as a useful defence against infections but they become dangerous and bring about septic shock, organ failure and mortality when excessive.

Pattern of lecithin-cholesterol-acyl-transferase (L-CAT) activity in the course of liver cirrhosis.

Considering liver cirrhosis a limit model, and therefore a condition suitable for the analysis of changes of lipid metabolism in liver disorders generally, the authors examined the L-CAT pattern, total and free cholesterol, HDL-cholesterol and APO-A in sixty-five subjects; fifty-three were suffering from liver cirrhosis, and were subdivided into those who were diabetic in addition, and those who were not, as well as according to the severity and duration of the liver disease; the remaining twelve were healthy controls. Analysis of the findings showed L-CAT to diminish significantly as the metabolic changes due to liver injury worsen. Contrary to the other parameters studied, L-CAT was the only one for which significant changes were found on analysis of variance comparing non-diabetic cirrhotics of varying severity. Further comparison suggested the idea that the reduction of L-CAT activity was correlated to the rate of progression of the disease rather than to the temporary condition of compensation or decompensation, so much so as to suggest itself as a valid parameter for the prognosis of liver cirrhosis.