Hypocholesterolemia in the acute phase of inflammation during sepsis
Hypocholesterolemia in the acute phase of inflammation during sepsis
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DOI：
10.1016/s0248-8663(97)80715-1
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发表时间：
1998-03-01
影响因子：
0.9
通讯作者：
Magnette, J
中科院分区：
文献类型：
--
作者：
Bentz, MH;Magnette, J
目标. - 长期以来，许多作者在细菌感染过程中观察到脂质、胆固醇和类胡萝卜素血浆水平的一过性变化，急性期出现低胆固醇血症、高胆固醇血症，增加了临床进展的第三天。它们的减少伴随着恢复正常。在细菌感染期间也观察到淋巴细胞减少症，并且由于胆固醇水平非常低，被认为是关键预后的因素，预测不利的演变，主要是在老年人中。C-反应蛋白（CRP）是脓毒症炎症反应的良好标志蛋白，其合成直接受细菌感染炎症反应急性期释放的细胞因子的影响。作者正在研究由CRP水平代表的急性期反应强度与胆固醇水平降低、高脂血症或淋巴细胞减少之间的相关性。- 在这项前瞻性研究中，采集了160例患者的空腹血样，根据CRP水平分为4组，每组40例，包括见证组（CRP水平低于10 mg/L）和3组表现为不同强度急性期反应的感染性疾病患者。所有患者均检测胆固醇、血脂、CRP水平及血细胞计数。三个病理组进行了比较，证人组和彼此：结果，-一个显着的相关性之间建立了脓毒症和胆固醇水平降低的急性期反应的强度。与目击组相比，所有三个病理组的胆固醇血症均降低（P < 0.05）;当观察到低强度炎症反应时存在差异（第1组的平均CRP水平为27.6（10.5）mg/L）。此外，第4组（平均CRP水平250（73）mg/L）和第1组之间存在显著的降低胆固醇水平的反应。在所有三个病理组中均观察到淋巴细胞减少，与CRP水平无明显联系。未观察到关于类胡萝卜素水平的改变。- 作者报道了在感染性疾病的早期阶段，总胆固醇与CRP水平呈负相关。先前的研究建立了细菌感染期间的炎症参数与总胆固醇和HDL分数之间的负相关性。考虑到血浆脂质途径，HDL组分由于其载脂蛋白A1、A2和C而在脂质转运和脂蛋白之间的交换中起主要作用。IL-1和TNF是参与急性期反应的两种细胞因子，具有降低血浆总胆固醇和HDL-2的代谢功能。IL-1还诱导淋巴细胞减少症。作者提出了脓毒症急性期反应与血浆胆固醇水平相关的假说，认为脓毒症急性期反应可由炎症介质或效应物引起。(C)1998年，爱思唯尔，巴黎。
Objectives. - Transitory changes in the plasma levels of lipids, cholesterol and triglycerids have been observed since a long time by many authors, in the course of bacterial infections, with hypocholesterolemia, hypertriglyceridemia in the acute phase, increasing the third day of clinical evolution. Their decrease accompanies the return to normal. Lymphopenia is also observed during bacterial infections and as the very low level of cholesterol, is considered to be a factor of critical prognosis, predicting an unfavorable evolution, essentially in elderly people. C-reactive proteine (CRP) proles to be a good marker protein in inflammation die to sepsis, its synthesis is directly influenced by the cytokines released during the acute phase response of inflammation in bacterial infection. The authors are researching a correlation between the intensity of the acute phase response represented by CRP levels, and a reduced cholesterol level, or a hypertriglyceridemia, or lymphocytopenia.Methods. - In this prospective study, blood samples at fasting state were obtained in 160 patients divided into four groups of 40 according to CRP levels, including a witness group (CRP levels lower than 10 mg/L) and three groups of patients presenting infectious diseases with acute phase response of different intensities. All patients were checked for cholesterol, triglycerid and CRP levels, blood cell count. The three pathologic groups were compared to the witness group and to each other:Results, - A significant correlation was established between the intensity of the acute phase response during sepsis and reduced levels of cholesterol. Cholesterolemia was reduced (P < 0.05) in all three pathologic groups when compared to the witness group; the difference existed when a low intensity inflammatory response was observed (mean CRP level 27.6 (10.5) mg/L in group 1). Moreover a significant response exists with reduced cholesterol levels between group 4 (mean CRP level 250 (73) mg/L) and group 1. Lymphocytopenia was observed in all three pathologic groups, without evident link with the CRP levels. No modification was observed concerning triglycerid levels.Conclusions. - The authors report a negative correlation of total cholesterol to CRP levels at the early stage of infections diseases. Prior studies established a negative correlation between inflammatory parameters during bacterial infections and total cholesterol and HDL fraction. Considering the plasma lipid pathways, HDL fraction plays a major role in lipid transport and exchanges between lipoproteins, thanks to its apolipoproteins A1, A2 and C. IL-1 and TNF, two cytokines involved in the acute phase response, have metabolic functions which could possibly contribute to reduce plasma total cholesterol and HDL2 fraction. IL-1 also induces lymphocytopenia. The authors propose the hypothesis of a correlation between plasma cholesterol levels and rite acute phase response during sepsis, wich could be induced by the mediators or effecters of inflammation. (C) 1998, Elsevier, Paris.