M H Bentz1, J Magnette. 1. Service de médecine interne à orientation pneumologique, centre hospitalier André-Boulloche, Montbéliard, France.
Abstract
OBJECTIVES: Transitory changes in the plasma levels of lipids, cholesterol and triglycerides 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 protein (CRP) proves to be a good marker protein in inflammation due 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, triglyceride 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 triglyceride 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 the acute phase response during sepsis, which could be induced by the mediators or effectors of inflammation.
OBJECTIVES: Transitory changes in the plasma levels of lipids, cholesterol and triglycerides 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 protein (CRP) proves to be a good marker protein in inflammation due 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, triglyceride 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 triglyceride 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 the acute phase response during sepsis, which could be induced by the mediators or effectors of inflammation.