Postsurgical reduction of serum lipoproteins: Interleukin-6 and the acute-phase response

Akgün, Suat; Ertel, Norman H.; Mosenthal, Anne C.; Oser, William

doi:10.1016/s0022-2143(98)90083-x

Cited by 60 publications

(48 citation statements)

References 12 publications

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“…Similar decreases were noted in serum concentrations of HDL and LDL-cholesterol 38 . There is increasing evidence that cholesterol metabolism is related to inflammation [39][40][41] , and indeed, may regulate and be regulated by proinfl ammatory cytokines [42][43][44][45] .…”

Section: Mechanisms Of Cholesterol Defi Ciencysupporting

confidence: 76%

Hypocholesterolemia in Clinically Serious Conditions - Review

Vyroubal¹,

Chiarla²,

Giovannini³

et al. 2008

BIOMED PAP

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Background:Cholesterol is an essential component of cell membranes, precursor of steroids, biliary acids and other components of serious importance in live organism. Cholesterol synthesis is a complicated and energy-demanding process. Real daily need of cholesterol and mechanisms of decline cholesterol levels in critical ill are unknown. During stressful situations a signifi cant hypocholesterolaemia may be found. Hypocholesterolemia has been known for a number of years to be a signifi cant prognostic indicator of increased morbidity and mortality connected with a whole spectrum of pathological conditions. The aim of article is the elucidation of the role and importance of hypocholesterolaemia during the intensive care. . Methods and Results:We examined studies that are engaged in problems of hypocholesterolemia in critically ill. Very low levels of total as well as LDL cholesterol are most frequently found in serious polytrauma, after extensive surgery, in serious infections, in protracted hypovolemic shock. It is still not clear whether hypocholesterolemia refl ects only a serious metabolic disorder, which results from a life-threatening condition, or whether it has an active role in evolution and outcome.Conclusions: Hypocholesterolemia is commonly observed in critically ill patients. Nevertheless, it is not known whether it is a secondary manifestation of disease, or whether it actively contributes to deterioration of the disease. Although the contribution of hypocholesterolemia to mortality is modest compared with known risk factors such as increased severity of illness and the development of nosocomial infection, low serum lipid concentrations represent a potential therapeutic target in sepsis.

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Section: Mechanisms Of Cholesterol Defi Ciencysupporting

confidence: 76%

Hypocholesterolemia in Clinically Serious Conditions - Review

Vyroubal¹,

Chiarla²,

Giovannini³

et al. 2008

BIOMED PAP

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“…18 Because the impact of major inflammatory response on Lp(a) had not been examined, we performed in the present study serial measurements of plasma levels of Lp(a) in subjects admitted to the intensive care unit (ICU) for sepsis or extensive burns, 2 conditions characterized by a pronounced systemic inflammatory response syndrome (SIRS), low plasma levels of total, HDL, and LDL cholesterol, 19,20 and high concentrations of cytokines, such as tumor necrosis factor-␣ (TNF-␣) 21 and interleukin (IL)-6. 22 To our surprise, we observed a pronounced reduction in plasma Lp(a) levels that closely paralleled the changes in LDL cholesterol levels.…”

mentioning

confidence: 55%

Major Reduction in Plasma Lp(a) Levels During Sepsis and Burns

Mooser¹,

Berger²,

Tappy³

et al. 2000

ATVB

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Abstract-Plasma levels of lipoprotein(a) [Lp(a)], an atherogenic particle, vary widely between individuals and are highly genetically determined. Whether Lp(a) is a positive acute-phase reactant is debated. The present study was designed to evaluate the impact of major inflammatory responses on plasma Lp(a) levels. Plasma levels of C-reactive protein (CRP), low density lipoprotein cholesterol, Lp(a), and apolipoprotein(a) [apo(a)] fragments, as well as urinary apo(a), were measured serially in 9 patients admitted to the intensive care unit for sepsis and 4 patients with extensive burns. Sepsis and burns elicited a major increase in plasma CRP levels. In both conditions, plasma concentrations of Lp(a) declined abruptly and transiently in parallel with plasma low density lipoprotein cholesterol levels and closely mirrored plasma CRP levels. In 5 survivors, the nadir of plasma Lp(a) levels was 5-to 15-fold lower than levels 16 to 18 months after the study period. No change in plasma levels of apo(a) fragments or urinary apo(a) was noticed during the study period. Turnover studies in mice indicated that clearance of Lp(a) was retarded in lipopolysaccharide-treated animals. Taken together, these data demonstrate that Lp(a) behaves as a negative acute-phase reactant during major inflammatory response. Nongenetic factors have a major, acute, and unexpected impact on Lp(a) metabolism in burns and sepsis. Identification of these factors may provide new tools to lower elevated plasma Lp(a) levels. (Arterioscler Thromb Vasc

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“…IL-6 is a cytokine with multiple and complex endocrine effects on lipid metabolism: administration of IL-6 to nonhuman primates 10 and cancer patients 11 resulted in a decrease of total cholesterol levels, whereas in healthy volunteers, it caused a significant increase in total cholesterol. 24 In patients with myocardial infarction, 25 after major surgery, 26,27 or on hemodialysis, 28 circulating IL-6 levels are correlated negatively with total cholesterol levels. Thus, the molecular and cellular mechanisms that elicit IL-6 effects on lipoprotein metabolism need further investigation.…”

Section: Schieffer Et Al Interleukin-6 In Experimental Atherosclerosimentioning

confidence: 99%

Impact of Interleukin-6 on Plaque Development and Morphology in Experimental Atherosclerosis

Schieffer

Selle²,

Hilfiker³

et al. 2004

Circulation

277

181

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Background— Vascular lipid accumulation and inflammation are hallmarks of atherosclerosis and perpetuate atherosclerotic plaque development. Mediators of inflammation, ie, interleukin (IL)-6, are elevated in patients with acute coronary syndromes and may contribute to the exacerbation of atherosclerosis. Methods and Results— To assess the role of IL-6 in atherosclerosis, ApoE −/− – IL-6 −/− double-knockout mice were generated, fed a normal chow diet, and housed for 53±4 weeks. Mortality and blood pressure were unaltered. However, serum cholesterol levels and subsequent atherosclerotic lesion formation (oil red O stain) were significantly increased in ApoE −/− – IL-6 −/− mice compared with ApoE −/− , wild-type (WT), and IL-6 −/− mice. Plaques of ApoE −/− – IL-6 −/− mice showed significantly reduced transcript and protein levels of matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, collagen I and V, and lysyl oxidase (by reverse transcriptase-polymerase chain reaction and immunohistochemistry). Recruitment of macrophages and leukocytes (Mac3- and CD45-positive staining) into the atherosclerotic lesion was significantly reduced in ApoE −/− – IL-6 −/− mice. The transcript and serum protein (ELISA) levels of IL-10 were significantly reduced. Conclusions— Thus, a lifetime IL-6 deficiency enhances atherosclerotic plaque formation in ApoE K −/− – IL-6 −/− mice and leads to maladaptive vascular developmental processes. These observations are consistent with the notion that baseline levels of IL-6 are required to modulate lipid homeostasis, vascular remodeling, and plaque inflammation in atherosclerosis.

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Postsurgical reduction of serum lipoproteins: Interleukin-6 and the acute-phase response

Cited by 60 publications

References 12 publications

Hypocholesterolemia in Clinically Serious Conditions - Review

Hypocholesterolemia in Clinically Serious Conditions - Review

Major Reduction in Plasma Lp(a) Levels During Sepsis and Burns

Impact of Interleukin-6 on Plaque Development and Morphology in Experimental Atherosclerosis

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