Pathophysiologic correlates of hypocholesterolemia in critically ill surgical patients

Giovannini, Ivo; Boldrini, Giuseppe; Chiarla, Carlo; Giuliante, Felice; Vellone, Maria; Nuzzo, Gennaro

doi:10.1007/s001340050940

Cited by 66 publications

(49 citation statements)

References 8 publications

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“…Also, some of the reported effects of statin drugs on cell signaling and immunity may reflect altered lipid raft structure and function due to decreased cholesterol availability. Conversely, cholesterol deficiency could limit inflammatory responses, and indeed where decreased serum cholesterol occurs in trauma, burns, and other critical illnesses, it appears to predispose to sepsis and death (45)(46)(47)(48)(49). Practically speaking, these findings suggest cholesterol excess and deficiency states may alter cell signaling in ways that are modifiable by dietary or pharmacologic cholesterol control.…”

Section: Discussionmentioning

confidence: 99%

Free Cholesterol Alters Lipid Raft Structure and Function Regulating Neutrophil Ca2+ Entry and Respiratory Burst: Correlations with Calcium Channel Raft Trafficking

Kannan

Barlos

Hauser

2007

The Journal of Immunology

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Recent studies associate cholesterol excess and atherosclerosis with inflammation. The link between these processes is not understood, but cholesterol is an important component of lipid rafts. Rafts are thought to concentrate membrane signaling molecules and thus regulate cell signaling through G protein-coupled pathways. We used methyl β-cyclodextrin to deplete cholesterol from polymorphonuclear neutrophil (PMN) rafts and thus study the effects of raft disruption on G protein-coupled Ca2+ mobilization. Methyl β-cyclodextrin had no effect on Ca2+ store depletion by the G protein-coupled agonists platelet-activating factor or fMLP, but abolished agonist-stimulated Ca2+ entry. Free cholesterol at very low concentrations regulated Ca2+ entry into PMN via nonspecific Ca2+ channels in a biphasic fashion. The specificity of cholesterol regulation for Ca2+ entry was confirmed using thapsigargin studies. Responses to cholesterol appear physiologic because they regulate respiratory burst in a proportional biphasic fashion. Investigating further, we found that free cholesterol accumulated in PMN lipid raft fractions, promoting formation and polarization of membrane rafts. Finally, the transient receptor potential calcium channel protein TRPC1 redistributed to raft fractions in response to cholesterol. The uniformly biphasic relationships between cholesterol availability, Ca2+ signaling and respiratory burst suggest that Ca2+ influx and PMN activation are regulated by the quantitative relationships between cholesterol and other environmental lipid raft components. The association between symptomatic cholesterol excess and inflammation may therefore in part reflect free cholesterol- dependent changes in lipid raft structure that regulate immune cell Ca2+ entry. Ca2+ entry-dependent responses in other cell types may also reflect cholesterol bioavailability and lipid incorporation into rafts.

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Section: Discussionmentioning

confidence: 99%

Free Cholesterol Alters Lipid Raft Structure and Function Regulating Neutrophil Ca2+ Entry and Respiratory Burst: Correlations with Calcium Channel Raft Trafficking

Kannan

Barlos

Hauser

2007

The Journal of Immunology

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“…49 ). In companion in vitro studies, TNF increased the degradation of 125 I-LDL in human fi broblasts and endothelial cells, and in HepG2 hepatoma cells 35 . Hypocholesterolemia in critically ill surgical patients has been found to correlate with decrease in plasma proteins and hepatic protein synthesis 36 .…”

Section: Mechanisms Of Cholesterol Defi Ciencymentioning

confidence: 91%

“…31 ). A number of papers have reported a critical level of cholesterol of between 2.6 and 3.5 mmol/l of total cholesterol [32][33][34][35] . The cause of the low cholesterol and lipoprotein concentrations in acute illness is most likely multifactorial, involving both decreased synthesis and enhanced catabolism.…”

Section: Mechanisms Of Cholesterol Defi Ciencymentioning

confidence: 99%

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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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“…Beslenme yetersizliği, hepatik sentezin azalması ve proinflamatuvar sitokinlerin (IL-6, IL-10, TNF) lipid metabozlizması üzerine etkileri hipolipidemiye yol açabilir (11)(12)(13)(14)(15) . Ayrıca akut faz yanıtı olarak hipolipidemi görülebilir (16) .…”

Section: Kronik Hastalıklar Onkolojik Hastalıklar Ve Yoğun Bakım Hasunclassified

Hypolipodemias in children

Erdur¹,

Güzin²

2016

Buch

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ÖZPlazma lipoprotein düzeylerinin düşüklüğü ile karşımıza çıkan hipolipidemiler primer (genetik) veya sekonder (kazanılmış) nedenlere bağlı olabilir. Hiperlipidemilerin aksine, hipolipidemilerin neden ve sonuçları konularında klinisyenlerin farkındalığı çoğu zaman yeterli olmamaktadır. Bununla birlikte, hipolipidemiler altta yatan ciddi bir sorunun göstergesi olabilir. Açıklanamayan hipolipidemilerin olası nedenleri kesinlikle araştırılmalıdır. Bu makalede, çocuklarda primer ve sekonder hipolipidemilerin nedenleri ve mekanizmaları tartışılmıştır. Anahtar kelimeler: Hipolipidemi, çocuklar ABSTRACTHypolipidemia is defined as a decrease in plasma lipoprotein caused by primary (genetic) or secondary (acquired) factors. Unlike hyperlipidemia, physicians are usually inadequately aware of hypolipidemia, its causes and consequences. However, hypolipidemias can be a marker for an underlying, serious problem. Unexplained hypolipidemias should always be investigated for their possible causes. In this report, causes and mechanisms of primary and secondary hypolipidemias in children were discussed.

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Pathophysiologic correlates of hypocholesterolemia in critically ill surgical patients

Abstract: These results help to explain the dynamics of the development, clinical relevance, and negative prognostic value of hypocholesterolemia in critical illness.

Cited by 66 publications

References 8 publications

Free Cholesterol Alters Lipid Raft Structure and Function Regulating Neutrophil Ca2+ Entry and Respiratory Burst: Correlations with Calcium Channel Raft Trafficking

Free Cholesterol Alters Lipid Raft Structure and Function Regulating Neutrophil Ca2+ Entry and Respiratory Burst: Correlations with Calcium Channel Raft Trafficking

Hypocholesterolemia in Clinically Serious Conditions - Review

Hypolipodemias in children

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