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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperlipidaemia has become generally accepted as a cause of coronary artery atherosclerosis, arterial occlusion and subsequent myocardial infarction. This may be true in a few people with lipid intolerance, but for the majority, hyperlipidaemia represents a normal physiological response to another pathological process. One such disease process involves the vessel wall, which appears to suffer injury. The cause of the injury may be associated with abnormal movement in the wall and this in turn can be provoked by stress. A hypothesis encompassing these observations is proposed. It would therefore appear that hyperlipidaemia is not a cause of arterial disease, but as part of normal homeostasis, it can be a risk indicator. It is dangerous to consider hyperlipidaemia as a cause of myocardial infarction as this leads to inappropriate treatment. The lowering of cholesterol and low density lipoproteins (LDL) by any means other than sensible dieting may be likened to attempts to lower elevated white blood cell counts in cases of bacterial pneumonia, without treating the pneumonia.
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PMID:Hyperlipidaemia and atherogenesis. 229 87

Hyperlipidemia has been extensively studied in the context of atherosclerosis, whereas the potential health consequences of the opposite extreme, hypolipidemia, remain largely uninvestigated. Circulating lipoproteins are essential carriers of insoluble lipid molecules and are increasingly recognized as innate immune effectors. Importantly, severe hypolipidemia, which may occur with trauma or critical illness, is clinically associated with bacterial pneumonia. To test the hypothesis that circulating lipoproteins are essential for optimal host innate defense in the lung, we used lipoprotein-deficient mice and a mouse model of Staphylococcus aureus pneumonia in which invasive infection requires virulence factor expression controlled by the accessory gene regulator (agr) operon. Activation of agr and subsequent virulence factor expression is inhibited by apolipoprotein B, the structural protein of low-density lipoprotein, which binds and sequesters the secreted agr-signaling peptide (AIP). In this article, we report that lipoprotein deficiency impairs early pulmonary innate defense against S. aureus quorum-sensing-dependent pathogenesis. Specifically, apolipoprotein B levels in the lung early postinfection are significantly reduced with lipoprotein deficiency, coinciding with impaired host control of S. aureus agr-signaling and increased agr-dependent morbidity (weight loss) and inflammation. Given that lipoproteins also inhibit LTA- and LPS-mediated inflammation, these results suggest that hypolipidemia may broadly impact posttrauma pneumonia susceptibility to both Gram-positive and -negative pathogens. Together with previous reports demonstrating that hyperlipidemia also impairs lung innate defense, these results suggest that maintenance of normal serum lipoprotein levels is necessary for optimal host innate defense in the lung.
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PMID:Serum Lipoproteins Are Critical for Pulmonary Innate Defense against Staphylococcus aureus Quorum Sensing. 2660 23