Dramatic atherosclerotic vascular burden in a patient with familial lecithin-cholesterol acyltransferase (LCAT) deficiency

Scarpioni, Roberto; Paties, Carlo; Bergonzi, G.

doi:10.1093/ndt/gfm760

Cited by 17 publications

(6 citation statements)

References 3 publications

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“…Serum LCAT activity is markedly reduced in end stage renal disease (ESRD) patients and may dramatically impact on the increased risk of premature atherosclerosis in familial LCAT deficiency, as previously reported in our experience [13].…”

Section: Pathophysiology Of Dyslipidemiasupporting

confidence: 69%

Dyslipidemia in Chronic Kidney Disease: Are Statins Still Indicated in Reduction Cardiovascular Risk in Patients on Dialysis Treatment?

Scarpioni¹,

Ricardi²,

Melfa³

et al. 2010

Cardiovascular Therapeutics

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SUMMARYBackground: Chronic kidney disease (CKD) is an increasingly health disease all around the world with a high burden of mortality and cardiovascular (CV) morbidity rate. Even when renal replacement therapy is reached, more than half patients die, mainly for CV causes due either to uremiarelated cardiovascular risk factors (such as anemia, hyperhomocysteinemia, mineral bone disease-CKD with hyperparathyroidism, oxidative stress, hypoalbuminemia, chronic inflammation, prothrombotic factors) or to traditional ones (age, male gender, diabetes, obesity, hypertension, smoking, insulin levels, family history, dyslipidemia). Among the latter causes dyslipidemia represents one of the major, potentially correctable risk factor. Methods and Results:Statins have demonstrated to effectively and safely reduce cholesterol levels in CKD patients. Here we will examine the effects of statins on CV risk factors in CKD patients and particularly in patients on dialysis treatment, in the light of the unfavorable results of the large trials 4D and AURORA, recently published, underlining the role of malnutrition/ inflammation as confounding factor. Probably it will be that only with a real prevention, starting statins even in the early stages of CKD, as indicated by post hoc analysis of large trials, that we will reach results in reducing the mortality rate in CKD patients. In the meanwhile, all the other remediable CV risk factors have to be at the same time corrected.

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Section: Pathophysiology Of Dyslipidemiasupporting

confidence: 69%

Dyslipidemia in Chronic Kidney Disease: Are Statins Still Indicated in Reduction Cardiovascular Risk in Patients on Dialysis Treatment?

Scarpioni¹,

Ricardi²,

Melfa³

et al. 2010

Cardiovascular Therapeutics

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“…Very recently, in obstruction with necrosis of two toes of his left foot and angina at rest with trivasal occlusive coronary artery disease at coronarography ( 110 ). Eventually this patient died at the age of 42 after a right femoral-axillo artery bypass and a thigh amputation.…”

Section: Lcat and Atherosclerosis In The General Populationmentioning

confidence: 95%

Lecithin:cholesterol acyltransferase: old friend or foe in atherosclerosis?

Kunnen

Eck

2012

Journal of Lipid Research

153

124

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“…Furthermore, overexpression of LCAT, even when coexpressed with scavenger receptor class B type I and CETP, failed to increase RCT in macrophages although HDL-C was significantly enhanced [ 77 ]. Measurement of the arterial intima media thickness in patients with LCAT genetic deficiencies, as well as other parameters, compared to normal controls, have been reported to both show [ 78 , 79 ] and not show [ 80 ] signs of atherosclerosis in the former. On the other hand, it has long been known that mutations in the LCAT gene in humans cause familial LCAT deficiency or fish eye disease [ 81 , 82 ].…”

Section: Hdl: the Goodmentioning

confidence: 99%

Cholesterol: The Good, the Bad, and the Ugly - Therapeutic Targets for the Treatment of Dyslipidemia

2013

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Maintaining cholesterol and triglyceride (TG) levels within healthy limits is critical for decreasing the risk of heart disease. Dyslipidemia refers to the abnormal levels of lipids in the blood, including low high-density lipoprotein cholesterol (HDL-C), also known as good cholesterol, high low-density lipoprotein cholesterol (LDL-C), also known as bad cholesterol, and/or high TG levels that contribute to the development and progression of atherosclerosis. In this article we reviewed some of the current therapeutic targets for the treatment of dyslipidemia, with a primary focus on endothelial lipase and lecithin cholesterol acyl transferase for raising HDL-C, and the proprotein convertase subtilisin-like kexin type 9 (PCSK9), microsomal triglyceride transfer protein, and the messenger RNA of apolipoprotein B for lowering LDL-C. In addition, we reviewed the role of apolipoprotein AI (apoAI) in raising HDL-C, where we discuss three apoAI-based drugs under development. These are its mutated dimer (apoAI-Milano), a complex with phospholipids, and a mimetic peptide. Atherosclerosis, mainly because of dyslipidemia, is a leading cause of cardiovascular disease. Regarding the title of this article, the ‘good' refers to HDL-C, the ‘bad' refers to LDL-C, and the ‘ugly' refers to atherosclerosis.

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Dramatic atherosclerotic vascular burden in a patient with familial lecithin-cholesterol acyltransferase (LCAT) deficiency

Cited by 17 publications

References 3 publications

Dyslipidemia in Chronic Kidney Disease: Are Statins Still Indicated in Reduction Cardiovascular Risk in Patients on Dialysis Treatment?

Dyslipidemia in Chronic Kidney Disease: Are Statins Still Indicated in Reduction Cardiovascular Risk in Patients on Dialysis Treatment?

Lecithin:cholesterol acyltransferase: old friend or foe in atherosclerosis?

Cholesterol: The Good, the Bad, and the Ugly - Therapeutic Targets for the Treatment of Dyslipidemia

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