Standardization of laboratory and lipid profile evaluation: A call for action with a special focus in 2016 ESC/EAS dyslipidaemia guidelines – Full report

Silva, Pedro Marqués da; Duarte, João Sequeira; Hafe, Pedro von; Gil, Víctor; Oliveira, Jorge Nunes de; Sousa, Germano de

doi:10.1016/j.atherosclerosissup.2018.04.001

Cited by 22 publications

(18 citation statements)

References 38 publications

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“…Clinically, lipid pro les such as TC and TG are routinely evaluated in patients with NS. De Silva et al recommended that the baseline lipid pro le, including TC, TG, HDL-C, and LDL-C, should be evaluated in children with SRNS [37]. Our results also propose the evaluation of lipid pro les and the need for careful characterization of patients.…”

Section: Resultssupporting

confidence: 52%

Markedly Increased Small Dense Low-Density Lipoprotein During Acute Phase in Childhood and Adolescent Nephrotic Syndrome

Sugimoto¹,

Miyazaki²,

Enya³

et al. 2020

Preprint

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Background: Hyperlipidemia is an important characteristic feature of idiopathic nephrotic syndrome (NS) in children. This study was conducted to examine the lipid profiles, including small dense low-density lipoprotein (sdLDL-C), in childhood-onset NS.Methods: This retrospective study enrolled patients diagnosed with initial-onset NS in childhood and adolescence. Study parameters included lipid profiles. The “alternative LDL window” comprises the number and sizes of LDL particles estimated according to non-HDL-C and TG levels.Results: A total of 39 patients were enrolled who exhibited markedly increased lipid abnormalities, including TC, TG, LDL-C, and non-HDL-C levels (TC, 409.7 TC, TG, and sizes of LDL particles estimated as non-HDL-C, 332.3). Of the 39 patients, 32 (82%) were categorized in the area of hyper-TG/-non-HDL levels, which is considered as sdLDL. A positive correlation was found between non-HDL-C and TC (r = 0.96, P < 0.001), TG (r = 0.38, P = 0.018), LDL-C (r = 0.84, P < 0.001), TC/HDL (r = 0.53, P < 0.001), and atherogenic index of plasma (r = 0.42, P = 0.008).Conclusions: Our study demonstrated markedly increased lipid profiles during the acute phase of NS. Evaluation of lipid profiles using the “alternative LDL window” may help understand the state of hyperlipidemia in NS.

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Section: Resultssupporting

confidence: 52%

Markedly Increased Small Dense Low-Density Lipoprotein During Acute Phase in Childhood and Adolescent Nephrotic Syndrome

Sugimoto¹,

Miyazaki²,

Enya³

et al. 2020

Preprint

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“…Diabetes was defined as symptoms and random blood glucose ≥11.1 mmol/L, or fasting plasma glucose ≥7.0 mmol/L, or 2-h oral glucose tolerance test level ≥11.1 mmol/L, or no diabetes symptoms and at least twice blood glucose meets the above criteria [ 12 ]. Dyslipidemia was defined as serum total cholesterol ≥5.18 mmol/L, high-density lipoprotein cholesterol (HDL-C) ≤1.04 mmol/L, low-density lipoprotein cholesterol (LDL-C) ≥3.37 mmol/L, or triglyceride ≥1.7 mmol/L or previous diagnosis of dyslipidemia in medication [ 13 ].…”

Section: Methodsmentioning

confidence: 99%

Association of lymphocyte-to-monocyte ratio with total coronary plaque burden in patients with coronary artery disease

Liu

Shan

et al. 2020

Coronary Artery Disease

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Background: Lymphocyte-to-monocyte ratio (LMR) is involved in all stages of coronary atherosclerosis and related to coronary artery disease (CAD). However, the correlation between LMR and the coronary plaque burden of CAD is not clearly elucidated. Therefore, this study aimed to investigate their correlation in patients with CAD. Methods: A total of 1953 consecutive eligible inpatients with suspected CAD were retrospectively included in this study. They were assigned into CAD (n = 564) and non-CAD groups (n = 1389). All patients underwent coronary computed tomographic angiography to evaluate coronary stenosis and coronary artery calcification (CAC). Spearman’s tests were used to analyze the correlation between CAC score and LMR. Multivariate logistic regression models were set up to assess the risk factors of CAD. Results: Patients with CAD had lower LMR value than patients without CAD ( P = 0.001). LMR was negatively correlated with CAC score and was an independent risk factor of CAC score ( P < 0.05). Multivariate logistic regression model showed that LMR ≤4.8 was a newly independent risk factor of CAD (all P < 0.05). Additionally, the new risk score model was compared with the Framingham model and showed that NRI was 4.9%, which proved that the new risk score model improved the prediction capability of CAD. Conclusion: LMR ≤4.8 is a new independent risk factor of CAD. LMR value was negatively correlated with CAC score and could be used as a new marker to evaluate the coronary plaque burden of CAD.

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“…Ethanol has a powerful influence and decrease bloodstream Lp(a) levels up to 60% [63] in dose-dependent manner independent of the size distribution of apo(a) isoforms [167]. Tobacco smoking reduces plasma Lp(a) by up to 20% [168,169] although tobacco smoking is one of the major risk factors for CVD, increasing plasma TG and lowering HDL-C [170].…”

Section: Factors That Influence Lp(a) Levels In the Bloodmentioning

confidence: 99%

“…e development of isoform-independent assays has helped to significantly improve Lp(a) measurements. Another important challenge is the contribution of Lp(a) cholesterol to LDL-C when using the Friedewald formula, which may require a mathematical correction before any interpretation is made [170].…”

Section: Ldl Receptor Removal or Uptakementioning

confidence: 99%

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

2020

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Lipoprotein(a) [Lp(a)], aka “Lp little a”, was discovered in the 1960s in the lab of the Norwegian physician Kåre Berg. Since then, we have greatly improved our knowledge of lipids and cardiovascular disease (CVD). Lp(a) is an enigmatic class of lipoprotein that is exclusively formed in the liver and comprises two main components, a single copy of apolipoprotein (apo) B-100 (apo-B100) tethered to a single copy of a protein denoted as apolipoprotein(a) apo(a). Plasma levels of Lp(a) increase soon after birth to a steady concentration within a few months of life. In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a).

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Standardization of laboratory and lipid profile evaluation: A call for action with a special focus in 2016 ESC/EAS dyslipidaemia guidelines – Full report

Cited by 22 publications

References 38 publications

Markedly Increased Small Dense Low-Density Lipoprotein During Acute Phase in Childhood and Adolescent Nephrotic Syndrome

Markedly Increased Small Dense Low-Density Lipoprotein During Acute Phase in Childhood and Adolescent Nephrotic Syndrome

Association of lymphocyte-to-monocyte ratio with total coronary plaque burden in patients with coronary artery disease

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

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