Clinical Lipidology最新文献

{"title":"Omega 3 fatty acids, inflammation and DNA methylation: an overview","authors":"Bethan Hussey, M. Lindley, S. Mastana","doi":"10.1080/17584299.2017.1319454","DOIUrl":"https://doi.org/10.1080/17584299.2017.1319454","url":null,"abstract":"ABSTRACT Omega-3 polyunsaturated fatty acids (n-3 PUFAs) are known to be anti-inflammatory and to alter gene expression within the cells. Emerging evidence indicates that one of the mechanisms for this process involves the alteration of epigenetic markers, such as DNA methylation. The focus of this overview is to document the current evidence for n-3 PUFA effects on DNA methylation and how these may impact on the inflammatory processes.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"81 4 1","pages":"24 - 32"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76038976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipoprotein X in autoimmune liver disease causing interference in routine and specialist biochemical investigations","authors":"N. Rao, A. Jain, A. Goyale, J. Persaud, K. Al-Musalhi, D. R. Nair","doi":"10.1080/17584299.2017.1308670","DOIUrl":"https://doi.org/10.1080/17584299.2017.1308670","url":null,"abstract":"ABSTRACT Primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are chronic, immune-mediated diseases which may be associated with the presence of lipoprotein X (LpX). This is an abnormal lipoprotein resulting in marked elevation of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) concentration. LpX is rich in free cholesterol (FC) and phospholipids (PL) and low in esterified cholesterol (CE). We describe two cases with florid lipid stigmata and presence of LpX. A patient with PBC presented with itching and palmar xanthomata. TC = 55.5 mmol/L, direct LDL-C = 14.9 mmol/L, high-density lipoprotein cholesterol (HDL-C) = 0.5 mmol and triglycerides (TG) = 11.3 mmol/L. Lipoprotein electrophoresis (LPE) showed the presence of LpX. An apolipoprotein E (Apo E) phenotype and genotype reported E2E3 and E3E3 isoforms, respectively. A patient with PSC presented with itchy eruptive xanthomata. TC = 22.8 mmol/L, calculated LDL-C = 21.7 mmol/L, HDL-C = 0.2 mmol/L and TG = 1.6 mmol/L. LPE was normal. Both Apo E phenotype and genotype showed E2E3 isoforms. Both patients were treated with statins and showed resolution of lipid stigmata and improvement of lipid parameters, including PL, FC and LpX. In the first case, Apo E phenotype showed an E3E3 phenotype like the genotype following the decrease in LpX. LpX can interfere with other routine biochemical measurements, falsely increase TC and LDL-C levels and in our patient with PBC, we believe that LpX interfered with Apo E phenotype analysis. This has not been previously described.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"41 1","pages":"13 - 8"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73884475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tagging SNPs within regulatory parts of APOA5 and CYP7A1 genes and their expression in human liver tissue: a pilot study","authors":"D. Dlouhá, M. Oliverius, J. Hubacek, I. Lesná, V. Lánská, R. Poledne","doi":"10.1080/17584299.2016.1261958","DOIUrl":"https://doi.org/10.1080/17584299.2016.1261958","url":null,"abstract":"Abstract Objective: Apolipoprotein A5 (lipoprotein lipase activator) and cholesterol 7α-hydroxylase (microsomal cytochrome P450) are almost exclusively expressed in liver tissue. Variants within the regulatory parts of these genes (rs662799 and rs3135506 within APOA5 and rs3808607 within CYP7A1) can probably affect levels of plasma lipids and may influence the success of the treatment of dyslipidaemia. Methods: In order to conduct a primary analysis of whether the effect of the variants is mediated through gene expression, we collected and analysed 25 anonymous samples of human liver tissue. Results: APOA5 expression levels of hepatic mRNA were lower in carriers of at least one less common APOA5 allele than in common alleles homozygotes, but the difference was not significant (p = 0.19), mainly due to the huge expression range in different samples. Similarly, CYP7A1 expression was also not significantly influenced by the promoter variant, regardless of the type of statistical model used (all p > 0.31). In our study, we have detected a huge inter-individual variation in the hepatic transcript levels of APOA5 and CYP7A1. These inter-individual variations were the main reasons why having even twice as high levels of expression between the compared groups with different genotypes was not significant. Conclusions: The results of our pilot study did not confirm a possible effect of promoter variants on the expression of APOA5 and CYP7A1 genes. The relatively small sample size could have affected our results. A central facility based on international collaboration that collects liver resection material may help increase the number of samples to provide meaningful results.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"79 1","pages":"28 - 32"},"PeriodicalIF":0.0,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74538951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Armolipid Plus® on small dense LDL particles","authors":"A. Magán-Fernández, G. Castellino, D. Nikolić, M. Rizzo","doi":"10.1080/17584299.2016.1261960","DOIUrl":"https://doi.org/10.1080/17584299.2016.1261960","url":null,"abstract":"Effects of Armolipid Plus® on small dense LDL particles particular importance in cases of FCHL. However, caution is recommended because of possible interactions with other medications. Some nutraceuticals, including Armolipid Plus, may have lipid-lowering effects similar to statins, but some supplements seem to have advantages compared with statins [11]; in any case, statin-related side effects are usually avoided. Future use of these natural supplements, alone or as a part of multifactorial treatment approach,[12] remains to be assessed.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"41 1","pages":"39 - 40"},"PeriodicalIF":0.0,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81380019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Takotsubo cardiomyopathy, acute myocardial infarction and dyslipidaemia: a comparison of studies","authors":"A. De Giorgi, M. Guarino, B. Boari, R. Cappadona, E. Maietti, F. Fabbian, R. Manfredini","doi":"10.1080/17584299.2016.1261959","DOIUrl":"https://doi.org/10.1080/17584299.2016.1261959","url":null,"abstract":"Abstract Background: Takotsubo cardiomyopathy (TTC) and acute myocardial infarction (AMI) share similar clinical presentation and risk of death, although one of the most important differences is the absence of obstructive coronary disease in TTC. We analysed the available literature and evaluated the prevalence of dyslipidaemia in patients with TTC compared with patients with AMI. Methods: A MEDLINE literature search to identify relevant papers focused on TTC and AMI was performed, evaluating the prevalence of dyslipidaemia in both groups. Systematic reviews, meta-analyses, controlled trials, cohort studies and case-control studies were considered for inclusion. We focused on studies reporting precise data on the prevalence of dyslipidaemia for both groups. Results: Out of a total of 511 articles found, 207 case reports, 24 comments, 56 letters and 57 articles in languages other than English were excluded. Of the remaining 167 papers, 23 articles providing the required information were selected. They included and compared 2247 TTC and 19,843 AMI patients. Cases with dyslipidaemia were 734 (32.7%) in the TTC group and 6592 (33.2%) in the AMI group. Conclusions: Patients with TTC showed a prevalence of dyslipidaemia comparable with that of patients with AMI. The prevalence of dyslipidaemia and clinical outcome in TTC and AMI may represent unrelated issues. It is likely that for TTC patients, other conditions and comorbidities, rather than dyslipidaemia alone and/or other established risk factors, are responsible for a risk of death comparable with that of AMI.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"4 1","pages":"33 - 38"},"PeriodicalIF":0.0,"publicationDate":"2016-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89123374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aggressive treatment of LDL-cholesterol and patients undergoing CABG: news from IMPROVE-IT","authors":"D. Mikhailidis, D. Nair","doi":"10.1080/17584299.2016.1254432","DOIUrl":"https://doi.org/10.1080/17584299.2016.1254432","url":null,"abstract":"taking S + Ez compared with those assigned to S + Pl (incidence-rate ratio, RR, 0.70: 0.59–0.84).[1] The corresponding RR for the group without prior CABG was 0.96 (0.89–1.03). Overall, there were 4231 additional primary endpoint events; 1050 in the prior CABG group (9% of the IMPROVE-IT population) and 3181 additional events in the non-prior CABG group (91% of the IMPROVE-IT population) (p < 0.001). The IMPROVE-IT trial “prior CABG” analysis [1] has several limitations. For example, patients with prior CABG represented only 9% of the participants; this limited the power to carry out any further detailed analysis within this population. Also, the time elapsed from the CABG was not available and there are no details regarding the type of grafts. Despite several limitations, IMPROVE-IT provides credible evidence that patients with prior CABG who develop an ACS are a high-risk subset with a substantial increased risk of recurrent CV ischemic events (56% at 7 years). These patients benefit more from adding ezetimibe to simvastatin (so as to achieve lower LDL-C levels) than patients without prior CABG. Future guidelines will need to consider this finding. Also, prior CABG + ACS patients may constitute an ideal population for assessing the effect of new potent LDL-C lowering drugs (e.g. proprotein convertase subtilisin/kexin nine inhibitors). The role of lipid lowering therapy for patients undergoing CABG was recognised several decades ago.[5–19] Also, of interest is that this literature includes evidence that high-density lipoprotein cholesterol (HDL-C), triglyceride and non-HDL-C levels may be relevant in terms of predicting disease progression in patients who underwent CABG. A meta-analysis also considered statin loading for CABG although it seems that the increased dose of statins was administered after CABG to achieve lower LDL-C levels long term; more aggressive statin treatment was superior.[20] It is of interest that even a recent study showed that post-CABG patients were undertreated with statins and aspirin. [21] In contrast, in IMPROVE-IT, at randomisation, 94.8% of those with prior CABG and 97.3% of those without prior CABG were on aspirin.[1] In addition, the corresponding % of patients on a thienopyridine was 79.0 and 87.2%, respectively.[1] There is evidence from IMPROVE-IT that more patients achieved the dual target of LDL-C (<70 mg/dl; 1.8 mmol/l) and high sensitivity C-reactive protein (<2 mg/l) with combination therapy than with monotherapy.[22] In turn, those achieving this dual target had fewer events than those not achieving this goal.[22] A dual target analysis was not carried out to the IMPROVE-IT CABG subgroup analysis probably because of the smaller number of participants in the CABG group.[1] OPEN ACCESS","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"1 1","pages":"26 - 27"},"PeriodicalIF":0.0,"publicationDate":"2016-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91305789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gender differences and statin therapy","authors":"G. Kolovou, S. Mavrogeni","doi":"10.1080/17584299.2016.1245478","DOIUrl":"https://doi.org/10.1080/17584299.2016.1245478","url":null,"abstract":"We read with interest the Pavanello et al. review on gender differences in the efficacy, safety and tolerability of statin therapy.[1] The authors reported differences between genders in cardiovascular (CV) risk factors, CV morbidity and mortality as well as in statin response and adverse events. These discrepancies may be attributed to hormonal, anthropometric and pharmacokinetic factors as discussed by the authors.[1] Pavanello et al. also commented on current CV guidelines in both men and women. Interestingly, apart from traditional CV predictors,[2] several emerging CV risk factors may differ between men and women.[3] Both atherosclerotic and non-atherosclerotic coronary heart disease may present gender differences.[4] Furthermore, gender may influence acute coronary syndrome (ACS) outcomes and thus it has been included in risk scores such as the CHA2DS2-VASc-HS score.[5] The rates and outcomes of coronary revascularisation procedures may also differ between genders.[6] In terms of genetic factors predisposing to CV diseases, gender differences have also been reported for polymorphisms in genes involved in lipid metabolism such as the ATP-binding cassette transporter A1 (ABCA1), cholesteryl ester transfer protein (CETP), lipoprotein lipase genes and apolipoprotein E genes.[7–9] With regard to drug therapy, CV risk factors are treated less aggressively and less frequently in women than in men,[2] thus contributing to the gender differences seen in CV disease morbidity and mortality. According to statin treatment and gender differences, data from the majority of studies [the Scandinavian Simvastatin Survival Study, the Prospective Pravastatin Pooling Project, the Women of Air Force/Texas Coronary Atherosclerosis Prevention Study, the Heart and Estrogen/Progestin Replacement Study, the Women of Intervention Trial Evaluating Rosuvastatin, the Women in the Pravastatin or Atorvastatin Evaluation and Infection Therapy Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial] [10–15] showed that both women and men had benefited from intensive statin therapy and thus, gender should not be a factor in determining who should be treated with intensive statin therapy.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"39 1","pages":"25 - 25"},"PeriodicalIF":0.0,"publicationDate":"2016-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82007688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D deficiency and metabolic syndrome: any link with statin intolerance and adipokines dysregulation?","authors":"N. Katsiki, A. Sahebkar, M. Banach","doi":"10.1080/17584299.2016.1243651","DOIUrl":"https://doi.org/10.1080/17584299.2016.1243651","url":null,"abstract":"We read with interest the Miñambres et al. review on hypovitaminosis D and the metabolic syndrome (MetS).[1] The authors describe evidence linking vitamin D (vit D) deficiency with MetS or its components, whereas inconsistent results have been reported with regard to vit D supplementation effects on metabolic parameters. The authors suggested that further research is needed to establish whether improving MetS components can increase vit D levels and vice versa. Vit D deficiency has been associated with statin-induced adverse effects.[reviewed in 2,3] In this context, a recent meta-analysis found that low vit D concentrations were related to myalgia in statin-treated patients.[4] Vit D supplementation has also been proposed as an option to manage statin intolerance in patients with vit D deficiency.[5] As MetS patients are at a high cardiovascular (CV) risk, they are often treated with statins.[6] Based on the link between MetS and vit D hypovitaminosis, it follows that measuring vit D levels may be clinically useful in MetS patients to either prevent or treat statin intolerance. In this context, it is also worth noting that statins can interfere with vit D metabolism through CYP3A4,[7] and also increase the availability of cholesterol biosynthesis precursors such as 7-dehydrocholesterol that mediate vitamin D production.[8] These interactions could confound the association between vit D status and MetS and should be considered before interpreting any observational data. On another issue, MetS has been associated with decreased adiponectin and increased leptin levels.[9] These adipokine abnormalities may further increase CV risk in MetS patients.[9] Vit D metabolism has been reported to influence the expression of leptin and adiponectin in adipose tissue.[10] In this context, there are data linking vit D positively with adiponectin and negatively with leptin levels.[11–13] However, a recent meta-analysis did not find any effect of vit D intake on leptin and adiponectin concentrations.[14] Further research is needed to elucidate such associations.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"15 1","pages":"23 - 24"},"PeriodicalIF":0.0,"publicationDate":"2016-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86014023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safe use of statins: focus on muscle toxicity","authors":"V. Kolovou, H. Bilianou, G. Kolovou","doi":"10.1080/17584299.2016.1239873","DOIUrl":"https://doi.org/10.1080/17584299.2016.1239873","url":null,"abstract":"Abstract Muscle toxicity can be classified as myopathy, myalgia, myositis or rhabdomyolysis (RM). RM can occur in patients with muscular dystrophy, alcoholic myopathy, peripheral artery disease and myocardial infarction as well as prolonged convulsions or immobility. Also, RM can occur, in otherwise healthy individuals, after viral illness, crush or high-voltage electrical injury, hyperthermia, severe exercise and taking certain drugs, particularly 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins). Muscle disorders provoked by statin use have been named “statin-associated myopathy (SAM)”. There is no commonly accepted definition of SAM, although recently a score system was introduced and the European Atherosclerosis Society (EAS) proposed a definition of SAM. There are several possible explanations for SAM; for example, genetic predisposition, decreased intracellular cholesterol levels, reduced production of coenzyme Q10 and related ubiquinones and decreased production of prenylated proteins. Due to the widespread use of statins, it is very important to diagnose SAM and particularly its severe presentation, RM. Early treatment will prevent serious complications. This review will focus on SAM.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"12 1","pages":"16 - 22"},"PeriodicalIF":0.0,"publicationDate":"2016-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81686831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cigarette smoking/cessation and metabolic syndrome","authors":"G. Kolovou, V. Kolovou, S. Mavrogeni","doi":"10.1080/17584299.2016.1228285","DOIUrl":"https://doi.org/10.1080/17584299.2016.1228285","url":null,"abstract":"Abstract The metabolic syndrome (MetS) is a common cluster of pre-morbid, modified metabolic–vascular risk factors/diseases (visceral obesity, hyperglycaemia, dyslipidaemia and hypertension) associated with increased cardiovascular (CV) morbidity, fatty liver and risk of cancer. Several studies reported a higher incidence of MetS in smokers. Cigarette smoking plays a substantial role in the pathogenesis of numerous chronic diseases such as CV disease (CVD), cancer, lung disease and others. However, due to the existence of the so-called “smoking paradox”, the impact of this risk factor on CVD mortality is still not clear. Smoking cigarettes may increase risk of MetS or worsen it by numerous mechanisms. Furthermore, individuals who quit smoking tend to increase their body weight. The possibility of gaining weight can stop smokers from quitting and increases the risk of relapse, particularly in women. Herein, we review the cigarette smoking status (active/cessation) in relation to the MetS.","PeriodicalId":55252,"journal":{"name":"Clinical Lipidology","volume":"51 1","pages":"14 - 6"},"PeriodicalIF":0.0,"publicationDate":"2016-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90420719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}