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We evaluated the effects of fasting during Ramadan on nutritional intake and plasma lipoproteins in 20 healthy adults of normal weight. A 5-day food questionnaire was completed for every participant. Clinical investigations, anthropometrical measurements and laboratory analysis were also undertaken. Body weight, blood pressure and blood glucose were not influenced by fasting but there were non-significant modifications in the plasma lipid fractions. The total cholesterol remained unchanged. Total daily energy intake was comparable before, during and after Ramadan despite the decrease in meal frequency during fasting. Thus fasting in Ramadan did not affect dietary intake, clinical, anthropometrical and most biological parameters

Quantitative plasma lipoprotein and metabolite profiles were measured on an autonomous community of the Basque Country (Spain) cohort consisting of hospitalized COVID-19 patients (n = 72) and a matched control group (n = 75) and a Western Australian (WA) cohort consisting of (n = 17) SARS-CoV-2 positives and (n = 20) healthy controls using 600 MHz 1H nuclear magnetic resonance (NMR) spectroscopy. Spanish samples were measured in two laboratories using one-dimensional (1D) solvent-suppressed and T2-filtered methods with in vitro diagnostic quantification of lipoproteins and metabolites. SARS-CoV-2 positive patients and healthy controls from both populations were modeled and cross-projected to estimate the biological similarities and validate biomarkers. Using the top 15 most discriminatory variables enabled construction of a cross-predictive model with 100% sensitivity and specificity (within populations) and 100% sensitivity and 82% specificity (between populations). Minor differences were observed between the control metabolic variables in the two cohorts, but the lipoproteins were virtually indistinguishable. We observed highly significant infection-related reductions in high-density lipoprotein (HDL) subfraction 4 phospholipids, apolipoproteins A1 and A2,that have previously been associated with negative regulation of blood coagulation and fibrinolysis. The Spanish and Australian diagnostic SARS-CoV-2 biomarkers were mathematically and biologically equivalent, demonstrating that NMR-based technologies are suitable for the study of the comparative pathology of COVID-19 via plasma phenotyping.

BACKGROUND Increased levels of plasma lipoproteins are among some of the modifiable risk factors for cardiovascular disease (CVD). Dietary changes and increased physical activity are the most powerful non-pharmacological interventions for achieving optimal plasma lipid levels. OBJECTIVES To investigate the effect of an intensive short-term lifestyle intervention on plasma lipid trajectories in overweight non-diabetic females. MATERIAL AND METHODS A total of 202 healthy overweight (body mass index (BMI) >27.5 kg/m2) females underwent an intensive short-term (ten-week) intervention (at least 4 units of one-hour exercise activity weekly at optimal energy intake) aimed at lowering body weight. Plasma lipid (total cholesterol (TC), low-density-lipoprotein cholesterol (LDL-C), high-density-lipoprotein cholesterol (HDL-C), and triglycerides (TG)) levels were examined at baseline and every 2 weeks over the course of the ten-week intervention. RESULTS There was a significant decrease in BMI (Δ -4.7%, p < 0.001) and body weight (Δ -4.9%, p < 0.001) after the intervention. Positive changes (decreases) in TC (Δ -8%, p < 0.001), TG (Δ -9%, p < 0.001) and LDL-C (Δ -11%, p < 0.001) were observed immediately after 2 weeks, but levels did not decrease further thereafter. In contrast, HDL-C did not increase as expected: after 2 weeks of intervention, we observed a significant decrease of about 6% (p < 0.001) followed by a slow return to baseline values. But even after 10 weeks of intervention, HDL-C values had not reached the values detected at baseline. CONCLUSIONS In overweight females, HDL-C decreased after short-term intensive lifestyle intervention. To confirm the protective effect of increased physical activity, plasma lipids need to be examined over a longer time period.

Purpose of review Contemporary polygenic scores, which summarize the cumulative contribution of millions of common single-nucleotide variants to a phenotypic trait, can have effects comparable to monogenic mutations. This review focuses on the emerging use of 'genome-wide' polygenic scores for plasma lipoproteins to define the etiology of clinical dyslipidemia, modify the severity of monogenic disease, and inform therapeutic options. Recent findings Polygenic scores for low-density lipoprotein cholesterol (LDL-C), triglycerides, and high-density lipoprotein cholesterol are associated with severe hypercholesterolemia, hypertriglyceridemia, or hypoalphalipoproteinemia, respectively. These polygenic scores for LDL-C or triglycerides associate with risk of incident coronary artery disease (CAD) independent of polygenic scores designed specifically for CAD and may identify individuals that benefit most from lipid-lowering medication. Additionally, the severity of hypercholesterolemia and CAD associated with familial hypercholesterolemia-a common monogenic disorder-is modified by these polygenic factors. The current focus of polygenic scores for dyslipidemia is to design predictive polygenic scores for diverse populations and determining how these polygenic scores could be implemented and standardized for use in the clinic. Summary Polygenic scores have shown early promise for the management of dyslipidemias, but several challenges need to be addressed before widespread clinical implementation to ensure that potential benefits are robust and reproducible, equitable, and cost-effective.

Background. Increasing evidence states that the plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) levels and apolipoprotein particles are regarded as the risk maker for cardiovascular heart disease. Nevertheless, the issue about whether Lp-PLA2 is associated with apolipoprotein particles in individuals who have been diagnosed as stable coronary artery disease (CAD) remains largely unexplored. Method. All 569 participants engaged in this research, who never took lipid-lowering drugs, had been divided into groups by the coronary angiography (CAG), namely, stable CAD: n=291; non-CAD: n=278. The results concerning Lp-PLA2 levels were calculated by Elisa Kit, while apolipoprotein particles were measured by the department of laboratory. Results. The plasma concentration of Lp-PLA2 was remarkably higher in stable CAD group than the non-CAD group (136.0±60.5 ng/mL vs. 113.2±65.6 ng/mL, P<0.001). Pearson correlation analyses explained the plasma Lp-PLA2 concentration was correlated with apoB (r=0.390, P<0.001) and apoB/apoA1 (r=0.450, P<0.001), not associated with apoA1 (r=−0.099, P=0.101). Conversely, the association remains unobserved among non-CAD patients except apoA1. Moreover, multiple linear regression revealed the relations between Lp-PLA2 concentrations and apoB (β=0.390, P<0.001), as well as apoB/apoA1 (β=0.450, P<0.001), but not apoA1 (β=−0.099, P=0.121). After adjustment for several risk factors regarding CAD, like hypertension, gender, smoking, age, and diabetes mellitus, there had still been positive associations between the Lp-PLA2 concentration and apoB (β=0.364, P<0.001), as well as apoB/apoA1 (β=0.390, P<0.001). Conclusion. The plasma levels of Lp-PLA2 provide positively a key link with apoB, apoB/apoA-1 among stable CAD, denoting the communication between Lp-PLA2 and apolipoprotein particles in the state of CAD.

The study aimed to assess the effects of dietary extruded linseed (ELS) and Lactobacillus acidophilus (LA) on performance, carcass traits, immune organ weights, plasma lipoprotein response, and caecal bacteria populations in broiler chickens. A total of 648 one-day-old chicks were divided into six groups in a 3 × 2 factorial arrangement consisting of three ELS levels (0, 6 and 12%) without or with probiotic L. acidophilus (0 and 20 g ton−1 feed). Each group had six replicates (18 birds/pen). Results showed no significant effects of ELS level nor LA supplementation on growth performance (body weight gain, feed intake, and feed conversion) of broilers during the overall period (1–42 days). The production efficiency factor increases (p = .045) with the LA addition. There were no effects of ELS level nor probiotic addition on carcase traits and immune organ weights, except for decreases in abdominal fat percentage (p = .027, respectively p = .035). The dietary ELS level significantly correlated with a decrease in the plasma total cholesterol (TC; p = .003), triglycerides, and very-low-density lipoprotein concentrations (p = .020), while the LA addition significantly correlated with a decrease (p = .015) in the plasma TC. The LA addition lowers the caecal pH (p = .007), Staphylococcus spp. and E. coli counts (p

The use of pesticides such as cypermethrin (Cyp) has become hazardous resulting into public and environmental health issues in the world with several studies pointing to a decline in reproductive health coupled with increased risk of infertility. Thus, pesticide safety and effects on human exposure in relation to general and reproductive health are of paramount concern. This study was aimed at investigating the biochemical alterations in the lipidomics of plasma components and reproductive organ of male rats exposed to cypermethrin. The animals were grouped into eight comprising seven animals each and orally treated for 28 days: control, 20 mg/kg body weight of Cyp, Cyp+JG(50 mg/kg), Cyp+JG(100 mg/kg), Cyp+ALA(50 mg/kg), JG(50 mg/kg), JG(100 mg/kg) and ALA(50 mg/kg). Lipid profile analyses were carried out on the plasma, HDL, vLDL+LDL, and testis homogenate of the rats as described by the diagnostic kit manual. Results obtained from this study showed that cypermethrin administration significantly elevated triglyceride (105.22%) and not significant cholesterol level (15.28%) in the plasma; significantly increased testicular triglyceride (96.46%) and cholesterol (64.99%) concentrations; significantly decreased HDL triglyceride (46.57%) and cholesterol (38.37%); significantly increased the concentration of vLDL+LDL triglyceride (126.28 %) and cholesterol (76.09%) in comparison with the control. Co-administration with both doses of J. gossypifolia (JG) leaf extract and alpha-lipoic acid (ALA) significantly reversed these alterations. Thus, the phytoconstituents of Jatropha gossypifolia plant extract possesses modulatory potentials that can mitigate the effect of cypermethrin on the reproductive organ and plasma lipidomics especially in the treatment of heart related disorders caused by hyperlipidemia.

Background and aims Familial hypercholesterolaemia (FH) and elevated plasma lipoprotein(a) [Lp(a)] are inherited conditions independently associated with atherosclerotic cardiovascular disease. This study investigated the detection of new cases of elevated Lp(a) during cascade testing of relatives of probands with a definite diagnosis of FH and elevated Lp(a) (≥50 mg/dL). Methods Relatives from 62 adult probands were tested for FH genetically and for elevated Lp(a) using an immunoassay. The prevalence and yield of new cases of FH with or without elevated Lp(a) (≥50 mg/dL) among relatives and the association between the detection of elevated Lp(a) and the Lp(a) concentration of the probands were assessed. Results Among 162 relatives tested (136 adults and 26 children), the prevalence of FH and elevated Lp(a) was 60.5% and 41.4%, respectively: FH alone was detected in 31.5%, elevated Lp(a) alone in 12.3%, FH with elevated Lp(a) in 29.0%, and neither disorder in 27.2% of the relatives. Cascade testing detected a new case of FH, elevated Lp(a) and FH with elevated Lp(a) for every 1.5, 2.1 and 3.0 relatives tested, respectively. The proportion of relatives detected with elevated Lp(a) was significantly higher when tested from probands with Lp(a) ≥100 mg/dL compared with those from probands with Lp(a) between 50-99 mg/dL (53% vs 34%, p = 0.018). The concordance between the detection of FH and elevated Lp(a) was 56.2% (kappa statistic 0.154), indicating a poor agreement. Conclusions A dual approach to cascade testing families for FH and high Lp(a) from appropriate probands can effectively identify not only new cases of FH, but also new cases of elevated Lp(a) with or without FH. The findings accord with the co-dominant and independent heritability of FH and Lp(a).

Background and aim Although some earlier studies have indicated the effect of phytosterol (PS) supplementation on serum lipoprotein(a) (Lp(a)) and free fatty acid (FFA) concentration, findings are still conflicting. We aimed to assess the impact of PS supplementation on serum Lp(a) and FFA concentration through a systematic review and meta-analysis of available RCTs. Methods and results We performed a systematic search of all available RCTs conducted up to 21 February 2019 in the following databases: PubMed, Scopus, and Cochrane. The choice of fixed- or random-effect model for analysis was determined according to the I2 statistic. Effect sizes were expressed as weighted mean difference (WMD) and 95% confidence interval (CI). Pooling of 12 effect sizes from seven articles revealed a significant reduction of Lp(a) levels following PS supplementation (MD: −0.025 mg/dl, 95% CI: −0.045, −0.004, p = 0.017) without significant heterogeneity among the studies (I2 = 0.0%, p = 0.599). Also, PS supplementation significantly lowered FFA (MD: −0.138 mg/dl, 95% CI: −0.195, −0.081, p = 0.000) without significant heterogeneity among the studies (I2 = 0.0%, p = 0.911). The results for meta-regression and sensitivity analysis were not significant. Conclusion The meta-analysis suggests that oral PS supplementation could cause a significant reduction in serum Lp(a) and FFA.

BackgroundLipoprotein(a) [Lp(a)] is a low-density lipoprotein‒like particle containing apolipoprotein(a) [apo(a)]. Patients with elevated Lp(a), even when treated with statins, are at increased risk of cardiovascular disease. We investigated the kinetic basis for elevated Lp(a) in these patients.ObjectivesApo(a) production rate (PR) and fractional catabolic rate (FCR) were compared between statin-treated patients with and without elevated Lp(a).MethodsThe kinetics of apo(a) were investigated in 14 patients with elevated Lp(a) and 15 patients with normal Lp(a) levels matched for age, sex, and body mass index using stable isotope techniques and compartmental modeling. All 29 patients were on background statin treatment. Plasma apo(a) concentration was measured using liquid chromatography–mass spectrometry.ResultsThe plasma concentration and PR of apo(a) were significantly higher in patients with elevated Lp(a) than in patients with normal Lp(a) concentration (all P < 0.01). The FCR of apo(a) was not significantly different between the groups. In univariate analysis, plasma concentration of apo(a) was significantly associated with apo(a) PR in both patient groups (r = 0.699 and r = 0.949, respectively; all P < 0.01). There was no significant association between plasma apo(a) concentration and FCR in either of the groups (r = 0.160 and r = −0.137, respectively).ConclusionElevated plasma Lp(a) concentration is a consequence of increased hepatic production of Lp(a) particles in these patients. Our findings provide a kinetic rationale for the use of therapies that target the synthesis of apo(a) and production of Lp(a) particles in patients with elevated Lp(a).

Lipoprotein(a) [Lp(a)] is a highly atherogenic lipoprotein characterized by apolipoprotein(a) [apo(a)] covalently bounded to apoB-100 (apoB). However, the metabolism of apo(a) and apoB within plasma Lp(a) particles in patients on statins remains unclear.The kinetics of Lp(a)-apo(a) and Lp(a)-apoB were determined in 20 patients with elevated Lp(a) (≥0.8 g/L; n = 10) and normal Lp(a) (≤0.3 g/L; n = 10) using stable isotope techniques and compartmental modeling. Plasma apo(a) concentration was measured using liquid chromatography-mass spectrometry. All patients were on statin therapy and were studied in the fasting state.The fractional catabolic rate (FCR) of Lp(a)-apo(a) was not significantly different from that of Lp(a)-apoB in statin-treated patients with elevated or normal Lp(a) (P 0.05 in both). Lp(a)-apo(a) FCR was significantly correlated with Lp(a)-apoB in patients with elevated and normal Lp(a) concentrations (r = 0.970 and r = 0.979, respectively; all P 0.001) with Lin's concordance test showing substantial agreement between the FCRs of Lp(a)-apo(a) and Lp(a)-apoB in patients with elevated and normal Lp(a) concentrations (rOur data indicate that the apo(a) and apoB proteins within Lp(a) particles have similar FCR and are therefore tightly coupled as an Lp(a) holoparticle in statin-treated patients with elevated and normal Lp(a) concentrations.

Introduction.The development of new and highly effective antitumor therapy is one of the priorities of pharmacology. The paper presents one of the solutions to the problem related to the development of transport forms of antitumor drugs.The aimof the study was to study the ability of various fractions of plasma lipoproteins (VLDLP, LDL, HDL) to interact with actinomycin D and show the role of HDL as a transport form of actinomycin D in the body cells.Material and methods. The studies were conducted using unlabeled and tritium-labeled actinomycin D, preparative ultracentrifugation of the rat plasma lipoprotein fractions, chromatography, and in vivo experiments with intravenous administration of HDL complexes with labeled actinomycin D.Results.The important role of HDL in the formation of complexes with actinomycin D in comparison with LDL and LPA was shown. The basic physicochemical characteristics of the interaction of HDL and apolipoprotein A-I with actinomycin were obtained. The constants of the association were of the order of 105 M-1, and the number of binding sites for the drug was 26 for HDL and 12 for apolipoprotein A-I. In vivo studies on rats, the highest radioactivity after intravenous injection of HDL complexes with tritium-labelled actinomycin D was observed in the adrenal glands, then in the liver and kidneys. The uptake of tritium-labelled actinomycin D was twice lower in the lungs, adipose tissue, thymus and spleen. The low uptake of the label was observed in the myocardial tissue.Conclusion.The results obtained demonstrate the feasibility of using HDL as a transport form of actinomycin D in body cells.

An experiment was conduct in order to investigate the effects of feed restriction level and duration and dietary coenzyme Q10 level on growth performance, organ characteristics and plasma lipoproteins. A factorial arangment based on a completely randomized design was performed using two levels of feed restriction (10 and 20% less than the standard Ross strain 308 guidelines), two levels of restriction duration (7 and 14 days) and three levels of coenzyme Q10 (0, 20 and 40 mg/kg feed). The results of the experiment showed that restriction intensity had significant effect on feed intake in first, second and sixth weeks of age (P

Subfractionation methods provide increased granularity for size and density plasma lipoproteins. The prevailing hypothesis is that this increased granularity will isolate the most atherogenic measure of cholesterol. Plasma lipoproteins continuously change in size and composition in order to transport cholesterol and triglycerides between tissues. Several methods for measuring lipoprotein subfractions are commercially available including electrophoresis, nuclear magnetic resonance, ion mobility, and direct homogeneous enzymatic methods. The various methods measure different lipoprotein components, separate subfractions by different means, and define small, medium, and large by different limits. Consequently, concordance across methods is relatively poor. Smaller low-density lipoprotein (LDL) subfractions are associated with increased risk of atherosclerosis. However, this association is attenuated in models that account for basic lipid parameters such as total LDL cholesterol or apolipoprotein B. This suggests that the information provided by LDL subfractions is neither independent nor additive to standard lipid assessments. Subfractions of high-density lipoproteins have been controversial and often conflicting regarding which size fractions are associated with risk. No clinical society has recommended the use of subfractionation and several relevant organizations including the American Heart Association and the National Lipid Association specifically recommend against use of lipoprotein subfraction testing in clinical practice.

We recently revealed that increases in particle sizes of very-low-density lipoproteins (VLDL) are highly correlated with the progression of nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH), and VLDL particle size may be a minimally invasive indicator of these hepatic disorders. Methionine and choline-deficient (MCD) diet fed animals are usually used as a NASH model; however, the application of this minimally invasive biomarker in MCD diet fed animals remains unclear. In the present study, we measured the levels of liver disease markers and plasma lipoprotein profiles in MCD diet fed rats, and compared them with those of normal diet fed rats. Assessing lipoprotein profiles showed marked increases in VLDL particle sizes in MCD diet fed rats with pathologically and biochemically NASH-like features.

Introduction: Elevated plasma lipoprotein (a) [Lp(a)] and coronary artery calcification (CAC) are established cardiovascular disease (CVD) risk factors that correlate with each other. In this study we hypothesized that other CVD risk factors could modify the relationship between baseline Lp(a) levels and CAC change over time. Methods: A total of 5975 participants from the Multi-Ethnic Study of Atherosclerosis were analyzed. All participants were 45-84 years old, free of apparent CVD at baseline and from one of four major ethnic groups (non-Hispanic white, African American, Hispanic American, and Chinese American). We tested for interactions of 24 study variables related to dyslipidemia, diabetes, insulin resistance, hypertension, inflammation and coagulation with baseline Lp(a) on change in CAC volume and density over 9.5 years. Results: Elevated Lp(a) was associated with larger annual absolute increase in CAC volume (3.21 and 4.45 mm 3 /year higher for Lp(a) ≥30 versus P P for interaction 3 /year in quartile 4, compared to -3.44, -0.59 and 1.91 mm 3 /year in quartile 1, respectively). A similar trend was seen when expressing Lp(a) ≥50 mg/dL as elevated levels. There were no associations for ln-transformed Lp(a) as a continuous variable, or when assessing the annual relative change in CAC volume and density. Conclusions: Elevated Lp(a) was associated with the progression of CAC volume, especially in participants with higher levels of selected markers of inflammation and coagulation. This study suggests that inflammation and coagulation may modify the relation between Lp(a) and CAC.

Arachidonic acid (AA) and docosahexaenoic acid (DHA) are important for neurological development. The aim was to determine the distribution and relative enrichment of AA and DHA among lipoprotein fractions prior to pregnancy, throughout gestation and in the post-partum period. Our hypothesis was that in pregnancy, in contrast to the non-pregnant state, AA and DHA are carried in highest concentration in the very low density lipoprotein (VLDL) fraction secondary to increased gestational liver triglyceride secretion. Two independent prospective, observational cohort studies carried out in Glasgow were combined; one early in pregnancy and one later in pregnancy with post-partum follow up. Across the pregnancy timeline plasma lipoproteins were isolated using sequential ultracentrifugation and lipoprotein fatty acids were extracted and analysed by gas chromatography. High density lipoprotein (HDL) had the highest concentration of AA and DHA compared to other lipoproteins. HDL became progressively enriched in the proportion of triglycerides at 16 weeks of gestation, which peaked at 35 weeks and returned to baseline at 13 weeks postpartum. HDL DHA per HDL-cholesterol and HDL DHA per apoA-I became progressively enriched at 16 weeks of gestation, peaked at 25 weeks and returned to baseline at 13 weeks postpartum, whereas HDL AA (per HDL-C or HDL-apoA-I) did not differ. DHA is carried primarily in HDL rather than VLDL. HDL has anti-oxidant properties that might afford DHA protection against oxidation.

Lipoprotein(a), Lp(a), is a modified low-density lipoprotein particle that contains apolipoprotein(a), encoded by LPA, and is a highly heritable, causal risk factor for cardiovascular diseases that varies in concentrations across ancestries. Here, we use deep-coverage whole genome sequencing in 8392 individuals of European and African ancestry to discover and interpret both single-nucleotide variants and copy number (CN) variation associated with Lp(a). We observe that genetic determinants between Europeans and Africans have several unique determinants. The common variant rs12740374 associated with Lp(a) cholesterol is an eQTL for SORT1 and independent of LDL cholesterol. Observed associations of aggregates of rare non-coding variants are largely explained by LPA structural variation, namely the LPA kringle IV 2 (KIV2)-CN. Finally, we find that LPA risk genotypes confer greater relative risk for incident atherosclerotic cardiovascular diseases compared to directly measured Lp(a), and are significantly associated with measures of subclinical atherosclerosis in African Americans.

Background Marked elevations of plasma lipoprotein X (Lp-X) levels have been reported in patients with cholestasis due to primary biliary cirrhosis, pancreatic cancer, hepatitis C, and quetiapine. We now report a patient with extreme elevation of plasma Lp-X due to alcohol-induced cholestasis. Case Presentation A 44 year-old African American male presented with painless jaundice and fatigue for one week. He denied nausea, vomiting, diarrhea, change in stool or urine color, or weight loss. He consumes 720-1080 mL of beer (2-3 cans) every night and admitted to heavier alcohol consumption in the past. On physical examination he had scleral icterus and hepatomegaly but no xanthomas or xanthelasmas. His serum total cholesterol was 1,126 mg/dL (normal range, 120-199 mg/dL), triglycerides were 238 mg/dL (50-150 mg/dL), calculated LDL-cholesterol was 1,072 mg/dL (39 mg/dL). His serum AST, 162 IU/L (10-50 IU/L); ALT, 79 IU/L (10-50 IU/L); alkaline phosphatase, 1,058 IU/L (40-129 IU/L); total bilirubin, 18.8 mg/dL (0.2-1.3 mg/dL); direct bilirubin, 13.5 mg/dL (0-0.3 mg/dL); and gamma glutamyl transferase, 4,583 IU/L (8-61 IU/L) were markedly elevated. His blood alcohol level was 34 mg/dL (not detected), sodium 124 mmol/L (135-145 mmol/L), and platelet count was 84,000/µL (150,000-459,000/µL). His TSH 2.89 µIU/mL (0.4-4.5 µIU/mL), UA without proteinuria, HBV immunized, HCV negative, and anti-mitochondrial antibody negative. CT abdomen revealed hepatic steatosis and gallbladder swelling without evidence of obstruction. MRCP showed cirrhosis without primary sclerosing cholangitis. Serum lipoprotein electrophoresis confirmed the presence of Lp-X. On day 3 of hospitalization, his cholestasis improved and his serum total bilirubin 10.0 mg/dL, direct bilirubin 7.4 mg/dL, AST 108 IU/L, ALT 66 IU/L, and alkaline phosphatase 663 IU/L had improved. The patient was advised to abstain from all alcohol consumption. Telephone follow up 2 months later with his wife revealed that he had stopped drinking alcohol and that his jaundice had resolved. Conclusions Although alcohol-induced cholestasis is a well-recognized entity, such presentation with extreme elevations of Lp-X has not been previously reported. In such patients, it is important to establish whether extreme hypercholesterolemia is due to LDL or Lp-X since, as opposed to LDL, Lp-X elevations are not considered to be atherogenic.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

ObjectiveThe present longitudinal study assessed whether changes in socio-economic status (SES) from infancy to adolescence were associated with plasma lipoprotein concentrations in adolescence, of which low HDL-cholesterol (HDL-C) and high LDL-cholesterol (LDL-C), TAG and total cholesterol (TC) concentrations are associated with higher cardiovascular risk.DesignSES, assessed using the modified Graffar Index, was calculated at 1, 5, 10 and 16 years. Principal components factor analysis with varimax rotation extracted two orthogonal SES factors, termed ‘environmental capital’ and ‘social capital’. Generalized linear models were used to analyse associations between environmental and social capital at 1 and 16 years and outcomes (HDL-C, LDL-C, TAG, TC) at 16 years, as well as changes in environmental and social capital from 1–5, 5–10, 10–16 and 1–16 years, and outcomes at 16 years.SettingSantiago, Chile.ParticipantsWe evaluated 665 participants from the Santiago Longitudinal Study enrolled at infancy in Fe-deficiency anaemia studies and examined every 5 years to age 16 years.ResultsSocial capital in infancy was associated with higher HDL-C in adolescence. Environmental capital in adolescence was associated with higher LDL-C and TC during adolescence. Changing environmental capital from 1–16 years was associated with higher LDL-C. Changing environmental capital from 1–5 and 1–16 years was associated with higher TC.ConclusionsImprovements in environmental capital throughout childhood were associated with less healthy LDL-C and TC concentrations in adolescence. We found no evidence of associations between changing environmental capital and HDL-C or TAG, or changing social capital and HDL-C, LDL-C, TAG or TC.