High Apolipoprotein Research Articles

Effect of aortic valve phenotype and sex on aorta dilation in patients with aortic stenosis

BackgroundBicuspid aortic valve (BAV) is often associated with a concomitant aortopathy. However, few studies have evaluated the effect of the aortic valve (AV) phenotype on the rate of dilation of...

Apolipoproteins, lipids, lipid-lowering drugs and risk of amyotrophic lateral sclerosis and frontotemporal dementia: a meta-analysis and Mendelian randomisation study.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) have clinical, pathological and genetic overlapping. Lipid pathways are implicated in ALS. This study examined the effect of blood lipid levels on ALS, FTD risk, and survival in ALS. A systematic review and meta-analysis of high and low-density lipoprotein cholesterol (HDL-c and LDL-c), total cholesterol, triglycerides, apolipoproteins B and A1 levels with ALS was performed. Two-sample Mendelian randomisation (MR) analysis sought the causal effects of these exposures on ALS, FTD, and survival in ALS. The effect of lipid-lowering drugs was also examined using genetic proxies for targets of lipid-lowering medications. Three cohort studies met the inclusion criteria for meta-analysis. Meta-analysis indicated an association between higher LDL-c (HRper mmol/L = 1.07, 95%CI:1.02-1.12; =18%) and lower HDL-c (HRper mmol/L = 0.83, 95%CI:0.74-0.94; =0%) with an increased risk of ALS. MR suggested causal effects of higher LDL-c (ORIVW = 1.085, 95%:CI 1.008-1.168, pFDR = 0.0406), total cholesterol (ORIVW = 1.081, 95%:CI 1.013-1.154, pFDR = 0.0458) and apolipoprotein B (ORIVW = 1.104, 95%:CI 1.041-1.171, pFDR = 0.0061) increasing ALS risk, and higher apolipoprotein B level increasing FTD risk (ORIVW = 1.424, 95%CI 1.072-1.829, pFDR = 0.0382). Reducing LDL-c through APOB inhibition was associated with lower ALS (ORIVW = 0.84, 95%CI 0.759-0.929, pFDR = 0.00275) and FTD risk (ORIVW = 0.581, 95%CI 0.387-0.874, pFDR = 0.0362). These data support the influence of LDL-c and total cholesterol on ALS risk and apolipoprotein B on the risk of ALS and FTD. Potential APOB inhibition might decrease the risk of sporadic ALS and FTD. Further work in monogenic forms of ALS and FTD is necessary to determine whether blood lipids influence penetrance and phenotype.

Coronary Artery Calcification Progression in Patients With Systemic Lupus Erythematosus.

To evaluate the progression of coronary artery calcification (CAC) and associated risk factors in a systemic lupus erythematosus (SLE) cohort. We reassessed the presence of CAC in patients with SLE who were screened 9 years before, using multidetector computed tomography. Clinical variables (cumulated disease activity and damage accrual), antiphospholipid syndrome and SLE serology, and cardiovascular (CV) risk factors (hypertension, BMI [kg/m2], modified Framingham risk score, lipid profile, menopausal status) were assessed longitudinally. We included 104 patients from the parent study. Most of them were women (94.2%), with a mean age of 41.0 (SD 8.3) years and mean disease duration of 14.8 (SD 2.9) years. We documented CAC in 17 patients (16.3%). Seven cases were from the parent study and 10 were incident cases. The cumulative incidence of CAC was 9% and the incidence density was 1 per 100 person-years. CAC occurred more frequently in the age groups 30-39 years and 40-44 years. All patients with previous CAC had worsening of their calcium indexes, and none developed clinical CV events. When comparing prevalent CAC cases (n = 17) vs patients without calcification (n = 87), both groups were similar in traditional CV risk factors, disease duration, Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) area under the curve (AUC), and Systemic Lupus International Collaborating Clinics (SLICC) score, but were more likely to be postmenopausal and have higher apolipoprotein B (apoB) levels. Patients with previous CAC had higher apoB levels, SLEDAI-2K AUC scores, and anticardiolipin IgG antibodies than incident cases. CAC in patients with SLE progressed over time but was not associated with adverse CV events during the first 9 years of follow-up. ApoB levels and postmenopausal status might be associated with this progression.

High Apolipoprotein B/Apolipoprotein A1 is Associated with Vitamin D Deficiency Among Type 2 Diabetes Patients.

To explore the relationship between vitamin D (VitD) deficiency and the apolipoprotein B/apolipoprotein A1 (apo B/A1) in type 2 diabetes mellitus (T2DM) patients. This was a retrospective study that lasted 2 years and 6 months, collecting information and laboratory data from 784 patients with T2DM. Patients were divided into VitD deficiency group (n = 433) and non-VitD deficiency group (n = 351) based on VitD levels. Calculated apo B/A1 ratio, and patients were further divided into high-apo B/A1 group (n = 392) and low-apo B/A1 group (n = 392) based on the median of the apo B/A1. All data were analyzed using Prism 8.0.1 and R version 4.3.1 software. Apo B/A1 levels of T2DM patients combined with VitD deficiency was significantly higher than that of non-VitD deficiency patients, and the VitD levels of patients with high apo B/A1 was significantly lower than that patients with low apo B/A1 (all P<0.001). Spearman correlation analysis showed that VitD levels were negatively correlated with apo B/A1 (r=-0.238, P<0.001). Multiple linear regression analysis revealed after adjusting other factors, VitD levels were significantly negatively associated with apo B/A1 (β=-0.123, P=0.001). Binary logistic regression analysis showed apoB/A1 was an independent risk factor for VitD deficiency in T2DM patients. Restrictive cubic spline indicated a significant linear relationship between apoB/A1 and VitD deficiency (P general trend <0.0001, P nonlinear = 0.0896), after stratification of gender, the results showed that apo B/A1 was more susceptible to VitD deficiency in female patients. The receiver operating characteristic (ROC) curve analysis showed that the area under the curve, sensitivity and specificity of the apo B/A1 for VitD deficiency were 0.654, 66.3% and 59.8%, respectively. The apo B/A1 was significantly negatively associated with VitD levels and an independent risk factor for VitD deficiency in patients with T2DM.

Association of High apoB/apoA1 Ratio with Increased Erythrocytes, Platelet/Lymphocyte Ratio, D-dimer, Uric Acid and Cardiac Remodeling in Elderly Heart Failure Patients: A Retrospective Study.

Previous studies have confirmed that high apolipoprotein B/apolipoprotein A1 (apoB/apoA1) ratio was associated with increased mortality from heart failure (HF). Furthermore, the association of plasma apoB/apoA1 ratio with clinical characteristics and adverse cardiac remodeling is still limited in chronic HF with mildly reduced ejection fraction (HFmrEF) elderly patients. Therefore, this study investigated the association of apoB/apoA1 ratio with clinical characteristics and adverse cardiac remodeling in chronic HFmrEF elderly patients. A total of 587 Chinese elderly (≥65 years) with coronary heart disease (CHD), HFmrEF (EF 40-50%) and related blood biochemical data were collected retrospectively. The cross-sectional data of echocardiographic and blood parameters were compared between binary apoB/apoA1 groups. In the elderly CHD patients with chronic HFmrEF, the univariate correlation analysis showed that apoB/apoA1 was correlated with younger age, increased prevalence of type 2 diabetes, erythrocytes, platelet/lymphocyte ratio (PLR), D-dimer, fibrinogen, high sensitivity C-reactive protein and uric acid, and adverse cardiac remodeling (All P < 0.05). However, multivariate logistic binary regression analysis found that high apoB/apoA1 ratio (≥0.62) was independently correlated with younger age, increased erythrocytes, PLR, D-dimer and uric acid, and adverse cardiac remodeling (All P < 0.05). In this retrospective study, the high apoB/apoA1 ratio is found to be associated with younger age, increased erythrocytes, PLR, D-dimer and uric acid, and adverse cardiac remodeling in Chinese CHD elderly with chronic HFmrEF.

Remnant cholesterol, LDL cholesterol, and apoB absolute mass changes explain results of the PROMINENT trial

Background and aimsThe PROMINENT trial, a cardiovascular outcome trial of the triglyceride- and remnant cholesterol-lowering agent pemafibrate, has shown neutral results despite reduction in plasma triglycerides and remnant cholesterol. We tested the hypothesis that absolute mass changes in remnant cholesterol, LDL cholesterol, and apolipoprotein B explain the results of the PROMINENT trial. MethodsAmong 108,431 individuals from the Copenhagen General Population Study (CGPS), those who met the key inclusion criteria of the PROMINENT trial were analyzed to mimic the trial design. Endpoint atherosclerotic cardiovascular disease (ASCVD) was cardiovascular death, myocardial infarction, ischemic stroke, and coronary revascularization as defined in PROMINENT. ResultsIn the PROMINENT trial, treatment with pemafibrate resulted in -7 mg/dL (−0.18 mmol/L; -18 %) change in remnant cholesterol, +10 mg/dL (+0.26 mmol/L; +12 %) LDL cholesterol, and +5 mg/dL (+0.05 g/L; +5 %) apolipoprotein B. In the CGPS mimicking PROMINENT, the estimated hazard ratios for ASCVD were 0.97 (95 % confidence interval: 0.94–0.99) for a -7 mg/dL (−0.18 mmol/L) change in remnant cholesterol, 1.04 (1.01–1.07) for a +10 mg/dL (+0.26 mmol/L) change in LDL cholesterol, and 1.02 (1.01–1.03) for a +5 mg/dL (+0.05 g/L) change in apolipoprotein B. When combining absolute changes in remnant cholesterol, LDL cholesterol, and apolipoprotein B, the estimated hazard ratio for ASCVD was 1.05 (0.96–1.14) in the CGPS mimicking PROMINENT compared to 1.03 (0.91–1.15) in the PROMINENT trial. ConclusionsAbsolute mass changes in remnant cholesterol, LDL cholesterol, and apolipoprotein B can explain results of the PROMINENT trial. The 3 mg/dL (0.08 mmol/L) higher total atherogenic cholesterol together with 5 mg/dL (0.05 g/L) higher apolipoprotein B seem to explain the trend toward more ASCVD in the pemafibrate arm.

FOXM1 Participates in Scleral Remodeling in Myopia by Upregulating APOA1 Expression Through METTL3/YTHDF2.

Apolipoprotein A1 (APOA1) is a potential crucial protein and treatment goal for pathological myopia in humans. This study set out to discover the function of APOA1 in scleral remodeling in myopia and its underlying mechanisms. A myopic cell model was induced using hypoxia. Following loss- and gain-of function experiments, the expression of the myofibroblast transdifferentiation-related and collagen production-related factors Forkhead box M1 (FOXM1), APOA1, and methyltransferase-like 3 (METTL3) in the myopic cell model was examined by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blotting. The proliferation and apoptosis were determined by Cell Counting Kit-8 assay and flow cytometry, respectively. Chromatin immunoprecipitation (ChIP) was employed to examine FOXM1 enrichment in the METTL3 promoter, methylated RNA immunoprecipitation (Me-RIP) to examine the N6-methyladenosine (m6A) modification level of APOA1, and photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP) to examine the binding between METTL3 and APOA1. Hypoxia-induced human scleral fibroblasts (HSFs) had high APOA1 and FOXM1 expression and low METTL3 expression. FOXM1 knockdown elevated METTL3 expression and downregulated APOA1 expression. FOXM1 was enriched in METTL3 promoter. APOA1 or FOXM1 knockdown or METTL3 overexpression reversed the hypoxia-induced elevation in vinculin, paxillin, and α-smooth muscle actin (α-SMA) levels and apoptosis and the reduction in collagen, type I, alpha 1 (COL1A1) level and cell proliferation in HSFs. METTL3 or YTH N6-methyladenosine RNA binding protein F2 (YTHDF2) knockdown or APOA1 overexpression reversed the impacts of FOXM1 knockdown on vinculin, paxillin, α-SMA, and COL1A1 expression and cell proliferation and apoptosis. FOXM1 elevated the m6A methylation level of APOA1 by repressing METTL3 transcription and enhanced APOA1 mRNA stability and transcription by reducing the YTHDF2-recognized m6A methylated transcripts.

Apolipoproteins as predictors of cardiovascular risk in patients with chronic pancreatitis.

Patients with pancreatic diseases are at increased risk of cardiovascular events. Investigating various apolipoprotein forms as important atherogenesis components may improve cardiovascular risk (CVR) prediction. This study aimed to investigate CVR factors in patients with chronic pancreatitis. The study enrolled 70 patients (40 males and 30 females, mean age 55.2 years) with chronic pancreatitis and treated pancreatic exocrine insufficiency. We assessed CVR by apolipoproteins A-I, A-II, B, and C-III, lipid profile; score systems [SCORE risk chart and Framingham Risk Score (FRS)], diabetes mellitus; chronic pancreatitis by M-ANNHEIM classification. Statistics were performed via SPSS v. 22. Low apolipoprotein A-I and high apolipoprotein B levels with increased atherogenic potential were observed in 37 and 26 patients. 45.71% demonstrated a high risk of myocardial infarction with high apolipoprotein B/apolipoprotein A-I ratio. Men are at higher CVR risk. Apolipoproteins A-I and A-II correlated with the cardioprotective high-density lipoprotein (HDL) in contrast to apolipoproteins B and C-III, which correlated strongly with low-density lipoprotein (LDL), total cholesterol (TC), and triglycerides (TG). Increased CVR assessed by FRS correlated with significantly lower apolipoprotein A-I and higher apolipoprotein B and apolipoprotein B/apolipoprotein A-I ratio. With the increase in chronic pancreatitis severity, we observed decreased apolipoproteins and increased apolipoprotein B/apolipoprotein A-I ratio. Apolipoproteins are valuable CVR indicators. Further studies are required to establish a CVR screening panel in this population.

Causal role of lipid metabolome on the risk of ischemic stroke, its etiological subtypes, and long-term outcome: A Mendelian randomization study

Background and aimsThe lipid profile is consistently associated with coronary artery disease (CAD) and ischemic stroke (IS). However, the lipoprotein subfractions have not been deeply explored in stroke subtypes, especially in IS outcome. MethodsWe performed two-sample Mendelian randomization (MR) analysis using 92 lipid traits measured by nuclear magnetic resonance in 115,000 subjects from the UK Biobank. Data for genetic associations with IS, its subtypes, and long-term outcome (LTO) were obtained from three cohorts of European ancestry: GIGASTROKE (73,652 cases, 1,234,808 controls), GODS (n = 1791) and GISCOME (n = 6165). Results obtained using CARDIoGRAMPlusC4D were used to identify differences with CAD. ResultsGenetically determined low concentration of medium high-density lipoprotein (HDL) particles (odds ratio (OR) = 0.92, 95% CI 0.88–0.96; p = 3.6 × 10−4) and its cholesterol content (OR = 0.92, 95% CI 0.88–0.96; p = 1.9 × 10−4) showed causal associations with an increased risk of stroke. Genetic predisposition to high apolipoprotein (apo)B to apoA-I ratio was causally associated with an increased risk of IS (OR = 1.12, 95% CI 1.06–1.18, p = 1.1 × 10−4), and a highly suggestive association was found between non-esterified cholesterol in low-density lipoprotein (LDL) and increased risk of atherothrombotic stroke (LAS) (OR = 1.35, 95% CI 1.10–1.66; p = 4.0 × 10−3). Low cholesterol in small and medium LDL was suggestively associated with poor LTO. ConclusionsOur results support that low medium HDL concentration was causally associated with an increased stroke risk, while high levels of non-esterified cholesterol in LDL were suggestively associated with an increased risk of LAS and with a better LTO.

The serum lipid profiles in immune thrombocytopenia: Mendelian randomization analysis and a retrospective study

BackgroundImmune thrombocytopenia (ITP) is an autoimmune hemorrhagic disease characterized by increased platelet destruction and impaired thrombopoiesis. The changes in platelet indices depend on the morphology and volume of platelets. Serum lipids have been found to affect platelet formation and activity in certain diseases, thus inducing the corresponding variation of platelet indices.MethodsMendelian randomization (MR) analysis was performed based on databases. The clinical data from 457 ITP patients were retrospectively collected and analyzed, including platelet indices, serum lipids, hemorrhages and therapeutic responses.ResultsMR analysis showed low high-density-lipoprotein-cholesterol (HDL-C), low apolipoprotein A-1, high triglyceride (TG) and high apolipoprotein B (ApoB) caused high platelet distribution width (PDW); high low-density-lipoprotein-cholesterol (LDL-C) increased mean platelet volume (MPV). In ITP, there were positive correlations between platelet count with TG, PDW with HDL-C and ApoB, and plateletcrit with TG and non-esterified fatty acid, and the correlation had gender differences. Bleeding scores were negatively correlated with cholesterol and LDL-C. LDL-C and homocysteine were risk factors for therapeutic responses.ConclusionsSerum lipids, especially cholesterol were tightly correlated with platelet indices, hemorrhage and therapeutic effects in ITP patients. These results provide clinical references for the management of serum lipids, and highlight the necessity to further explore the relationship between lipids and pathogenesis of ITP.Trial registrationNo: NCT05095896, October 14, 2021, retrospectively registered.

Genetic scores associated with favourable and unfavourable adiposity have consistent effect on metabolic profile and disease risk across diverse ethnic groups.

This study aims to investigate the associations between genetic risk scores (GRS) for favourable and unfavourable adiposity and a wide range of adiposity-related outcomes across diverse populations. We utilised previously identified variants associated with favourable (36 variants) and unfavourable (38 variants) adiposity to create GRS for each adiposity phenotype. We used summary statistics from 39 outcomes generated by the Pan-UKB genome-wide association studies Version 0.3, incorporating covariates such as age, sex and principal components in six populations: European (n = 420,531), African (6636), American (980), Central/South Asian (8876), East Asian (2709) and Middle Eastern (1599). The favourable adiposity GRS was associated with a healthy metabolic profile, including lower risk of type 2 diabetes, lower liver enzyme levels, lower blood pressure, higher HDL-cholesterol, lower triglycerides, higher apolipoprotein A, lower apolipoprotein B, higher testosterone, lower calcium and lower insulin-like growth factor 1 generally consistently across all the populations. In contrast, the unfavourable adiposity GRS was associated with an adverse metabolic profile, including higher risk of type 2 diabetes, higher random glucose levels, higher HbA1c, lower HDL-cholesterol, higher triglycerides, higher liver enzyme levels, lower testosterone, and higher C-reactive protein generally consistently across all the populations. The study provides evidence that the genetic scores associated with favourable and unfavourable adiposity have consistent effects on metabolic profiles and disease risk across diverse ethnic groups. These findings deepen our understanding of distinct adiposity subtypes and their impact on metabolic health.

Hypertriglyceridemic hyperapoB and the development and resolution of nonalcoholic fatty liver disease: a cohort study

Hypertriglyceridemic hyperapoB is an adverse lipoprotein phenotype characterized by low high density lipoprotein (HDL) cholesterol, high triglycerides, high apolipoprotein B (ApoB), and low low density lipoprotein (LDL) cholesterol to ApoB ratio. We investigated whether and to what extent hypertriglyceridemic hyperapoB associates with the incidence and resolution of nonalcoholic fatty liver disease (NAFLD). This prospective cohort study included 9,019 Chinese participants 40 years or older, from 2010 to 2015. Logistic regression models were used to examine the odds ratios (ORs) for the incidence and resolution of NAFLD associated with the hypertriglyceridemic hyperapoB lipoprotein phenotype and individual lipid and lipoprotein parameters. During a median 4.3 years of follow-up, compared with participants with optimal phenotype, the fully adjusted ORs (95% CIs) for participants with hypertriglyceridemic hyperapoB were 2.75 (1.91, 3.95) and 0.57 (0.33, 1.00) for incidence and resolution of NAFLD, respectively. These associations were consistent across subgroup participants with varied demographic, lifestyle, and metabolic status. Individually, each unit increase in HDL cholesterol (OR: 0.98; 95% CI: 0.97, 0.99), natural logarithm-transformed triglycerides (1.89; 1.52, 2.36), and ApoB (1.006; 1.002, 1.011) was independently associated with NAFLD incidence, and only triglycerides (0.77; 0.60, 0.99) was independently associated with NAFLD resolution. Our findings suggest that Chinese adults with hypertriglyceridemic hyperapoB have a higher risk of NAFLD incidence and a lower likelihood of NAFLD resolution. These associations were stable among adults with different demographic, lifestyle, and metabolic status, supporting hypertriglyceridemic hyperapoB as a valuable clinical marker for the prevention and control of NAFLD.

Impact of apolipoprotein A1 on tumor immune microenvironment, clinical prognosis and genomic landscape in hepatocellular carcinoma.

Current knowledge on apolipoprotein A1 (APOA1) in hepatocellular carcinoma (HCC) is fragmented and even contradictory. Multi-dimensional analyses are required to comprehensively elucidate its value and underlying mechanism. We collected 49 RNA-seq datasets, 40 cell line types data and 70 scRNA pan-cancer datasets public available, including 17 HCC datasets (1754 tumor samples), and enrolled 73 pairs of HCC tissue and 516 blood samples independently from our clinics. APOA1 impacting on the HCC tumor microenvironment (TME) was analyzed using intensive data mining. Methylation sequencing, flow cytometry, quantitative PCR, western blot, immunohistochemistry and clinical chemistry assays were conducted for wet experimental investigation. The APOA1 ontology fingerprint indicated that it played various crucial biological roles in HCC, primarily involved in cholesterol efflux. Consistent findings at histology, serology, and clinical follow-up revealed that high APOA1 was a good prognosis indicator of HCC. Hypermethylation in the APOA1 promoter region was found in clinical samples which is in accordance with the reduction of APOA1 in HCC. The cell cycle, DNA replication, mismatch repair pathways, and tumor cell proliferation were less observed in the HCC APOA1high subgroup. The favorable immunoregulatory abilities of APOA1 showed interesting findings: a positive correlation between APOA1 and anti-tumor immune cells (NK, CD8+T cells) and a negative association with immune cells exerting immunosuppressive effects, including M2 macrophages. This is an integrative multidimensional exploration of APOA1 using bioinformatics and experiments. Both the prognostic value and anti-tumor effects based on APOA1 panoramic exploration in the HCC TME demonstrate a new potential clinical target for HCC assessment and intervention in the future.

Obesity Indices Could Predict High Apolipoprotein B/Apolipoprotein A1 Ratio in Non-menopausal Indonesian Adult Females

Previous researches have demonstrated associations between high obesity indices with increased risk of metabolic and cardiovascular disorders. It has also been established that abnormalities of lipoprotein metabolism have an important role in atherogenesis and that non-menopausal females are protected from atherosclerotic cardiovascular events relative to menopausal females and males. This study aimed to investigate the relationship between obesity indices such as body mass index (BMI), waist circumference (WC), body fat percentage (BF), and visceral fat (VF) with apolipoprotein B/apolipoprotein A1 ratio in non-menopausal Indonesian adult females. A total of 75 non-menopausal Indonesian adult females were included as subjects in this cross-sectional study. Measured indices included BMI, WC, BF, and VF. Measurement of apolipoprotein B and A1 were performed by immunoturbidimetry, followed by calculation of the ratio. A cut-off value of 0.8 was used to define high apolipoprotein B/apolipoprotein A1 ratio. Apolipoprotein B/Apolipoprotein A1 ratio was significantly correlated with BMI (r=0.384, p=0.001), WC (r=0.363, p=0.001), BF (r=0.385, p=0.001), VF (r=0.380, p=0.001). The area under curve of BF (0.754) was slightly larger than BMI (0.722), VF (0.721), and WC (0.686) in predicting high apolipoprotein B/apolipoprotein A1 ratio. A positive significant correlation was observed between obesity indices with the apolipoprotein B/apolipoprotein A1 ratio. Obesity indices could be used to predict high apolipoprotein B/apolipoprotein A1 ratio.

Etiology and clinical characteristics of primary epistaxis.

Primary epistaxis (rupture of nasal artery vessels) is a common emergency, but the related factors are still controversial. This study collected the data on primary epistaxis patients and healthy people undergoing a physical examination at the same center to explore and classify primary epistaxis by its characteristics. Primary epistaxis was divided into septal epistaxis and non-septal epistaxis, and logistic regression was performed to determine the risk factors. In total, 196 cases of septal epistaxis and 127 cases of non-septal epistaxis, and the control group was 182 healthy subjects. There were significant differences in sex, drinking history, hypertension history and hyperlipidemia between the bleeding group and the control group, but no correlation with smoking, diabetes, cardiovascular and cerebrovascular events, or anticoagulant drug use. In the age group of 26-40 years it was related to alcohol consumption and hypertension, for those aged 41-55 years it was related to hypertension, in the age group of 56-70 years it was related to hypertension, high triglyceride and high apolipoprotein B levels, and no related factors were found in the age group >70 years. The risk factors for non-septal cases were increased low-density lipoprotein (LDL) [P=0.035; odds ratio (OR), 2.450; 95% confidence interval (CI): 1.067-5.624], male sex (P=0.002; OR, 3.136; 95% CI: 1.501-6.554), and younger age (P=0.000; OR, 0.941; 95%CI: 0.920-0.962). All patients with nosebleed underwent nasal endoscopy and the bleeding site was successfully located and treated with electrocoagulation. No further bleeding or serious complications occurred after 6 months of follow-up. Primary epistaxis is more common in males and is related to alcohol consumption, hypertension, and hyperlipidemia. In the young age groups, male sex, and increased LDL were high risk factors for non-septal hemorrhage in winter and spring. Nasal endoscopy and electrocoagulation are safe and effective.

Correlation between Apolipoprotein A1 and the Occurrence and Prognosis of Cardiovascular Events in Peritoneal Dialysis Patients.

This study investigates the value of apolipoprotein A1 in assessing the occurrence and prognosis of cardiovascular events in peritoneal dialysis patients. A retrospective analysis was conducted based on the clinical information of 80 end-stage renal disease patients who underwent peritoneal dialysis at Zhuji People's Hospital Zhejiang Province from January 2015 to December 2016. Based on the median value of apolipoprotein A1, patients were evenly distributed as either High Apolipoprotein A1 Group (H-ApoA1, > 1.145g/L, n = 40) or Low Apolipoprotein A1 Group (L-ApoA1, < 1.145g/L, n = 40). When compared with the H-ApoA1 group, the L-ApoA1 group patients were observed to have higher BMI, total Kt/V, hemoglobin, AKP, glycated hemoglobin, HOMA-IR, HDL levels, while simultaneously having lower total Ccr, triglycerides, total cholesterol, LDL, CRP levels (p < 0.05). Further analysis found that the all-cause mortality rate, cardiovascular death rate, and cardiovascular event rates were significantly higher in L-ApoA1 group patients than the H-ApoA1 group (p < 0.05); no statistical significance was found for mortality rates due to infection, abandon treatment, tumor, failure, gastrointestinal bleeding or undetermined reasons between the two groups (p > 0.05). In addition, the median all-cause mortality and median occurrence of cardiovascular events of L-ApoA1 group patients were observed to be shorter than the H-ApoA1 group (p < 0.05), and apolipoprotein A1 is a risk factor for all-cause mortality rate and cardiovascular occurrence end-point events (p < 0.05). Peritoneal dialysis patients with a reduced level of apolipoprotein A1 have a poorer prognosis and more severe cardiovascular events.

Cholesterols, Apolipoproteins, and Their Associations with the Presence and Severity of Diabetic Retinopathy: A Systematic Review.

Serum apolipoproteins have been reported as a more significant marker for diabetic retinopathy (DR) compared with serum cholesterols. This article aims to review the associations between serum cholesterols and apolipoproteins, and the presence and severity of DR. The protocol of this systematic review was registered at the PROSPERO registry (CRD42022303331). We conducted a systematic search of literature published between 2011 to 2022 using the search terms "serum cholesterol" AND/OR "lipoprotein" AND/OR "apolipoprotein" AND/OR "diabetic retinopathy". Fifteen studies were included in this review. Six studies assessed the association between serum cholesterols, apolipoproteins, and the presence of DR. Three studies reported lower levels of apolipoprotein A1, and one study reported higher levels of apolipoprotein B in patients with DR. The remaining nine studies compared serum cholesterol and apolipoprotein levels according to DR severity. Patients with more severe grades of DR presented with lower apolipoprotein A1 in six (66.7%) studies, higher apolipoprotein B levels in seven (77.8%) studies, and a higher apolipoprotein B/apolipoprotein A1 ratio in six out of seven (85%) studies. In conclusion, serum apolipoproteins, in particular the apolipoprotein B/apolipoprotein A1 ratio, were a more consistent marker for DR severity compared with serum cholesterols.

Characteristics of primary age‐related tauopathy defined by neuroimaging biomarkers

AbstractBackgroundPrimary age‐related tauopathy (PART) is a neuropathological entity with neurofibrillary tangles (NFTs) in the absence of amyloid (Aβ) plaques in the brain. Recent advance of neuroimaging makes it possible to identify PART in living human brain. We tried to investigate the frequency and clinical characteristics including rate of cognitive decline of non‐demented older adults with PART defined by neuroimaging biomarkers.MethodA total of 113 non‐demented older individuals recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE) were included in the analysis. All participants underwent [11C] PiB PET and [18F] AV‐1451 PET with comprehensive clinical assessment. Global cognition was measured annually using MMSE, from 2 years before to 2 years after the PET scans. PART was defined when beta‐amyloid deposition is negative and tau burden corresponds to Braak stage I‐IV.ResultAmong 113 participants, 40 (35.4%) were classified as PART, 29 (25.7%) as no Alzheimer's disease (AD)‐ pathology (amyloid‐negative, Tau Braak stage 0), and 44 (38.9%) as AD (amyloid‐positive). Compared to PART and no‐AD associated pathology group, AD group had higher apolipoprotein E ε4 positivity (13.8%, 12.5%, and 59.1% for PART, no‐AD pathology, and AD, respectively). In regard of cognitive decline rate over 4 years, PART was similar to no‐AD pathology, but significantly slower than AD.ConclusionOur findings indicate that PART is relatively common in non‐demented older adults. In regard of genetic risk and progression rate, PART appears closer to no‐AD pathology condition rather than AD.

Prevalence and clinical characteristics of metabolically healthy obese versus metabolically unhealthy obese school children.

IntroductionChildren with obesity in the absence of traditional cardiometabolic risk factors (CRF) have been described as metabolically healthy obese (MHO). Children with MHO phenotype has a favorable metabolic profile with normal glucose metabolism, lipids, and blood pressure compared to children with metabolically unhealthy obese (MUO) phenotype. This study aimed to compare several parameters related to obesity between these two groups and to examine the predictors associated with the MHO phenotype.MethodsThis study included a cross-sectional baseline data of 193 children with obesity (BMI z-score > +2 SD) aged 8-16 years enrolled in MyBFF@school program, a school-based intervention study conducted between January and December 2014. Metabolic status was defined based on the 2018 consensus-based criteria with MHO children had no CRF (HDL-cholesterol > 1.03 mmol/L, triglycerides ≤ 1.7 mmol/L, systolic and diastolic blood pressure ≤ 90th percentile, and fasting plasma glucose ≤ 5.6 mmol/L). Those that did not meet one or more of the above criteria were classified as children with MUO phenotype.ResultsThe prevalence of MHO was 30.1% (95% CI 23.7 – 37.1) among schoolchildren with obesity and more common in younger and prepubertal children. Compared to MUO, children with MHO phenotype had significantly lower BMI, lower waist circumference, lower uric acid, higher adiponectin, and higher apolipoprotein A-1 levels (p < 0.01). Multivariate logistic regression showed that adiponectin (OR: 1.33, 95% CI 1.05 – 1.68) and apolipoprotein A-1 (OR: 1.02, 95% CI 1.01 – 1.03) were independent predictors for MHO phenotype in this population.ConclusionsMHO phenotype was more common in younger and prepubertal children with obesity. Higher serum levels of adiponectin and apolipoprotein A-1 increased the possibility of schoolchildren with obesity to be classified into MHO phenotype.

An adverse lipoprotein phenotype—hypertriglyceridaemic hyperapolipoprotein B—and the long-term risk of type 2 diabetes: a prospective, longitudinal, observational cohort study

This study examines the risk of new-onset diabetes in patients with hypertriglyceridaemic hyperapolipoprotein B (high triglycerides, high apolipoprotein B [apoB], low LDL cholesterol to apoB ratio, and low HDL cholesterol). The aim was to establish whether this lipoprotein phenotype identified a substantial group at high risk of developing diabetes over the next 20 years. In this prospective, longitudinal, observational cohort study, we used data from the Framingham Offspring cohort (recruited in Framingham, MA, USA). Participants were aged 40-69 years and free of diabetes and cardiovascular disease at a baseline examination done between April, 1987, and November, 1991, and were followed up until March, 2014. Cox proportional hazards regression with hierarchical adjustment for age and sex, waist circumference, and fasting blood glucose were used to model the relationship between each lipid marker and incident diabetes, as well as the relationship between hypertriglyceridaemic hyperapoB (defined as values greater than sample medians of triglycerides and apoB, and less than medians of HDL cholesterol and LDL cholesterol to apoB ratio) and incident diabetes. Of 3446 individuals aged 40-69 years who completed baseline examination, 2515 participants were eligible and included in all analyses. During median 21·1 years (IQR 11·1-23·1) of follow-up, 402 (16·0%) individuals developed diabetes. Age (p=0·032), waist circumference (p<0·0001), fasting blood glucose (p<0·0001), and natural logarithm-transformed triglycerides (p<0·0001) were associated with new-onset diabetes, as were apoB (p=0·0016), LDL cholesterol to apoB ratio (p=0·0018), and HDL cholesterol (p=0·0016) when added to this model. The age and sex-adjusted incidence of diabetes in the hypertriglyceridaemic hyperapoB group was 32·4% (95% CI 27·8-37·7) versus 5·5% (3·5-8·6) in the optimal lipid phenotype group and 15·5% (13·5-17·7) in the mixed lipid phenotype group. The fully adjusted hazard ratio, including glucose and waist circumference, for individuals with hypertriglyceridaemic hyperapoB was 3·30 (95% CI 2·06-5·30; p=0·0008) and for mixed lipid phenotype was 2·17 (1·38-3·40; p<0·0001) compared with those with the optimal lipid phenotype. Our findings suggest that individuals with hypertriglyceridaemic hyperapoB are at high risk of new-onset diabetes and might benefit from intensive measures to prevent diabetes. The association between this phenotype and incident diabetes is consistent with a pro-diabetic effect due to increased clearance of apoB particles from plasma, which could injure pancreatic islet cells. This mechanism might explain the increased risk of diabetes with statin therapy. Doggone Foundation.