OBJECTIVE: To explore the co-morbid influencing factors of postmenopausal osteoporosis(PMOP) and dyslipidemia, and to provide evidence-based basis for clinical co-morbidity management. METHODS: Based on the 2017 to 2018 Beijing community cross-sectional survey data, PMOP patients were included and divided into the dyslipidemia group and the uncomplicated dyslipidemia group according to whether they were comorbid with dyslipidemia. Demographic characteristics, living habits and disease history were collected through questionnaires, and bone mineral density and bone metabolism biomarkers (osteocalcin, blood calcium, serum typeⅠprocollagen N-terminal prepeptide, etc.) were detected on site. Co-morbidity risk factors were analyzed using binary logistic regression. RESULTS: Three hundred and twenty patients with PMOP were included, including the comorbid group (75 patients) and the uncomplicated group (245 patients). The results showed that history of cardiovascular disease [<i>ORi>=1.801, 95%<i>CIi>(1.003, 3.236), <i>Pi>=0.049], history of cerebrovascular disease [<i>ORi>=2.923, 95%<i>CIi>(1.460, 5.854), <i>Pi>=0.002], frying and cooking methods[<i>ORi>=5.388, 95%<i>CIi>(1.632, 17.793), <i>Pi>=0.006], OST results[<i>ORi>=0.910, 95%<i>CIi>(0.843, 0.983), <i>Pi>=0.016], and blood Ca results [<i>ORi>=60.249, 95%<i>CIi>(1.862, 1 949.926), <i>Pi>=0.021] were the influencing factors of PMOP complicated with dyslipidemia. CONCLUSION Focus should be placed on the influencing factors of PMOP and dyslipidemia co-morbidities, with emphasis on multidimensional assessment, combining lifestyle interventions with bone metabolism marker monitoring to optimize co-morbidity management.
Humans ; Dyslipidemias/epidemiology* ; Female ; Middle Aged ; Osteoporosis, Postmenopausal/metabolism* ; Aged ; Cross-Sectional Studies ; Risk Factors ; Bone Density

This review examines strategies for the prevention and management of obesity, hypertension, type 2 diabetes mellitus and dyslipidaemia, conditions that are increasing in Singapore, as components of individualised health plans in 'Healthier SG' and beyond. We describe cardiometabolic disease prevention and management initiatives in Changi General Hospital (CGH), including collaborations with SingHealth Polyclinics, Active SG, Exercise is Medicine Singapore and community partners in the Eastern Community Health Outreach programme, and highlight advances in curable hypertension (e.g., primary hyperaldosteronism) and novel cardiovascular risk markers such as lipoprotein(a). We also outline technology-based interventions, notably the CGH Health Management Unit, which demonstrate the utility and convenience of telemedicine, and digital therapeutics in the form of apps that have been shown to improve treatment adherence and clinical outcomes. Individual empowerment, in partnership with community and healthcare providers and supported by research and innovation of care delivery, is key to building a healthier and stronger nation.
Humans ; Singapore ; Diabetes Mellitus, Type 2/therapy* ; Hypertension/therapy* ; Obesity/therapy* ; Dyslipidemias/therapy* ; Telemedicine ; Cardiovascular Diseases/prevention & control* ; Exercise ; Metabolic Diseases/prevention & control*

Asthma is a diverse disease that can be categorized into various phenotypes and endotypes, including obesity-re-lated asthma and allergic asthma. "Treatable traits (TTs)" represent a new approach to managing asthma. Asthma accompanied by dyslipidemia would be a distinct asthma phenotype that is becoming increasingly common. Therefore, dyslipidemia can potentially serve as a target for the management of asthma. Nevertheless, it remains highly under-researched compared to other observable traits. Gaining knowledge about the clinical and inflammatory characteristics, underlying mechanisms, and potential therapeutic medications for asthma with dyslipidemia is crucial for its effective management. This review aimed to provide a comprehensive overview of asthma with dyslipidemia, consolidating existing knowledge and ongoing research.
Humans ; Asthma/complications* ; Dyslipidemias/epidemiology*

This study aims to investigate the potential effect of the water extract of fresh Rehmanniae Radix on hypercholesterolemia in mice that was induced by a high-fat and high-cholesterol diet and explore its possible mechanism from bile acid reabsorption. Male C57BL/6 mice were randomly assigned into the following groups: control, model, low-and high-dose(4 and 8 g·kg~(-1), respectively) fresh Rehmanniae Radix, and positive drug(simvastatin, 0.05 g·kg~(-1)). Other groups except the control group were fed with a high-fat and high-cholesterol diet for 6 consecutive weeks to induce hypercholesterolemia. From the 6th week, mice were administrated with corresponding drugs daily via gavage for additional 6 weeks, while continuing to be fed with a high-fat and high-cholesterol diet. Serum levels of total cholesterol(TC), triglycerides(TG), low density lipoprotein-cholesterol(LDL-c), high density lipoprotein-cholesterol(HDL-c), and total bile acid(TBA), as well as liver TC and TG levels and fecal TBA level, were determined by commercial assay kits. Hematoxylin-eosin(HE) staining, oil red O staining, and transmission electron microscopy were performed to observe the pathological changes in the liver. Three livers samples were randomly selected from each of the control, model, and high-dose fresh Rehmanniae Radix groups for high-throughput transcriptome sequencing. Differentially expressed genes were mined and KEGG pathway enrichment analysis was performed to predict the key pathways and target genes of the water extract of fresh Rehmanniae Radix in the treatment of hypercholesterolemia. RT-qPCR was employed to measure the mRNA levels of cholesterol 7α-hydroxylase(CYP7A1) and cholesterol 27α-hydroxylase(CYP27A1) in the liver. Western blot was employed to determine the protein levels of CYP7A1 and CYP27A1 in the liver as well as farnesoid X receptor(FXR), apical sodium-dependent bile acid transporter(ASBT), and ileum bile acid-binding protein(I-BABP) in the ileum. The results showed that the water extract of fresh Rehmanniae Radix significantly lowered the levels of TC and TG in the serum and liver, as well as the level of LDL-c in the serum. Conversely, it elevated the level of HDL-c in the serum and TBA in feces. No significant difference was observed in the level of TBA in the serum among groups. HE staining, oil red O staining, and transmission electron microscopy showed that the water extract reduced the accumulation of lipid droplets in the liver. Further mechanism studies revealed that the water extract of fresh Rehmanniae Radix significantly down-regulated the protein levels of FXR and bile acid reabsorption-related proteins ASBT and I-BABP. Additionally, it enhanced CYP7A1 and CYP27A1, the key enzymes involved in bile acid synthesis. Therefore, it is hypothesized that the water extract of fresh Rehmanniae Radix may exert an anti-hypercholesterolemic effect by regulating FXR/ASBT/I-BABP signaling, inhibiting bile acid reabsorption, and increasing bile acid excretion, thus facilitating the conversion of cholesterol to bile acids.
Animals ; Male ; Bile Acids and Salts/metabolism* ; Mice, Inbred C57BL ; Mice ; Diet, High-Fat/adverse effects* ; Cholesterol/metabolism* ; Drugs, Chinese Herbal/administration & dosage* ; Hypercholesterolemia/genetics* ; Receptors, Cytoplasmic and Nuclear/genetics* ; Rehmannia/chemistry* ; Liver/drug effects* ; Humans ; Cholesterol 7-alpha-Hydroxylase/genetics* ; Plant Extracts

OBJECTIVES: To clarify the causal relationship between the level of cytoplasmic unactivated mineralocorticoid receptor (MR) and the development of tubulointerstitial nephritis (TIN), and to evaluate the impact of MR on dyslipidemia, particularly secondary hyperlipemia, in patients with diabetic kidney disease. METHODS: We conducted a two-sample Mendelian randomization study using genome-wide association study (GWAS) summary data. Genetic variants associated with MR levels were selected as exposures, with TIN and lipid profiles [including low-density lipoprotein cholesterol (LDL-C), triglyceride, and high-density lipoprotein cholesterol] as outcomes. A two-step Mendelian randomization approach was used to assess TIN as a mediator, employing inverse variance weighted regression as the primary analysis, supplemented by Mendelian randomization-Egger, weighted median, and sensitivity analyses. RESULTS: Cytoplasmic unactivated MR level exhibited a significant causal association with a decreased risk of TIN (<i>ORi> = 0.8598, 95% <i>CIi> [0.7775-0.9508], <i>Pi> < 0.001). Although no significant causal relationship was identified between MR level and secondary hyperlipemia, a potential association of cytoplasmic unactivated MR level with lower LDL-C levels was observed (<i>OR =i> 0.9901, 95% <i>CIi> [0.9821-0.9983], <i>Pi> = 0.018). Additionally, TIN exhibited causal links with secondary hyperlipemia (<i>OR =i> 1.0016, 95% <i>CIi> [1.0002-1.0029], <i>Pi> = 0.020) and elevated LDL-C (<i>OR =i> 1.0111, 95% <i>CIi> [1.0024-1.0199], <i>Pi> = 0.012), particularly LDL-C in European males (<i>OR =i> 1.0230, 95% <i>CIi> [1.0103-1.0358], <i>Pi> < 0.001). Inverse Mendelian randomization analysis revealed causal relationships between TIN and genetically predicted triglyceride (<i>OR =i> 0.7027, 95% <i>CIi> [0.6189-0.7978], <i>Pi> < 0.001), high-density lipoprotein cholesterol (<i>OR =i> 1.1247, 95% <i>CIi> [1.0019-1.2626], <i>Pi> = 0.046), and LDL-C (<i>OR =i> 0.8423, 95% <i>CIi> [0.7220-0.9827], <i>Pi> = 0.029). Notably, TIN mediated 16.7% of the causal association between MR and LDL-C levels. CONCLUSIONS MR plays a critical role in the development of TIN and lipid metabolism, highlighting the potential of MR-antagonists in reducing renal damage and lipid metabolism-associated complications.
Humans ; Mendelian Randomization Analysis ; Nephritis, Interstitial/metabolism* ; Receptors, Mineralocorticoid/genetics* ; Lipid Metabolism/genetics* ; Genome-Wide Association Study ; Male ; Female ; Polymorphism, Single Nucleotide ; Dyslipidemias/metabolism*

OBJECTIVE: To investigate the gene detection results of 2 patients with familial hypercholesterolemia (FH) caused by complex heterozygous variation, and to clarify the relationship between clinical manifestations and gene variation. METHODS: Two patients (patient 1 and 2) with FH who visited Beijing Anzhen Hospital Affiliated to Capital Medical University in 2018 were selected as research subjects. A retrospective study method was used to collect clinical and family history data of the two patients. And 2 mL of peripheral venous blood from each of the two patients was collected, and genomic DNA extraction was performed on the blood samples. Sanger sequencing was used to validate the variant sites of the two patients detected by whole-exome sequencing (WES). Pathogenicity of variants was classified based on the American College of Medical Genetics and Genomics (ACMG) Standards and Guidelines for the Classification of Genetic Variants (hereinafter referred to as the "ACMG Guidelines"), and the impact of variant was analyzed using multiple bioinformatics tools including SIFT, PolyPhen-2, and SWISS-MODEL. This study has been approved by Beijing Anzhen Hospital Affiliated to Capital Medical University (Ethics No. 2024215X). RESULTS: Patient 1 initially presented with early-onset coronary heart disease, with initial lipid levels of serum total cholesterol (TC) 9.86 mmol/L (normal reference value: 3.10~5.20 mmol/L) and serum low-density lipoprotein cholesterol (LDL-C) 8.37 mmol/L (normal reference value: 1.27~3.12 mmol/L) on admission. Patient 1 initially underwent treatment with rosuvastatin combined with ezetimibe for one month, but the lipid-lowering effect was not significant. The lipid-lowering therapy was then adjusted to atorvastatin combined with ezetimibe and probucol. After one year of treatment, the patient developed paroxysmal chest pain symptoms. A follow-up lipid profile showed a serum TC level of 4.50 mmol/L and a LDL-C level of 3.55 mmol/L. The lipid-lowering regimen was continued, and the serum LDL-C levels were maintained between 2.65 and 3.66 mmol/L. Patient 2 was found to have an abnormally high blood lipid level and carotid artery hardening during physical examination, with an initial blood lipid level of serum TC 11.82 mmol/L and serum LDL-C 9.63 mmol/L. After receiving rosuvastatain therapy, the lipid-lowering effect was significant. WES revealed that patient 1 carried the heterozygous variants c.1871_1873del(p.Ile624del) and c.1747C>T (p.His583Tyr) in the LDLR gene (NM_000527.4), while patient 2 carried the heterozygous variants c.1747C>T (p.His583Tyr) in the LDLR gene and c.6936_6937inv (p.Ile2313Val) in the APOB gene (NM_000384). According to the ACMG Guidelines, the LDLR gene c.1747C>T (p.His583Tyr) was classified as a pathogenic variant (PS3+PM1+PM2_supporting+PM5+PP2+PP3), and c.1871_1873del (p.Ile624del) was classified as a pathogenic variant (PS3+PS4+PM2_supporting+PM1+PM4); the APOB gene c.6936_6937inv (p.Ile2313Val) was classified as a variant of uncertain clinical significance (PM2_supporting BP4). CONCLUSION Patients 1 and 2 in this study were patients with complex heterozygous variant FH, and their genotypic differences may be related to the differences in clinical serum LDL-C levels and the efficacy of hypolipidemic agents.
Humans ; Hyperlipoproteinemia Type II/drug therapy* ; Male ; Female ; Heterozygote ; Adult ; Middle Aged ; Receptors, LDL/genetics* ; Retrospective Studies ; Mutation ; Exome Sequencing

Objectives: We determined the clinical characteristics and prevalence of metabolic syndrome among adult Filipinos with overt hypothyroidism. Methodology: This is a cross-sectional study of 151 adults. Patients were recruited by sequential enrollment. Anthropometric and blood pressure measurements were performed followed by blood extraction for metabolic parameters and thyroid function tests. Clinical and laboratory characteristics were compared between patients with and without metabolic syndrome. Results: The prevalence of metabolic syndrome is 40.4% (95%CI: 32.5%, 48.7%). Patients with metabolic syndrome have a waist circumference of 88.4 ± 7.7 cm in females and 93.3 ± 9.0 cm in males. The median fasting blood glucose was 111.4 (52.2) mg/dL, median systolic blood pressure of 120 (30) mm Hg and diastolic blood pressure of 80 (20) mmHg, median serum triglycerides of 174.3 (114.2) mg/dL, median HDL-C of 42.3 (19.2) mg/dL and a proportion of patients with diabetes (23.0%) and hypertension (44.3%), respectively. The presence of increased waist circumference is the most prevalent component seen among hypothyroid patients. There were no differences in terms of age, sex, etiology of hypothyroidism and anti-TPO levels in those with and without metabolic syndrome. Conclusion The prevalence of metabolic syndrome in adult Filipinos with hypothyroidism is high. Emphasis must be placed on early screening using waist circumference and metabolic parameters among hypothyroid patients who are at high risk of developing metabolic syndrome.
Dyslipidemias ; Hypothyroidism ; Metabolic Syndrome ; Prevalence

BACKGROUND: Tri-ponderal mass index (TMI) has been reported to be a more accurate estimate of body fat than body mass index (BMI). This study aims to compare the effectiveness of TMI and BMI in identifying hypertension, dyslipidemia, impaired fasting glucose (IFG), abdominal obesity, and clustered cardio-metabolic risk factors (CMRFs) in 3- to 17-year-old children. METHODS: A total of 1587 children aged 3 to 17 years were included. Logistic regression was used to evaluate correlations between BMI and TMI. Area under the curves (AUCs) were used to compare discriminative capability among indicators. BMI was converted to BMI- z scores, and accuracy was compared by false-positive rate, false-negative rate, and total misclassification rate. RESULTS: Among children aged 3 to 17 years, the mean TMI was 13.57 ± 2.50 kg/m 3 for boys and 13.3 ± 2.33 kg/m 3 for girls. Odds ratios (ORs) of TMI for hypertension, dyslipidemia, abdominal obesity, and clustered CMRFs ranged from 1.13 to 3.15, higher than BMI, whose ORs ranged from 1.08 to 2.98. AUCs showed similar ability of TMI (AUC: 0.83) and BMI (AUC: 0.85) in identifying clustered CMRFs. For abdominal obesity and hypertension, the AUC of TMI was 0.92 and 0.64, respectively, which was significantly better than that of BMI, 0.85 and 0.61. AUCs of TMI for dyslipidemia and IFG were 0.58 and 0.49. When 85th and 95th of TMI were set as thresholds, total misclassification rates of TMI for clustered CMRFs ranged from 6.5% to 16.4%, which was not significantly different from that of BMI- z scores standardized according to World Health Organization criteria. CONCLUSIONS TMI was found to have equal or even better effectiveness in comparison with BMI in identifying hypertension, abdominal obesity, and clustered CMRFs TMI was more stable than BMI in 3- to 17-year-old children, while it failed to identify dyslipidemia and IFG. It is worth considering the use of TMI for screening CMRFs in children and adolescents.
Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Male ; Body Mass Index ; Dyslipidemias ; East Asian People ; Hypertension ; Obesity, Abdominal ; Pediatric Obesity/diagnosis* ; Cardiometabolic Risk Factors

OBJECTIVE: To investigate the spatial patterns of the prevalence, awareness, treatment, and control rates of dyslipidemia at the provincial level in China. METHODS: A national and provincial representative cross-sectional survey was conducted among 178,558 Chinese adults in 31 provinces in mainland China in 2018-2019, using a multi-stage, stratified, cluster-randomized sampling design. Subjects, as households, were selected, followed by a home visit to collect information. Both descriptive and linear regression procedures were applied in the analyses. RESULTS: The overall prevalence of dyslipidemia was 35.6%, and wide geographic variations of prevalence, treatment, and control rates of dyslipidemia were identified among 178,558 eligible participants with a mean age of 55.1 ± 13.8 years. The highest-lowest difference regarding the provincial level prevalence rates were 19.7% <i>vs.i> 2.1% for high low-density lipoprotein cholesterol, 16.7% <i>vs.i> 2.5% for high total cholesterol, 35.9% <i>vs.i> 5.4% for high triglycerides, and 31.4% <i>vs.i> 10.5% for low high-density lipoprotein cholesterol. The treatment rate of dyslipidemia was correlated with the socio-demographic index ( <i>Pi> < 0.001), urbanization rate ( <i>Pi> = 0.01), and affordable basic technologies and essential medicines ( <i>Pi> < 0.001). CONCLUSION Prevailing dyslipidemia among the Chinese population and its wide geographic variations in prevalence, treatment, and control suggest that China needs both integrated and localized public health strategies across provinces to improve lipid management.
Humans ; Adult ; Middle Aged ; Aged ; Cross-Sectional Studies ; Prevalence ; East Asian People ; Dyslipidemias/prevention & control* ; China/epidemiology* ; Cholesterol, HDL ; Risk Factors ; Triglycerides

OBJECTIVE: To analyze variant of LDLR gene in a patient with familial hypercholesterolemia (FH) in order to provide a basis for the clinical diagnosis and genetic counseling. METHODS: A patient who had visited the Reproductive Medicine Center of the First Affiliated Hospital of Anhui Medical University in June 2020 was selected as the study subject. Clinical data of the patient was collected. Whole exome sequencing (WES) was applied to the patient. Candidate variant was verified by Sanger sequencing. Conservation of the variant site was analyzed by searching the UCSC database. RESULTS: The total cholesterol level of the patient was increased, especially low density lipoprotein cholesterol. A heterozygous c.2344A>T (p.Lys782*) variant was detected in the LDLR gene. Sanger sequencing confirmed that the variant was inherited from the father. CONCLUSION The heterozygous c.2344A>T (p.Lys782*) variant of the LDLR gene probably underlay the FH in this patient. Above finding has provided a basis for genetic counseling and prenatal diagnosis for this family.
Humans ; Cholesterol, LDL/genetics* ; Heterozygote ; Hyperlipoproteinemia Type II/genetics* ; Mutation ; Pedigree ; Phenotype ; Receptors, LDL/genetics*