Pub Date : 2026-01-01DOI: 10.1016/j.jacl.2025.10.059
Akos Berthold MMSc, CGC, Rebecca Miller MS, CGC, Christopher Jordan MD, Jared Spitz MD
Familial hypercholesterolemia (FH) is a genetic disorder leading to elevated low-density lipoprotein cholesterol (LDL-c) and increased risk for early atherosclerotic cardiovascular disease (ASCVD). While the 3 primary genes (LDLR, APOB, and PCSK9) associated with monogenic FH have been well established, rare variants remain challenging to interpret. We report a novel APOB variant, c.9498G>C (p.Lys3166Asn) in the region of the apolipoprotein B100 that is involved in the binding to the LDL receptor (LDLR). This variant was identified in multiple unrelated families with FH. We initially observed this variant in the proband with severe hypercholesterolemia and early ASCVD. Familial testing showed complete segregation of the variant with FH in the proband’s family in all tested individuals with hypercholesterolemia. Further collaboration with diagnostic laboratories revealed 3 additional probands with the same variant and severe hypercholesterolemia. These findings suggest that this variant causes FH; however, functional studies are needed for definitive confirmation. This case underscores the importance of collaborative data sharing in variant interpretation and the role of case reports in enhancing genetic diagnosis for FH.
{"title":"Novel APOB variant causes familial hypercholesterolemia in multiple unrelated families","authors":"Akos Berthold MMSc, CGC, Rebecca Miller MS, CGC, Christopher Jordan MD, Jared Spitz MD","doi":"10.1016/j.jacl.2025.10.059","DOIUrl":"10.1016/j.jacl.2025.10.059","url":null,"abstract":"<div><div>Familial hypercholesterolemia (FH) is a genetic disorder leading to elevated low-density lipoprotein cholesterol (LDL-c) and increased risk for early atherosclerotic cardiovascular disease (ASCVD). While the 3 primary genes (<em>LDLR, APOB</em>, and <em>PCSK9</em>) associated with monogenic FH have been well established, rare variants remain challenging to interpret. We report a novel <em>APOB</em> variant, c.9498G>C (p.Lys3166Asn) in the region of the apolipoprotein B100 that is involved in the binding to the LDL receptor (LDLR). This variant was identified in multiple unrelated families with FH. We initially observed this variant in the proband with severe hypercholesterolemia and early ASCVD. Familial testing showed complete segregation of the variant with FH in the proband’s family in all tested individuals with hypercholesterolemia. Further collaboration with diagnostic laboratories revealed 3 additional probands with the same variant and severe hypercholesterolemia. These findings suggest that this variant causes FH; however, functional studies are needed for definitive confirmation. This case underscores the importance of collaborative data sharing in variant interpretation and the role of case reports in enhancing genetic diagnosis for FH.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 215-219"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145582012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.jacl.2025.09.029
Daniela Junqueira PharmD, MSc, PhD , Victoria Molenkamp BSc , Rajat Goel MPharm , Joshua Ikuemonisan MD, MPH , Patrick J. Campbell PharmD, PhD
BACKGROUND
Implementation strategies can enhance the utilization of lipid-lowering therapies (LLTs), such as proprotein convertase subtilisin/kexin type 9 inhibitors. However, the effectiveness of these strategies, particularly for nonstatin add-on LLTs, remains unclear. This global systematic review examined implementation strategies to optimize the uptake, adherence, and persistence of nonstatin add-on LLTs, their associated clinical outcomes, and the barriers and enablers to the success of these strategies.
METHODS
Implementation strategy studies were identified from bibliographic databases and additional sources not indexed in bibliographic databases, including conference proceedings and clinical trial registries. The review included observational, interventional, and implementation science studies that described implementation strategies targeted for patients, prescribers, or other healthcare providers to improve the adoption of LLTs. Data elements of the implementation strategy and outcomes were extracted and narratively synthesized.
FINDINGS
Twenty-one studies were included, primarily from North America, with most being retrospective. Prescriber-driven, pharmacist-driven, multidisciplinary healthcare provider-driven, remote patient programs, and pill formulation strategies were evaluated. Prescriber-driven strategies enhanced uptake of nonstatin LLTs, leading to improvements in achieving low-density lipoprotein cholesterol (LDL-C) goals. Pharmacist-driven interventions, including motivational interviews and continuous care, enhanced adherence and LDL-C control. Multidisciplinary approaches and remote patient programs also enhanced use of optimized guideline-directed add-on LLTs and lowered LDL-C levels. Pill formulation strategies yielded mixed results. Barriers to adoption of nonstatin LLTs included high costs, patient refusal, and comorbidities, while enablers included reduced skepticism and supportive clinical environments.
CONCLUSIONS
All strategies positively influenced the optimization of nonstatin add-on LLT use, particularly by reducing LDL-C levels and improving adherence. These strategies can be implemented in various healthcare contexts, depending on factors such as gaps in care, geographic and health system landscapes, local context, acceptability, and costs.
{"title":"Implementation strategies to optimize the use of nonstatin add-on lipid-lowering therapies in individuals with dyslipidemia: A systematic review","authors":"Daniela Junqueira PharmD, MSc, PhD , Victoria Molenkamp BSc , Rajat Goel MPharm , Joshua Ikuemonisan MD, MPH , Patrick J. Campbell PharmD, PhD","doi":"10.1016/j.jacl.2025.09.029","DOIUrl":"10.1016/j.jacl.2025.09.029","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Implementation strategies can enhance the utilization of lipid-lowering therapies (LLTs), such as proprotein convertase subtilisin/kexin type 9 inhibitors. However, the effectiveness of these strategies, particularly for nonstatin add-on LLTs, remains unclear. This global systematic review examined implementation strategies to optimize the uptake, adherence, and persistence of nonstatin add-on LLTs, their associated clinical outcomes, and the barriers and enablers to the success of these strategies.</div></div><div><h3>METHODS</h3><div>Implementation strategy studies were identified from bibliographic databases and additional sources not indexed in bibliographic databases, including conference proceedings and clinical trial registries. The review included observational, interventional, and implementation science studies that described implementation strategies targeted for patients, prescribers, or other healthcare providers to improve the adoption of LLTs. Data elements of the implementation strategy and outcomes were extracted and narratively synthesized.</div></div><div><h3>FINDINGS</h3><div>Twenty-one studies were included, primarily from North America, with most being retrospective. Prescriber-driven, pharmacist-driven, multidisciplinary healthcare provider-driven, remote patient programs, and pill formulation strategies were evaluated. Prescriber-driven strategies enhanced uptake of nonstatin LLTs, leading to improvements in achieving low-density lipoprotein cholesterol (LDL-C) goals. Pharmacist-driven interventions, including motivational interviews and continuous care, enhanced adherence and LDL-C control. Multidisciplinary approaches and remote patient programs also enhanced use of optimized guideline-directed add-on LLTs and lowered LDL-C levels. Pill formulation strategies yielded mixed results. Barriers to adoption of nonstatin LLTs included high costs, patient refusal, and comorbidities, while enablers included reduced skepticism and supportive clinical environments.</div></div><div><h3>CONCLUSIONS</h3><div>All strategies positively influenced the optimization of nonstatin add-on LLT use, particularly by reducing LDL-C levels and improving adherence. These strategies can be implemented in various healthcare contexts, depending on factors such as gaps in care, geographic and health system landscapes, local context, acceptability, and costs.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 4-20"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145573797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.jacl.2025.10.073
Antonina Giammanco MD, PhD , Laura D’Erasmo MD , Gabriella Iannuzzo MD , Davide Noto MD, PhD , Anna Montali , Alberto Zambon MD, PhD , Francesco Forte MD , Patrizia Suppressa MD , Stefano Giannini MD , Carlo M. Barbagallo MD, PhD , Carola M. Gagliardo MD , Emilio Nardi MD , Daniele Tramontano MD , Giuseppe Brancatelli MD , Marcello Arca MD , Angelo B. Cefalù MD, PhD , Maurizio Averna MD
BACKGROUND
Familial chylomicronemia syndrome (FCS) is a rare, severe, autosomal recessive disorder characterized by extremely high triglyceride (TG) levels and an increased risk of acute and/or recurrent pancreatitis. Lomitapide, a microsomal triglyceride transfer protein (MTP) inhibitor, is approved for the treatment of homozygous familial hypercholesterolemia. The open-label, single-arm LOCHNES study (EudraCT 2018-002911-80) investigated lomitapide in adult patients with genetically confirmed FCS and a history of pancreatitis, demonstrating its efficacy and tolerability.
METHODS
Fourteen patients previously enrolled in the LOCHNES study were admitted to the Lomitapide Expanded Access Program 2 months after study completion. They were followed every 3 months over a nearly 3-year period (median follow-up: 33 months), continuing lomitapide at the maximum tolerated dose established during the trial. Evaluations included lipid profile, liver function tests, hepatic fat content, and liver stiffness.
RESULTS
At the start of the follow-up period (after a 2-month lomitapide washout), median TG levels were 1899.5 mg/dL (range: 1013.5-2572 mg/dL). At the last observation, median fasting TGs were reduced to 376.5 mg/dL (range: 195-1328 mg/dL), representing a 80.2% decrease; 9 patients achieved TG levels ≤750 mg/dL. Adverse events were mostly mild-to-moderate, predominantly gastrointestinal (n = 11). Two patients experienced an episode of acute pancreatitis during follow-up. Liver enzymes ≥3 × the upper limit of normal were observed in 2 patients. Hepatic fat content increased in 3 patients, while median liver stiffness remained within the normal range.
CONCLUSIONS
Lomitapide effectively and safely reduced TG levels in FCS patients with a history of pancreatitis over a nearly 3-year follow-up period. These findings are consistent with those of the open-label trial, despite the use of a lower median daily dose (27 mg). No new safety signals were observed.
{"title":"Long-term efficacy and safety of lomitapide in patients with familial chylomicronemia syndrome: Data from an expanded access program","authors":"Antonina Giammanco MD, PhD , Laura D’Erasmo MD , Gabriella Iannuzzo MD , Davide Noto MD, PhD , Anna Montali , Alberto Zambon MD, PhD , Francesco Forte MD , Patrizia Suppressa MD , Stefano Giannini MD , Carlo M. Barbagallo MD, PhD , Carola M. Gagliardo MD , Emilio Nardi MD , Daniele Tramontano MD , Giuseppe Brancatelli MD , Marcello Arca MD , Angelo B. Cefalù MD, PhD , Maurizio Averna MD","doi":"10.1016/j.jacl.2025.10.073","DOIUrl":"10.1016/j.jacl.2025.10.073","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Familial chylomicronemia syndrome (FCS) is a rare, severe, autosomal recessive disorder characterized by extremely high triglyceride (TG) levels and an increased risk of acute and/or recurrent pancreatitis. Lomitapide, a microsomal triglyceride transfer protein (MTP) inhibitor, is approved for the treatment of homozygous familial hypercholesterolemia. The open-label, single-arm LOCHNES study (EudraCT 2018-002911-80) investigated lomitapide in adult patients with genetically confirmed FCS and a history of pancreatitis, demonstrating its efficacy and tolerability.</div></div><div><h3>METHODS</h3><div>Fourteen patients previously enrolled in the LOCHNES study were admitted to the Lomitapide Expanded Access Program 2 months after study completion. They were followed every 3 months over a nearly 3-year period (median follow-up: 33 months), continuing lomitapide at the maximum tolerated dose established during the trial. Evaluations included lipid profile, liver function tests, hepatic fat content, and liver stiffness.</div></div><div><h3>RESULTS</h3><div>At the start of the follow-up period (after a 2-month lomitapide washout), median TG levels were 1899.5 mg/dL (range: 1013.5-2572 mg/dL). At the last observation, median fasting TGs were reduced to 376.5 mg/dL (range: 195-1328 mg/dL), representing a 80.2% decrease; 9 patients achieved TG levels ≤750 mg/dL. Adverse events were mostly mild-to-moderate, predominantly gastrointestinal (n = 11). Two patients experienced an episode of acute pancreatitis during follow-up. Liver enzymes ≥3 × the upper limit of normal were observed in 2 patients. Hepatic fat content increased in 3 patients, while median liver stiffness remained within the normal range.</div></div><div><h3>CONCLUSIONS</h3><div>Lomitapide effectively and safely reduced TG levels in FCS patients with a history of pancreatitis over a nearly 3-year follow-up period. These findings are consistent with those of the open-label trial, despite the use of a lower median daily dose (27 mg). No new safety signals were observed.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 104-111"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Familial hypercholesterolemia (FH) is caused by genetic mutations in lipid metabolism that increase atherosclerotic cardiovascular disease (ASCVD) risk.
OBJECTIVE
We wanted to assess lipid profile effects of liver transplant in i) a donor patient with heterozygous FH (HeFH), and ii) a HeFH recipient patient with colorectal adenocarcinoma with isolated liver metastasis.
METHODS
A 34-year-old donor female with HeFH and intolerance to all lipid lowering therapies underwent living donor HeFH-negative liver transplant. Her HeFH liver was subsequently transplanted into a 49-year-old recipient female with colorectal adenocarcinoma with isolated liver metastasis, despite surgery and chemotherapy.
RESULTS
Donor patient with HeFH who got HeF H negative liver transplant had significant improvement in lipid panel to the point of no longer requiring lipid lowering therapy. Post-liver transplant, hyperlipidemia developed in the recipient of the HeFH liver, though not quite to the level of the donor baseline, suggesting physiologically functioning extrahepatic LDL receptors' contribution to some LDL-C clearance.
CONCLUSION
Utilizing HeFH liver transplant, combined with aggressive treatment of dyslipidemia can be used to potentially salvage higher risk patients with isolated liver metastasis from colon cancer.
{"title":"Lipid profile effects on donor and recipient of a domino liver transplant with heterozygous familial hypercholesterolemia","authors":"Dinesh Poudyal MD, MPH , Idris Yakubu PharmD , Vinay Kumaran MD , Mohammad Siddiqui MD , Stéphanie B. Mayer MD, MHSc","doi":"10.1016/j.jacl.2025.10.060","DOIUrl":"10.1016/j.jacl.2025.10.060","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Familial hypercholesterolemia (FH) is caused by genetic mutations in lipid metabolism that increase atherosclerotic cardiovascular disease (ASCVD) risk.</div></div><div><h3>OBJECTIVE</h3><div>We wanted to assess lipid profile effects of liver transplant in i) a donor patient with heterozygous FH (HeFH), and ii) a HeFH recipient patient with colorectal adenocarcinoma with isolated liver metastasis.</div></div><div><h3>METHODS</h3><div>A 34-year-old donor female with HeFH and intolerance to all lipid lowering therapies underwent living donor HeFH-negative liver transplant. Her HeFH liver was subsequently transplanted into a 49-year-old recipient female with colorectal adenocarcinoma with isolated liver metastasis, despite surgery and chemotherapy.</div></div><div><h3>RESULTS</h3><div>Donor patient with HeFH who got HeF H negative liver transplant had significant improvement in lipid panel to the point of no longer requiring lipid lowering therapy. Post-liver transplant, hyperlipidemia developed in the recipient of the HeFH liver, though not quite to the level of the donor baseline, suggesting physiologically functioning extrahepatic LDL receptors' contribution to some LDL-C clearance.</div></div><div><h3>CONCLUSION</h3><div>Utilizing HeFH liver transplant, combined with aggressive treatment of dyslipidemia can be used to potentially salvage higher risk patients with isolated liver metastasis from colon cancer.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 200-203"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145743003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.jacl.2025.10.002
Jelani K. Grant MD, MHS , Pooja Selvam MD , Margaret Koester MD, MPH , Thorsten M. Leucker MD, PhD , Andreas S. Barth MD, PhD
OBJECTIVES
Patients with muscular dystrophies are at increased cardiometabolic risk due to reduced mobility, increased adiposity, glucose intolerance, and dyslipidemia. While statins remain the cornerstone of cardiovascular disease prevention in the general population, their use in muscular dystrophies is complicated by the presence of underlying muscle symptoms, which can be difficult to distinguish from statin-associated myopathy. This overlap contributes to heightened concerns about statin tolerance and may impair long-term adherence. The emergence of nonstatin lipid-lowering therapies presents an important opportunity to revisit the conventional “statin-first” approach. Therefore, we sought to highlight the under-recognized issue of atherosclerotic cardiovascular disease (ASCVD) prevention in patients with muscular dystrophy, and explore alternative lipid-lowering strategies beyond statins, given the unique challenges in this population.
METHODS
We conducted a comprehensive review of the existing literature on dyslipidemia and ASCVD risk in muscular dystrophies, evaluated current management guidelines, and shared our institutional experience by presenting the largest known case series of patients with muscular dystrophies treated with nonstatin lipid-lowering therapies.
RESULTS
Statin use in muscular dystrophy is complicated by the difficulty in distinguishing baseline muscle symptoms from statin-associated myopathy, leading to concerns about tolerance and adherence. Our case series demonstrates that nonstatin therapies are a viable and well-tolerated alternative in this population.
CONCLUSIONS
There is a critical need to expand the focus of cardiovascular care in muscular dystrophy to include ASCVD prevention. Nonstatin therapies represent a promising and practical option for managing dyslipidemia in patients with muscular dystrophy. Tailored approaches are needed to balance cardiovascular risk reduction with the unique neuromuscular challenges in this population.
{"title":"Tailoring strategies for dyslipidemia management and atherosclerotic cardiovascular disease prevention in muscular dystrophy patients","authors":"Jelani K. Grant MD, MHS , Pooja Selvam MD , Margaret Koester MD, MPH , Thorsten M. Leucker MD, PhD , Andreas S. Barth MD, PhD","doi":"10.1016/j.jacl.2025.10.002","DOIUrl":"10.1016/j.jacl.2025.10.002","url":null,"abstract":"<div><h3>OBJECTIVES</h3><div>Patients with muscular dystrophies are at increased cardiometabolic risk due to reduced mobility, increased adiposity, glucose intolerance, and dyslipidemia. While statins remain the cornerstone of cardiovascular disease prevention in the general population, their use in muscular dystrophies is complicated by the presence of underlying muscle symptoms, which can be difficult to distinguish from statin-associated myopathy. This overlap contributes to heightened concerns about statin tolerance and may impair long-term adherence. The emergence of nonstatin lipid-lowering therapies presents an important opportunity to revisit the conventional “statin-first” approach. Therefore, we sought to highlight the under-recognized issue of atherosclerotic cardiovascular disease (ASCVD) prevention in patients with muscular dystrophy, and explore alternative lipid-lowering strategies beyond statins, given the unique challenges in this population.</div></div><div><h3>METHODS</h3><div>We conducted a comprehensive review of the existing literature on dyslipidemia and ASCVD risk in muscular dystrophies, evaluated current management guidelines, and shared our institutional experience by presenting the largest known case series of patients with muscular dystrophies treated with nonstatin lipid-lowering therapies.</div></div><div><h3>RESULTS</h3><div>Statin use in muscular dystrophy is complicated by the difficulty in distinguishing baseline muscle symptoms from statin-associated myopathy, leading to concerns about tolerance and adherence. Our case series demonstrates that nonstatin therapies are a viable and well-tolerated alternative in this population.</div></div><div><h3>CONCLUSIONS</h3><div>There is a critical need to expand the focus of cardiovascular care in muscular dystrophy to include ASCVD prevention. Nonstatin therapies represent a promising and practical option for managing dyslipidemia in patients with muscular dystrophy. Tailored approaches are needed to balance cardiovascular risk reduction with the unique neuromuscular challenges in this population.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 179-195"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145957743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.jacl.2025.10.054
Jee Ah Kim MD, PhD, Min-Seung Park MD, PhD, Eun Hye Cho MD, PhD, Min-Jung Kwon MD, PhD, Hyosoon Park MD, PhD, Hee-Yeon Woo MD, PhD
BACKGROUND
Discordance between apolipoprotein B (apoB) and low-density lipoprotein cholesterol (LDL-C) levels is frequently observed in individuals with metabolic disorders and may contribute to underestimated cardiovascular risk. Population-based data on LDL-C discordance in East Asians, particularly in metabolically healthy individuals, remain limited.
OBJECTIVE
We aimed to investigate the distribution of apoB relative to LDL-C and non-high-density lipoprotein cholesterol (non-HDL-C) levels and assess the prevalence and determinants of apoB–LDL-C discordance.
METHODS
We analyzed data from 411,125 Korean adults who underwent health checkups between 2011 and 2023. Participants with a history of cardiovascular disease or lipid-lowering therapy were excluded from the study. ApoB–LDL-C (and apoB–non-HDL-C) discordance was quantified using residuals from a linear regression model. Individuals were classified as discordant-high (residuals > 75th percentile), discordant-low (residuals < 25th percentile), or concordant (residuals between the 25th and 75th percentiles). Subgroup analyses were performed for metabolic status, obesity phenotype, and lifestyle or family risk factors.
RESULTS
Substantial variability in apoB levels was observed at each LDL-C and non-HDL-C level. ApoB–LDL-C discordance patterns between apoB and non-HDL-C were similar to those observed with apoB and LDL-C, though with smaller residual differences. Discordance was most pronounced in metabolically unhealthy obese individuals, followed by metabolically unhealthy lean individuals, and metabolically healthy individuals (P < .001), indicating that metabolic health is a stronger determinant of discordance than obesity.
CONCLUSIONS
ApoB–LDL-C discordance is common, even among metabolically healthy individuals, and is primarily driven by metabolic dysfunction rather than by obesity. ApoB measurements should be included in routine cardiovascular risk assessments.
{"title":"Associations of metabolic health and obesity with apolipoprotein B and low-density lipoprotein cholesterol discordance in a large Korean cohort","authors":"Jee Ah Kim MD, PhD, Min-Seung Park MD, PhD, Eun Hye Cho MD, PhD, Min-Jung Kwon MD, PhD, Hyosoon Park MD, PhD, Hee-Yeon Woo MD, PhD","doi":"10.1016/j.jacl.2025.10.054","DOIUrl":"10.1016/j.jacl.2025.10.054","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Discordance between apolipoprotein B (apoB) and low-density lipoprotein cholesterol (LDL-C) levels is frequently observed in individuals with metabolic disorders and may contribute to underestimated cardiovascular risk. Population-based data on LDL-C discordance in East Asians, particularly in metabolically healthy individuals, remain limited.</div></div><div><h3>OBJECTIVE</h3><div>We aimed to investigate the distribution of apoB relative to LDL-C and non-high-density lipoprotein cholesterol (non-HDL-C) levels and assess the prevalence and determinants of apoB–LDL-C discordance.</div></div><div><h3>METHODS</h3><div>We analyzed data from 411,125 Korean adults who underwent health checkups between 2011 and 2023. Participants with a history of cardiovascular disease or lipid-lowering therapy were excluded from the study. ApoB–LDL-C (and apoB–non-HDL-C) discordance was quantified using residuals from a linear regression model. Individuals were classified as discordant-high (residuals > 75th percentile), discordant-low (residuals < 25th percentile), or concordant (residuals between the 25th and 75th percentiles). Subgroup analyses were performed for metabolic status, obesity phenotype, and lifestyle or family risk factors.</div></div><div><h3>RESULTS</h3><div>Substantial variability in apoB levels was observed at each LDL-C and non-HDL-C level. ApoB–LDL-C discordance patterns between apoB and non-HDL-C were similar to those observed with apoB and LDL-C, though with smaller residual differences. Discordance was most pronounced in metabolically unhealthy obese individuals, followed by metabolically unhealthy lean individuals, and metabolically healthy individuals (<em>P</em> < .001), indicating that metabolic health is a stronger determinant of discordance than obesity.</div></div><div><h3>CONCLUSIONS</h3><div>ApoB–LDL-C discordance is common, even among metabolically healthy individuals, and is primarily driven by metabolic dysfunction rather than by obesity. ApoB measurements should be included in routine cardiovascular risk assessments.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 123-134"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145742996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Recent cohort studies demonstrated that higher levels of serum remnant cholesterol (remnant-C) were a predictor of kidney outcomes in diabetes; however, these studies did not take into account triglycerides, highly correlated with remnant-C.
OBJECTIVE
This study aimed to elucidate whether serum remnant-C predicts kidney disease progression in people with diabetes when considering triglycerides.
METHODS
This was a retrospective cohort study of 5214 adults with type 2 diabetes, classified into 4 groups by median of remnant-C and triglycerides levels. Exposures were remnant-C and triglycerides, defined as their geometric means within individuals at baseline and during the follow-up period. The outcome was a composite of a ≥40% decrease in estimated glomerular filtration rate or the initiation of kidney replacement therapy. Hazard ratios (95% CI) were estimated by the multivariable Fine-Gray model treating death as a competing risk.
RESULTS
During the median follow-up period of 8.8 years, 1070 people reached the outcome. Hazard ratios (vs people with both below-median remnant-C and triglycerides) for the outcome were 1.21 (0.88-1.65), 1.48 (1.07-2.05), and 1.33 (1.13-1.58) in those with only above-median triglycerides, only above-median remnant-C, and both above-median remnant-C and triglycerides, respectively. When classifying participants by quartile of remnant-C, outcome hazards gradually increased from the first to fourth quartile. The association for triglycerides was similar, but weaker. By adjusting for both 4-category dummy variables for remnant-C and triglycerides, the gradual increase was observed only in remnant-C.
CONCLUSION
Remnant-C can predict kidney disease progression in type 2 diabetes, even considering triglycerides.
{"title":"Remnant cholesterol and kidney disease progression in type 2 diabetes: A retrospective cohort study","authors":"Tomomi Mori MD, PhD , Yui Yamamoto MD, PhD , Ko Hanai MD, PhD , Yurika Yamashige MD , Hidekazu Murata MT , Tomohiro Shinozaki MPH, PhD , Tomoko Nakagami MD, PhD","doi":"10.1016/j.jacl.2025.10.075","DOIUrl":"10.1016/j.jacl.2025.10.075","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Recent cohort studies demonstrated that higher levels of serum remnant cholesterol (remnant-C) were a predictor of kidney outcomes in diabetes; however, these studies did not take into account triglycerides, highly correlated with remnant-C.</div></div><div><h3>OBJECTIVE</h3><div>This study aimed to elucidate whether serum remnant-C predicts kidney disease progression in people with diabetes when considering triglycerides.</div></div><div><h3>METHODS</h3><div>This was a retrospective cohort study of 5214 adults with type 2 diabetes, classified into 4 groups by median of remnant-C and triglycerides levels. Exposures were remnant-C and triglycerides, defined as their geometric means within individuals at baseline and during the follow-up period. The outcome was a composite of a ≥40% decrease in estimated glomerular filtration rate or the initiation of kidney replacement therapy. Hazard ratios (95% CI) were estimated by the multivariable Fine-Gray model treating death as a competing risk.</div></div><div><h3>RESULTS</h3><div>During the median follow-up period of 8.8 years, 1070 people reached the outcome. Hazard ratios (vs people with both below-median remnant-C and triglycerides) for the outcome were 1.21 (0.88-1.65), 1.48 (1.07-2.05), and 1.33 (1.13-1.58) in those with only above-median triglycerides, only above-median remnant-C, and both above-median remnant-C and triglycerides, respectively. When classifying participants by quartile of remnant-C, outcome hazards gradually increased from the first to fourth quartile. The association for triglycerides was similar, but weaker. By adjusting for both 4-category dummy variables for remnant-C and triglycerides, the gradual increase was observed only in remnant-C.</div></div><div><h3>CONCLUSION</h3><div>Remnant-C can predict kidney disease progression in type 2 diabetes, even considering triglycerides.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 135-144"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145634016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Recent evidence suggests that visit-to-visit low-density lipoprotein cholesterol (LDL-C) variability—a measure of intraindividual lipid fluctuation over time—may independently influence cardiovascular risk. This study evaluated the impact of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) and inclisiran on LDL-C variability compared to standard lipid-lowering therapy (LLT) in a real-world population of very high-risk patients.
METHODS
We conducted a longitudinal, observational study including 618 patients at very high cardiovascular risk, treated at a single tertiary center. Patients were stratified into 3 groups: standard LLT (statins ± ezetimibe), PCSK9i, or inclisiran. LDL-C variability was assessed at 4 follow-up time points using both SD and coefficient of variation (CV), excluding the first lipid measurement to minimize early response bias. High variability was defined as SD or CV above the population median. Major adverse cardiovascular events (MACE) were collected as exploratory outcomes.
RESULTS
Patients receiving PCSK9i or inclisiran had significantly lower LDL-C variability compared to those on standard LLT (mean SD: 8.2 and 8.5 vs 20.5 mg/dL; P < .001; mean CV: 0.17 and 0.16 vs 0.31; P < .001). High variability in both SD and CV was observed in 77.3% of patients on standard LLT, but only in 17.2% and 17.1% of patients on PCSK9i and inclisiran, respectively. MACE incidence was higher in patients with high variability (12.5% vs 6.1%, P = .012). Multivariate analysis confirmed that treatment with PCSK9i or inclisiran was independently associated with lower LDL-C variability.
CONCLUSIONS
In patients at very high cardiovascular risk, PCSK9i and inclisiran therapies are associated with significantly lower visit-to-visit LDL-C variability compared to standard statin-based regimens. These findings support the importance of not only achieving LDL-C targets but also maintaining lipid stability over time, which may contribute to improved cardiovascular outcomes.
背景：最近的证据表明，每次就诊的低密度脂蛋白胆固醇（LDL-C）变异性——一种衡量个体内部脂质随时间波动的指标——可能独立影响心血管风险。本研究评估了与标准降脂治疗（LLT）相比，蛋白转化酶枯草杆菌素/酮素9型抑制剂（PCSK9i）和inclisiran对现实世界高危患者LDL-C变异性的影响。方法：我们进行了一项纵向观察性研究，包括618名在单一三级中心治疗的心血管风险极高的患者。患者分为3组：标准LLT（他汀类药物±依折替米贝）、PCSK9i或inclisiran。在4个随访时间点使用SD和变异系数（CV）评估LDL-C变异性，排除第一次脂质测量以减少早期反应偏差。高变异性定义为SD或CV高于总体中位数。收集主要不良心血管事件（MACE）作为探索性结果。结果：与接受标准LLT治疗的患者相比，接受PCSK9i或inclisiran治疗的患者LDL-C变异性显著降低（平均SD: 8.2和8.5 vs. 20.5 mg/dL; P < 0.001；平均CV: 0.17和0.16 vs. 0.31; P < 0.001）。在标准LLT治疗的患者中，77.3%的SD和CV具有高度可变性，而在PCSK9i和inclisiran治疗的患者中，SD和CV分别只有17.2%和17.1%。高变异性患者的MACE发生率更高（12.5%比6.1%,P = 0.012）。多因素分析证实，PCSK9i或inclisiran治疗与较低的LDL-C变异性独立相关。结论：在心血管风险极高的患者中，与标准的他汀类药物治疗方案相比，PCSK9i和inclisiran治疗与更低的访间LDL-C变异性相关。这些发现支持不仅达到LDL-C目标，而且随着时间的推移保持脂质稳定的重要性，这可能有助于改善心血管结果。
{"title":"Reduction of visit-to-visit LDL-C intraindividual variability in patients treated with PCSK9 inhibitors and inclisiran vs standard lipid-lowering therapy","authors":"Arturo Cesaro MD, PhD , Vincenzo Acerbo MD , Francesco Scialla MD , Andrea Zito MD , Gennaro Porcelli MD , Domenico Panico MD , Giovanni Argenziano MD , Demetrio Iaria MD , Maria Grazia Monaco PharmD , Vincenzo De Sio MD , Felice Gragnano MD, PhD , Michele Golino MD, PhD , Massimiliano Ruscica PharmD, PhD , Stefano Carugo MD , Alberto Corsini PharmD, PhD , Paolo Calabrò MD, PhD","doi":"10.1016/j.jacl.2025.10.066","DOIUrl":"10.1016/j.jacl.2025.10.066","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Recent evidence suggests that visit-to-visit low-density lipoprotein cholesterol (LDL-C) variability—a measure of intraindividual lipid fluctuation over time—may independently influence cardiovascular risk. This study evaluated the impact of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) and inclisiran on LDL-C variability compared to standard lipid-lowering therapy (LLT) in a real-world population of very high-risk patients.</div></div><div><h3>METHODS</h3><div>We conducted a longitudinal, observational study including 618 patients at very high cardiovascular risk, treated at a single tertiary center. Patients were stratified into 3 groups: standard LLT (statins ± ezetimibe), PCSK9i, or inclisiran. LDL-C variability was assessed at 4 follow-up time points using both SD and coefficient of variation (CV), excluding the first lipid measurement to minimize early response bias. High variability was defined as SD or CV above the population median. Major adverse cardiovascular events (MACE) were collected as exploratory outcomes.</div></div><div><h3>RESULTS</h3><div>Patients receiving PCSK9i or inclisiran had significantly lower LDL-C variability compared to those on standard LLT (mean SD: 8.2 and 8.5 vs 20.5 mg/dL; <em>P</em> < .001; mean CV: 0.17 and 0.16 vs 0.31; <em>P</em> < .001). High variability in both SD and CV was observed in 77.3% of patients on standard LLT, but only in 17.2% and 17.1% of patients on PCSK9i and inclisiran, respectively. MACE incidence was higher in patients with high variability (12.5% vs 6.1%, <em>P</em> = .012). Multivariate analysis confirmed that treatment with PCSK9i or inclisiran was independently associated with lower LDL-C variability.</div></div><div><h3>CONCLUSIONS</h3><div>In patients at very high cardiovascular risk, PCSK9i and inclisiran therapies are associated with significantly lower visit-to-visit LDL-C variability compared to standard statin-based regimens. These findings support the importance of not only achieving LDL-C targets but also maintaining lipid stability over time, which may contribute to improved cardiovascular outcomes.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 66-74"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145582068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.jacl.2025.10.063
Sebastian Holländer MD , Evelyn Marth MA , Philipp Robert Scherber MD, MHBA , Antonios Spiliotis MD, MSc , Ammar Al-Ali MD , Gereon Gäbelein MD , Matthias Glanemann MD
BACKGROUND/OBJECTIVES
The increasing incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) poses a major healthcare challenge. This condition is particularly prevalent in patients with obesity. Artichoke leaf extract (ALE) has known hepatoprotective, antioxidant, and lipid-lowering properties. While ALE has been studied for its impact on liver metabolism, its specific effectiveness in individuals with obesity and MASLD remains unclear. This study investigates the effectiveness of ALE in reducing liver steatosis in patients scheduled for bariatric surgery. To our knowledge, this is the first study to examine ALE's “antisteatotic” efficacy in this clinical context.
METHODS
Forty participating bariatric surgery candidates received either ALE or a placebo for 6 weeks before measurements. Steatosis was quantified using FibroScan (controlled attenuation parameter, CAP), and liver size was assessed via ultrasound. Secondary outcomes included serum laboratory parameters and body composition, measured through bioelectrical impedance analysis.
RESULTS
ALE intake significantly reduced CAP values and liver lobe diameters compared to placebo, indicating decreased steatosis and liver volume. Improvements were already evident after 3 weeks. In female participants, total and low-density lipoprotein cholesterol levels improved. However, transaminase levels—particularly aspartate aminotransferase—increased in the ALE group. Body composition improved, with reductions in fat mass percentage.
CONCLUSIONS
ALE effectively reduces liver steatosis and size and improves body composition in patients with obesity and MASLD. Unlike prior studies, we observed a significant transaminase increase, suggesting a distinct hepatic response in individuals with obesity. Further research is needed to evaluate ALE's metabolic and hepatic effects specifically in this population beyond the prebariatric setting.
{"title":"Artichoke leaf extract reduces steatosis and decreases liver size in prebariatric patients: A randomized placebo-controlled pilot trial—The “SteatoChoke-Study”","authors":"Sebastian Holländer MD , Evelyn Marth MA , Philipp Robert Scherber MD, MHBA , Antonios Spiliotis MD, MSc , Ammar Al-Ali MD , Gereon Gäbelein MD , Matthias Glanemann MD","doi":"10.1016/j.jacl.2025.10.063","DOIUrl":"10.1016/j.jacl.2025.10.063","url":null,"abstract":"<div><h3>BACKGROUND/OBJECTIVES</h3><div>The increasing incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) poses a major healthcare challenge. This condition is particularly prevalent in patients with obesity. Artichoke leaf extract (ALE) has known hepatoprotective, antioxidant, and lipid-lowering properties. While ALE has been studied for its impact on liver metabolism, its specific effectiveness in individuals with obesity and MASLD remains unclear. This study investigates the effectiveness of ALE in reducing liver steatosis in patients scheduled for bariatric surgery. To our knowledge, this is the first study to examine ALE's “antisteatotic” efficacy in this clinical context.</div></div><div><h3>METHODS</h3><div>Forty participating bariatric surgery candidates received either ALE or a placebo for 6 weeks before measurements. Steatosis was quantified using FibroScan (controlled attenuation parameter, CAP), and liver size was assessed via ultrasound. Secondary outcomes included serum laboratory parameters and body composition, measured through bioelectrical impedance analysis.</div></div><div><h3>RESULTS</h3><div>ALE intake significantly reduced CAP values and liver lobe diameters compared to placebo, indicating decreased steatosis and liver volume. Improvements were already evident after 3 weeks. In female participants, total and low-density lipoprotein cholesterol levels improved. However, transaminase levels—particularly aspartate aminotransferase—increased in the ALE group. Body composition improved, with reductions in fat mass percentage.</div></div><div><h3>CONCLUSIONS</h3><div>ALE effectively reduces liver steatosis and size and improves body composition in patients with obesity and MASLD. Unlike prior studies, we observed a significant transaminase increase, suggesting a distinct hepatic response in individuals with obesity. Further research is needed to evaluate ALE's metabolic and hepatic effects specifically in this population beyond the prebariatric setting.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 167-178"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145581967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.jacl.2025.09.027
Nouran Y. Salah MD , Dina Abdel Hakam MD , Sara I. Taha MD , Marwa Samir Hamza PhD , Eman Aly Ramadan PhD
BACKGROUND
Proprotein convertase subtilisin/kexin type-9 (PCSK9) has recently emerged as an important vasculopathy modulator. However, limited data exist on its level and expression in children and adolescents with type 1 diabetes (T1D).
AIM
To assess serum PCSK9 and gene expression among children and adolescents with T1D and correlate them with glycemia, dyslipidemia, and microvascular complications.
METHODS
Fifty children and adolescents with T1D were compared to 50 matched healthy controls. Serum PCSK9 enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR) gene expression, glycated-hemoglobin, fundus, urinary albumin-to-creatinine ratio (uACR) and fasting lipids were assessed with calculation of the estimated-glucose disposal rate (eGDR).
RESULTS
Children and adolescents with T1D, particularly those with microvascular complications, have significantly higher PCSK9 and PCSK9 gene expression than controls (P < .05). Serum PCSK9 and PCSK9 gene expression were significantly correlated with diabetes-duration, insulin dose, time above range (TAR), diastolic blood pressure percentile, low-density lipoprotein cholesterol (LDL-C) and uACR (P < .05), being independently correlated with diabetes-duration, LDL-C, and uACR using multivariate regression.
CONCLUSION
Serum PCSK9 and PCSK9 gene expression are elevated among children and adolescents with T1D showing significant association with dyslipidemia and microvascular complications. Further studies are warranted to explore the potential role of PCSK9 inhibitors in prevention and treatment of dyslipidemia and vasculopathy in T1D.
{"title":"PCSK9–dyslipidemia interplay in children and adolescents with type 1 diabetes: A potential modulator of vasculopathy","authors":"Nouran Y. Salah MD , Dina Abdel Hakam MD , Sara I. Taha MD , Marwa Samir Hamza PhD , Eman Aly Ramadan PhD","doi":"10.1016/j.jacl.2025.09.027","DOIUrl":"10.1016/j.jacl.2025.09.027","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Proprotein convertase subtilisin/kexin type-9 (PCSK9) has recently emerged as an important vasculopathy modulator. However, limited data exist on its level and expression in children and adolescents with type 1 diabetes (T1D).</div></div><div><h3>AIM</h3><div>To assess serum PCSK9 and gene expression among children and adolescents with T1D and correlate them with glycemia, dyslipidemia, and microvascular complications.</div></div><div><h3>METHODS</h3><div>Fifty children and adolescents with T1D were compared to 50 matched healthy controls. Serum PCSK9 enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR) gene expression, glycated-hemoglobin, fundus, urinary albumin-to-creatinine ratio (uACR) and fasting lipids were assessed with calculation of the estimated-glucose disposal rate (eGDR).</div></div><div><h3>RESULTS</h3><div>Children and adolescents with T1D, particularly those with microvascular complications, have significantly higher PCSK9 and PCSK9 gene expression than controls (<em>P</em> < .05). Serum PCSK9 and PCSK9 gene expression were significantly correlated with diabetes-duration, insulin dose, time above range (TAR), diastolic blood pressure percentile, low-density lipoprotein cholesterol (LDL-C) and uACR (<em>P</em> < .05), being independently correlated with diabetes-duration, LDL-C, and uACR using multivariate regression.</div></div><div><h3>CONCLUSION</h3><div>Serum PCSK9 and PCSK9 gene expression are elevated among children and adolescents with T1D showing significant association with dyslipidemia and microvascular complications. Further studies are warranted to explore the potential role of PCSK9 inhibitors in prevention and treatment of dyslipidemia and vasculopathy in T1D.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 1","pages":"Pages 56-65"},"PeriodicalIF":4.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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