Journal of clinical lipidology最新文献

{"title":"Associations of serum omega-3 polyunsaturated fatty acids with apolipoprotein B and atherogenic lipoprotein lipids","authors":"Meredith Wilcox MPH,&nbsp;Liana Guarneiri PhD,&nbsp;Peter Attia MD,&nbsp;David Allison PhD,&nbsp;Kevin Maki PhD,&nbsp;Carol Kirkpatrick PhD","doi":"10.1016/j.jacl.2025.04.085","DOIUrl":"10.1016/j.jacl.2025.04.085","url":null,"abstract":"<div><h3>Funding</h3><div>The Indiana University Foundation funded this research.</div></div><div><h3>Background/Synopsis</h3><div>Observational evidence supports associations between higher intakes of omega-3 polyunsaturated fatty acids (PUFAs), primarily eicosapentaenoic acid and docosahexaenoic acid (DHA), and reduced risk for atherosclerotic cardiovascular disease. Serum levels of omega-3 PUFAs correlate with dietary intakes.</div></div><div><h3>Objective/Purpose</h3><div>Aegis was a prospective cohort study that investigated immunological and other biomarker changes after incident severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This cross-sectional analysis of baseline data from the Aegis cohort examined the relationships between serum total omega-3 PUFA and DHA levels and selected biomarkers of cardiovascular risk, including apolipoprotein B (apoB) and lipoprotein lipid concentrations.</div></div><div><h3>Methods</h3><div>Baseline fasting serum levels of omega-3 PUFAs, apoB, low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), and triglycerides were assessed. Multivariate linear models were used to assess trends in biomarker levels across quintile categories of serum fatty acids with body mass index (BMI), age, and sex as covariates.</div></div><div><h3>Results</h3><div>Analyses included 1894 participants for whom relevant biomarker data were available (65% female, mean age: 50 y, mean BMI: 29.0 kg/m², 62% Non-Hispanic White, 11% Black/African American, 7% Hispanic/Latino, 10% Asian, 10% mixed/other). The 20^th and 80^th percentiles for total omega-3 PUFAs as a percentage of total circulating fatty acids were 3.00% and 4.73%, respectively, and for DHA were 1.51% and 2.26%, respectively. Least squares geometric means (LSGMs) in mg/dL for serum omega-3 PUFA level quintile (Q)1 and Q5, respectively, were: apoB, 94.0 and 98.0 (P = 0.047); LDL-C, 102 and 105 (P = 0.381); non-HDL-C, 124 and 128 (P = 0.283); and triglycerides, 99.2 and 105 (P = 0.055). LSGMs for serum DHA level Q1 and Q5, respectively, were: apoB, 103 and 91.4; LDL-C, 114 and 97.5; non-HDL-C, 143 and 116; and triglycerides, 152 and 80.1 (all P &lt; 0.001).</div></div><div><h3>Conclusions</h3><div>A higher serum DHA level was linked to lower apoB, LDL-C, non-HDL-C, and triglyceride concentrations. In contrast, a higher serum total omega-3 PUFA level was modestly associated with a higher apoB concentration and showed no significant relationships with other lipoprotein lipid biomarkers, highlighting potential differential relationships for specific omega-3 PUFAs.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e62"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168320","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}

{"title":"Adult onset very long chain acyl-CoA dehydrogenase deficiency: A case report","authors":"Katherine Anderson Other,&nbsp;Amanda Doran MD,&nbsp;Macrae Linton MD,&nbsp;Melis Sahinoz MD","doi":"10.1016/j.jacl.2025.04.100","DOIUrl":"10.1016/j.jacl.2025.04.100","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Very long chain acyl-CoA dehydrogenase deficiency (VLCAD) is a rare autosomal recessive lipid disorder caused by biallelic pathogenic variants in the ACADVL gene, leading to impaired fatty acid metabolism. This report presents a compelling case of VLCAD diagnosed in adulthood.</div></div><div><h3>Objective/Purpose</h3><div>Here, we present an interesting case with VLCAD, a rare autosomal recessive lipid disorder, and hyperlipidemia.</div></div><div><h3>Methods</h3><div>Case Presentation: A 35-year-old woman was referred to the lipid clinic due to elevated LDL levels. Historically healthy, she began experiencing recurrent episodes of rhabdomyolysis requiring hospitalization over the last 5-6 years. Further evaluations revealed multiple vitamin and mineral deficiencies, including vitamin D, folic acid, cobalamin, and iron. Notably, there was no family history of premature atherosclerotic cardiovascular disease. Laboratory results indicated total cholesterol of 276 mg/dL, triglycerides of 63 mg/dL, HDL of 56 mg/dL, and LDL of 207 mg/dL. Genetic testing identified a c.848T&gt;C (p.Val283Ala) pathogenic variant and a c.938_940del (p.Asp313del) variant of unknown significance in the ACADVL gene. Cardiac assessments, including EKG and transthoracic echocardiogram, revealed normal sinus rhythm and normal biventricular size and function without significant valvular disease.</div></div><div><h3>Results</h3><div>The patient was initiated on medium-chain triglyceride (MCT) replacement therapy and adjusted her diet to increase protein and fiber while reducing fat intake. She was initially tolerating approximately 20 mL of MCT three times daily, constituting 22% of her daily caloric intake. However, she experienced severe nausea, vomiting, and bloating, which limited her adherence to the treatment.</div></div><div><h3>Conclusions</h3><div>This case illustrates the complexities of diagnosing VLCAD in adulthood and the challenges in managing treatment due to side effects. Further research is warranted to explore additional therapeutic options for VLCAD.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e71"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167956","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}

{"title":"Increased risk of ASCVD in women with PCOS is only partially mediated by incident metabolic comorbidities","authors":"Julia Ditosto MS,&nbsp;Kyle Busse PhD,&nbsp;Jennifer Lewey MD,&nbsp;Sunni Mumford PhD,&nbsp;Daniel Soffer MD,&nbsp;Qing Liu BS,&nbsp;Anuja Dokras MD,&nbsp;Snigdha Alur-Gupta MD","doi":"10.1016/j.jacl.2025.04.079","DOIUrl":"10.1016/j.jacl.2025.04.079","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background/Synopsis&lt;/h3&gt;&lt;div&gt;Women with polycystic ovary syndrome (PCOS) have a high prevalence of cardiovascular disease risk factors such as diabetes and dyslipidemia. Previous research suggests PCOS status may be associated with increased hazards of individual CVD events.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective/Purpose&lt;/h3&gt;&lt;div&gt;To determine ASCVD risk associated with PCOS and address whether incident intermediate conditions including diabetes and hyperlipidemia mediate ASCVD risk.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We performed a retrospective cohort study using the nationwide claims database Optum Clinformatics® Data Mart (2000-2022). Women aged 18-50 with PCOS were identified through ICD9/10 codes for PCOS and matched 1:5 by age and visit month to women without PCOS. The primary outcome was composite ASCVD (coronary artery disease, angina, myocardial infarction, carotid artery disease, ischemic stroke, and transient ischemic attack). Causal mediation analyses were conducted for incident intermediate conditions (defined as hypertension, hyperlipidemia, obesity, and type 2 diabetes [T2DM]) developed after PCOS diagnosis to determine whether these conditions mediated the association between PCOS and composite ASCVD. Confounders of the exposure-outcome, exposure-mediator, and mediator-outcome associations were considered in the analysis, and interactions were also considered. Adjusted hazard was determined by controlling for race, ethnicity, education and history of smoking, infertility, depression, metabolic dysfunction associated steatotic liver disease, oral contraception and metformin use, and the other intermediate conditions which were not the outcome.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;420,756 unique patients with PCOS matched to 2,103,780 patients without PCOS. Mean age in both groups was 31.2 ± 7.1 years. The crude incidence per 1000 person-years of compositive ASCVD was 4.64 in women with PCOS compared to 0.79 in those without PCOS with an adjusted HR of 4.44, 95% CI 4.28-4.62. The incidence of each individual component of ASCVD was also increased. Those with PCOS had a significantly higher hazards for each of the incident intermediate conditions as well: hypertension: (aHR 1.47, 95% CI 1.45-1.48), T2DM: (aHR 2.22, 95% CI 2.19-2.25), hyperlipidemia: (aHR 1.35, 95% CI 1.33-1.36), obesity: (aHR 2.19, 95% CI 2.18-2.21). When controlling for the covariates, incident hypertension mediated 14.9% of the association between PCOS and ASCVD, T2DM mediated 9.6% of the association, hyperlipidemia mediated 12.0%, and obesity mediated 13.3% of the association. A combined mediator variable for any one of these conditions mediated 35.3% of the association.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;In the largest longitudinal study of pre-menopausal women with PCOS residing in the United States, PCOS was independently associated with ASCVD and incident intermediate conditions partially mediated this risk. Our findings indicate that PCOS is a CVD risk","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e58-e59"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167959","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}

{"title":"Maximizing LDL management: The power of EHR alerts and patient follow-up","authors":"Mazhar Afaq MD,&nbsp;Katie Coons MBA,&nbsp;Tara Kelly MSN,&nbsp;Zaydan Ahmed,&nbsp;Mohammed Abualenain MD","doi":"10.1016/j.jacl.2025.04.023","DOIUrl":"10.1016/j.jacl.2025.04.023","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Previous studies have shown that automated electronic health record (EHR) alerts alone do not significantly improve lipid profiles in patients with hyperlipidemia. Our study suggests additional patient engagement strategies may be necessary to optimize LDL management. Personalized follow-up interventions, such as phone calls, may enhance adherence to treatment plans and improve lipid control outcomes.</div></div><div><h3>Objective/Purpose</h3><div>This study evaluates the effectiveness of combining follow-up phone calls with automated EHR alerts containing guideline-based lipid management recommendations to improve LDL outcomes in an outpatient setting.</div></div><div><h3>Methods</h3><div>A total of 250 patients were analyzed between October 2022 and October 2023. Baseline and post-intervention LDL levels, along with demographic variables (age, sex, race, and ethnicity), were collected. Statistical analyses included correlation tests, t-tests, and regression modeling to assess the impact of baseline LDL, age, and sex on post-intervention LDL changes.</div></div><div><h3>Results</h3><div>A moderate negative correlation was observed between baseline LDL levels and LDL reduction (r = -0.517), indicating that patients with higher initial LDL experienced greater reductions. The study population was 56% male, with a mean age of 68 years (SD 11). Neither age (r = 0.007) nor sex (p = 0.362) significantly influenced LDL changes. Regression analysis showed that baseline LDL accounted for 26.9% of the variation in LDL reduction (p &lt; 0.001), suggesting that patients with higher initial LDL benefited the most from the intervention.</div></div><div><h3>Conclusions</h3><div>The integration of follow-up phone calls with automated EHR alerts may enhance LDL management, particularly in patients with elevated baseline LDL levels. Age and sex had minimal impact on LDL reduction. These findings highlight the potential benefits of combining digital health interventions with direct patient engagement to optimize lipid control. Future studies should explore the long-term impact and cost-effectiveness of this combined approach.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e16-e17"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166975","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}

{"title":"Statin use among uninsured individuals in a charity community clinic","authors":"Zahid Ahmad MD,&nbsp;Christie Tran BS,&nbsp;Michael Pannell BS,&nbsp;Tanvi Ingle MS","doi":"10.1016/j.jacl.2025.04.071","DOIUrl":"10.1016/j.jacl.2025.04.071","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Limited data exist on lipid-lowering treatment in vulnerable populations, particularly those receiving primary care at charity community clinics. These clinics serve uninsured individuals with little to no access to healthcare providers, including safety-net healthcare systems.</div></div><div><h3>Objective/Purpose</h3><div>To assess statin therapy among statin-eligible patients at a primary care charity clinic (North Dallas Shared Ministry, NDSM; Dallas, TX).</div></div><div><h3>Methods</h3><div>We queried the electronic medical records (Athena Health) at NDSM (2016-2024) to extract demographic data, ICD-10 diagnoses, laboratory values, and statin prescriptions for both children and adults. Patients were categorized into four statin benefit groups per the 2018 AHA/ACA cholesterol guidelines. Multivariate logistic regression was performed to identify factors associated with statin prescriptions.</div></div><div><h3>Results</h3><div>Among 5,097 children (51% female, 89% Hispanic), 28 had lipids checked. One child had LDL-C ≥ 130 mg/dL, potentially qualifying for statin therapy. Among 34,982 adults (median age 41 years, 61% female, 86% Hispanic), 985 had lipids testing and sufficient data to determine if they belong to a statin benefit group. Statin prescription rates by benefit group were: ASCVD (n=43): 70%; diabetes (n=597): 58%; LDL-C ≥ 190 mg/dL (n=39): 87%; ASCVD risk ≥ 7.5%: 41%. Overall, 54% of statin-eligible patients were prescribed statins. In multivariate analysis, factors associated with statin prescriptions included age (OR 2.6, 95% CI 1.8, 3.6), diabetes diagnosis (OR 6.0, 95% CI 3.2, 11.5), total cholesterol (OR 2.5, 95% CI 2.1, 3.0), and HDL-C (OR 0.7, 95% CI 0.5, 0.7), (p &lt; 0.0001, C-index 0.889).</div></div><div><h3>Conclusions</h3><div>Among uninsured patients in a primary care, charity community clinic, statin prescription rates were slightly higher than those reported in insured populations (∼50%), with similar predictors of statin prescriptions (<em>e.g.,</em> age, diabetes diagnosis, lipid levels). However, lipid screening was infrequent – only 3% of adult patients had lipids checked – suggesting most statin-eligible patients likely remain unidentified. These findings highlight a critical gap: the need to improve lipid screening in uninsured populations to ensure at-risk individuals are identified and treated appropriately. In addition, future analyses should assess not only statin prescription rates but also whether patients receive appropriate statin intensity and non-statin therapies like ezetimibe and PCSK9 inhibitors.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e53"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168252","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}

{"title":"A case of dysbetalipoproteinemia: diagnostic and therapeutic strategies","authors":"Swathi Bolneni MSHS,&nbsp;Adedoyin Akinlonu MD,&nbsp;Ann Yilmaz MSN,&nbsp;James Underberg MD,&nbsp;Astrid Jara Pernia MD,&nbsp;Kalyani Dhar MD","doi":"10.1016/j.jacl.2025.04.013","DOIUrl":"10.1016/j.jacl.2025.04.013","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background/Synopsis&lt;/h3&gt;&lt;div&gt;Dysbetalipoproteinemia (DBL) is an underdiagnosed inherited disorder of remnant lipoprotein metabolism associated with high levels of cholesterol and triglycerides (TG). In DBL, dysfunctional apolipoprotein E (apoE) impairs LDL receptor-mediated clearance of apoB-containing lipoproteins.   &lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective/Purpose&lt;/h3&gt;&lt;div&gt;Describe a case with dysbetalipoproteinemia including diagnosis, management and treatment. Highlight the role of specialty lipid clinics in optimizing care for patients with uncommon lipid disorders. &lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Case report about dysbetalipoproteinemia.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;A 40-year-old male with a history of hypertension, pre-diabetes, and obesity (BMI 32) first learned he had high cholesterol in his 20s. His mother and 15-year-old son also have elevated cholesterol. He smokes four to five cigarettes intermittently and drinks two to three beers monthly.&lt;/div&gt;&lt;div&gt;The patient's baseline lipid values showed TG 582 mg/dL, non-HDL-cholesterol (non-HDL-C) 365 mg/dL, total cholesterol (TC) 403 mg/dL. Atorvastatin 80 mg was initiated with subsequent labs noting TG 358 mg/dL, LDL 174.3 mg/dL (Martin-Hopkins method), apoB 85 mg/dL, TC 275 mg/dL, HDL 40 mg/dL. Lp(a) was within normal limits. &lt;/div&gt;&lt;div&gt;He returned to the clinic three years later, off lipid lowering therapy (LLT), complaining of firm, yellow nodules at the elbows. Labs revealed TG 764 mg/dL, non-HDL-C 515 mg/dL, TC 548 mg/dL. Atorvastatin 80 mg, non-prescribed omega-3 fatty acid 1 gram, and fenofibrate 48 mg were initiated. Biopsy confirmed xanthomas, which prompted referral to lipid clinic. &lt;/div&gt;&lt;div&gt;In lipid clinic, discordance between LDL-C and apoB raised suspicion for dysbetalipoproteinemia. Genetic testing  demonstrated homozygosity for the APOE2 allele and heterozygosity for a risk variant in the APOA5 gene, consistent with familial dysbetalipoproteinemia. A non-contrast CT coronary returned with a calcium score of 38, placing him in the 93rd percentile based on age/sex. Omega-3 supplement was discontinued, and ezetimibe was added to LLT. Repeat labs demonstrated TG 340 mg/dL, non-HDL-C 149 mg/dL.  Lifestyle counseling was provided, fenofibrate discontinued. Further LDL-C/apoB lowering is being considered. &lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Patients with suspected DBL should be seen expeditiously in specialty lipid clinics to manage lipid levels and long-term cardiovascular risk. Dysbetalipoproteinemia should be considered in patients with elevated levels of cholesterol and TG, especially if xanthomas are present. Diagnosis is supported by normal or mildly elevated apoB levels. If genetic testing confirms APOE2 homozygosity, a secondary metabolic “hit” is still needed to express DBL phenotype. Treatment of DBL focuses on lifestyle modifications, including a traditional type III diet, alcohol limitation, exercise, and weight loss. LLT should be initiated when life","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e8-e9"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167928","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}

{"title":"Effective treatment of statin- and ezetimibe-resistant hyperlipidemia in a patient with active membranous nephrotic syndrome using a PCSK9 inhibitor","authors":"Verity Ramirez MD,&nbsp;Yongkang Zhang MD","doi":"10.1016/j.jacl.2025.04.039","DOIUrl":"10.1016/j.jacl.2025.04.039","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Hyperlipidemia is a characteristic of nephrotic syndrome (NS), contributing to increased cardiovascular risk. Proprotein convertase subtilisin kexin 9 (PCSK9) is upregulated in NS, leading to dysregulated lipid metabolism. Consequently, PCSK9 inhibitors are emerging as promising therapeutic agents for NS-associated hyperlipidemia. This case report describes the effectiveness of a PCSK9 inhibitor in treating statin- and ezetimibe-resistant hyperlipidemia in a patient with active membranous nephropathy (MN).</div></div><div><h3>Objective/Purpose</h3><div>To highlight the efficacy of PCSK9 inhibitors in managing NS-associated hyperlipidemia.</div></div><div><h3>Methods</h3><div>A chart review was conducted.</div></div><div><h3>Results</h3><div>A 40-year-old male with MN-type nephrotic syndrome complicated by recurrent pulmonary emboli and chronic thromboembolic pulmonary hypertension (CTEPH), and insulin-dependent diabetes presented with severe hyperlipidemia on high-dose statin and ezetimibe. His immunotherapy for NS was delayed due to a planned pulmonary thromboembolectomy for CTEPH.</div><div>The patient did not drink alcohol and smoked half a pack of cigarettes daily. He was unable to exercise due to dyspnea from CTEPH. His lipid panel before medical therapy was total cholesterol (TC) 295 mg/dL, triglycerides (TG) 172 mg/dL, and LDL 195 mg/dL. After initiation of atorvastatin 80 mg and ezetimibe 10 mg, his lipid panel remained elevated with TC 296 mg/dL, TG 323 mg/dL, and LDL 174 mg/dL. Lipoprotein(a) was 69 mg/dL.</div><div>Given persistent hyperlipidemia, he was started on the PCSK9 inhibitor Evolocumab. Within one month, his lipid profile dramatically improved to TC 120 mg/dL, TG 131 mg/dL, and LDL 44 mg/dL, representing a 74% reduction in LDL and 59% reduction in TG. The patient underwent planned pulmonary thromboembolectomy and started NS treatment post-surgery.</div></div><div><h3>Conclusions</h3><div>This case highlights the efficacy of Evolocumab in managing hyperlipidemia in a patient with active MN-type nephrotic syndrome who had not yet started immunotherapy. Previous case reports have shown similar successes with PCSK9 inhibitors in immunotherapy-refractory nephrotic syndrome not responding to statins, including a Japanese report where Evolocumab reduced LDL by 78% in a patient with refractory minimal change disease (MCD) on atorvastatin. Another case series showed a 36.8% reduction in LDL with PCSK9 inhibitors in 12 patients with refractory MN-, MCD-, or focal segmental glomerulosclerosis (FSGS)-type NS not at LDL goal with statin ± ezetimibe. Our case adds to the existing literature by demonstrating that PCSK9 inhibitors can effectively treat NS-associated hyperlipidemia even before immunotherapy initiation, supporting the need for future studies on PCSK9 inhibitors as a potent therapeutic for NS-associated hyperlipidemia.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e29"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167942","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}

{"title":"Clinical outcomes in patients hospitalized with diabetic ketoacidosis and acute pancreatitis: A nationwide analysis","authors":"Michael Fatuyi MD,&nbsp;Mohammad Amin Eshghabadi MD,&nbsp;Gregory Pierce BS,&nbsp;Brenda Pierce MD,&nbsp;Natalie Assaf BA,&nbsp;M Kenan Rahima MD,&nbsp;ReyhanehSadat Rahima MD,&nbsp;Borna Mansouri MD,&nbsp;Sila Mateo Faxas MD,&nbsp;Jason Pichardo MD,&nbsp;Fayaz Khan MD,&nbsp;Mohammed Najdat Seijari MD,&nbsp;Muayad Alzamara MD,&nbsp;Shahla Mallick MD,&nbsp;Mian Hammas MD","doi":"10.1016/j.jacl.2025.04.090","DOIUrl":"10.1016/j.jacl.2025.04.090","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Despite the clinical relevance, there is a scarcity of comprehensive studies evaluating the clinical outcomes of patients hospitalized with both diabetic ketoacidosis (DKA) and acute pancreatitis (AP).</div></div><div><h3>Objective/Purpose</h3><div>Consequently, this study aims to assess the clinical outcomes in this specific patient population.</div></div><div><h3>Methods</h3><div>We queried the National Inpatient Sample from 2017-2021 for adult patients hospitalized with diabetic ketoacidosis (DKA) and acute pancreatitis (AP). The primary outcome was inpatient mortality. Secondary outcomes included cardiac arrest, gastrointestinal bleeding (GIB), intubation, length of stay (LOS), and total hospital charge. A multivariable logistic regression analysis was used to estimate clinical outcomes. P-value &lt; 0.05 was considered significant.</div></div><div><h3>Results</h3><div>We analyzed 1,593,213 hospitalizations with diabetic ketoacidosis (DKA) and identified 75,769 cases (4.8%) with concurrent acute pancreatitis (AP). The cohorts with DKA and AP versus DKA without AP had a mean age of 44.7 vs. 46.4 years; male prevalence of 39.7% vs. 49.1%; and White ethnicity distribution of 50.2% vs. 54.8%. Clinical outcomes indicated a hospitalization mortality rate of 3.8% vs. 3.7% (OR 1.22, CI 1.12 - 1.33); a cardiac arrest incidence of 1.8% vs. 1.7% (OR 1.15, CI 1.01 - 1.30); an intubation requirement of 9.7% vs. 6.4% (OR 1.69, CI 1.60 - 1.79); a gastrointestinal bleeding rate of 5.7% vs. 3.9% (OR 1.54, CI 1.44 - 1.66); a length of stay (LOS) of 6.7 days vs. 5.1 days (IRR 1.36, CI 1.34 - 1.40); and total hospital charges of $20,727.41 vs. $14,586.77 (IRR 1.44, CI 1.40 - 1.48). All p-values were less than 0.05.</div></div><div><h3>Conclusions</h3><div>This study highlights the significant differences in clinical outcomes between patients hospitalized with diabetic ketoacidosis (DKA) and acute pancreatitis (AP) compared to those with DKA alone. Patients with concurrent DKA and AP exhibited higher rates of mortality, cardiac arrest, intubation, gastrointestinal bleeding, longer hospital stays, and increased hospital charges. These findings underscore the need for heightened clinical awareness and proactive management strategies for patients with both DKA and AP to mitigate these adverse outcomes. Further research is warranted to explore the underlying mechanisms and develop targeted interventions to improve prognosis in this high-risk population.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e65"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167945","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}

{"title":"Trends and experience with lipoprotein(a) testing in a large academic medical center","authors":"Victoria Clair BA,&nbsp;David Saxon MD,&nbsp;Steven Simon MD,&nbsp;Edward Gill MD,&nbsp;Francis Zirille MD","doi":"10.1016/j.jacl.2025.04.088","DOIUrl":"10.1016/j.jacl.2025.04.088","url":null,"abstract":"<div><h3>Funding</h3><div>Kaneka Corporation</div></div><div><h3>Background/Synopsis</h3><div>Evidence has grown around the relationship between lipoprotein(a) [Lp(a)] and cardiovascular disease risk. The 2024 focused update on Lp(a) from the National Lipid Association recognizes elevated plasma Lp(a) as an important independent, causal risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis.</div></div><div><h3>Objective/Purpose</h3><div>We hypothesize that there has been slow adoption of recommended Lp(a) screening and aim to understand current testing rates and trends within a large healthcare system, especially in higher risk patients.</div></div><div><h3>Methods</h3><div>Within a university-based health system, a large data extraction model was used to identify all patients who had undergone Lp(a) testing. Relevant high-risk patient populations, including all those with known histories of coronary artery disease, cerebral vascular accident, peripheral arterial disease, aortic stenosis, LDL-C &gt;190, coronary artery calcium score &gt;100, and familial hypercholesterolemia (FH) across the system were identified using diagnosis and procedural codes.</div></div><div><h3>Results</h3><div>In a health system with an estimated number of 4,553,100 unique patients, Lp(a) testing has been done 3,361 times on 1,976 unique patients between 12/2013 and 11/2023, representing approximately 0.04% of patients. Since 2016, Lp(a) measurement has increased on average by 23.6% year-over-year, as detailed in Figure 1, with rates of Lp(a) testing in each specific comorbidity group outlined in Figure 2. Most notably, patients with FH have a significantly higher rate of Lp(a) testing (25.7%) while patients with known aortic stenosis have a significantly lower rate of Lp(a) testing (0.7%) despite recommendations.</div></div><div><h3>Conclusions</h3><div>In a large academic medical center, Lp(a) measurement remains low, though with notable increase in just the last few years. Each of the patient comorbidity groups outlined have a higher rate of Lp(a) testing than the general population but remain significantly lower than recommended by recent guidelines regarding Lp(a) testing. The exception is patients with a diagnosis of FH, who have significantly higher rates of testing, likely influenced by following in a specialty lipid clinic. Our group postulates that the number of patients undergoing Lp(a) testing will exponentially increase, prompting the need for clearer guidelines for the management of each subpopulation of patients, notably as novel therapeutic agents directed at Lp(a) become approved and the experience with apheresis for Lp(a) continues to grow.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e63-e64"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167949","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}

{"title":"Genetic mutations and associated phenotypes in familial hypercholesterolemia: A biobank study","authors":"Steven Simon MD,&nbsp;David Madison BA,&nbsp;David Saxon MD,&nbsp;Shannon Christen BA,&nbsp;Carolyn Watts BS","doi":"10.1016/j.jacl.2025.04.099","DOIUrl":"10.1016/j.jacl.2025.04.099","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Familial hypercholesterolemia (FH) is the most common monogenic disease, affecting 1:250-300 people in the general population. Despite the high prevalence of FH, it is often under-recognized and under-treated, which can lead to premature cardiovascular morbidity and mortality in affected individuals. This study explores the relationship between genetic mutations and phenotypic manifestations in familial hypercholesterolemia.</div></div><div><h3>Objective/Purpose</h3><div>To investigate the phenotypic characteristics associated with genetic mutations in familial hypercholesterolemia, focusing on lipid levels, coronary atherosclerosis, and use of pharmacotherapy. The study aims to provide insights into how genetic variants contribute to clinical outcomes in FH.</div></div><div><h3>Methods</h3><div>The University of Colorado's Center for Personalized Medicine maintains a genetic biobank of over 235,000 patients, from which a total of 27 participants with mutations consistent with familial hypercholesterolemia were examined. A retrospective analysis was conducted to evaluate the phenotypes including clinical diagnosis, lipid levels, medication usage of these individuals using chart review.</div></div><div><h3>Results</h3><div>The mean age of participants was 64 years. 96% (26/27) of participants had mutations of the LDL receptor gene (LDL-R). 66% (18/27) had chart identification of heterozygous FH. The most recent mean LDL level was 117 mg/dL (SD = 56 mg/dL), with the average highest recorded LDL-C in the chart of 183 mg/dL. 40% (11/27) of participants had documented coronary atherosclerosis. 70% (19/27) of participants were on statin therapy, and 44% (12/27) were using additional lipid-lowering treatments.</div></div><div><h3>Conclusions</h3><div>This study highlights the clinical diversity in familial hypercholesterolemia patients based on their genetic mutations and associated phenotypes. Identifying genetic variants in this cohort reveals that while elevated LDL levels and coronary atherosclerosis are common, there is significant variability in clinical presentation, including medication use and clinical identification of heterozygous FH. This approach of identifying genetic mutations first, rather than focusing on phenotypic presentation, offers a unique perspective on FH and its management.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e71"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167955","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}