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Curbside Consult Optimizing Statin Therapy in the Elderly: A Personalized Approach to Cardiovascular Disease Prevention.
Cardiol Rev
January 2025
Departments of Cardiology and Medicine, Westchester Medical Center and New York Medical College, Valhalla, NY.
Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) play a vital role in managing and preventing cardiovascular disease, particularly in elderly populations who face elevated risks for atherosclerosis and related conditions. This review delves into the mechanisms of statin action, emphasizing their impact on low-density lipoprotein cholesterol levels, anti-inflammatory properties, and potential genetic factors influencing efficacy and drug tolerability. Consideration is given to statin intolerance and management strategies, drug interactions, and guidelines for primary and secondary prevention of cardiovascular events.
View Article and Find Full Text PDFComparative efficacy, toxicity, and insulin-suppressive effects of simvastatin and pravastatin in fatty acid-challenged mouse insulinoma MIN6 β-cell model.
Front Endocrinol (Lausanne)
November 2024
Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Kuwait City, Kuwait.
Article Synopsis
- - Familial hypercholesterolemia is a common condition that can lead to early heart disease and stroke, with statins being the primary treatment, but they might also increase the risk of type 2 diabetes due to effects on β-cells.
- - The study used a mouse insulinoma model to analyze the effects of simvastatin and pravastatin on β-cells in the presence of fatty acids, revealing that simvastatin reduced cholesterol more effectively but was also more cytotoxic and suppressed insulin levels.
- - While simvastatin lowered insulin content significantly, this effect was reversible and not dependent on its main action, indicating that it may impact insulin secretion through mechanisms beyond just blocking HMG-CoA reductase. *
Absence of Pathogenic Mutations and Strong Association With HLA-DRB1*11:01 in Statin-Naïve Early-Onset Anti-HMGCR Necrotizing Myopathy.
Neurol Neuroimmunol Neuroinflamm
September 2024
From the Department of Neurology (L.L., C.L., M.C.-Á., Á.C., A.V., L.Q., E.G., M.O.), Neuromuscular Diseases Unit; Department of Genetics (A.S.-C., B.R.-S.), Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona; Department of Neurology (C.D.-G.), Neuromuscular Diseases Unit, Hospital Universitario 12 de Octubre. Research Institute imas12, Biomedical Network Research Centre on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Madrid, Spain; Université Paris-Est Créteil (E.M.), INSERM, U955 IMRB; AP-HP, Hôpital Mondor, FHU SENEC, Service d'Histologie, Créteil, France; Department of Neurology (S.K.), Neuromuscular Diseases Unit, Osakidetza Basque Health Service, Basurto University Hospital, Universidad del País Vasco, Bilbao; Institut de Recerca Sant Pau (IR Sant Pau) (B.R.-S., R.B., C.L., L.Q., E.G., M.O.), Barcelona; Biomedical Network Research Centre on Rare Diseases (CIBERER), Madrid; Genomic Instability Syndromes and DNA Repair Group and Join Research Unit on Genomic Medicine UAB (B.R.-S.), Institut de Recerca Sant Pau (IR Sant Pau), Hospital de la Santa Creu i Sant Pau; Immunology Department (O.C., A.M.), Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Institut de Recerca Sant Pau (IR Sant Pau), Barcelona, Spain; Department of Genetics (A.D.), Craiova University Hospital, Romania; Neuropaediatrics Department (A.N.O.), Neuromuscular Diseases Unit, Hospital Sant Joan de Déu, Fundación Sant Joan de Déu, CIBERER - ISC III; Neurology Department (A.P., L.G.-M.), Neuromuscular Unit, IDIBELL-Hospital de Bellvitge, Hospitalet de Llobregat, Barcelona; Pathology Department (A.H.-L.), Neuropathology Unit, Hospital Universitario 12 de Octubre, Madrid; Pathology Department (C.J.), Institut Pediàtric de Recerca, Hospital Sant Joan de Déu, and MetabERN, Barcelona; Biomedical Network Research Centre on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Madrid; Department of Neurology (L.G.-M.), Hospital de Viladecans, Barcelona; and Department of Genetics (A.A.), Hospital Universitario 12 de Octubre, Research Institute imas12, Madrid, Spain.
Background And Objectives: Immune-mediated necrotizing myopathy (IMNM) caused by antibodies against 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) is an inflammatory myopathy that has been epidemiologically correlated with previous statin exposure. We characterized in detail a series of 11 young statin-naïve patients experiencing a chronic disease course mimicking a limb-girdle muscular dystrophy. With the hypothesis that HMGCR upregulation may increase immunogenicity and trigger the production of autoantibodies, our aim was to expand pathophysiologic knowledge of this distinct phenotype.
View Article and Find Full Text PDFPathologic Features of Anti-Ku Myositis.
Neurology
April 2024
From the Department of Neurology (M.O., S. Suzuki), Keio University School of Medicine, Tokyo, Japan; Department of Medicine for Nephrology, Rheumatology and Endocrinology (M.-T.H.), Division of Rheumatology and Systemic Inflammatory Diseases, III, University Medical Center Hamburg-Eppendorf, Germany; Department of Medical Ethics (Y.O.), Tokai University School of Medicine; Department of Clinical Genetics (Y.O.), Tokai University Hospital, Kanagawa; Department of Neuromuscular Research (Y.S., Y.N., I.N.), National Institute of Neuroscience, and Department of Genome Medicine Development (Y.S., Y.N., I.N.), Medical Genome Center, National Center of Neurology and Psychiatry, Tokyo; Department of Neurology (Y.N.), Nara Medical University; Department of Molecular Life Science (S. Suzuki, T.S.), Tokai University School of Medicine, Kanagawa, Japan; Department of Neuropathology (S.L.-L.), Sorbonne Université, Assistance Publique-Hôpitaux de Paris, Pitié-Salpêtrière University Hospital; Department of Neuromyology (S.L.-L.), National Reference Center of Neuromuscular Disorders, Sorbonne Université, Assistance Publique-Hôpitaux de Paris, Pitié-Salpêtrière University Hospital; Department of Internal Medicine and Clinical Immunology (O.B.), Inflammatory Myopathies Reference Center, Research Center in Myology UMR974, Sorbonne Université, Assistance Publique-Hôpitaux de Paris, Pitié-Salpêtrière Universi, France; Department of Rheumatology (U.S.), and Department of Neuropathology (W.S.), Charité-Universitätsmedizin, Freie Universität Berlin, Humboldt-Universtät zu Berlin, and Berlin Institute of Health; Leibniz ScienceCampus Chronic Inflammation (W.S.), Berlin, Germany; and Department of Neurology (A.U.), Tokyo Metropolitan Neurological Hospital, Japan.
Objective: Characteristics of myositis with anti-Ku antibodies are poorly understood. The purpose of this study was to elucidate the pathologic features of myositis associated with anti-Ku antibodies, compared with immune-mediated necrotizing myopathy (IMNM) with anti-signal recognition particle (SRP) and anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) antibodies, in muscle biopsy-oriented registration cohorts in Japan and Germany.
Methods: We performed a retrospective pathology review of patients with anti-Ku myositis samples diagnosed in the Japanese and German cohorts.
Immune-Mediated Necrotizing Myopathy (IMNM): A Story of Antibodies.
Antibodies (Basel)
February 2024
INSERM U1234, PAn'THER FOCIS Center of Excellence, Université de Rouen, F-76000 Rouen, France.
Immune-mediated necrotizing myopathy (IMNM) is a rare and severe disease that corresponds to a specific entity of idiopathic inflammatory myopathy. Patients with IMNM suffer from proximal muscle weakness, and present high levels of creatine kinase and necrotic myofibers. Anti-Signal Recognition Particle (SRP) and anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase autoantibodies (HMGCR) have recently been identified in two thirds of patients with IMNM and are used as a hallmark of the disease.
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