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[PMID]:28391878
[Au] Autor:Koopal C; Marais AD; Westerink J; Visseren FL
[Ad] Endereço:Department of Vascular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
[Ti] Título:Autosomal dominant familial dysbetalipoproteinemia: A pathophysiological framework and practical approach to diagnosis and therapy.
[So] Source:J Clin Lipidol;11(1):12-23.e1, 2017 Jan - Feb.
[Is] ISSN:1933-2874
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Familial dysbetalipoproteinemia (FD) is a genetic disorder of lipoprotein metabolism associated with an increased risk for premature cardiovascular disease. In about 10% of the cases, FD is caused by autosomal dominant mutations in the apolipoprotein E gene (APOE). This review article provides a pathophysiological framework for autosomal dominant FD (ADFD) and discusses diagnostic challenges and therapeutic options. The clinical presentation and diagnostic work-up of ADFD are illustrated by two cases: a male with premature coronary artery disease and a p.K164Q mutation in APOE and a female with mixed hyperlipidemia and a p.R154H mutation in APOE. ADFD is characterized by a fasting and postprandial mixed hyperlipidemia due to increased remnants. Remnants are hepatically cleared by the low-density lipoprotein receptor and the heparan sulfate proteoglycan receptor (HSPG-R). Development of FD is associated with secondary factors like insulin resistance that lead to HSPG-R degradation through sulfatase 2 activation. Diagnostic challenges in ADFD are related to the clinical presentation; lipid phenotype; dominant inheritance pattern; genotyping; and possible misdiagnosis as familial hypercholesterolemia. FD patients respond well to lifestyle changes and to combination therapy with statins and fibrates. To conclude, diagnosing ADFD is important to adequately treat patients and their family members. In patients presenting with mixed hyperlipidemia, (autosomal dominant) FD should be considered as part of the diagnostic work up.
[Mh] Termos MeSH primário: Hiperlipoproteinemia Tipo III/fisiopatologia
[Mh] Termos MeSH secundário: Genótipo
Proteoglicanas de Heparan Sulfato/metabolismo
Seres Humanos
Hiperlipoproteinemia Tipo III/diagnóstico
Hiperlipoproteinemia Tipo III/genética
Hiperlipoproteinemia Tipo III/terapia
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Heparan Sulfate Proteoglycans)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE


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[PMID]:28336558
[Au] Autor:Bernelot Moens SJ; Verweij SL; Schnitzler JG; Stiekema LCA; Bos M; Langsted A; Kuijk C; Bekkering S; Voermans C; Verberne HJ; Nordestgaard BG; Stroes ESG; Kroon J
[Ad] Endereço:From the Departments of Vascular Medicine (S.J.B.M., S.L.V., L.C.A.S., M.B., S.B., E.S.G.S., J.K.), Experimental Vascular Medicine (J.G.S.), and Nuclear Medicine (H.J.V.), AMC, Amsterdam, The Netherlands; The Copenhagen General Population Study (A.L., B.G.N.) and Department of Clinical Biochemistry
[Ti] Título:Remnant Cholesterol Elicits Arterial Wall Inflammation and a Multilevel Cellular Immune Response in Humans.
[So] Source:Arterioscler Thromb Vasc Biol;37(5):969-975, 2017 May.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Mendelian randomization studies revealed a causal role for remnant cholesterol in cardiovascular disease. Remnant particles accumulate in the arterial wall, potentially propagating local and systemic inflammation. We evaluated the impact of remnant cholesterol on arterial wall inflammation, circulating monocytes, and bone marrow in patients with familial dysbetalipoproteinemia (FD). APPROACH AND RESULTS: Arterial wall inflammation and bone marrow activity were measured using F-FDG PET/CT. Monocyte phenotype was assessed with flow cytometry. The correlation between remnant levels and hematopoietic activity was validated in the CGPS (Copenhagen General Population Study). We found a 1.2-fold increase of F-FDG uptake in the arterial wall in patients with FD (n=17, age 60±8 years, remnant cholesterol: 3.26 [2.07-5.71]) compared with controls (n=17, age 61±8 years, remnant cholesterol 0.29 [0.27-0.40]; <0.001). Monocytes from patients with FD showed increased lipid accumulation (lipid-positive monocytes: Patients with FD 92% [86-95], controls 76% [66-81], =0.001, with an increase in lipid droplets per monocyte), and a higher expression of surface integrins (CD11b, CD11c, and CD18). Patients with FD also exhibited monocytosis and leukocytosis, accompanied by a 1.2-fold increase of F-FDG uptake in bone marrow. In addition, we found a strong correlation between remnant levels and leukocyte counts in the CGPS (n=103 953, for trend 5×10-276). In vitro experiments substantiated that remnant cholesterol accumulates in human hematopoietic stem and progenitor cells coinciding with myeloid skewing. CONCLUSIONS: Patients with FD have increased arterial wall and cellular inflammation. These findings imply an important inflammatory component to the atherogenicity of remnant cholesterol, contributing to the increased cardiovascular disease risk in patients with FD.
[Mh] Termos MeSH primário: Artérias/imunologia
Arterite/imunologia
Colesterol/imunologia
Hiperlipoproteinemia Tipo III/imunologia
Imunidade Celular
Lipoproteínas/imunologia
Triglicerídeos/imunologia
[Mh] Termos MeSH secundário: Idoso
Artérias/diagnóstico por imagem
Artérias/metabolismo
Arterite/sangue
Arterite/diagnóstico por imagem
Células da Medula Óssea/imunologia
Células da Medula Óssea/metabolismo
Estudos de Casos e Controles
Células Cultivadas
Colesterol/sangue
Dinamarca
Feminino
Fluordesoxiglucose F18
Células-Tronco Hematopoéticas/imunologia
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
Hiperlipoproteinemia Tipo III/sangue
Hiperlipoproteinemia Tipo III/diagnóstico por imagem
Integrinas/imunologia
Integrinas/metabolismo
Lipoproteínas/sangue
Masculino
Meia-Idade
Monócitos/imunologia
Monócitos/metabolismo
Fenótipo
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Compostos Radiofarmacêuticos
Transdução de Sinais
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Integrins); 0 (Lipoproteins); 0 (Radiopharmaceuticals); 0 (Triglycerides); 0 (remnant-like particle cholesterol); 0Z5B2CJX4D (Fluorodeoxyglucose F18); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.308834


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[PMID]:27494723
[Au] Autor:Peng W; Qiang F; Peng W; Qian Z; Ke Z; Yi L; Jian Z; Chongrong Q
[Ad] Endereço:Department of Cardiology, Xuzhou Hospital Affiliated East South University School of Medicine, Xuzhou Cardiovascular Disease Institute, 199 Jiefang Road, Xuzhou 221009, PR China.
[Ti] Título:Therapeutic efficacy of PCSK9 monoclonal antibodies in statin-nonresponsive patients with hypercholesterolemia and dyslipidemia: A systematic review and meta-analysis.
[So] Source:Int J Cardiol;222:119-29, 2016 Nov 01.
[Is] ISSN:1874-1754
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVE: Heterozygous familial hypercholesterolemia and dyslipidemia are the predominant causes for cardiovascular disease (CVD). Clinical guidelines for lowering CVD risk have advocated that low density lipoprotein-cholesterol (LDL-C) must be reduced. The primary choice of therapy for controlling lipidemia has been statins, which are not completely effective. Proprotein convertase subtilisin/kexin type-9 (PCSK9), which interferes with LDL clearance from circulation, inversely relates to the LDL-C levels. The loss of statin efficacy is likely due to increased circulating PCSK9 and antibody therapy against PCSK9 has been found to be efficacious in lowering LDL-C. In this study, we evaluated the efficacy of PCSK9-mAbs for lowering LDL-C, in statin non-responsive hypercholesterolemia patients. STUDY DESIGN AND METHODS: PubMed, EMBASE, Scholar, Web of Science and Scopus databases were searched to identify randomized controlled trials of PCSK9 antibody-statin combination vs statin, published till 2015. Two reviewers independently screened the articles, and a collective decision was reached about the included studies in the metaanalysis. Parameters analyzed: change from baseline in LDL-C, high-density lipoprotein cholesterol (HDL-C) and total cholesterol (TC); ApoB and ApoA1 levels. RESULTS: A total of 12 studies with 4909 patients were selected. Overall, add-on therapy with PCSK9-mAb to the ongoing statin therapy was found to achieve greater reduction in LDL-C, ApoB, TC, compared to statin therapy. There were no major treatment emergent adverse effects due to PCSK9-mAb therapy. CONCLUSIONS: In adult patients with heterozygous familial hypercholesterolemia and dyslipidemia, PCSK9-mAb therapy in combination with statins was able to achieve the goal of lowering LDL-C.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Doenças Cardiovasculares/prevenção & controle
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Hiperlipoproteinemia Tipo III
Pró-Proteína Convertase 9/imunologia
[Mh] Termos MeSH secundário: LDL-Colesterol/metabolismo
Quimioterapia Combinada/métodos
Seres Humanos
Hiperlipoproteinemia Tipo III/tratamento farmacológico
Hiperlipoproteinemia Tipo III/metabolismo
Hipolipemiantes/farmacologia
Conduta do Tratamento Medicamentoso
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Cholesterol, LDL); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Hypolipidemic Agents); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160806
[St] Status:MEDLINE


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[PMID]:27481046
[Au] Autor:Blum CB
[Ad] Endereço:Columbia University College of Physicians and Surgeons, New York, NY 10019, USA. Electronic address: cbb1@cumc.columbia.edu.
[Ti] Título:Type III Hyperlipoproteinemia: Still Worth Considering?
[So] Source:Prog Cardiovasc Dis;59(2):119-124, 2016 Sep - Oct.
[Is] ISSN:1873-1740
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Familial type III hyperlipoproteinemia (HLP) was first recognized as a distinct entity over 60 years ago. Since then, it has proven to be instructive in identifying the key role of apolipoprotein E (apoE) in removal of the remnants of very low density lipoproteins and chylomicrons produced by the action of lipoprotein lipase on these triglyceride-transporting lipoproteins. It has additionally shed light on the potent atherogenicity of the remnant lipoproteins. This review describes the history of development of our understanding of type III HLP, discusses the several genetic variants of apoE that play roles in the genesis of type III HLP, and describes the remarkable responsiveness of this fascinating disorder to lifestyle modification, especially carbohydrate restriction and calorie restriction, and, when required, the addition of pharmacotherapy.
[Mh] Termos MeSH primário: Hiperlipoproteinemia Tipo III
Hipolipemiantes/farmacologia
Comportamento de Redução do Risco
[Mh] Termos MeSH secundário: Apolipoproteínas E/metabolismo
Gerenciamento Clínico
Seres Humanos
Hiperlipoproteinemia Tipo III/genética
Hiperlipoproteinemia Tipo III/psicologia
Hiperlipoproteinemia Tipo III/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Hypolipidemic Agents)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170517
[Lr] Data última revisão:
170517
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160803
[St] Status:MEDLINE


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[PMID]:26968187
[Au] Autor:Oral A; Bambul N
[Ad] Endereço:Department of Internal Medicine, Goztepe Training and Research Hospital, Istanbul Medeniyet University, Istanbul, Turkey.
[Ti] Título:Xanthoma striatum palmare.
[So] Source:Korean J Intern Med;31(5):1008, 2016 Sep.
[Is] ISSN:2005-6648
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Mh] Termos MeSH primário: Hiperlipoproteinemia Tipo III/patologia
Xantomatose/patologia
[Mh] Termos MeSH secundário: Feminino
Mãos/patologia
Seres Humanos
Hiperlipoproteinemia Tipo III/diagnóstico
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE
[do] DOI:10.3904/kjim.2015.277


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[PMID]:26343209
[Au] Autor:Shah AS; Wilson DP
[Ad] Endereço:Department of Pediatric Endocrinology and Diabetes, Cincinnati Children's Hospital Medical Center & the University of Cincinnati, Cincinnati, OH, USA. Electronic address: amy.shah@cchmc.org.
[Ti] Título:Primary hypertriglyceridemia in children and adolescents.
[So] Source:J Clin Lipidol;9(5 Suppl):S20-8, 2015 Sep-Oct.
[Is] ISSN:1933-2874
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary disorders of lipid metabolism causing hypertriglyceridemia (HyperTG) result from genetic defects in triglyceride synthesis and metabolism. With the exception of lipoprotein lipase deficiency, these primary HyperTG disorders usually present in adulthood. However, some are unmasked earlier by precipitating factors, such as obesity and insulin resistance, and can be diagnosed in adolescence. Physical findings may be present and can include eruptive, palmer, or tuberoeruptive xanthomas. Triglyceride levels are very high to severe and can occur in the absence or the presence of other lipid abnormalities. Each of the causes of HyperTG is associated with an increased risk to develop recurrent pancreatitis and some may increase the risk of premature cardiovascular disease. Adoption of a healthy lifestyle that includes a low-fat diet, optimizing body weight, smoking avoidance/cessation, and daily physical activity is the first line of therapy. Pharmacologic therapies are available and can be beneficial in select disorders. Here, we review the causes of primary HyperTG in children and adolescents, discuss their clinical presentation and associated complications including the risk of pancreatitis and premature cardiovascular disease, and conclude with management and novel therapies currently in development. The goal of this article is to provide a useful resource for clinicians who may encounter primary HyperTG in the pediatric population.
[Mh] Termos MeSH primário: Hipertrigliceridemia/patologia
[Mh] Termos MeSH secundário: Adolescente
Criança
Seres Humanos
Hiperlipoproteinemia Tipo I/complicações
Hiperlipoproteinemia Tipo III/complicações
Hipertrigliceridemia/complicações
Hipertrigliceridemia/diagnóstico
Hipertrigliceridemia/enzimologia
Programas de Rastreamento
Pancreatite/complicações
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150908
[St] Status:MEDLINE


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[PMID]:26103610
[Au] Autor:Marais D
[Ad] Endereço:Chemical Pathology, University of Cape Town Health Science Faculty, National Health Laboratory Service and Medical Research Council Cape Heart Group, Cape Town, South Africa.
[Ti] Título:Dysbetalipoproteinemia: an extreme disorder of remnant metabolism.
[So] Source:Curr Opin Lipidol;26(4):292-7, 2015 Aug.
[Is] ISSN:1473-6535
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Lipoprotein metabolism and the role of apolipoprotein E in the pathogenesis of dysbetalipoproteinemia. RECENT FINDINGS: Remnant lipoproteins, modulated by lifestyle and genetic factors, are atherogenic. Dysbetalipoproteinemia could be viewed as a monogenic disorder of remnant metabolism. SUMMARY: Elevated plasma triglyceride and cholesterol concentrations (mixed hyperlipidemias) are commonly encountered and dysbetaliproteinemia should be considered in this setting. Dysbetalipoproteinemia (remnant clearance disease, Fredrickson type III hyperlipidemia) is an uncommon dyslipoproteinemia related to mutations in apolipoprotein E that disrupt the clearance of remnants of triglyceride-rich lipoproteins; it may be overlooked because xanthomata of the skin and/or tendons occur in a minority of patients. The diagnosis ideally requires the demonstration of remnant lipoprotein accumulation and a genetic cause. Genotyping for apolipoprotein E2 may not prove the diagnosis as it may be associated with low plasma lipid values. The recent association of remnant lipoproteins with atherosclerosis along with many factors that modulate remnant lipoprotein metabolism underscores the importance of recognising dysbetalipoproteinemia as an extreme state of remnant lipoprotein accumulation. Although there may be some differences between remnants in the general population and dysbetalipoproteinemia, it is clear that remnants promote atherosclerosis. Current treatment strategies are adequate but new strategies could also be of benefit in dysbetalipoproteinemia.
[Mh] Termos MeSH primário: Hiperlipoproteinemia Tipo III/metabolismo
[Mh] Termos MeSH secundário: Apolipoproteínas E/metabolismo
Aterosclerose/complicações
Aterosclerose/metabolismo
Seres Humanos
Hiperlipoproteinemia Tipo III/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Apolipoproteins E)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150713
[Lr] Data última revisão:
150713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150624
[St] Status:MEDLINE
[do] DOI:10.1097/MOL.0000000000000192


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[PMID]:25867729
[Au] Autor:Malloy M; Miller B; Kane J
[Ad] Endereço:Cardiovascular Research Institute, University of California, San Francisco.
[Ti] Título:Apolipoprotein E and neurocognitive function--in reply.
[So] Source:JAMA Neurol;72(4):479, 2015 Apr.
[Is] ISSN:2168-6157
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Apolipoproteínas E/genética
Hiperlipoproteinemia Tipo III/genética
Lipase/genética
Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; LETTER
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Multidrug Resistance-Associated Proteins); EC 3.1.1.3 (Lipase)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150414
[Lr] Data última revisão:
150414
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150414
[St] Status:MEDLINE
[do] DOI:10.1001/jamaneurol.2014.4699


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[PMID]:25867727
[Au] Autor:Cullum CM; Weiner MF
[Ad] Endereço:Department of Psychiatry and Neurology, University of Texas Southwestern Medical Center at Dallas.
[Ti] Título:Apolipoprotein E and neurocognitive function.
[So] Source:JAMA Neurol;72(4):478, 2015 Apr.
[Is] ISSN:2168-6157
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Apolipoproteínas E/genética
Hiperlipoproteinemia Tipo III/genética
Lipase/genética
Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; LETTER
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Multidrug Resistance-Associated Proteins); EC 3.1.1.3 (Lipase)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150414
[Lr] Data última revisão:
150414
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150414
[St] Status:MEDLINE
[do] DOI:10.1001/jamaneurol.2014.4702


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[PMID]:25768710
[Au] Autor:Koopal C; Retterstøl K; Sjouke B; Hovingh GK; Ros E; de Graaf J; Dullaart RP; Bertolini S; Visseren FL
[Ad] Endereço:Department of Vascular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
[Ti] Título:Vascular risk factors, vascular disease, lipids and lipid targets in patients with familial dysbetalipoproteinemia: a European cross-sectional study.
[So] Source:Atherosclerosis;240(1):90-7, 2015 May.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Familial dysbetalipoproteinemia (FD), also known as type III hyperlipoproteinemia, is a genetic dyslipidemia characterized by elevated very low density lipoprotein (VLDL) and chylomicron remnant particles that confers increased risk of cardiovascular disease (CVD). The objective of this study was to evaluate the prevalence of vascular risk factors, CVD, lipid values, treatment and lipid targets in patients with FD across Europe. METHODS: This cross-sectional study was performed in 305 patients with FD from seven academic hospitals in four European countries. Information was collected from clinical records. RESULTS: Patients mean (±standard deviation) age was 60.9±14.4 years, 201 (66%) were male, 69 (23%) had diabetes mellitus (DM) and 87 (29%) had a prior history of CVD. Mean body mass index was 28.5±5.0 kg/m2. Lipid-lowering medication was used by 227 (74%) patients (27% usual dose (theoretical low-density lipoprotein cholesterol (LDL-C) reduction≤40%) and 46% intensive dose (theoretical LDL-C reduction>40%)). Non high-density lipoprotein cholesterol (non-HDL-C) levels below treatment target (<3.3 mmol/L) were present in 123 (40%) patients and 163 patients (53%) had LDL-C levels below target (<2.5 mmol/L). No significant determinants were found for having non-HDL-C levels below target, while a prior history of CVD (OR 1.90, 95%CI 1.05-3.47) and presence of DM (OR 2.00, 95%CI 1.08-3.70) were associated with having LDL-C levels below treatment target. CONCLUSION: The majority of FD patients had non-HDL-C levels above the treatment target of 3.3 mmol/L. Intensive dose lipid-lowering medication was used by only half of the patients, leaving them at increased cardiovascular risk.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/epidemiologia
Doenças Cardiovasculares/prevenção & controle
HDL-Colesterol/sangue
LDL-Colesterol/sangue
Hiperlipoproteinemia Tipo III/tratamento farmacológico
Hiperlipoproteinemia Tipo III/epidemiologia
Hipolipemiantes/uso terapêutico
[Mh] Termos MeSH secundário: Centros Médicos Acadêmicos
Idoso
Biomarcadores/sangue
Doenças Cardiovasculares/diagnóstico
Comorbidade
Estudos Transversais
Diabetes Mellitus/epidemiologia
Europa (Continente)/epidemiologia
Feminino
Seres Humanos
Hiperlipoproteinemia Tipo III/sangue
Hiperlipoproteinemia Tipo III/diagnóstico
Modelos Logísticos
Masculino
Meia-Idade
Razão de Chances
Prevalência
Medição de Risco
Fatores de Risco
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cholesterol, HDL); 0 (Cholesterol, LDL); 0 (Hypolipidemic Agents)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150413
[Lr] Data última revisão:
150413
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150314
[St] Status:MEDLINE



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