Browsing by Subject "Hypercholesterolemia"

Now showing 1 - 3 of 3
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    Current Management Guidelines on Hyperlipidemia: The Silent Killer
    (Hindawi, 2021-07-31) Su, Lilly; Mittal, Rea; Ramgobin, Devyani; Jain, Rahul; Jain, Rohit; Medicine, School of Medicine
    Given the high incidence of cardiovascular events in the United States, strict control of modifiable risk factors is important. Pharmacotherapy is helpful in maintaining control of modifiable risk factors such as elevated lipids or hypercholesterolemia. Hypercholesterolemia can lead to atherosclerotic disease which may increase the risk of acute coronary events. Statin therapy has long been a mainstay in the treatment of hypercholesterolemia, but while highly regarded, statin therapy also has side effects that may lead to patient noncompliance. Therefore, various medicines are being developed to manage hypercholesterolemia. This paper will discuss the role that lipids play in the pathophysiology of atherosclerotic disease, review the current lipid management guidelines, and discuss new treatment options that are alternatives to statin therapy.
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    Impairment of exercise hyperaemia in familial hypercholesterolaemia: complex interplay of vasodilators vs. vasoconstrictors
    (Wiley, 2014-04-14) Tune, Johnathan D.; Department of Cellular & Integrative Physiology, IU School of Medicine
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    Interrogation of selected genes influencing serum LDL-Cholesterol levels in patients with well characterized NAFLD
    (Elsevier, 2021) Vilar-Gomez, Eduardo; Gawrieh, Samer; Liang, Tiebing; McIntyre, Adam D.; Hegele, Robert A.; Chalasani, Naga; Medicine, School of Medicine
    Background: The clinical significance of rare mutations in LDL metabolism genes on nonalcoholic fatty liver disease (NAFLD) severity is not well understood. Objective: To examine the significance of mutations in LDL metabolism genes including apolipoprotein B (APOB), proprotein convertase subtilisin kexin 9 (PCSK9) and LDL receptor (LDLR) in patients with NAFLD. Methods: Patients with biopsy-confirmed NAFLD from the NASH Clinical Research Network studies were stratified into 3 groups of LDL-C (≤50 mg/dL, 130-150 mg/dL, ≥ 190 mg/dL) and then 120 (40 per group) were randomly selected from the strata. We examined the presence of mutations on LDL genes and analyzed its association with selected NAFLD-related features. Multivariable analyses were adjusted for age, race, gender and use of statins. Results: Among 40 patients with LDL-C ≤ 50 mg/dL, 7 (18%) patients had heterozygous variants in APOB and 2 had heterozygous variants in PCSK9 (5%). We also found heterozygous mutations in 3 (8%) patients with LDL-C ≥ 190 mg/dL; 2 and 1 located in LDLR and APOE genes, respectively. Compared to wild-type controls with LDL-C ≤ 50, APOB carriers displayed higher levels of alanine aminotransferase (85.86 ± 35.14 U/L vs 45.61 ± 20.84 U/L, Adj. P = 0.002) and steatosis >66% (57% vs 24%, Adj. P = 0.050). These associations remained statistically significant after excluding statin users. Other histological features of NAFLD severity were not different between wild-type controls and APOB mutation carriers. Conclusion: Mutations in the APOB gene are common among NAFLD patients with very low LDL-C and may be associated with increased aminotransferase levels and steatosis severity.