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Articles by Daniel J. Rader
Total Records ( 5 ) for Daniel J. Rader
  W. Virgil Brown , H. Bryan Brewer , Daniel J. Rader and Ernst J. Schaefer
  Not available
  Prabhjot S. Nijjar , Frances M. Burke , Annette Bloesch and Daniel J. Rader
  Coronary heart disease (CHD) remains a major source of morbidity and mortality. As the epidemic of obesity, diabetes, and hypertension continues to grow among young adults, the population at risk for atherosclerotic CHD is ever increasing. More than a century of laboratory and human findings link cholesterol levels with a propensity to develop atherosclerosis. Low-density lipoprotein (LDL) is the major atherogenic lipoprotein, and numerous clinical trials have shown the efficacy of lowering LDL-cholesterol (LDL-C) for reducing CHD risk. New trial data have resulted in LDL-C goals being lowered over time and expansion of the population of patients that are candidates for LDL-lowering therapy to decrease their lifetime risk of CHD. Although statins are relatively safe and well tolerated, there are still significant numbers of patients who cannot tolerate them and many others who only require mild LDL-C reduction and prefer nonprescription alternatives to statin therapy. A number of dietary supplements and functional foods have been suggested to reduce LDL-C levels, but only a few have withstood the rigors of randomized controlled trials. Here we review the evidence in support of dietary supplements and their LDL-C−lowering effects. We also review supplements that, after initial excitement about their purported effect, were not found to lower LDL-C significantly.
  Anne C. Goldberg , Paul N. Hopkins , Peter P. Toth , Christie M. Ballantyne , Daniel J. Rader , Jennifer G. Robinson , Stephen R. Daniels , Samuel S. Gidding , Sarah D. de Ferranti , Matthew K. Ito , Mary P. McGowan , Patrick M. Moriarty , William C. Cromwell , Joyce L. Ross and Paul E. Ziajka
  The familial hypercholesterolemias (FH) are a group of genetic defects resulting in severe elevations of blood cholesterol levels and increased risk of premature coronary heart disease. FH is among the most commonly occurring congenital metabolic disorders. FH is a treatable disease. Aggressive lipid lowering is necessary to achieve the target LDL cholesterol reduction of at least 50% or more. Even greater target LDL cholesterol reductions may be necessary for FH patients who have other CHD risk factors. Despite the prevalence of this disease and the availability of effective treatment options, FH is both underdiagnosed and undertreated, particularly among children. Deficiencies in the diagnosis and treatment of FH indicate the need for greatly increased awareness and understanding of this disease, both on the part of the public and of healthcare practitioners. This document provides recommendations for the screening, diagnosis and treatment of FH in pediatric and adult patients developed by the National Lipid Association Expert Panel on Familial Hypercholesterolemia. This report goes beyond previously published guidelines by providing specific clinical guidance for the primary care clinician and lipid specialist with the goal of improving care of patients with FH and reducing their elevated risk for CHD.
  W. Virgil Brown , Daniel J. Rader and John Kane
  The diagnosis of familial hypercholesterolemia is usually straightforward. The severely elevated low-density lipoprotein cholesterol and the occurrence of high concentrations of low-density lipoprotein cholesterol in the parents provide the diagnosis. The presence of tendon xanthomata is confirmation but not necessary. However, this relatively simple picture becomes much more complicated when one attempts to define the genetic variants that actually produced this clinical syndrome. In this Roundtable discussion, I am joined by two experts in the identification of genetic abnormalities discovered in those with phenotypic familial hypercholesterolemia. Dr. John Kane from the University of California, San Francisco, and Dr. Daniel Rader from the University of Pennsylvania share their knowledge in and experience with this topic.
  W. Virgil Brown , Daniel J. Rader and Anne C. Goldberg
  Clinical lipidologists are often asked to manage patients with severely elevated low-density lipoprotein cholesterol (LDL-C) and other apolipoprotein B-containing lipoproteins. Statins at maximum doses and in combination with other drugs may not achieve adequate reductions in LDL-C in such patients. The most dramatic elevations are usually in patients with genetic abnormalities in the LDL receptor gene on both chromosome pairs. LDL-C values well in excess of 400 mg/dL are not fully responsive to current treatments. In the past few months, the Food and Drug Administration has approved 2 new drugs for special use in such patients; these are mipomersen and lomitapide. During the National Lipid Association's Scientific Sessions, 2 highly experienced clinician scientists who have completed research studies with these agents agreed to answer questions pertinent to the prescription use of these agents. These scientists are Dr Anne Goldberg from Washington University in St. Louis and Dr Daniel Rader from the University of Pennsylvania.
 
 
 
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