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Articles by E. J. Schaefer
Total Records ( 2 ) for E. J. Schaefer
  E. L Berson , B Rosner , M. A Sandberg , C Weigel DiFranco , R. J Brockhurst , K. C Hayes , E. J Johnson , E. J Anderson , C. A Johnson , A. R Gaudio , W. C Willett and E. J. Schaefer
 

Objective  To determine whether lutein supplementation will slow visual function decline in patients with retinitis pigmentosa receiving vitamin A.

Design  Randomized, controlled, double-masked trial of 225 nonsmoking patients, aged 18 to 60 years, evaluated over a 4-year interval. Patients received 12 mg of lutein or a control tablet daily. All were given 15 000 IU/d of vitamin A palmitate. Randomization took into account genetic type and baseline serum lutein level.

Main Outcome Measures  The primary outcome was the total point score for the Humphrey Field Analyzer (HFA) 30-2 program; prespecified secondary outcomes were the total point scores for the 60-4 program and for the 30-2 and 60-4 programs combined, 30-Hz electroretinogram amplitude, and Early Treatment Diabetic Retinopathy Study acuity.

Results  No significant difference in rate of decline was found between the lutein plus vitamin A and control plus vitamin A groups over a 4-year interval for the HFA 30-2 program. For the HFA 60-4 program, a decrease in mean rate of sensitivity loss was observed in the lutein plus vitamin A group (P = .05). Mean decline with the 60-4 program was slower among those with the highest serum lutein level or with the highest increase in macular pigment optical density at follow-up (P = .01 and P = .006, respectively). Those with the highest increase in macular pigment optical density also had the slowest decline in HFA 30-2 and 60-4 combined field sensitivity (P = .005). No significant toxic effects of lutein supplementation were observed.

Conclusion  Lutein supplementation of 12 mg/d slowed loss of midperipheral visual field on average among nonsmoking adults with retinitis pigmentosa taking vitamin A.

Application to Clinical Practice  Data are presented that support use of 12 mg/d of lutein to slow visual field loss among nonsmoking adults with retinitis pigmentosa taking vitamin A.

Trial Registration  ClinicalTrials.gov Identifier: NCT00346333

  M. E Brousseau , J. S Millar , M. R Diffenderfer , C Nartsupha , B. F Asztalos , M. L Wolfe , J. P Mancuso , A. G Digenio , D. J Rader and E. J. Schaefer
 

This study was designed to establish the mechanism responsible for the increased apolipoprotein (apo) A-II levels caused by the cholesteryl ester transfer protein inhibitor torcetrapib. Nineteen subjects with low HDL cholesterol (<40 mg/dl), nine of whom were also treated with 20 mg of atorvastatin daily, received placebo for 4 weeks, followed by 120 mg of torcetrapib daily for the next 4 weeks. Six subjects in the nonatorvastatin cohort participated in a third phase, in which they received 120 mg of torcetrapib twice daily for 4 weeks. At the end of each phase, subjects underwent a primed-constant infusion of [5,5,5-2H3]l-leucine to determine the kinetics of HDL apoA-II. Relative to placebo, torcetrapib significantly increased apoA-II concentrations by reducing HDL apoA-II catabolism in the atorvastatin (–9.4%, P < 0.003) and nonatorvastatin once- (–9.9%, P = 0.02) and twice- (–13.2%, P = 0.02) daily cohorts. Torcetrapib significantly increased the amount of apoA-II in the -2-migrating subpopulation of HDL when given as monotherapy (27%, P < 0.02; 57%, P < 0.003) or on a background of atorvastatin (28%, P < 0.01). In contrast, torcetrapib reduced concentrations of apoA-II in -3-migrating HDL, with mean reductions of –14% (P = 0.23), –18% (P < 0.02), and –18% (P < 0.01) noted during the atorvastatin and nonatorvastatin 120 mg once- and twice-daily phases, respectively. Our findings indicate that CETP inhibition increases plasma concentrations of apoA-II by delaying HDL apoA-II catabolism and significantly alters the remodeling of apoA-II-containing HDL subpopulations.

 
 
 
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