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In a 2-year clinical trial, the addition of ezetimibe to simvastatin had no effect on the progression of atherosclerosis, as measured by carotid-artery intima–media thickness, despite the additional lowering of levels of low-density lipoprotein cholesterol and C-reactive protein by ezetimibe when added to simvastatin. However, the study was not powered to assess clinical end points.
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Among pregnant women in a large U.S. group-practice health maintenance organization, overweight and obese women had a significantly longer mean length of hospital stay and higher rates of prenatal testing, medications dispensed from the outpatient pharmacy, telephone calls, and prenatal visits than did women with a normal BMI. Most of the increase in length of stay was related to increased rates of cesarean deliveries and obesity-related high-risk conditions.
The genetic basis of a defect in the metabolism of vitamin B12 (the cblD defect) was studied in cultured skin fibroblasts from seven patients with the defect. The defect was localized to chromosome 2q23.2, and a candidate gene (designated MMADHC) was identified in this region. Mutations in MMADHC were found in all seven patients. Transfection of the gene into fibroblasts from patients rescued the affected metabolic pathways.
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The efficacy of local treatment of vulvar intraepithelial neoplasia with imiquimod, an immune-response modifier, was tested in a double-blind, randomized trial. As compared with placebo, imiquimod cream was effective in reducing or eliminating the lesion, relieving symptoms, and clearing the lesion of human papillomavirus.
A 65-year-old asymptomatic man is concerned about his risk of osteoporosis. His mother died after a hip fracture at 74 years of age. The patient has no history of fractures but has lost 3 inches in height; he does not smoke and has never taken corticosteroids. He drinks two glasses of beer per day. His body-mass index is 25. Measurements of bone mineral density are consistent with osteoporosis. What should you recommend?
This comprehensive account of the genetic and environmental factors that cause atopic dermatitis reconciles two hypotheses concerning the origin of the disease — IgE-mediated sensitization, or an intrinsic defect in epithelial cells that causes dysfunction of the skin barrier — with evidence that both mechanisms contribute. Clinical implications are discussed.
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The authors review potential strategies to contain health care costs and assess each proposal's potential for success. Modifications in reimbursement to reward the practice of evidence-based medicine, expansion of the use of electronic medical records, and standardization of billing transactions to reduce administrative costs are among the strategies they view as most promising.
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