To assess the effect of fiber supplementation on blood pressure (BP), Streppel et al conducted a meta-analysis of 24 randomized, placebo-controlled trials. Increased intake of fiber (around 12 g/d, mainly through supplements) reduced systolic BP by –1.1 mm Hg (95% confidence interval, –2.5 to 0.2 mm Hg) and diastolic BP by –1.3 mm Hg (–2.0 to –0.5 mm Hg). The data suggested a somewhat larger effect of dietary fiber on BP in older (>40 years) and hypertensive populations. The authors conclude that fiber supplementation may contribute to the prevention of hypertension in Western populations, where intake of dietary fiber is far below recommended levels.
Patients often blame their prescription medications for adverse effects, but little is known about the incidence or validity of these reports. Weingart and colleagues studied 286 medication-related symptoms reported by 661 adult primary care patients, surveyed their physicians, and determined whether patients’ symptoms represented true adverse drug events. Investigators found that patients discussed two thirds of medication symptoms with a physician. Physicians confirmed most patient-reported medication symptoms but failed to address one quarter of confirmed symptoms. Adverse drug events were common among patients who failed to report symptoms or whose physicians failed to address symptom reports. As many as 7.8 million adverse drug events could be prevented or ameliorated each year in the United States if patients and their physicians communicated better and physicians acted more reliably to address medication symptoms.
C-reactive protein (CRP), a marker of inflammation, is increasingly advocated to stratify coronary artery disease risk and guide clinical management, but little is known about how inflammatory markers fluctuate over time in subjects with stable ischemic heart disease. Bogaty et al found considerable fluctuations in short-term and long-term serum CRP values in 159 clinically stable patients. Relatively important CRP fluctuations in patients with stable ischemic heart disease may be problematic for risk stratification and treatment monitoring. Similar interleukin 6 variability suggests that these patients have a dynamic inflammatory status that may modulate acute coronary risk.
Treatment of impaired glucose tolerance (IGT) represents a promising new approach for preventing vascular disease, particularly among high-risk individuals such as those who had had a previous stroke or myocardial infarction. The potential impact of IGT therapy, however, will depend on the prevalence of IGT among target populations. In this cross-sectional study, Kernan et al examined the prevalence of IGT among men and women older than 45 years with no history of diabetes who were hospitalized for transient ischemic attack (TIA) or nondisabling ischemic stroke. The authors’ results indicate that IGT and diabetic glucose tolerance are common after TIA or ischemic stroke, even among persons with no history of diabetes and a fasting blood glucose level in the nondiabetic range.
Sowers and colleagues conducted a double-blind, randomized trial to evaluate the effects of celecoxib, rofecoxib, and naproxen on 24-hour systolic blood pressure (SBP) in 404 treated hypertensive patients with osteoarthritis and type 2 diabetes mellitus. Reductions in osteoarthritis symptoms, including pain, mobility, and stiffness, were similar in all treatment groups. Increases in 24-hour SBP occurred for rofecoxib compared with celecoxib (3.78 mm Hg; 95% confidence interval, 1.18-6.38 mm Hg; P = .005) and for rofecoxib compared with naproxen (3.85 mm Hg; 95% confidence interval, 1.15-6.55 mm Hg; P = .005). These effects were primarily related to changes in the daytime SBP. Thus, at equally efficacious doses for osteoarthritis management, treatment with rofecoxib is more likely than celecoxib and naproxen to induce a significant increase in 24-hour SBP in patients with type 2 diabetes mellitus receiving antihypertensive therapies.
Distribution of changes from baseline in ambulatory SBP at week 6.
In This Issue of Archives of Internal Medicine. Arch Intern Med. 2005;165(2):136. doi:10.1001/archinte.165.2.136