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Correction
to
Knopp,
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Joan Dorn, Ph.D.
John Naughton, M.D.
State University of New York at Buffalo
Buffalo, NY 14214-3000
Catarina Galletti, M.D.
University of Bologna
40059 Bologna, Italy
References
Although the mechanisms leading to the increased serum urea and creatinine concentrations are unknown, this side effect is important for two reasons. First, awareness of this change may prevent unnecessary studies in patients in whom it develops. Second, high serum concentrations of homocysteine, an important cardiovascular risk factor, have recently been reported in patients taking either fenofibrate or bezafibrate.2 This increase has been ascribed to a fibrate-induced impairment of renal function, and it may counteract the benefits expected from the lipid-lowering action of fenofibrate, bezafibrate, and ciprofibrate. This might explain why gemfibrozil, which is devoid of renal side effects, is the only fibrate that has resulted in a significant reduction of major cardiac events in both primary-prevention trials3 and secondary-prevention trials.4
Nilufer Broeders, M.D.
Christiane Knoop, M.D.
Daniel Abramowicz, M.D.
Hôpital Erasme
B-1070 Brussels, Belgium
References
To the Editor: Dorn et al. make the worthy point that exercise is an important element in caring for patients with hyperlipidemia. However, substantial physical effort is required, such as five hours of aerobic exercise per week, to raise the serum HDL cholesterol concentration by 5 mg per deciliter (0.1 mmol per liter).1 Obese, inactive patients, in whom the beneficial effects of exercise on serum triglyceride and HDL concentrations would be the greatest, are least likely to engage in such activity. In general, my colleagues and I inquire about and encourage exercise. A specific recommendation of exercise can be beneficial when dietary and drug interventions have been maximally implemented and when the patient can clearly recognize the potential benefit of greater physical effort.
The mechanism and clinical importance of the increase in serum creatinine associated with the use of some fibric acid drugs are unclear. The effect appears to be entirely reversible. The studies in which increases in serum homocystine concentrations were reported in patients receiving fibric acid derivatives were not controlled.2,3 It is also unclear whether the reported increases in serum creatinine and homocystine concentrations are related.
There is an error in Table 2 of the article, on page 500, which lists risk factors for cardiovascular disease. In the right-hand column, the serum homocystine concentration should have been >10 µmol per liter, not >10 nmol per liter, as printed.
Robert H. Knopp, M.D.
Northwest Lipid Research Clinic
Seattle, WA 98104
References
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