Correspondence

Saw Palmetto for Benign Prostatic Hyperplasia

N Engl J Med 2006; 354:1950-1951May 4, 2006

Article

To the Editor:

Bent et al. (Feb. 9 issue)1 report that 160 mg of saw palmetto taken twice daily did not improve symptoms of benign prostatic hyperplasia. The authors indicate that the fatty-acid fraction of saw palmetto may be the active ingredient of the berry extract and that most products contain 85 to 95 percent fatty acids. Since saw palmetto is available in higher doses than 160 mg, would it not be expected that the higher-dose capsules contain more of the supposed active ingredient and thus would be more effective than the 160-mg dose?

Paul R. Casner, M.D., Ph.D.
Texas Tech University Health Sciences Center, El Paso, TX 79905
paul.casner@ttuhsc.edu

1 References

1. 1

   Bent S, Kane C, Shinohara K, et al. Saw palmetto for benign prostatic hyperplasia. N Engl J Med 2006;354:557-566
   Full Text | Web of Science | Medline

To the Editor:

The study by Bent et al. should remind us that in everyday practice, it is not always clear whether the clinician is treating benign prostatic hyperplasia, lower urinary tract symptoms (LUTS), LUTS from benign prostatic hyperplasia, or a combination of conditions involving more than benign prostatic hyperplasia and LUTS. In reality, symptoms of benign prostatic hyperplasia fall across a spectrum of several overlapping clinical conditions.1 The pathologic diagnosis of benign prostatic hyperplasia may or may not be associated with an anatomical diagnosis of benign prostatic enlargement, which may or may not cause urinary symptoms. Benign prostatic obstruction, a urodynamic condition, may or may not be related to either benign prostatic hyperplasia or benign prostatic enlargement. Bladder-outlet obstruction includes both benign prostatic obstruction and bladder-neck pathology. Therefore, the clinical syndrome of LUTS may or may not be related to any of the other benign prostatic conditions or bladder-outlet obstruction.

Jordan D. Dimitrakov, M.D., Ph.D.
Harvard Medical School, Boston, MA 02115
jordan.dimitrakov@childrens.harvard.edu

1 References

1. 1

   Lepor H. Insights into the natural history and treatment of benign prostatic hyperplasia. J Urol 2006;175:815-816
   CrossRef | Web of Science | Medline

Author/Editor Response

With regard to the comments of Dr. Casner: the dose of 160 mg of saw palmetto was selected because almost all previous clinical trials of saw palmetto used this dose. A recent systematic review of 21 randomized, controlled trials of saw palmetto found that 15 studies used a dose of 160 mg twice a day, and 5 studies used lower doses; only 1 study used a higher dose.1 Although it is interesting to consider whether higher doses of saw palmetto might be effective for the treatment of symptoms of benign prostatic hyperplasia, our goal was to evaluate the safety and efficacy of the most commonly used dose while paying particular attention to the methodologic weaknesses of previous studies. Therefore, we tested a large population over a long period and used a standard measure of symptoms of benign prostatic hyperplasia, a well-matched placebo capsule, and an assessment of the adequacy of blinding. Given the contrast between our negative results and the positive findings of many previous studies, we believe it is important to conduct validation studies that could include a dose-ranging protocol and an active control (alpha-blockade).

We agree with Dr. Dimitrakov that LUTS may be caused by a number of different types of obstruction of the urethra or bladder outlet and that patients with certain forms of obstruction may not be expected to benefit from medications or herbs that reduce the size of the prostate or promote smooth-muscle relaxation. However, most previous clinical trials of saw palmetto and other medical therapies for patients with LUTS probably caused by benign prostatic hyperplasia simply enrolled patients who reported some threshold of severity of urinary symptoms, with other causes of LUTS excluded through history, physical examination, and directed laboratory testing, without an evaluation of the specific pathophysiological cause of those symptoms.

The patients who were enrolled in our study had characteristics (including the size of the prostate and transitional zone) that were similar to those of patients in earlier studies of pharmaceutical drugs for the treatment of LUTS caused by benign prostatic hyperplasia.2,3 It is probably correct to say that our study found that saw palmetto was not effective for LUTS caused by benign prostatic hyperplasia,4 but we chose to follow the precedent in previous studies of saw palmetto and used the term benign prostatic hyperplasia.

Stephen Bent, M.D.
University of California, San Francisco, San Francisco, CA 94143
stephen.bent@ucsf.edu

Christopher Kane, M.D.
San Francisco Veterans Affairs Medical Center, San Francisco, CA 94121

Andrew L. Avins, M.D., M.P.H.
Northern California Kaiser Permanente, Oakland, CA 94612

4 References

1. 1

   Wilt T, Ishani A, Mac Donald R. Serenoa repens for benign prostatic hyperplasia. Cochrane Database Syst Rev 2002;3:CD001423-CD001423
   Medline

2. 2

   Roehrborn CG, Siegel RL. Safety and efficacy of doxazosin in benign prostatic hyperplasia: a pooled analysis of three double-blind, placebo-controlled studies. Urology 1996;48:406-415
   CrossRef | Web of Science | Medline

3. 3

   McConnell JD, Roehrborn CG, Bautista OM, et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med 2003;349:2387-2398
   Full Text | Web of Science | Medline

4. 4

   Denis L, McConnell J, Khoury S, et al. Recommendations of the International Scientific Committee: the evaluation and treatment of lower urinary tract symptoms (LUTS) suggestive of benign prostatic obstruction. In: Denis L, Griffiths K, Khoury S, et al., eds. Proceedings of the Fourth International Consultation on Benign Prostatic Hyperplasia. London: Health Publications, 1998:669-84.
   

Citing Articles (2)

Citing Articles

1. 1

   Michael R. Freeman, Keith R. Solomon. (2011) Cholesterol and benign prostate disease. Differentiation 82:4-5, 244-252
   CrossRef

2. 2

   Peyman Tavassoli, Rob Snoek, Mira Ray, Leticia Gomez Rao, Paul S. Rennie. (2007) Rapid, non-destructive, cell-based screening assays for agents that modulate growth, death, and androgen receptor activation in prostate cancer cells. The Prostate 67:4, 416-426
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