Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2004;6 Suppl 9(Suppl 9):S3-S10.

Pathophysiology, epidemiology, and natural history of benign prostatic hyperplasia

Pathophysiology, epidemiology, and natural history of benign prostatic hyperplasia

Herbert Lepor. Rev Urol. 2004.

Abstract

The pathophysiology, epidemiology, and natural history of benign prostatic hyperplasia (BPH) are incompletely understood; however, the development of reliable instruments to measure symptom severity, prostatic enlargement, and bladder outlet obstruction has allowed major advances in their elucidation. The development of lower urinary tract symptoms (LUTS) in the aging male is influenced to some degree by the severity of bladder outlet obstruction and prostatic enlargement. Although the development of LUTS, bladder outlet obstruction, and BPH are age-dependent, they are not necessarily causally related; there are many other factors involved in the pathophysiology of LUTS. The clinically important parameters of disease progression in men with moderate to severe LUTS and low peak flow rates are symptom progression and the development of acute urinary retention (AUR). The risk of AUR is related to both baseline serum prostate-specific antigen level and prostate volume. In men with moderate prostate enlargement, the risk of AUR appears to be high enough to justify intervention with a 5alpha-reductase inhibitor in order to reduce this risk.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Age-stratified autopsy prevalence of histologic benign prostatic hyperplasia (BPH). Reproduced with permission from Roehrborn CG, McConnell JD.
Figure 2
Figure 2
Proposed pathophysiology of benign prostatic hyperplasia (BPH). A number of studies have challenged the paradigm that prostatic enlargement causes bladder outlet obstruction, leading to lower urinary tract symptoms (LUTS). Although BPH and bladder outlet obstruction clearly contribute to the development of LUTS, there are other unrecognized factors that also cause LUTS.
Figure 3
Figure 3
Investigators in different countries have reported cross-sectional studies designed to determine the prevalence of clinical benign prostatic hyperplasia (BPH), as defined by an International Prostate Symptom Score (IPSS) > 7, peak urinary flow rate (Qmax) < 15 mL/sec, and prostate volume > 20 cc. The prevalence of BPH in these studies was consistently shown to be age-dependent, as well as fairly uniform across the world. Reproduced with permission from Roehrborn CG, McConnell JD.
Figure 4
Figure 4
The Medical Therapy of Prostatic Symptoms (MTOPS) study represents the longest placebo-controlled trial to date of men with benign prostatic hyperplasia (BPH). The placebo arm provides insights into the natural history of men with moderate to severe lower urinary tract symptoms and decreased peak urinary flow rates, which imply some level of bladder outlet obstruction. Adapted with permission from McConnell JD et al. Copyright ©2003 Massachusetts Medical Society. All rights reserved.
Figure 5
Figure 5
The incidence of acute urinary retention (AUR) at 4 years among placebo-treated patients in finasteride clinical studies was clearly related to baseline prostate volume (PV) and prostate-specific antigen (PSA) levels. Adapted from Roehrborn CG et al. with permission from Elsevier.
Figure 6
Figure 6
The dutasteride clinical studies showed a clear relationship between baseline prostate-specific antigen (PSA) levels and the development of acute urinary retention (AUR) at 2 years in placebo-treated patients. Data from Roehrborn CG et al.

References

    1. McNeal JG. The prostate gland: morphology and pathobiology. Monogr Urol. 1983;4:3–33.
    1. Jepsen JV, Bruskewitz RC. Clinical manifestation and indications for treatment. In: Lepor H, editor. Prostatic Diseases. Philadelphia, PA: WB Saunders Co; 2000. pp. 123–142.
    1. Berry SJ, Coffey DS, Walsh PC, et al. The development of human prostatic hyperplasia with age. J Urol. 1984;132:474–479. - PubMed
    1. Roehrborn CG, McConnell JD. Etiology, pathophysiology, epidemiology and natural history of benign prostatic hyperplasia. In: Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ, editors. Campbell’s Urology. 8th ed. Philadelphia, PA: WB Saunders Co; 2002. pp. 1297–1336.
    1. McConnell JD. Prostatic growth: new insights into hormonal regulation. Br J Urol. 1995;76(suppl 1):5–10. - PubMed

LinkOut - more resources