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SOURCE

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Source: Norris LB, Kolesar JM. Prostate cancer. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146075273. Accessed March 9, 2017.

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DEFINITION

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  • Malignant neoplasm that arises from prostate gland.

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ETIOLOGY

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  • Hormonal, dietary, and genetic differences may contribute to altered susceptibility in certain populations.

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PATHOPHYSIOLOGY

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  • Normal prostate composed of acinar secretory cells altered when invaded by cancer.

    • Adenocarcinoma found in >95% of cases.

  • Metastatic spread can occur by:

    • Local extension.

    • Lymphatic drainage.

    • Hematogenous dissemination.

      • Skeletal metastases most common sites of distant spread.

  • Rationale for hormone therapy based on effect of androgens on growth and differentiation of normal prostate (Figure 1).

  • Testes and adrenal glands are major sources of androgens, specifically dihydrotestosterone (DHT).

  • Luteinizing hormone–releasing hormone (LH-RH) from the hypothalamus stimulates release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from anterior pituitary gland.

    • LH stimulates production of testosterone.

    • Active, unbound testosterone penetrates prostate cell and is converted to DHT by 5-α-reductase.

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FIGURE 1.

Hormonal regulation of prostate gland. (ACTH, adrenocorticotropic hormone; DHT, dihydrotestosterone; FSH, follicle-stimulating hormone; GH, growth hormone; LH, luteinizing hormone; LH-RH, luteinizing hormone–releasing hormone; mRNA, messenger RNA; PROL, prolactin; R, receptor.) Reprinted with permission from Wells BG, DiPiro JT, Schwinghammer TL, et al. Pharmacotherapy Handbook. 10th ed. New York, NY: McGraw-Hill, 2017.

Graphic Jump Location
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EPIDEMIOLOGY

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  • Most commonly diagnosed cancer in American men, and second leading cause of cancer-related deaths in males.

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PREVENTION AND SCREENING

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CHEMOPREVENTION
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  • Use of finasteride for treatment of benign prostatic hypertrophy (BPH) decreased prostate cancer risk by ~25%.

    • Prostate cancer diagnosed in patients on finasteride is more aggressive.

    • Current guidelines do not recommend use of finasteride or dutasteride for prostate cancer chemoprevention.

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SCREENING
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  • US Preventive Services Task Force recommends against screening for prostate cancer.

  • American Urologic Association does not recommend routine screening between ages 40 and 54 for men of average risk; between 55 and 69, men should discuss the risks and benefits of screening. If men elect to screen, the frequency should be no more than every 2 years.

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RISK FACTORS

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  • Possible risk factors include:

    • Age (>70% of cases in men >65 years old)

    • Race-ethnicity (African American has highest incidence and death rate)

    • Family history (can be inheritable)

  • Other risk factors include:

    • Environment (incidence varies worldwide)

    • Occupation (associated with cadmium exposure)

    • Diet (Mediterranean diet associated with reduced risk)

    • Hormonal (does not occur in castrated men)

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CLINICAL PRESENTATION

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  • Most prostate cancers identified prior to development of symptoms.

    • Localized prostate cancer usually asymptomatic.

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