Abstract and Introduction
Abstract
Benign prostatic hyperplasia (BPH) is one of the most common genitourinary complications in men over 50 years of age and typically presents with lower urinary tract symptoms (LUTS). Classes of medications include α1-adrenoceptor blockers, 5α-reductase inhibitors, and phosphodiesterase 5 inhibitors. Today, α1-adrenoceptor blockers and 5α-reductase inhibitors are often combined to give a synergistic effect. A review of the current literature identified several adverse sexual side effects, including erectile dysfunction (ED), decreased libido, orgasmic disorders, and ejaculatory disorders. We believe it is important to know the extent of these side effects, as the clinician and patient will need to decide the cost of improved voiding symptoms. The chief adverse effect is ejaculatory disorders, including the absence of ejaculation. Clinical consideration for BPH should include the elements of male sexual function, patients' age, and the characteristics and comprehensive effects of each group of drugs. Methodological bias in clinical studies, such as the subjective evaluation of the sexual side effect, makes it difficult to determine the ideal drug for treatment.
Introduction
Benign prostatic hyperplasia (BPH) is a clinical syndrome which includes prostate enlargement and lower urinary tract symptoms (LUTS). The aim of BPH treatment is alleviating urination problems, preventing prostatic disease progression, and improving the quality of life. Over the past two decades, the standard of treatment has shifted from surgery to drug therapy. A greater understanding of detrusor physiology as well as the development of effective drugs for solving the dynamic and static components of the obstruction in the prostate and bladder neck have paved the path for the ubiquity of pharmacological therapy for BPH. However, clinical studies in the 1990s reported that despite the amelioration of LUTS, adverse effects of BPH drug therapy began to surface.[1] These effects were noted as sexual dysfunction, which can be divided into erectile dysfunction (ED), ejaculatory dysfunction (EjD), orgasmic disorders, as well as sexual desire disorders.
Pharmacological BPH therapy protocols advocate the use of α-blockers (ABs) and 5α-reductase inhibitors (5ARI), individually or in combination, as well as phosphodiesterase-5 (PDE5) inhibitors, individually or concomitantly with ABs. Adverse sexual side effects can occur as a result of the drug group itself or specific drugs within the group.[2] Watchful Waiting is usually utilized in patients with an AUA symptom score <10. ABs bind to α1-adrenoceptors and act by relaxing the smooth muscles of the prostate and bladder neck to improve urine flow and facilitate urination. They do not reduce prostatic volume or curb the natural progression of BPH. Nonetheless, ABs do vary in uroselectivity and the production of adverse effects.[3] They can be nonselective (e.g., doxazosin, terazosin, and alfuzosin) and selective (e.g., tamsulosin and silodosin). 5ARIs cause the inhibition of 5α-reductase enzymes and prevent the conversion of non-active forms testosterone to DHT, the androgen steroid compound mainly responsible for the initial and subsequent enlargement of the prostate gland.[4] The enzyme has two isoforms: type 1 (found in the liver and skin) and 2 (found in reproductive tissues). 5ARIs are prominently available as finasteride and dutasteride, with both exhibiting similar clinical effects. 5ARIs may lead to ED, EjD, and decreased libido compared to placebo.[5] The combination of AB and 5ARI is an increasingly popular mode of treatment which incorporates the combined effect of both components, including combined sexual side effects. Lastly, PDE5 inhibitors (e.g., tadalafil) are commonly used in order to treat ED as well as inhibit PDE11, which is found in the prostate and testes.[6] As of yet, PDE11 inhibition with therapeutic doses of tadalafil has shown no clinical significance.[7] Nonetheless, findings from studies have revealed that PDE5 is highly expressed in the lower urinary tract and supporting vasculature, and that PDE5 inhibition potentially decreases smooth muscle cell proliferation in the prostate, relaxes smooth muscle in the prostate, bladder neck, and supporting vasculature, increases blood perfusion to the lower urinary tract, and modulates bladder afferent nerve activity.[8] For these reasons, in 2011, the FDA approved tadalafil to also treat the signs and symptoms of BPH as well as a combination of BPH and ED when the conditions coincide.
Management of sexual dysfunction in men treated with BPH/LUTS should be focused and symptom-dependent. A validated questionnaire of enquiry, such as the international index of erectile function or male sexual health questionnaire, should be used to assess sexual function before beginning pharmacological therapy for BPH/LUTS. The clinician then must assess co-morbidities and concomitant medications, particularly those that affect erectile capacity, as well as address any risk factors for cardiovascular disease before initiating any sort of therapy. Also before pharmacological therapy, the physician must advise the patient on lifestyle modifications to improve sexual function, such as weight loss and an appropriate exercise regimen. The physician may even consider PDE5 inhibitors if necessary, especially if the patient presents with true symptoms of ED. If the patient has EjD, he must be advised to transform his BPH/LUTS therapy to an alternative AB or 5ARI. Once the relevant sexual dysfunction is tended to, the physician must provide the apposite counseling on the safety and tolerability of pharmacological therapies for BPH/LUTS. Follow up can be done in 4–8 weeks to check sexual function, after which 6-month checkups are adequate.[9]
Transl Androl Urol. 2017;6(2):295-304. © 2017 AME Publishing Company
