Men's Health: ED, Testosterone, Peyronie's, Infertility

Men's-health visits are a growing part of urology and a natural fit for APPs. Beyond treating the specific complaint, these visits are a rare opportunity to catch cardiovascular and metabolic disease in men who otherwise avoid doctors — erectile dysfunction in particular is an early and independent marker of cardiovascular disease.

13.1 Erectile dysfunction (ED)

ED is the consistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance. The physiology is straightforward: an erection requires intact arterial inflow, veno-occlusion, neural signaling, adequate testosterone for libido, and the psychological substrate. Failure anywhere in that chain produces ED — and the most common cause by far is vascular.

Evaluate

• History: onset (abrupt vs. gradual), situational vs. constant, presence of nocturnal/morning erections (their PRESENCE suggests an intact vascular/neural apparatus and points toward a psychogenic or situational cause), libido, ejaculatory function, relationship factors, depression, and performance anxiety.

• Vascular risk factors: diabetes, hypertension, hyperlipidemia, smoking, obesity, sedentary lifestyle. Check a lipid panel, A1c, and blood pressure — ED is a cardiovascular warning shot.

• Medications that cause it: thiazides, beta-blockers, SSRIs, antiandrogens, finasteride, and alcohol/recreational drugs.

• Labs: morning total testosterone if there is low libido or fatigue (Chapter 22); consider prolactin and thyroid if indicated.

• Quantify: use the IIEF-5 (SHIM) to score baseline severity and track response.

Treat — a stepwise menu

• First-line: PDE5 inhibitors (sildenafil, tadalafil, vardenafil, avanafil) plus aggressive risk-factor modification (exercise and weight loss genuinely improve erectile function). Counsel on the details that determine success: sildenafil needs an empty stomach and ~1 hour lead time; tadalafil lasts up to 36 hours and can be dosed daily at 5 mg; and — critically — these drugs require sexual stimulation to work. Many “failures” are simply dosing errors. Try a maximum dose at least 4–6 times before calling it a failure.

• Second-line: intracavernosal injection therapy (alprostadil or Trimix — papaverine/phentolamine/alprostadil). Injections are highly effective even in severe or neurogenic ED, and they work when pills do not. Counsel every injection patient on priapism (Chapter 2). The vacuum erection device (VED) is drug-free, inexpensive, and effective, and is also used for penile rehabilitation.

• Low-intensity shockwave therapy (LISWT): an AU regenerative option that applies low-intensity acoustic waves to stimulate neovascularization and improve penile blood flow in appropriate men with mild-to-moderate vasculogenic ED.

• Third-line: penile prosthesis (semirigid, or a three-piece inflatable such as the Coloplast Titan) for refractory ED. Patient satisfaction with prostheses is among the highest of any procedure in urology — do not treat it as a last resort to be ashamed of.

13.2 Testosterone deficiency (hypogonadism) — overview

• Diagnose correctly: consistent symptoms (low libido, fatigue, ED, loss of morning erections, reduced motivation, decreased muscle mass) PLUS at least TWO low early-morning total testosterone levels. One low level is not a diagnosis.

• Work up the cause: LH/FSH (to separate primary testicular failure — high LH — from secondary/central causes — low or inappropriately normal LH), prolactin (a pituitary adenoma is a treatable cause), and consider iron studies. Reversible contributors: obesity, obstructive sleep apnea, opioids, alcohol, and glucocorticoids.

• Before starting therapy: baseline hematocrit and PSA, and an explicit fertility conversation — exogenous testosterone suppresses the HPG axis and spermatogenesis.

• Enclomiphene: for hypogonadal men who wish to preserve fertility, enclomiphene raises the body's own testosterone while MAINTAINING sperm production — an AU-favored alternative to exogenous testosterone.

Testosterone therapy is covered in depth — formulations and our preference order, anastrozole for estrogen control, targets, the monitoring schedule, and contraindications, alongside women's hormone therapy — in Chapter 22.

13.3 Peyronie's disease

• What it is: a fibrous plaque of the tunica albuginea, thought to follow repetitive microtrauma during intercourse in genetically susceptible men, causing penile curvature, pain, shortening, indentation/hourglass deformity, and often ED. Associated with Dupuytren's contracture and diabetes.

• Two phases — and the phase determines the treatment: the ACTIVE phase (evolving deformity, often painful, lasting ~6–18 months) and the STABLE phase (deformity fixed, pain resolved, stable for ≥ 3 months). Do NOT operate during the active phase.

• Assess: objectively document curvature (a photograph of an erection, or an in-office intracavernosal injection with goniometry), plaque location, penile length, and erectile function.

• Manage: reassurance and observation for mild, non-bothersome curvature (a minority improve spontaneously); intralesional collagenase (Xiaflex) injections for stable, bothersome dorsal/lateral curvature of 30–90° with intact erections; penile traction therapy (which genuinely helps with length preservation and is underprescribed); and surgery for stable, significant deformity — plication for simpler curves, grafting for complex ones, or a penile prosthesis when significant ED coexists.

13.4 Male infertility

• Frame it correctly: infertility is failure to conceive after 12 months of unprotected intercourse (6 months if the partner is over 35). A male factor is present in roughly HALF of couples — evaluate the man in parallel with the female partner, never sequentially.

• Start with: a reproductive history (puberty, prior paternity, testicular injury/torsion/cryptorchidism, infections, chemotherapy or radiation, medications, anabolic steroid or testosterone use, heat exposure, tobacco/marijuana) and at least TWO semen analyses collected after 2–5 days of abstinence.

• Exam: testicular size and consistency (a small, soft testis suggests impaired spermatogenesis), the presence of the vas deferens on both sides (congenital bilateral absence of the vas is associated with CFTR/cystic fibrosis mutations — test both partners), and varicocele.

• Hormones: testosterone and FSH at a minimum; add LH and prolactin as indicated. A high FSH with small testes indicates primary spermatogenic failure; a low FSH/LH with low testosterone indicates a central cause.

• Azoospermia: separate obstructive (normal testicular size and FSH — think vasal absence, prior vasectomy, ejaculatory duct obstruction) from non-obstructive (small testes, high FSH — testicular failure). Obtain karyotype and Y-chromosome microdeletion testing before proceeding to surgical sperm retrieval.

• Treat what is treatable: varicocele repair (improves semen parameters and pregnancy rates in appropriately selected men), stopping exogenous testosterone/anabolic steroids, treating infection, and lifestyle change. Refer to our reproductive urology (male-fertility) specialist for azoospermia, surgical sperm retrieval, or complex cases.

13.5 Premature ejaculation

• Very common (the most common male sexual dysfunction) and very treatable, yet rarely volunteered — you have to ask.

• Options: behavioral techniques (stop-start, squeeze), topical anesthetics (lidocaine/prilocaine spray or cream applied 10–15 minutes before, with a condom to avoid transferring numbness to the partner), and off-label SSRIs (daily paroxetine/sertraline, or on-demand dosing). Tramadol is an alternative. Treat any concurrent ED FIRST — men who lose erections often rush to ejaculate.

13.6 Vasectomy

• Safe, effective, in-office permanent contraception, typically performed via a no-scalpel technique under local anesthesia in about 15–20 minutes.

• Counsel on: permanence (consider it irreversible, even though reversal exists); the failure rate (~1 in 2,000 after confirmed sterility); post-vasectomy pain syndrome (1–2%); and — most importantly — that it is NOT immediately effective.

• The critical instruction: use another form of contraception until a post-vasectomy semen analysis (typically at ~8–12 weeks and after ~20 ejaculations) confirms azoospermia. Unplanned pregnancies after vasectomy are almost always a failure of this instruction, not of the surgery.

• Reassure: vasectomy does not affect testosterone, libido, erections, or ejaculate volume in any meaningful way (sperm contribute < 5% of the volume), and it does not increase the risk of prostate cancer.