Complications
POME may occur with intramuscular injections of long-acting testosterone undecanoate, and less commonly with other oil-based intramuscular testosterone injections. Symptoms may include cough, dyspnea, throat tightening, chest pain, dizziness, and syncope.[78] These episodes typically occur within 30 minutes of administration and resolve spontaneously.
POME is much less frequent if the injection is given slowly (e.g., over 60-90 seconds for long-acting intramuscular testosterone undecanoate). Long-acting testosterone undecanoate should be administered in a healthcare setting (rather than at home).
Patients who receive long-acting intramuscular testosterone undecanoate should be monitored for 30 minutes after injection in the clinic for clinical symptoms of embolization, such as cough or chest pain.[54]
Hypogonadism in adults can lead to loss of bone mass in adults, while in childhood it can result in failure to reach bone mass peak.[79][80]
Long-standing hypogonadism is associated with osteoporosis that can result in fractures occurring with unusually low levels of trauma. Men who have had, or are at risk for, falls and bone fractures should have an assessment of their bone mineral density.
Testosterone therapy has been shown to increase bone mineral density in older men with low testosterone.[81][82] However, the evidence for reducing fracture risk is limited and inconsistent.[83] One subtrial of a large, randomized, controlled trial showed that testosterone therapy did not result in lower incidence of fracture compared with placebo in middle-aged and older men with hypogonadism; fracture incidence was found to be higher among men who received testosterone (follow-up median 3 years).[84] The study did not evaluate bone density and structure, or assess possible mechanisms for fracture. Long-term studies are needed to determine the effect of testosterone on fracture risk.
Men with hypogonadism and osteoporosis should receive treatment for osteoporosis, regardless of testosterone therapy, in order to most effectively reduce fracture risk.[83]
See Osteoporosis
This is particularly common with intramuscular testosterone preparations.
In most patients (without increased risk of cardiovascular disease), elevated hematocrit may be managed by reducing testosterone dose or changing the formulation (e.g., from intramuscular to transdermal preparation). Risk factors should be addressed (cessation of smoking, weight loss, identification and treatment of sleep apnea, and hypertension).
If hematocrit is greater than 50%, testosterone may need to be temporarily discontinued. Consider reducing testosterone dose and/or changing the formulation when hematocrit decreases to a safe level.[2][37]
It is expected that patients with functional hypogonadism will experience testicular shrinkage as a result of negative feedback of testosterone on gonadotropin secretion. However, men with pathological hypogonadism will either already have small testes at baseline, or develop shrinkage irrespective of testosterone treatment.
Occurs less frequently with gels/creams than with transdermal patches; the mechanism is unclear.
Obtain urology consultation if: PSA increases to above 4.0 nanograms/mL; PSA velocity is above 0.4 nanograms/mL/year; there is an increase in PSA above 1.4 nanograms/mL within a 12-month period of testosterone treatment.[37]
PSA elevation may occur from causes other than testosterone therapy: for example, exercise (in particular cycling), urinary tract infection (check urine), prostatitis, benign prostatic hypertrophy, urinary retention, urinary catheterization, digital rectal exam, sigmoidoscopy/colonoscopy, inflammatory bowel disease, ejaculation, anal intercourse, and recent surgery.
Men with pathological hypogonadism will have subfertility at baseline and this will be largely unaffected by testosterone treatment. For men with functional hypogonadism, who may retain spermatogenesis, it is likely that there will be a reduction in sperm count on testosterone therapy, which could cause or exacerbate subfertility.
Patients with congenital hypogonadotropic hypogonadism should be advised that there is no evidence that testosterone therapy is detrimental to their fertility if later switched to human chorionic gonadotropin combined with follicle-stimulating hormone for fertility treatment.[75]
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