Beste apotheek van Nederland

ED as a main complaint. In only one of four small trials, the intramuscular injection of
testosterone improved erectile function compared with placebo. Gel testosterone (50 mg and 100
mg doses) was found to have increased sexual intercourse frequency compared with placebo or
patch testosterone.
Two RCTs compared testosterone treatment (alone or combined) with PDE–5 inhibitors in
hypogonadal patients with ED that was refractory to prior sildenafil therapy (this was also
relevant to Question 1). In both trials, patients treated with the combination of testosterone
(either patch 5 mg/d or gel 1 percent) and 100 mg sildenafil had statistically significantly greater
IIEF scores compared with those treated with sildenafil alone (endpoint: 21.8 versus 14.4, p
<0.05 and mean change: 4.4 versus 2.1, p = 0.029).
KQ 3. What are the harms of pharmaceutical treatments for patients
with ED?
What is the evidence on specific harms such as nonarteritic ischemic
optic neuropathy (NAION) and penile fibrosis related to
pharmaceutical treatments in patients with ED?
All-cause adverse events were more frequent in patients treated with PDE–5 inhibitors
compared with those treated with placebo. In particular, meta-analyses demonstrated that
patients receiving sildenafil (any dose) were at higher risk of any adverse (RR = 1.51, 95 percent
CI: 1.32–1.72). The 12-week use of 20 mg tadalafil was also associated with an increased risk of
any adverse events (RR = 1.61, 95 percent CI: 1.37–1.89). The most common adverse events in
PDE–5 inhibitor-treated patients were headache, flushing, dyspepsia, and rhinitis. The use of
both sildenafil and vardenafil was associated with an increased risk of headache, dyspepsia, or
flushing compared with placebo. Patients treated with sildenafil had an increased risk of visual
disturbances (RR = 3.66, 95 percent CI: 2.27–5.92).
Serious adverse events were not statistically different between PDE–5 inhibitor and placebo
groups. For example, patients treated with vardenafil experienced a statistically non-significant
34 percent increase in risk of serious adverse events (RR = 1.34, 95 percent CI: 0.76–2.36).
Although the rate of withdrawals due to adverse events was slightly increased in patients
receiving vardenafil versus those on placebo, the pooled RR estimate did not reach the level of
statistical significance (RR = 1.29, 95 percent CI: 0.78–2.13).
The incidence of adverse events increased with the dose of PDE–5 inhibitors. Meta-analyses
demonstrated a statistically significant increase in the risk of any adverse events between patients
receiving 20 mg versus 10 mg of either tadalafil (RR = 1.21, 95 percent CI: 1.05–1.38) or
vardenafil (RR = 1.15, 95 percent CI: 1.06–1.25). The pooled RR estimates for specific events in
sildenafil treated patients were: flushing (50 mg versus 25 mg; RR = 1.65, 95 percent CI: 1.13-
2.42), headache (100 mg versus 50 mg; RR = 1.31, 95 percent CI: 0.93-1.84), and visual
disturbances (100 mg versus 50 mg; RR = 4.18, 95 percent CI: 0.44-39.54). The differences in
the incidence of any adverse events between treatment and placebo groups did not vary
significantly among four head-to-head trials with patients treated with sildenafil, tadalafil, or
vardenafil.
Penile pain or priapism was more frequent in patients treated with alprostadil injections
compared with those who received placebo. Patients who received a testosterone patch had a
higher rate of skin reactions at the application site compared with those who received the
placebo. One trial reported prostate cancer in two patients treated with a testosterone patch. The
use of gel testosterone did not show a dose-related increase in adverse events.
4