A Review of Antipsychotics and Priapism

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REVIEW

A Review of Antipsychotics and Priapism


Thomas Hwang, MD, Tejash Shah, MD, and Hossein Sadeghi-Nejad, MD, FACS

ABSTRACT

Introduction: Pharmacologically induced priapism is now the most common cause of priapism, with approx-
imately 50% of drug-related priapism being attributed to antipsychotic usage. The majority of pharmacologic
priapism is believed to result in ischemic priapism (low flow), which may lead to irreversible complications, such
as erectile dysfunction. It is imperative that prescribing physicians be aware of potentially inciting medications.
Objectives: To identify medications, specifically antipsychotics, associated with priapism and prolonged erec-
tions and understand the rates and treatment of these side effects.
Methods: A PubMed search of all articles available on the database relating to priapism, prolonged erections,
and antipsychotics was performed.
Results: Various typical and atypical antipsychotic drugs (APDs) have been implicated in pharmacologically
induced priapism. In addition to dopaminergic and serotoninergic receptors, APDs have affinities for a wide array
of other receptors in the central nervous system, including histaminergic, noradrenergic, and cholinergic re-
ceptors. Although the exact mechanism is unknown, the most commonly proposed mechanism of priapism
associated with APDs is a-adrenergic blockade in the corpora cavernosa of the penis. Priapism appears in only a
small fraction of men using medications with a1-receptoreblocking properties, indicating differential sensitiv-
ities to the a-blocking effect among men, and/or additional risk factors that may contribute to the development
of priapism. The best predictor for the subsequent development of priapism is a past history of having prolonged
and painless erections. The acute management algorithm of APD-induced priapism is the same as for other causes
of low-flow priapism.
Conclusion: Clinicians should educate patients treated with antipsychotics about the potential for priapism and
its sequelae including permanent erectile dysfunction. Appropriate patient education will raise awareness,
encourage early reporting, and help reduce the long-term consequences associated with priapism through early
intervention. Hwang T, Shah T, Sadeghi-Nejad H. A Review of Antipsychotics and Priapism. Sex Med Rev
2020;XX:XXXeXXX.
Copyright  2020, International Society for Sexual Medicine. Published by Elsevier Inc. All rights reserved.
Key Words: Priapism; Antipsychotics; Prolonged Erections; Medication Side Effects

INTRODUCTION arterial (high-flow or nonischemic) priapism, and stuttering


Priapism is characterized by a prolonged penile erection lasting (recurrent or intermittent) priapism.1
more than 4 hours that is unrelated to sexual stimulation or in- Ischemic priapism, or low flow priapism, is the most common
terest.1 Although the incidence of priapism is low in the general form of priapism, accounting for >95% of all priapism episodes.2,3
population (0.5e0.9 cases per 100,000 person-years), when It is the result of venous occlusion leading to a backup of blood and
stratified for specific populations with increased baseline risk, such decreased cavernous arterial inflow.4 The blockage of fresh blood
as those with sickle cell anemia, the rates of priapism significantly induces tissue hypoxia that may lead to irreversible complications of
increase.1 Depending on the etiology of priapism, it can be further ischemic penile fibrosis and subsequent erectile dysfunction.4
classified into ischemic (low-flow or veno-occlusive) priapism, Ischemic priapism is a urologic emergency that requires a medi-
cal intervention to minimize potentially irreversible consequences.1
The etiology of ischemic priapism is idiopathic in most cases but
Received August 1, 2020. Accepted October 13, 2020. has been associated with illicit drugs such as cocaine, hematological
Department of Urology, Rutgers New Jersey Medical School, Newark, NJ, disorders such as sickle-cell anemia, malignancy, and commonly
USA
prescribed medications, including antipsychotic drugs (APDs).1,5
Copyright ª 2020, International Society for Sexual Medicine. Published by
Elsevier Inc. All rights reserved. Arterial priapism, or high-flow priapism, is a persistent erection
https://doi.org/10.1016/j.sxmr.2020.10.003 caused by unregulated cavernous arterial inflow, often secondary

Sex Med Rev 2020;-:1e8 1


2 Hwang et al

to penile trauma or iatrogenic injury.1,4 Arterial priapism is not a clinically effective doses.8 Atypical antipsychotics are serotonergic
medical emergency as the corporal tissue is adequately antagonists at the 5-hydroxytryptamine 2A receptors receptors as
perfused.1,4 Stuttering priapism, or intermittent priapism, in- well as being D2 receptor antagonists.10 Commonly prescribed
volves recurrent painful episodes of prolonged erections, usually atypical antipsychotics include clozapine, risperidone, ziprasi-
for less than 3 hours.1 Erections are usually self-limited with done, olanzapine, aripiprazole, and quetiapine.5
intervening periods of detumescence.6 Both typical and atypical APDs have been implicated in
Pharmacologically induced priapism is now the most common pharmacologically induced priapism. In addition to dopami-
cause of priapism, with approximately 50% of drug-related pri- nergic and serotoninergic receptors, APDs have affinities for a
apism being attributed to antipsychotic usage.4,7 The majority of wide array of other receptors in the CNS, including histamin-
pharmacologic priapism is believed to result in ischemic priapism ergic, noradrenergic, and cholinergic receptors.10e12 The
(low flow), which may lead to irreversible complications, such as receptor-binding profile of APDs has been published previously
erectile dysfunction.4 Therefore, it is important that prescribing in pharmacological literature and demonstrates the varying af-
physicians be aware of potentially inciting medications. In this finities APDs have for adrenergic receptors, as well as other CNS
review, we will focus on APDs and its relation to priapism. receptors. The differing binding affinities between APDs is
proposed to be related to its side effect profile.5,13 Although the
exact mechanism is unknown, the most commonly proposed
MATERIALS AND METHODS mechanism of priapism associated with APDs is a-adrenergic
A thorough PubMed search was performed of all articles blockade in the corpora cavernosa of the penis.14
available on the database relating to priapism and antipsychotic During the flaccid state, the penile arterioles are in a tonic
medications. The search included case reports, case series, and state of contraction mediated by a-adrenergic activity.15 Induc-
reviews. Review articles were cross-referenced to search for tion of a penile erection is a result of increased sacral para-
further available detailed individual reports. Additional publica- sympathetic tone leading to relaxation of the cavernous and
tions were reviewed for general background on pathophysiology, arteriolar smooth muscles.15 The relaxation of smooth muscle
evaluation, and management. Only articles published in English increases blood flow into the arterioles and sinusoids and com-
were considered. The quality of evidence reviewed is limited by presses the emissary veins against the tunica albuginea with a
the observational and uncontrolled nature of case reports, case consequent decrease in venous outflow.10,15 The inflow of blood
series, and review articles. and decrease in outflow lead to an erection. Detumescence oc-
curs when the process is reversed with sympathetic stimulation
by norepinephrine at a1- and, to a smaller extent, a2-adrenergic
RESULTS receptors.10 In general, antipsychotics are more potent in
Pharmacology blocking a1-adrenoreceptors than a2-adrenoreceptors.16 APDs
APDs are often classified as “typical” and “atypical” and are block a1-adrenergic receptors in the corpora cavernosa inhibiting
typically used to treat patients with neuropsychiatric disorders, the sympathetic system that mediates smooth muscle contraction
particularly, schizophrenia and bipolar disorder, and can help and detumescence.14,The a-2-blockade exacerbates the a1-
ameliorate psychosis.4,8 Off label, APDs are used in the treat- mediated priapism by stimulating the release of nitric
ment of many other ailments, including treatment-resistant oxideelike substance, a potent muscle relaxant.10 The blockade
depression, dementia, obsessive-compulsive disorder, aggres- of these receptors shifts the penile vascular equilibrium into the
sion, autism spectrum disorders, sleep disorders, and pervasive direction of prolonged erection and intracavernosal stasis, which
developmental disorders.8 All APDs antagonize dopaminergic consequently may result in ischemic priapism. It is important to
transmission at the dopamine type 2 (D2) receptors in the central note, however, that priapism only appears in a small fraction of
nervous system (CNS) but are heterogeneous as a drug group.9 men using medications with a-1 receptor-blocking properties,
The functional distinction between classes is based solely on indicating differential sensitivity to the a-1 blockade and/or
their ability to cause extrapyramidal symptoms (EPS), including additional factors that must be present for priapism to manifest.9
tardive dyskinesia.8
Typical APDs, or first-generation antipsychotics, are charac- Typical vs Atypical Antipsychotics
terized by a strong affinity for the D2 receptors in the CNS.9 Priapism with APDs can occur soon after starting APDs, with
Typical APDs are associated with a higher incidence of EPS at chronic APD use, or after a change in dose or addition of another
usual clinical dosages than atypical APDs.8 Commonly prescribed medication.5,7,17e19 Drug-induced priapism accounts for
typical antipsychotics include phenothiazines (chlorpromazine, ~15e41% of all cases, of which antipsychotic-induced priapism
thioridazine, fluphenazine, perphenazine, mesoridazine, thio- is most commonly implicated.9 The incidence of priapism
thixene) and butyrophenones (haloperidol, zuclopenthixol).5 relating to APDs has not been estimated in the literature. In
Atypical APDs, or second-generation antipsychotics, are most comparison, trazodone has been estimated at between 1 in 1,000
accurately described as one that produces minimal EPS at and 1 in 10,000, and it is likely the incidence in antipsychotics is

Sex Med Rev 2020;-:1e8


Antipsychotics and Priapism 3

lower.5 Priapism associated with APD use may be considered an Risperidone and ziprasidone have the highest affinities for a1-
idiosyncratic reaction, as there has been no conclusive evidence adrenoreceptors among atypical antipsychotics and have been
of correlation between priapism and the dosage or duration of associated with priapism in over 20 cases when administered as a
APD use.10,20 Andersohn et al21 found a correlation between the monotherapy or in combination with other drugs.5,21,29
drug affinities for the a1 receptor of different antipsychotics and
their relative propensities for causing priapism. In addition, there Associated Risk Factors
have been reports of increased risk of priapism secondary to Priapism appears in only a small fraction of men using med-
polypharmacy with APDs and one reported case of clitoral ications with a1-receptor blocking properties, indicating differ-
priapism.10,22,23 ential sensitivities to the a-blocking effect among men, and/or
Approximately 50% of medication-induced priapism cases additional risk factors that may contribute to the development of
are due to APDs, in which phenothiazines are the most priapism.9,30 The best predictor, however, for the subsequent
commonly implicated ones.20 Although atypical antipsychotics development of priapism is a past history of having prolonged
were initially thought to be less likely to cause priapism than and painless erections. It has been noted that a history of delayed
their typical counterparts, almost all atypical antipsychotics, detumescence is present in approximately 50% of any subse-
including risperidone, olanzapine, aripiprazole, clozapine, and quent case of priapism.31 Therefore, it is important to regularly
quetiapine, have been linked to priapism in the literature.20,24 inquire and counsel the patient taking antipsychotics about the
The potential for any individual antipsychotic to cause pria- occurrence of this side effect to increase awareness and to pro-
pism is believed to be dependent on their affinity to block mote early reporting of symptoms.
adrenergic receptors.21 Among the older typical antipsychotics, Diabetes has been implicated as a possible risk factor for the
mesoridazine, chlorpromazine, levomepromazine, thioridazine, development of ischemic priapism in patients using atypical
and fluphenazine have the highest propensity to block a1- antipsychotics. In one case report, a 44-year-old man with a 23-
adrenoreceptors.21 Within the newer atypical antipsychotics, year history of schizophrenia developed priapism when separately
ziprasidone, risperidone, clozapine, and quetiapine have a high trialed on risperidone and trazodone, quetiapine, and olanzapine.
affinity.21 However, even among the APDs with reported low During this time, his blood sugar was found to be elevated. In
affinity, such as aripiprazole, there have been case reports of the past, the patient had been on risperidone and trazodone for
priapism.21,25,26 2 years, and quetiapine and trazodone for 4 months with no
Historically, among typical antipsychotics, the phenothiazine documented episodes of priapism. During that period, his blood
class is most commonly implicated to cause priapism.5 In sugar had been stable. After his diabetes was controlled with
comparing the pharmacology of phenothiazines to butrophe- insulin, the patient was stabilized on loxapine.32 The implication
nones, the phenothiazines are low-potency dopamine receptor is that there is a possible increased risk of developing priapism in
antagonists with higher a-adrenergic blockade, whereas butro- patients on atypical antipsychotics with elevated blood glucose
phenones are higher potency D2 antagonists with lower a- levels.32
adrenergic blockade.21 In the literature, this is reflected in the In theory, polypharmacy may increase the risk of priapism
higher number of case reports associated with phenothiazines, either through the synergistic effect of combining drugs that can
when compared to higher potency D2 antagonists, such as, independently cause priapism or by combining drugs that may
haloperidol.5,21 affect another drug’s metabolism.24 The effect of a-adrenergic
Clozapine was the first atypical antipsychotic to be associated antagonism leading to priapism has been demonstrated in men
with priapism and was first reported in 1992. Since that time, using other medications with a-antagonistic activity, such as, a-
there have been over 10 case reports.5 Clozapine is often used in blockers for the management of blood pressure or lower urinary
patients with schizophrenia who have failed trials with other tract symptoms (LUTS), and trazodone, an antidepressant.4,33,34
drugs and is considered treatment resistant.5 Patients who In one case, terazosin, a a-1-selective adrenergic antagonist, was
develop priapism on clozapine present a challenge to the pre- prescribed to an otherwise healthy male for LUTS. As his dose of
scribing psychiatrist. In cases of clozapine-associated priapism, terazosin was titrated from 1 to 5 mg, the duration of his erec-
one patient was attempted to be switched to quetiapine but did tions increased from 1 to 3.5 hours. Ultimately, the patient
not achieve a good control of his symptoms. Consequently, the suffered an acute priapism episode lasting 17.5 hours, and he
patient requested to restart clozapine despite the risks and was subsequently developed postpriapism erectile dysfunction.33
able to gradually increase his dose with no recurrence of pria- Given the selective action of terazosin on a-adrenergic re-
pism.27 In another case, a 25-year-old patient developed priapism ceptors, this report gives support to the proposed mechanism of
after 1 year of taking clozapine. His dose was reduced to half his APD-induced priapism through a-adrenergic blockade.
original dose successfully with no further episodes. However, it is Although one may expect a high incidence of priapism in pa-
important to note that his initial episode of priapism had lasted tients using a-blockers, this is not the case. It is proposed that
33 hours, and it is likely the patient was subsequently this may be related to dosage, where there is a greater incidence
impotent.28 of priapism in patients taking a-blockers for hypertension than

Sex Med Rev 2020;-:1e8


4 Hwang et al

for LUTS. It is also likely that there are factors in addition to a- side effect of medications. However, clitoral priapism associated
blockade that plays a role in the development of priapism.4 In with antidepressants, including trazodone, nefazodone, cit-
APDs, those with higher affinities for a-adrenergic blockade have alopram, and bupropion, has been reported.5 Olanzapine is the
been implicated to have a higher association with priapism and only antipsychotic that has been reported in the literature to
have been reported with more frequency than their low-a-affinity cause clitoral priapism.47 In this case, a 27-year-old female with
counterparts.21 Given the proposed etiology of APD-induced bipolar disorder was maintained on sodium valproate for
priapism, the combination of APDs with other medications 6 months. She developed a manic episode with psychotic features
with a-blocking properties, such as antidepressants and a- and was prescribed olanzapine for the first time. 4 weeks after
blockers such as tamsulosin, may increase the risk of starting olanzapine, she developed painful swelling of her clitoris.
priapism.4,21,35 Olanzapine was discontinued, and the swelling resolved in
In many patients with psychotic disorders, the practice of 2 days. Of note, the patient did not have any clitoris-related
combining APDs or taking them concurrently with other psy- pathology previously in her medical history.47
chiatric medications such as serotonin-specific reuptake in-
hibitors (SSRIs) is very common and increases the risk of side
Acute Evaluation and Treatment
effects, thereby making it more difficult to ascertain the In the evaluation of a patient with acute priapism, a
offending agent.9 Combining antipsychotics with SSRIs, highly comprehensive history is the mainstay in diagnosis.2,48 The
active antiretroviral therapy (HAART), and lithium have been history can help determine the underlying type of priapism
implicated in increasing the risk for priapism through alterations (ischemic vs arterial) and should include the duration of erection,
in drug metabolism.5,22,32 presence and degree of pain, previous episodes of priapism and
Risperidone is metabolized by the cytochrome P450 (CYP450) method of treatment, current erectile function, use of erectogenic
2D6 enzymatic system, and to a lesser extent, 3A4.36 There is some therapies, medications, recreational drug use, history of sickle cell
evidence suggesting that CYP450 enzyme inducers or inhibitors disease, hemoglobinopathies, hypercoagulable states, and
could impact risperidone plasma levels.37e39 SSRIs inhibit the trauma.1,2 APD-induced priapism is thought to induce ischemic
CYP450 2D6 system and can lead to a higher plasma level of ris- priapism, and our review will focus on the treatment of low-flow
peridone, and in turn, a greater a-adrenergic blockade.40 There priapism.
have been case reports of priapism developing in patients taking The physical examination should include the genitalia, peri-
risperidone concurrently with paroxetine, citalopram, or fluvox- neum, and abdomen.1 The abdominal and perineal examination
amine.23,41,42 However, it is important to note that risperidone has may reveal evidence of trauma or malignancy.1 In ischemic pri-
caused priapism even when used as a monotherapy.43 apism, the corpora are fully rigid and tender, but the glans penis
HAART has also been implicated in interacting with anti- is soft. In comparison, the corpora in arterial priapism are not
psychotic medications through the alteration of CYP450 en- fully rigid.1 Laboratory testing should include a complete blood
zymes leading to increased plasma levels of antipsychotic.22,44 count, white blood count with blood cell differential, platelet
Although case reports exist, there is a paucity of definitive data count, and coagulation profile.2,48 Corporal blood gas analysis is
regarding interactions between HAART and antipsychotic essential to differentiate arterial and ischemic priapism. In
medications. ischemic priapism, the corporal aspirate will usually reflect pO2
Lithium is not directly associated with priapism, but a number (mmHg) < 30, pCO2 (mmHg) > 60, and pH < 7.25.2
of cases have occurred in patients taking lithium and risperidone The management of APD-induced ischemic priapism requires
concurrently.45,46 A suggested mechanism of action is that emergent intervention to restore penile flaccidity and prevent
lithium acts synergistically to increase a-adrenergic antago- damage to the corpora cavernosa.1 The first step in the man-
nism.5,45,46 In one case, a patient had been taking risperidone for agement of ischemic priapism is decompression of the corpora
2 years without developing priapism. Once the patient was cavernosa by penile aspiration until fresh red oxygenated blood is
started on lithium, he began developing prolonged erections obtained.1 Decompression promotes the recovery of the intra-
between 1 and 3 hours. His risperidone was tapered from corporal blood circulation, which should relieve the penile pain.1
1.5 mg/day to 1 mg/day with resolution of symptoms.46 If priapism persists or recurs after penile aspiration, the next step
Although it is unclear to what extent polypharmacy increases is intracavernosal injection of sympathomimetic agents.1 Phen-
the risk of priapism, clinicians must be cognizant of the theo- ylephrine is suggested as the drug of choice because of its high
retical risk when prescribing drugs that interact metabolically, or selectivity for the a1-adrenergic receptor, without concomitant
may act synergistically. b-mediated ionotropic and chronotropic cardiac effects.49,50
Phenylephrine is usually diluted in normal saline to a concen-
tration of 100e500 mg/mL and given in 1-ml doses every
Clitoral Priapism 3e5 minutes. It is administered directly into the corpus cav-
Clitoral priapism has been associated with perineal malig- ernosum with a maximum dosage of 1 mg over 1 hour.1 Patients’
nancies and radiation but is much less frequently reported as a vital signs should be monitored every 15 minutes; side effects of

Sex Med Rev 2020;-:1e8


Antipsychotics and Priapism 5

sympathomimetic agents include headache, dizziness, hyperten- most serious complication of priapism is impotence secondary to
sion, reflex bradycardia, tachycardia, palpitations, and irregular ischemia and corporal fibrosis.5 The prognosis is dependent on
cardiac rhythm.1,51 the promptness of treatment, but even with treatment, 40e50%
If detumescence is not achieved after aspiration and intra- of patients can develop erectile dysfunction and permanent
cavernosal injection of a sympathomimetic drug, surgical inter- damage.5,60 On acute presentation of priapism, a urologic
vention in the form of penile shunt surgery should be performed consultation should be obtained on an emergent basis to restore
to relieve penile ischemia and avoid corporal fibrosis in priapism penile flaccidity.5 Detumescence can normally be achieved
cases 72 hours.2,52,53 through corporal aspiration and intracavernosal injection of an a-
adrenergic agonist.1
The type of shunt procedure performed is selected by the
surgeon’s preference and familiarity. As a rule, it is preferable to With the increasing use of APDs in various disorders, the
try distal shunts first.1 It is important to note, however, that clinician must be conscious of the risk of priapism associated
prolonged priapism events >36 hours appear to irreversibly with these medications, although the overall risk may be low.
damage erectile tissue structurally and functionally. In these Priapism can occur in patients starting APDs, in those who have
cases, any shunt procedure may only serve to decrease pain been on stable doses for long periods of time, and with the
without preserving erectile function.1 addition of other medications.5,7,17e19 It has been hypothesized
that APDs with higher affinities for a1-adrenoreceptors have a
In intractable cases of acute ischemic priapism lasting
higher propensity to cause priapism; however, even APDs with
>48e72 hours, immediate penile prosthesis surgery has been
low a-adrenergic antagonism have been linked to the side ef-
recommended.1 Ischemic episodes of that duration will usually
fect.21 It should be mentioned that the incidence of priapism
result in complete erectile function impairment and major penile
with APDs is based on published case reports and reported
fibrosis/deformity. By performing immediate prosthesis place-
adverse drug reactions submitted to the US Food and Drug
ment, one may avoid surgical difficulties and complications (eg,
Administration. As a result, the reported incidence of priapism
urethral injury, tunical erosions, infection, penile shortening)
with any individual APD may partially be the result of the fre-
associated with corporal fibrosis.54e57
quency of use in the population and the length of time the drug
has been on the market. Regardless, baseline risk factors should
Preventing Future Episodes be considered when starting a patient on APDs. These include
After the acute presentation of priapism associated with an personal history of prolonged erections, sickle cell anemia, sub-
APD, future occurrences may be avoided by discontinuing the stance abuse, diabetes, and polypharmacy with drugs that are
offending medication, decreasing the dosage, or changing to an independently linked to priapism or may alter the metabolism of
APD with a lower affinity for a-adrenergic receptors.5,21 In cases APDs.5
of stuttering priapism, hormonal manipulation and the use of a-
Patients prescribed APDs should be made aware of the po-
adrenergic agonists, digoxin, terbutaline, gabapentin, baclofen,
tential side effects before the initiation of treatment, as the lack of
hydroxyurea, or phosphodiesterase type 5 inhibitors have been
awareness may lead to a delay in seeking medical attention or
reported in the literature.1 Given the proposed mechanism of
reduce adherence to their therapy. Sexual dysfunction is preva-
APD-induced priapism, the use of a-adrenergic agonists, such as
lent in users of antipsychotics and may be attributed to the effects
pseudoephedrine, has been suggested.58 In one case, a 36-year-
of this class of medications on a1- and a2-adrenergic, histamine-
old male with schizophrenia had been trialed on several anti-
H1, and dopaminergic receptors.9 Sexual side effects are espe-
psychotics, including risperidone, fluphenazine, aripiprazole,
cially important to recognize and address in patients with psy-
haloperidol, and quetiapine. The patient had poor psychiatric
chosis, as this patient population is less likely to spontaneously
response to these medications and had developed priapism to
report these symptoms because of the sensitive nature of the
each of these antipsychotics. The patient was started on chlor-
pathology.9 It is also important to be aware that these side effects
promazine with improvement of his psychiatric symptoms;
can reduce patient adherence to APDs, a major cause of psy-
however, once the medication was titrated to 400 mg/day, the
chotic relapse and rehospitalization for psychosis.61
patient again developed priapism. The patient’s dose of chlor-
promazine was reduced to 200 mg/day, and he was started on Unfortunately, it seems likely that patients starting psycho-
pseudoephedrine ER 120 mg nightly. The patient did not tropic medications will not be counseled appropriately regarding
develop any further episodes of priapism and was able to sub- the side effects of prolonged erections and priapism.62 In a study
sequently increase his dosage of chlorpromazine to 450 mg/ performed at the VA New Jersey Health Care System in New
day.58 Jersey, all male patients younger than 50 years taking trazodone
were surveyed regarding their counseling before initiating ther-
apy. It was found that only 43 of 229 (18.78%) patients were
DISCUSSION informed about the side effects of prolonged erections, 37 of 229
It is estimated that between 15% and 26% of priapism cases (16.16%) were informed about the risk priapism, and only 17 of
are associated with the use of antipsychotic medications.59 The 229 (7.42%) patients were asked if they had a history of

Sex Med Rev 2020;-:1e8


6 Hwang et al

prolonged erections or priapism.62 Although the study was 2. Broderick GA, Kadioglu A, Bivalacqua TJ, et al. Priapism:
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Corresponding Author: Tejash Shah, MD, Department of 11. Roth BL, Sheffler DJ, Kroeze WK. Magic shotguns versus
Urology, Rutgers New Jersey Medical School, 185 S Orange magic bullets: selectively non-selective drugs for mood dis-
Ave, Newark, NJ 07103, USA. Tel: (973)972-4488; Fax: (973) orders and schizophrenia. Nat Rev Drug Discov 2004;3:353-
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12. Miyamoto S, Duncan GE, Marx CE, et al. Treatments for
Conflict of Interest: The authors report no conflicts of interest.
schizophrenia: a critical review of pharmacology and mecha-
Funding: None. nisms of action of antipsychotic drugs. Mol Psychiatry 2005;
10:79-104.
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