We evaluate the efficacy and safety of tamsulosin a selective α1A-receptor antagonist in patients with painful ejaculation (PE) as a sole entity. A total of 118 men with PE were included in the study. Patients were randomly assigned to receive 0.4 mg oral daily tamsulosin (group 1, n=59) or placebo (group 2, n=59), during a 6-week period for each agent. Pretreatment evaluation included history and physical examination, International Index of Erectile Function (IIEF) and a visual analog scale (VAS) for pain. The efficacy of two treatments was assessed every 2 weeks during treatment, and at the end of the study using responses to IIEF, VAS evaluation, mean intercourse satisfaction domain, mean weekly coitus episodes and adverse drug effects. In all, 104 patients (88%) completed the whole treatment schedule. Pain resolved in 16 and 13% of the patients treated with tamsulosin and placebo, respectively (P=0.1). Baseline mean intercourse satisfaction domain values of IIEF 10 and 11 reached to 12 and 10 at 6-week treatment in groups 1 and 2, respectively (P=0.08). The VAS after tamsulosin and placebo decreased from 5.7 and 5.8 to 5.1 and 5.5, respectively (P=0.1). The mean weekly intercourse episodes increased from pretreatment values of 1.8 and 1.6 to 1.9 and 1.7, for tamsulosin and placebo, respectively (P=0.08). Mean number of adverse events was 11 for tamsulosin and 5 for placebo (P<0.05). Tamsulosin is no better than placebo in improvement of PE as a sole entity.
Painful ejaculation (PE) is an uncommon problem that may have psychological or organic causes. Although ejaculatory pain in the general male population is considered to be 1%,1 it is presented a serious problem for 88–91% of men who experience it.2, 3 It can be caused by prostatectomy,4, 5 a history of prostatitis,6 pelvic radiation,7, 8 lower urinary tract symptoms (LUTS) diagnosed with clinical benign prostatic hyperplasia (BPH),9, 10 chronic pelvic pain disorder,11 and neuroleptics.12, 13, 14, 15, 16, 17, 18
On the other hand, PE as a sole entity is rare, and its etiology often remains unknown. No urogenital, infectious, psychological or neurological diseases are associated with the symptoms. The pain is refractory to conventional analgesics and several neuropathic pain therapies. The proposed theory for etiology of this problem in men is that pelvic floor muscle and/or bladder neck spasm are key to the development of this condition.
Three α1-adrenoceptor subtypes α1A, α1B and α1D exist.19 Another α1-adrenoceptor subtype with a low-affinity prazosin adrenoceptor termed α1L also exists.19 α1-receptors predominate in the prostate gland, prostatic capsule, prostatic urethra and bladder.20 Electrophysiological study of prostate and smooth muscles have shown that the α1A and α1L-adrenoceptor subtype predominates in the prostate capsule and it is responsible for mediating smooth muscle tone.21, 22, 23, 24, 25 Another study demonstrates that α1-adrenoceptors in the human detrusor are of the α1D and, to a lesser extent, the α1A subtypes.26 Tamsulosin is an α1-adrenoceptor antagonist that exhibits selectivity for α1A – and, somewhat lesser extent, α1D – over α1B-adrenoceptors.26, 27, 28, 29 In addition, tamsulosin has 12 times greater affinity for α1-adrenoceptors in the human prostate than in the aorta in contrast to prazosin, which has comparable affinity for those in the prostate and aorta.30 This can be referred to as receptor pharmacological uroselectivity.31
A randomized, placebo-controlled, multi-center clinical trial studying the efficacy of tamsulosin in treating patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) has demonstrated improvement in pain using tamsulosin.11 Also tamsulosin was superior to placebo in providing symptomatic relief in men with CP/CPPS in few studies.11, 32 Case reports have also suggested tamsulosin to be effective in alleviating PE in clinically depressed patients.33 Given the aforementioned postulated theory for the origin of PE and the uroselectivity of tamsulosin, we decided to test its potential therapeutic effect on PE as a sole entity. To our knowledge this is the first double-blind placebo controlled study on the efficacy of tamsulosin for treating PE in patients without any urogenital, infectious, psychological or neurological causes.
Materials and methods
This study comprised 118 married men (aged 21–40 years) with PE as a sole entity. All patients gave their written informed consent to participate in the study after procedures, and possible side effects were explained to them. All couples were in a stable relationship for at least 6 months. The primary diagnostic criterion was pain or discomfort during or immediately after ejaculation in more than 90% of coitus for at least 3 months in the previous 6 months.
All patients underwent preliminary assessment, including a medical and sexual history, physical examination, and structured interview diagnostic of mental and physical disorders. To be able to exclude organic causes, urine analysis, urine culture, urine cytology, semen culture, and expressed prostatic secretions analysis were done and serum chemistries, serum prostate-specific antigen (PSA) level, and complete blood count were measured. We used ligase chain reaction to screen for Chlamydia in urethral urine samples and excluded men whose tests yielded positive results. All patients had undergone cystoscopy to exclude lower urinary tract pathology.
Men 40 years old or younger diagnosed with PE and with negative urine and semen cultures and normal expressed prostatic secretions at baseline were eligible for study. Age limits were selected to exclude men from the study who might have helped from α-blocker therapy for symptoms associated with BPH. Only patients without any obvious organic, psychogenic, neurogenic, infectious and drug-induced causes of PE, and serum PSA level of ⩽4 ng/ml were included in the study. We presumed that for preventing bias in study protocol, the patients had to have adequate frequency of intercourse, therefore only patients with possible sexual intercourse equal or greater than one per week were included.
Patients with chronic or acute bacterial and nonbacterial prostatitis, CPPS, prostatodynia, abnormal digital rectal examination (DRE), bacteriuria within 3 months of screening, any urogenital disease, prior prostate or pelvic surgery or pelvic radiotherapy, a history of another chronic pain disorder or using any therapy for chronic pelvic pain disorders such as central analgesic agents, a history of active genital herpes within the previous year, a history of genitourinary cancer, inflammatory bowel disease, abnormal serum chemistries or complete blood count, history of allergy to α-adrenergic antagonists or hypersensitivity to tamsulosin, postural hypotension, cancer diagnosed within 5 years of baseline, finasteride use within 3 months, or cardiac, endocrine, or neurological disorders, were excluded. Medications known to cause PE (such as imipramine, desipramine, clomipramine, protriptyline, amoxapine, fluoxetine and venlafaxine) or interference with the study drug or influence the symptom of PE (such as α-adrenergic blocking drugs, α-adrenergic agents, drugs with anticholinergic activity, antispasmodics or muscle relaxants, parasympathomimetics or cholinomimetics, nonsteriodal anti-inflammatory drugs, antibiotics, warfarin, cimetidine, herbal medications and intravesical bacillus Calmette-Guerin) were not permitted.
The patients were randomly assigned to either group of 59 subjects each. Each eligible patient was given a randomization number using an interactive voice response system, which followed a randomization table generated by the method of random permuted blocks. Persons who were geographically and operationally independent from the study investigator did the randomization of the study. Group 1 was given 0.4 mg tamsulosin (Omnic, Yamanouchi Europe, The Netherlands) orally daily for 6 weeks. Group 2 received a similar regimen of placebo. The placebo capsules were a starch compound with the same color and size of tamsulosin. All the men were asked not to consume alcoholic drinks within 6 h of sexual activity. Treatment was administered in a randomized sequence that remained unknown to the patient and to the physician.
Patients were screened on day −14. Baseline measurements were obtained on day −1, and efficacy assessments were made every 2 weeks after the initial dose of tamsulosin on day 1. At baseline, every 2-week after the commencement of medical therapy and at the end of 6-week treatment period, patients completed two inventories (i) the international index of erectile function (IIEF), and (ii) a visual analog scale (VAS) for pain. The IIEF is a 15-question validated inventory, which has five domains, erectile function, libido, orgasmic function, sexual satisfaction and overall satisfaction (Table 1). The questionnaire addresses the patient's sexual function over the 4-week period before completing the inventory. The efficacy of the placebo and tamsulosin was assessed using responses to the questions 6–11. Each question is scored on a Likert scale (maximum score of 5), with higher scores indicating better function. The VAS used was a standard 1–10 scale with a score of 10 representing the worst pain. The safety and tolerability of tamsulosin were monitored by physical examinations, sitting vital signs, recording adverse events and concomitant medications throughout the trial. Adverse events were graded according to National Cancer Institute Common Toxicity Criteria (version 2.0).34 Patients were asked at each visit to report any adverse events that had occurred since the previous visit. The questions were open-ended, and patients were not asked about any specific types of adverse but all of the ejaculation disorders (premature ejaculation, retrograde ejaculation, anejaculation and PE) were included in questions.
All events, regardless of whether they were likely reactions to the study drugs, were recorded.
The study sample size of 118 patients (59 per group) was powered for a difference of approximately 1 standard deviation between the tamsulosin and placebo group with a statistical power of 85% (β=0.15) and assuming an overall 10% dropout rate.
Sexual satisfaction rates of patients and comparison of the incidence of side effects were tested using the χ2-test. Scores for all scales were compared between pre and post-treatment time periods using a two-tailed Student's t-test. A P-value less than 0.05 was considered statistically significant. Statistical analysis was performed using the computer statistical package SPSS/10.0 (SPSS, Chicago, IL, USA) and SAS/6.4 (SAS Institute Cary, NC, USA).
All patients were seen with their wives and interviewed about their sexual activity and patient's ejaculation function. In all 118 patients were recruited, but only 104 (88%) completed the whole randomized trial study (50 of 59 in the tamsulosin group and 54 of 59 in the placebo group) (Figure 1).
Fourteen patients were non-completer. Reasons for non-completion included four adverse effects (tamsulosin group), six cases of lack of effect on pain (three from each group) and four were lost for follow-up (two from each group). The dropout rates was significantly higher in tamsulosin group compared with placebo group) (9 versus 5) (P=0.04). Pain was located in the penis (87%), testis (10%), or abdomen (3%). Most patients (82%) experienced pain for a duration of 1–5 min post ejaculation. Pain lasted less than a minute in 12%, but more than 5 min in 6%. There were no statistical differences in patients' characteristics in the two groups (Table 2). Mean patient age was 28.7 years (range 21–40) in group 1 and 27.6 years (range 21–40) in group 2 (P=0.09, not significant). Mean serum PSA level was 1.4 ng/ml (range 0.02–4). None of the patients had abnormal serum PSA level.
Efficacy of tamsulosin
After 6 weeks of treatment, pain improvement did not differ significantly between the two treatment groups. Neither treatment had significant effect in pain relief. During the study, from week one onward and at the study endpoint (week 6), there were no significant differences between the treatment groups (P=0.1) (Table 3).
In 50 patients who received tamsulosin, eight (16%) noticed a decrease in pain, five (10%) reported an increase and 37 (74%) found no change. When treated with placebo (n=54), seven (13%) reported a decrease in pain, five (9.3%) noticed an increase and 42 (77.7%) had no change. The statistical analysis showed that tamsulosin was not statistically superior to placebo (P=0.1). The mean pretreatment VAS was decreased from baseline 5.7 in the tamsulosin group to 5.1 compared with a mild decrease in the placebo group (from 5.8 to 5.5). Again the difference was not statistically significant (P=0.1).
Baseline and 6-week mean intercourse satisfaction domain values of the IIEF were 10, 11 and 12, 10 in groups 1 and 2, respectively. Tamsulosin group did not report significantly greater intercourse satisfaction than those in placebo group (P=0.08).
The mean pretreatment intercourse frequency was 1.8 per week for tamsulosin compared to 1.6 per week for placebo. Tamsulosin did not demonstrate superiority in increasing mean pretreatment intercourse frequency. The mean intercourse frequency at 6-week treatment was 1.9 and 1.7 for tamsulosin and placebo, respectively (P=0.08).
More adverse effects were associated with tamsulosin treatment (P=0.01) (Table 4). Eleven (22%) tamsulosin and five (9.3%) placebo patients reported treatment-related adverse events; the most common in the tamsulosin group were dizziness (4%), retrograde ejaculation (4%), and headache (4%). Among these 11 men, 2 (18.2%) reported grade 1 (‘mild’), and 3 (27.3%) reported grade 2 (‘moderate’) adverse events. None of the patients reported grade 3 (‘severe’) adverse events. Retrograde ejaculations were confirmed by post-ejaculation urine analysis.
Asthenia, rhinitis, gastrointestinal disorders, impotence, postural hypotension and palpitation were seen less frequently (1–2% of patients). Except for dizziness, rhinitis and abnormal ejaculation, statistical analysis did not show significant difference between two groups. In our study, 4 of 50 patients (8%) in group 1 discontinued medication because of intolerable side effects, namely retrograde ejaculation in one, dizziness in two, and headache in one.
Despite many advances in our understanding of the pathophysiology of erectile dysfunction, the true pathogenesis of PE remains unknown. Although a number of medical therapies are available for CP/CPPS, the lack of significant prospective and double-blind, placebo-controlled studies makes it difficult to individualize efficacy rates in PE without any known risk factors.
Tamsulosin was not superior to placebo in providing symptomatic relief of PE as measured by VAS. None of the treatment had demonstrated significant pain relief effect. Our hypothesis has been that PE is the result of primarily of bladder neck spasm; however, we have no electrophysiological data to support this. Ejaculation comprises two phases: sympathetically mediated emission of seminal fluid into the posterior urethra, followed by somatically mediated true ejaculation with expulsion of the ejaculate. α-Adrenergic receptor blockers such as tamsulosin have proven to be effective in treating voiding symptoms attributed to benign prostatic hypertrophy due to the inhibition of these receptors in smooth muscles of the prostate capsule.35 Ejaculation is mediated by α1A-adrenoceptors and it is also known that α-adrenergic antagonists can cause ejaculatory problems.36
It is generally agreed that CP/CPPS is the most likely inciting factor.37 Vallancien et al.3 reported an incidence of pain or discomfort on ejaculation of 23% in a European survey. The cases presented in our study are not associated with a particular urogenital disease. In these patients, pain was not due to specific nerve damage or urethral disease, as evidenced by the absence of sensory abnormality or sexual dysfunction, as well as normal results obtained from cultures, cytologies, and cystoscopies.
Baranas et al.32 recently published their report on the use of this agent in 98 men with orgasmic pain. In this prospective, non-placebo controlled study, patients with orgasmic pain were interviewed and administered tamsulosin 0.4 mg p.o. q.h.s. for at least 4 weeks. Patients were separated into groups based on etiology of the problem (radical prostatectomy, radiation therapy, and other). Seventy-six (77%) patients reported significant improvement in pain (⩾2 points on pain VAS) and 12 (12%) noted complete resolution of their pain. Questions regarding the true efficacy of the reported studies without a proper control arm are valid. Nickel et al.11 assessed the effect of tamsulosin in men with CP/CPPS. In this study, men with a diagnosis of chronic pelvic pain disorder were treated with either tamsulosin or placebo in a randomized fashion. At 45 days, tamsulosin exerted a greater positive impact on patients' pain compared to placebo using a validated pain inventory. In the current study, we prescribed tamsulosin (without any sponsorship) in a placebo-controlled fashion to men who reported pain associated with ejaculation but without any known etiological factor. However, the beneficial effects of tamsulosin were not produced in our study. None of our analyses showed a significant response in patients with PE as a sole entity. Alexander et al. conducted a randomized double-blind trial in 196 men with CP/CPPS. Men were randomly assigned in equal proportions within a 2 × 2 factorial design to receive placebo; ciprofloxacin alone, 500 mg twice daily; tamsulosin alone, 0.4 mg once daily; or a combination of both drugs. The primary outcome was the change in the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) total score from baseline to 6 weeks. Secondary outcomes included changes in the pain, voiding, and quality-of-life subscales of the NIH-CPSI; physical and mental summary scores on the Medical Outcomes Study 12-Item Short-Form Health Survey; and a 7-point patient-reported global response assessment. No statistically significant difference in the primary outcome was seen for ciprofloxacin versus no ciprofloxacin (P=0.15) or tamsulosin versus no tamsulosin (P>0.2). Treatments also did not differ significantly for any of the secondary outcomes.38 This agrees with our study.
The cause of CP/CPPS remains unknown. As bacterial infections of the prostate do occur,39 it has long been accepted that CP/CPPS is due to bacterial infection. However, recent studies have demonstrated that the presence of bacteria in prostate has no relationship with symptoms40 and that the presence of bacteria in prostatic secretions is identical in men with CP/CPPS and age-matched asymptomatic men.41 The current body of medical literature is almost devoid of information pertaining to orgasmic dysfunction and orgasm-associated pain in men. The neurophysiology of the male orgasm is even less well understood than that of erection. More specifically, the physiology of PE is not known. Two theoretical mechanisms have formerly been proposed to clarify PE. The first explanation was that a partial blockade of peripheral sympathetic adrenergic receptors such as that observed during administration of the tricyclic antidepressants, could impede the coordinated contractions of the smooth muscles implicated in semen carrying and thus induce painful spasms.42 The second explanation is that noradrenaline potentiation could interfere with the ejaculatory mechanism, thereby inducing a painful spasm. This suggestion can in fact elucidate why PE has principally been described with desipramine, imipramine, nortriptyline and clomipramine (the metabolite desmethylclomipramine is a powerful noradrenaline reuptake inhibitor) and emission. It could also explain why PE has been described with the dual uptake inhibitor venlafaxine.18
To our knowledge this study is the first to look at ejaculatory pain as a sole entity. If indeed ejaculatory pain is related to a specific mechanism, and is not simply more at the extreme end of a common CP/CPPS spectrum, then a neuromuscular origin, an inflammatory mechanism (involving cytokines or oxidative stress not reflected in the measured white count) or an otherwise unknown mechanism may be at work.43 Other potential etiology for ejaculatory pain might include neuromuscular spasm instigated by the muscular contractions of emission.
There was only a modest placebo effect in this study. Placebo effect of any oral medication for this problem is unknown. This study demonstrated that there was no difference between active and placebo medication in the treatment of PE as a sole entity. The placebo effect has repeatedly been shown to be a significant factor in drug treatments for some lower urinary tract diseases such as overactive bladder, interstitial cystitis and BPH and is, therefore, an obstacle that must be considered with any treatment modality by performing randomized placebo-controlled trials. Our design was double-blind, and the blinding of study was strictly controlled throughout the study. We believe that most of the patients did not guess the arm to which they were assigned. Placebo theory suggests that those who guessed that they were on active drugs were biased toward disease improvement compared with those who guessed they were receiving placebo. These features may be even more notable in a disease in which symptoms tend to wax and wane with time. Further research will be required to quantify the incidence and etiology of PE as a sole entity.
It is possible that the patients we select to study, men with PE without any known risk factors, represent a small subpopulation of the overall group of men with orgasmic pain. Nevertheless, further study of such men is warranted, because they have an unrelenting problem of unknown cause for which there is least evidence to conduct therapy. Thus, the purpose of the study was to determine whether this therapy for men with longstanding symptoms is more effective than placebo. There was significant drug-related adverse effect in this study. Clearly, the issue of placebo-controlled trials will remain the ultimate litmus test of treatment efficacy. However, we present our study as the largest group of men treated and evaluated following tamsulosin therapy. These were not significantly different from the results obtained with placebo. We agree that further studies must be done on this drug and other α-blockers to define the role of these drugs in PE as a sole entity.
We concluded that 6 weeks of therapy with 0.4 mg tamsulosin daily in patients with PE as a sole entity, has no beneficial effect. Larger randomized double-blind placebo controlled studies would be the next logical step in further confirming the efficacy of this drug and other α-blockers.
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I am indebted to the patients who participated in this study.
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Safarinejad, M. Safety and efficacy of tamsulosin in the treatment of painful ejaculation: a randomized, double-blind, placebo-controlled study. Int J Impot Res 18, 527–533 (2006). https://doi.org/10.1038/sj.ijir.3901466
- painful ejaculation
- ejaculation disorders
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