VA Class:GU900
ATC Class:G04CA02
Tamsulosin hydrochloride is an α1-adrenergic blocking agent1, 2, 3, 5, 6, 8, 9, 10, 11, 12, 13, 14, 15, 32, 33 with selectivity for α1A-adrenergic receptors, which are mainly located in nonvascular smooth muscle (e.g., prostate).1, 8, 9, 10, 11, 12, 33
Tamsulosin is used to reduce urinary obstruction and relieve associated manifestations in hypertensive or normotensive patients with symptomatic benign prostatic hyperplasia (BPH, benign prostatic hypertrophy).1, 2, 3, 5, 6, 8, 9, 10, 11, 12, 13, 35 Tamsulosin relieves mild to moderate obstructive manifestations (e.g., hesitancy, terminal dribbling of urine, interrupted or weak stream, impaired size and force of stream, sensation of incomplete bladder emptying or straining) and improves urinary flow rates1, 5, 8, 9, 13, 14, 15 in a substantial proportion of patients and may be a useful alternative to surgery, particularly in those who are awaiting or are unwilling to undergo surgical correction of the hyperplasia (e.g., via transurethral resection of the prostate [TURP]) or who are not candidates for such surgery.8, 11, 12 Therapy with α1-adrenergic blocking agents appears to be less effective in relieving irritative (e.g., nocturia, daytime frequency, urgency, dysuria) than obstructive symptomatology,17, 18, 19 although tamsulosin also has been shown to be effective in relieving irritative symptoms.9, 34 In addition, therapy with α1-adrenergic blocking agents generally can be expected to produce less subjective and objective improvement than prostatectomy,20, 21 and periodic monitoring (e.g., performance of digital rectal examinations, serum creatinine determinations, serum prostate specific antigen [PSA] assays) is indicated in these patients to detect and manage other potential complications of or conditions associated with BPH (e.g., obstructive uropathy, prostatic carcinoma).16, 18, 20, 22, 23, 24, 25
Results of several controlled studies indicate that tamsulosin is more effective than placebo1, 2, 3, 8, 9, 12, 13, 14, 15, 32 and limited data suggest that the drug is at least as effective as other α1-adrenergic blocking agents (e.g., doxazosin, prazosin, terazosin) in the management of BPH.8, 9, 12 While symptomatic improvement has been maintained for up to at least 60 weeks of tamsulosin therapy in some patients,8, 11, 13 the long-term effects of α-blockers on the need for surgery and on the frequency of developing BPH-associated complications such as acute urinary obstruction remain to be established.22, 26, 27 Although tamsulosin appears to be associated with a decreased incidence of adverse cardiovascular effects including hypotension, dizziness, and syncope,8, 9, 10, 11, 12, 13 patients should be warned of the possibility of tamsulosin-induced postural dizziness and measures to take if it develops (e.g., sitting, lying down).1 During initiation of tamsulosin therapy, patients should be cautioned to avoid situations where injury could result if syncope occurs.1 If syncope occurs, the patient should be placed in a recumbent position and treated supportively as necessary.1, 29, 30
Combination therapy with an α1-blocker and 5α-reductase inhibitor (e.g., finasteride) has been more effective than therapy with either drug alone in preventing long-term BPH symptom progression; combined therapy also can reduce the risks of long-term acute urinary retention and the need for invasive therapy compared with α-blocker monotherapy.35
For additional information on the use of α1-blockers in the management of BPH, see Uses: Benign Prostatic Hyperplasia, in Doxazosin 24:20.
Allergic-type reactions, including skin rash, pruritus, urticaria, and angioedema of the tongue, lips, and face, have been reported in some patients with positive rechallenge of tamsulosin therapy.
The possibility of carcinoma of the prostate and other conditions associated with manifestations that mimic those of BPH should be excluded in any patient for whom tamsulosin therapy for presumed BPH is being considered.1
The manufacturer states that tamsulosin should not be used in the management of hypertension.1
Tamsulosin is administered orally.1 Because food may decrease peak plasma concentrations of tamsulosin and lengthen the time to achievement of peak plasma concentrations and decrease oral bioavailability of the drug, the manufacturer recommends that tamsulosin be taken 30 minutes after a meal; it is recommended that the drug be taken after the same meal each day.1, 8 Patients should be advised that the capsules must be swallowed intact and not be opened, chewed, or crushed.1
Risk of Intraoperative Floppy Iris Syndrome
A condition termed intraoperative floppy iris syndrome (IFIS) has been observed during phacoemulsification cataract surgery in some patients receiving α1-adrenergic blocking agents, including tamsulosin.1, 36 IFIS is a variant of small pupil syndrome and is characterized by the combination of a flaccid iris that billows in response to intraoperative irrigation currents, progressive intraoperative miosis despite preoperative dilation with mydriatics, and potential prolapse of the iris toward the phacoemulsification incisions.1, 36 Most reported cases of IFIS were in patients who continued α1-blocker therapy at the time of cataract surgery.1, 36 A few cases also were reported in patients who had discontinued such therapy prior to surgery, generally 2-14 days prior to surgery but occasionally 5 weeks to 9 months prior to surgery.1, 36 The manufacturer of tamsulosin recommends that male patients being considered for cataract surgery be specifically questioned to ascertain whether they have received tamsulosin or other α1-blockers.36 If a patient has received such agents, the ophthalmologist should be prepared to modify the surgical technique (e.g., through use of iris hooks, iris dilator rings, or viscoelastic substances) to minimize complications of IFIS.1, 36 The benefit of discontinuing α1-blockers, including tamsulosin, prior to cataract surgery has not been established.1, 36
The manufacturer states that safety and efficacy of tamsulosin in children younger than 18 years of age have not been established, and clinical experience in these patients is not available.1, 34
For the management of benign prostatic hyperplasia (BPH), the usual initial adult dosage of tamsulosin is 0.4 mg once daily.1 About 2-4 weeks may be needed to adequately assess the response at this dosage.1 To achieve the desired improvement in symptoms and/or urinary flow rates, subsequent dosage may be increased to 0.8 mg daily as needed.1 If tamsulosin is discontinued for several days at either dosage (i.e., 0.4 or 0.8 mg daily), therapy with the drug should be reinstituted at the lower daily dosage.1 Although the elimination half-life may be slightly prolonged and intrinsic clearance of tamsulosin may be decreased in patients 55 years of age and older, the manufacturer makes no specific recommendations for dosage adjustment in such patients.1, 34
The manufacturer states that tamsulosin should not be used concomitantly with other α-adrenergic blocking agents.1
Dosage in Renal and Hepatic Impairment
Although protein binding of tamsulosin may be altered in patients with mild to moderate (i.e., creatinine clearance of 30-70 mL/minute per 1.73 m2) or severe (i.e., creatinine clearance of 10 to less than 30 mL/minute per 1.73 m2) renal impairment and in patients with moderate hepatic impairment resulting in changes of overall plasma concentrations of the drug, alterations in intrinsic clearance and concentrations of unbound tamsulosin do not appear to be substantial.1, 8, 13 Therefore, the manufacturer states that dosage adjustment in such patients is not necessary.1 However, tamsulosin has not been studied in patients with end-stage (i.e., creatinine clearance of less than 10 mL/minute per 1.73 m2) renal disease.1
Known hypersensitivity to tamsulosin or any ingredient in the formulation.1
Potential for postural hypotension, dizziness, or vertigo; syncope may occur.1
Priapism reported rarely; treat promptly.1
Rash, pruritus, urticaria, and angioedema of the tongue, lips, and face reported; positive rechallenge in some patients.1
Allergic reaction to tamsulosin reported rarely in patients with sulfa sensitivity.1 Use with caution in patients with serious or life-threatening sulfa sensitivity.1
Exclude possibility of prostate cancer prior to initiation of therapy.1
Intraoperative Floppy Iris Syndrome
Intraoperative floppy iris syndrome (IFIS) observed during phacoemulsification cataract surgery in some patients receiving α1-adrenergic blocking agents, including tamsulosin.1, 36 Most reported cases were in patients who continued such therapy at the time of cataract surgery.1, 36
Manufacturer recommends that male patients being considered for cataract surgery be specifically questioned to ascertain whether they have received tamsulosin or other α1-blockers.36 If the patient has received α1-blockers, the ophthalmologist should be prepared to modify the surgical technique (e.g., through use of iris hooks, iris dilator rings, or viscoelastic substances) to minimize complications of IFIS.1, 36
Benefit of discontinuing α1-blockers prior to cataract surgery not established.1, 36
Category B.1 Not indicated for use in women.1
Not indicated for use in women.1
Not indicated for use in children.1
No substantial differences in safety and efficacy relative to younger adults, but increased sensitivity cannot be ruled out.1
Headache, infection, asthenia, back pain, chest pain, dizziness, somnolence, insomnia, decreased libido, rhinitis, pharyngitis, increased cough, sinusitis, diarrhea, nausea, tooth disorder, abnormal ejaculation, blurred vision.1
Additive effects; concomitant use not recommended.1
No change in blood pressure or pulse rate; dosage adjustment not necessary.1
Increased plasma tamsulosin concentrations.1 Use with caution, particularly with doses >0.4 mg.1
Pharmacokinetic interaction unlikely.1
No change in blood pressure or pulse rate; dosage adjustment not necessary.1
Decreased plasma tamsulosin concentrations; not clinically important.1
No change in blood pressure or pulse rate; dosage adjustment not necessary.1
Pharmacokinetic interaction unlikely.1
Possible pharmacokinetic interaction.1 Available data inconclusive; use with caution.1
Essentially completely absorbed following oral administration under fasting conditions; peak plasma concentrations attained within 4-5 hours.1
Food delays time to peak plasma concentration by about 2 hours.1 When administered under fasting conditions, bioavailability and peak plasma concentration are increased by 30 and 40-70%, respectively, compared with fed state.1
Appears to distribute into extracellular fluids in humans.1 In animals, distributed into kidney, prostate, liver, gallbladder, heart, aorta, and brown fat, with minimal distribution into brain, spinal cord, and testes.1
94-99% (mainly to α1-acid glycoprotein).1
In patients with moderate hepatic impairment, protein binding is altered, resulting in changes in overall plasma concentrations; however, no substantial alterations in intrinsic clearance and concentrations of unbound drug.1, 8, 13
In patients with renal impairment, protein binding is altered, resulting in changes in overall plasma concentrations, however, no substantial alterations in intrinsic clearance and concentrations of unbound drug.1, 8, 13
Extensively metabolized by CYP enzymes (specific isoenzyme[s] not identified) in the liver.1 Metabolites undergo further conjugation prior to excretion.1
Excreted in urine (76%) and feces (21%).1
Because of absorption rate-controlled pharmacokinetics of tamsulosin capsules, apparent half-life is about 9-13 hours in healthy individuals and 14-15 hours in patients with BPH.1
In males 55-75 years of age, intrinsic clearance is decreased and elimination half-life is prolonged, resulting in a 40% increase in AUC compared with males 20-32 years of age.1, 34
Tamsulosin hydrochloride is a sulfamoylphenethylamine-derivative α1-adrenergic blocking agent.1, 2, 3, 5, 6, 8, 9, 10, 11, 12, 13, 14, 15, 32, 33 Commercially available tamsulosin hydrochloride is a racemic mixture of 2 isomers.8 The drug is pharmacologically related to doxazosin, prazosin, and terazosin;8, 9, 10, 11, 12, 13 however, unlike these drugs, tamsulosin has higher affinity and selectivity for α1A-adrenergic receptors, which are mainly located in nonvascular smooth muscle (e.g., prostate), than for α1B-adrenergic receptors located in vascular smooth muscle (e.g., internal iliac artery).1, 8, 9, 10, 11, 12, 33 Results of in vitro studies indicate that tamsulosin has 7-38 times greater affinity for α1A-adrenoceptors than for α1B-adrenoceptors;8, 13 the drug has about 12 times greater affinity for α1-adrenergic receptors in the prostate than for those in the aorta.8, 10, 11, 13 Such selectivity of tamsulosin for α1A-receptors may result in a reduced incidence of adverse cardiovascular effects (e.g., syncope, dizziness, hypotension).8, 9, 10, 11, 12, 13 On a molar basis, the α1-adrenergic receptor affinity of tamsulosin is about 6 times that of prazosin when tested in human prostatic tissue.8, 10, 11, 28, 31
Because of the prevalence of α-receptors on the prostate capsule, prostate adenoma, and bladder trigone and the relative absence of these receptors on the bladder body,6α-adrenergic blocking agents decrease urinary outflow resistance in men.2, 5, 8, 9, 11, 12
Additional Information
SumMon® (see Users Guide). For additional information on this drug until a more detailed monograph is developed and published, the manufacturer's labeling should be consulted. It is essential that the labeling be consulted for detailed information on the usual cautions, precautions, and contraindications.
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Capsules | 0.4 mg |
AHFS® Drug Information. © Copyright, 1959-2025, Selected Revisions June 9, 2011. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
1. Boehringer Ingelheim. Flomax® (tamsulosin hydrochloride) capsules prescribing information. Ridgefield, CT; 2006 Jul 19.
2. Geller J, Kirschenbaum A, Lepor H et al. Therapeutic controversies: clinical treatment of benign prostatic hyperplasia. J Clin Endocrinol Metab . 1995; 80:745-53. [PubMed 7533770]
3. Oesterling JE. Benign prostatic hyperplasia: medical and minimally invasive treatment options. N Engl J Med . 1995; 332:99-109. [PubMed 7527494]
4. Nacey J, Delahunt B. Changing perspectives in benign prostatic hyperplasia. N Z Med J . 1995; 108:283-4. [PubMed 7543666]
5. Kawabe K, Ueno A, Takimoto Y et al et al. Use of an α1-blocker, YM617, in the treatment of benign prostatic hypertrophy. J Urol . 1990; 144:908-12. [PubMed 1697914]
6. Eri LM, Tveter KJ. α-blockade in the treatment of symptomatic benign prostatic hyperplasia. J Urol . 1995; 154:923-34. [PubMed 7543612]
7. Narayan P, Indudhara R. Pharmacotherapy for benign prostatic hyperplasia. West J Med . 1994; 161:495-506. [PubMedCentral][PubMed 7528957]
8. Wilde MI, McTavish D. Tamsulosin: a review of its pharmacological properties and therapeutic potential in the management of symptomatic benign prostatic hyperplasia. Drugs . 1996; 52:883-98. [PubMed 8957159]
9. Chapple CR, Wyndaele JJ, Nordling J et al et al. Tamsulosin, the first prostate-selective α1A-adrenoceptor antagonist: a meta-analysis of two randomized, placebo-controlled, multicentre studies in patients with benign prostatic obstruction (symptomatic BPH). Eur Urol . 1996; 29:155-67. [PubMed 8647141]
10. Hieble JP, Ruffolo RR Jr. The use of α-adrenoceptor antagonists in the pharmacological management of benign prostatic hypertrophy: an overview. Pharmacol Res . 1996; 33:145-60. [PubMed 8880886]
11. Schulman CC, Cortvriend J, Jonas U et al. Tamsulosin, the first prostate-selective α1A-adrenoceptor antagonist: analysis of a multinational, multicentre, open-label study assessing the long-term efficacy and safety in patients with benign prostatic obstruction (symptomatic BPH). Eur Urol . 1996; 29:145-54. [PubMed 8647140]
12. Abrams P, Schulman CC, Vaage S and the European Tamsulosin Study Group. Tamsulosin, a selective α1c-adrenoceptor antagonist: a randomized, controlled trial in patients with benign prostatic 'obstruction' (symptomatic BPH). Br J Urol . 1995; 76:325-336. [PubMed 7551841]
13. Rabasseda X, Fitzpatrick JM. Tamsulosin: the first prostate-selective α1A-adrenoceptor antagonist for the treatment of symptomatic benign prostatic hyperplasia. Drugs Today . 1996; 32(Suppl C):1-12.
14. Lepor H and the Tamsulosin Investigator Group. Clinical evaluation of tamsulosin, a prostate selective alpha 1c antagonist. J Urol . 1995; 153(Suppl):274A.
15. Lepor H and the Tamsulosin Investigator Group. Long-term evaluation of tamsulosin, a prostate selective alpha1 antagonist. J Urol . 1996; 155(Suppl):585A.
16. Wasson JH, Reda DJ, Bruskewitz RC et al et al. A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia. N Engl J Med . 1995; 332:75-9. [PubMed 7527493]
17. Lepor H. The emerging role of alpha antagonists in the therapy of benign prostatic hyperplasia. J Androl . 1991; 12:389-94. [PubMed 1722795]
18. Wilde MI, Fitton A, Sorkin EM. Terazosin: a review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in benign prostatic hyperplasia. Drugs Aging . 1993; 3:258-77. [PubMed 7686794]
19. Lepor H, Meretyk S, Knapp-Maloney G. The safety, efficacy and compliance of terazosin therapy for benign prostatic hyperplasia. J Urol . 1992; 147:1554-7. [PubMed 1375659]
20. Chapple C. Medical treatment for benign prostatic hyperplasia. BMJ . 1992; 304:1198-9. [PubMedCentral][PubMed 1381250]
21. Chapple CR, Christmas TJ, Milroy EJG. A twelve-week placebo-controlled study of prazosin in the treatment of prostatic obstruction. Urol Int . 1990; 45(Suppl 1):47-55. [PubMed 1690482]
22. Lepor H. Role of long-acting selective alpha-1 blockers in the treatment of benign prostatic hyperplasia. Urol Clin North Am . 1990; 17:651-9. [PubMed 1695785]
23. Chisholm GD. Benign prostatic hyperplasia: the best treatment. BMJ . 1989; 299:215-6. [PubMedCentral][PubMed 2475197]
24. Geller J. Nonsurgical treatment of prostatic hyperplasia. Cancer . 1992; 70(Suppl 1):339-45. [PubMed 1376202]
25. Bostwick DG, Cooner WH, Denis L et al. The association of benign prostatic hyperplasia and cancer of the prostate. Cancer . 1992; 70(Suppl 1):291-301. [PubMed 1376199]
26. Hill SJ, Lawrence SL, Lepor H. New use for alpha blockers: benign prostatic hyperplasia. Am Fam Physician . 1994; 49:1885-8. [PubMed 7515555]
27. Kirby RS. Alpha-adrenoceptor inhibitors in the treatment of benign prostatic hyperplasia. Am J Med . 1989; 87(Suppl 2A):26-30S.
28. Yamada S, Suzuki M, Tanaka C et al. Comparative study on α1-adrenoreceptor antagonist binding in human prostate and aorta. Clin Exp Pharmacol Physiol . 1994; 21:405-11. [PubMed 7955549]
29. Abbott Laboratories. Hytrin® (terazosin hydrochloride) tablets prescribing information. North Chicago, IL; 1993 Aug.
30. Pfizer Roerig. Cardura® (doxazosin mesylate) tablets prescribing information. New York, NY; 1994 Dec.
31. Hayashida S, Hirasawa T, Uchiyama K et al. Effect of tamsulosin hydrochloride on benign prostatic hyperplasia-comparison with prazosin hydrochloride. Proceedings of the 23rd Congress of the Societe Internationale d'Urologie. Sydney, Australia. 1994:99. Abstract No. 93.
32. Anon. Tamsulosin for benign prostatic hyperplasia. Med Lett Drugs Ther . 1997; 29:96.
33. Lowe FC. Coadministration of tamsulosin and three antihypertensive agents in patients with benign prostatic hyperplasia: pharmacodynamic effect. Clin Ther . 1997; 19:730-57. [PubMed 9377617]
34. Reviewers' comments (personal observations).
35. American Urological Association. Guideline on the management of benign prostatic hyperplasia (BPH)(2003/updated 2006). From website. Accessed 2006 Aug 10. [Web]
36. Boodee HW. Dear doctor letter regarding intraoperative floppy iris syndrome associated with tamsulosin. Ridgefield, CT: Boehringer Ingelheim; 2005 Nov.