Benign prostatic hyperplasia
SynonymsBenign enlargement of the prostate (BEP, BPE), adenofibromyomatous hyperplasia, benign prostatic hypertrophy,[1] benign prostatic obstruction[1]
FieldUrology
SymptomsFrequent urination, trouble starting to urinate, weak stream, inability to urinate, loss of bladder control[1]
ComplicationsUrinary tract infections, bladder stones, kidney failure[2]
OnsetAge over 40[1]
CausesUnclear[1]
RisksFamily history, obesity, type 2 diabetes, not enough exercise, erectile dysfunction[1]
DiagnosisBased on symptoms and examination after ruling out other possible causes[2]
DifferentialHeart failure, diabetes, prostate cancer[2]
TreatmentLifestyle changes, medications, several procedures, surgery[1][2]
MedicationAlpha blockers such as terazosin, 5α-reductase inhibitors such as finasteride[1]
Frequency94 million men affected globally (2019)[3]

Benign prostatic hyperplasia (BPH), also called prostate enlargement, is a noncancerous increase in size of the prostate gland.[1] Symptoms may include frequent urination, trouble starting to urinate, weak stream, inability to urinate, or loss of bladder control.[1] Complications can include urinary tract infections, bladder stones, and chronic kidney problems.[2]

The cause is unclear.[1] Risk factors include a family history, obesity, type 2 diabetes, not enough exercise, and erectile dysfunction.[1] Medications like pseudoephedrine, anticholinergics, and calcium channel blockers may worsen symptoms.[2] The underlying mechanism involves the prostate pressing on the urethra thereby making it difficult to pass urine out of the bladder.[1] Diagnosis is typically based on symptoms and examination after ruling out other possible causes.[2]

Treatment options include lifestyle changes, medications, a number of procedures, and surgery.[1][2] In those with mild symptoms, weight loss, decreasing caffeine intake, and exercise are recommended, although the quality of the evidence for exercise is low.[2][4] In those with more significant symptoms, medications may include alpha blockers such as terazosin or 5α-reductase inhibitors such as finasteride.[1] Surgical removal of part of the prostate may be carried out in those who do not improve with other measures.[2] Some studies have suggested that certain plant extracts may help mitigate symptoms of BPH.[5] Examples include saw palmetto (Serenoa repens),[6] stinging nettle (Urtica dioica) root,[7] beta-sitosterol[8] from African star grass (Hypoxis rooperi), and pygeum (extracted from the bark of Prunus africana).[9] However, meta-analyses have called these conclusions into question,[10] highlighting methodological problems showing no difference from a placebo, and lack of support from larger scale trials.[11]

As of 2019, about 94 million men aged 40 years and older are affected globally.[3] BPH typically begins after the age of 40.[1] The prevalence of clinically diagnosed BPH peaks at 24% in men aged 75–79 years.[3] Based on autopsy studies, half of males aged 50 and over are affected, and this figure climbs to 80% after the age of 80.[3] Although prostate-specific antigen levels may be elevated in males with BPH, the condition does not increase the risk of prostate cancer.[12]

Signs and symptoms

BPH is the most common cause of lower urinary tract symptoms (LUTS), which are divided into storage, voiding, and symptoms which occur after urination.[13] Storage symptoms include the need to urinate frequently, waking at night to urinate, urgency (compelling need to void that cannot be deferred), involuntary urination, including involuntary urination at night, or urge incontinence (urine leak following a strong sudden need to urinate).[14] Voiding symptoms include urinary hesitancy (a delay between trying to urinate and the flow actually beginning), intermittency (not continuous),[15] involuntary interruption of voiding, weak urinary stream, straining to void, a sensation of incomplete emptying, and uncontrollable leaking after the end of urination.[16][17][18] These symptoms may be accompanied by bladder pain or pain while urinating, called dysuria.[19]

Bladder outlet obstruction (BOO) can be caused by BPH.[20] Symptoms are abdominal pain, a continuous feeling of a full bladder, frequent urination, acute urinary retention (inability to urinate), pain during urination (dysuria), problems starting urination (urinary hesitancy), slow urine flow, starting and stopping (urinary intermittency), and nocturia.[21]

BPH can be a progressive disease, especially if left untreated. Incomplete voiding results in residual urine or urinary stasis, which can lead to an increased risk of urinary tract infection.[22]

Causes

Hormones

Most experts consider androgens (testosterone and related hormones) to play a permissive role in the development of BPH. This means that androgens must be present for BPH to occur, but do not necessarily directly cause the condition. This is supported by evidence suggesting that castrated boys do not develop BPH when they age. In a study of 26 eunuchs from the palace of the Qing dynasty still living in Beijing in 1960, the prostate could not be felt in 81% of the studied eunuchs.[23] The average time since castration was 54 years (range, 41–65 years). On the other hand, some studies suggest that administering exogenous testosterone is not associated with a significant increase in the risk of BPH symptoms, so the role of testosterone in prostate cancer and BPH is still unclear. Further randomized controlled trials with more participants are needed to quantify any risk of giving exogenous testosterone.[24]

Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2. DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is ten times more potent than testosterone because it dissociates from the androgen receptor more slowly. The importance of DHT in causing nodular hyperplasia is supported by clinical observations in which an inhibitor of 5α-reductase such as finasteride is given to men with this condition. Therapy with a 5α-reductase inhibitor markedly reduces the DHT content of the prostate and, in turn, reduces prostate volume and BPH symptoms.[25][26]

Testosterone promotes prostate cell proliferation,[27] but relatively low levels of serum testosterone are found in patients with BPH.[28][29] One small study has shown that medical castration lowers the serum and prostate hormone levels unevenly, having less effect on testosterone and DHT levels in the prostate.[30]

Besides testosterone and DHT, other androgens are also known to play a crucial role in BPH development. C21 11-oxygenated steroids (pregnanes) have been identified are precursors to 11-oxygenated androgens which are also potent agonists for the androgen receptor.[31] Specifically, steroids like 11β-hydroxyprogesterone and 11-ketoprogesterone can be converted to 11-ketodihydrotestosterone, an 11-oxo form of DHT with the same potency. These precursors have also been detected in tissue biopsy samples from patients with BPH, as well as in their serum levels.[32][33][34] Besides that, androgens biosynthesized via a backdoor pathway can contribute to the development of BPH.[32]

While there is some evidence that estrogen may play a role in the cause of BPH, this effect appears to be mediated mainly through local conversion of androgens to estrogen in the prostate tissue rather than a direct effect of estrogen itself.[35] In canine in vivo studies castration, which significantly reduced androgen levels but left estrogen levels unchanged, caused significant atrophy of the prostate.[36] Studies looking for a correlation between prostatic hyperplasia and serum estrogen levels in humans have generally shown none.[29][37]

In 2008, Gat et al. published evidence that BPH is caused by failure in the spermatic venous drainage system resulting in increased hydrostatic pressure and local testosterone levels elevated more than 100-fold above serum levels.[38] If confirmed, this mechanism explains why serum androgen levels do not seem to correlate with BPH and why giving exogenous testosterone would not make much difference.

Diet

Studies indicate that dietary patterns may affect the development of BPH, but further research is needed to clarify any important relationship.[39] Studies from China suggest that greater protein intake may be a factor in the development of BPH. Men older than 60 in rural areas had very low rates of clinical BPH, while men living in cities and consuming more animal protein had a higher incidence.[40][41] On the other hand, a study in Japanese-American men in Hawaii found a strong negative association with alcohol intake, but a weak positive association with beef intake.[42] In a large prospective cohort study in the US (the Health Professionals Follow-up Study), investigators reported modest associations between BPH (men with strong symptoms of BPH or surgically confirmed BPH) and total energy and protein, but not fat intake.[43] There is also epidemiological evidence linking BPH with metabolic syndrome (concurrent obesity, impaired glucose metabolism and diabetes, high triglyceride levels, high levels of low-density cholesterol, and hypertension).[44]

Degeneration

Benign prostatic hyperplasia is an age-related disease. Misrepair-accumulation aging theory[45] suggests that the development of benign prostatic hyperplasia is a consequence of fibrosis and weakening of the muscular tissue in the prostate.[46] The muscular tissue is important in the functionality of the prostate, and provides the force for excreting the fluid produced by prostatic glands. However, repeated contractions and dilations of myofibers will unavoidably cause injuries and broken myofibers. Myofibers have a low potential for regeneration; therefore, collagen fibers need to be used to replace the broken myofibers. Such misrepairs make the muscular tissue weak in functioning, and the fluid secreted by glands cannot be excreted completely. Then, the accumulation of fluid in glands increases the resistance of muscular tissue during the movements of contractions and dilations, and more and more myofibers will be broken and replaced by collagen fibers.[47]

Pathophysiology

As men age, the enzymes aromatase and 5-alpha reductase increase in activity. These enzymes are responsible for converting androgen hormones into estrogen and DHT, respectively. This metabolism of androgen hormones leads to a decrease in testosterone but increased levels of DHT and estrogen.

Both the glandular epithelial cells and the stromal cells (including muscular fibers) undergo hyperplasia in BPH.[2] Most sources agree that of the two tissues, stromal hyperplasia predominates, but the exact ratio of the two is unclear.[48]: 694

Anatomically the median and lateral lobes are usually enlarged, due to their highly glandular composition. The anterior lobe has little in the way of glandular tissue and is seldom enlarged. (Carcinoma of the prostate typically occurs in the posterior lobe – hence the ability to discern an irregular outline per rectal examination). The earliest microscopic signs of BPH usually begin between the age of 30 and 50 years old in the PUG, which is posterior to the proximal urethra.[48]: 694 In BPH, the majority of growth occurs in the transition zone (TZ) of the prostate.[48]: 694 In addition to these two classic areas, the peripheral zone (PZ) is also involved to a lesser extent.[48]: 695 Prostatic cancer typically occurs in the PZ. However, BPH nodules, usually from the TZ are often biopsied anyway to rule out cancer in the TZ.[48]: 695 BPH can be a progressive growth that in rare instances leads to exceptional enlargement.[49] In some males, the prostate enlargement exceeds 200 to 500 grams.[49] This condition has been defined as giant prostatic hyperplasia (GPH).[49]

Diagnosis

The clinical diagnosis of BPH is based on a history of LUTS (lower urinary tract symptoms), a digital rectal exam, and the exclusion of other causes of similar signs and symptoms. The degree of LUTS does not necessarily correspond to the size of the prostate. An enlarged prostate gland on rectal examination that is symmetric and smooth supports a diagnosis of BPH.[2] However, if the prostate gland feels asymmetrical, firm, or nodular, this raises concern for prostate cancer.[2]

Validated questionnaires such as the American Urological Association Symptom Index (AUA-SI), the International Prostate Symptom Score (I-PSS), and more recently the UWIN score (urgency, weak stream, incomplete emptying, and nocturia) are useful aids to making the diagnosis of BPH and quantifying the severity of symptoms.[2][50][51]

Laboratory investigations

Urinalysis is typically performed when LUTS are present and BPH is suspected to evaluate for signs of a urinary tract infection, glucose in the urine (suggestive of diabetes), or protein in the urine (suggestive of kidney disease).[2] Bloodwork including kidney function tests and prostate-specific antigen (PSA) are often ordered to evaluate for kidney damage and prostate cancer, respectively.[2] However, checking blood PSA levels for prostate cancer screening is controversial and not necessarily indicated in every evaluation for BPH.[2] Benign prostatic hyperplasia and prostate cancer are both capable of increasing blood PSA levels and PSA elevation is unable to differentiate these two conditions well.[2] If PSA levels are checked and are high, then further investigation is warranted. Measures including PSA density, free PSA, rectal examination, and transrectal ultrasonography may help determine whether a PSA increase is due to BPH or prostate cancer.[2]

Imaging and other investigations

Uroflowmetry is done to measure the rate of urine flow and total volume of urine voided when the subject is urinating.[52]

Abdominal ultrasound examination of the prostate and kidneys is often performed to rule out hydronephrosis and hydroureter. Incidentally, cysts, tumours, and stones may be found on ultrasound. Post-void residual volume of more than 100 ml may indicate significant obstruction.[53] Prostate size of 30 cc or more indicates enlargement of the prostate.[54]

Prostatic calcification can be detected through transrectal ultrasound (TRUS). Calcification is due to solidification of prostatic secretions or calcified corpora amylacea (hyaline masses on the prostate gland). Calcification is also found in a variety of other conditions such as prostatitis, chronic pelvic pain syndrome, and prostate cancer.[55][56] For those with elevated levels of PSA, TRUS guided biopsy is performed to take a sample of the prostate for investigation.[57] Although MRI is more accurate than TRUS in determining prostate volume, TRUS is less expensive and almost as accurate as MRI. Therefore, TRUS is still preferred to measure prostate volume.[58]

Differential diagnosis

Medical conditions

The differential diagnosis for LUTS is broad and includes various medical conditions, neurologic disorders, and other diseases of the bladder, urethra, and prostate such as bladder cancer, urinary tract infection, urethral stricture, urethral calculi (stones), chronic prostatitis, and prostate cancer.[2] Neurogenic bladder can cause urinary retention and cause symptoms similar to those of BPH. This may occur as a result of uncoordinated contraction of the bladder muscle or impairment in the timing of bladder muscle contraction and urethral sphincter relaxation.[2] Notable causes of neurogenic bladder include disorders of the central nervous system such as Parkinson's disease, multiple sclerosis, and spinal cord injuries as well as disorders of the peripheral nervous system such as diabetes mellitus, vitamin B12 deficiency, and alcohol-induced nerve damage.[2] Individuals affected by heart failure often experience nighttime awakenings to urinate due to redistribution of fluid accumulated in swollen legs.[2]

Medications

Certain medications can increase urination difficulties by increasing bladder outlet resistance due to increased smooth muscle tone at the prostate or bladder neck and contribute to LUTS.[2] Alpha-adrenergic agonist medications, such as decongestants with pseudoephedrine can increase bladder outlet resistance.[2] In contrast, calcium channel blockers and anticholinergic medications can worsen urinary retention by promoting bladder muscle relaxation.[2] Diuretic medications such as loop diuretics (e.g., furosemide) or thiazides (e.g., chlorthalidone) can cause or worsen urinary frequency and nighttime awakenings to urinate.[2]

Management

When treating and managing benign prostatic hyperplasia, the aim is to prevent complications related to the disease and improve or relieve symptoms.[59] Approaches used include lifestyle modifications, medications, catheterization, and surgery.

Lifestyle

Lifestyle alterations to address the symptoms of BPH include physical activity,[4] decreasing fluid intake before bedtime, moderating the consumption of alcohol and caffeine-containing products, and following a timed voiding schedule.

Patients can also attempt to avoid products and medications with anticholinergic properties that may exacerbate urinary retention symptoms of BPH, including antihistamines, decongestants, opioids, and tricyclic antidepressants; however, changes in medications should be done with input from a medical professional.[60]

Physical activity

Physical activity has been recommended as a treatment for urinary tract symptoms. A 2019 Cochrane review of six studies involving 652 men assessing the effects of physical activity alone, and physical activity as a part of a self-management program, among others. However, the quality of evidence was very low and therefore it remains uncertain whether physical activity is helpful in men experiencing urinary symptoms caused by benign prostatic hyperplasia.[61]

Voiding position

Voiding position when urinating may influence urodynamic parameters (urinary flow rate, voiding time, and post-void residual volume).[62] A meta-analysis found no differences between the standing and sitting positions for healthy males, but that, for elderly males with lower urinary tract symptoms, voiding in the sitting position[63]

  • decreased the post-void residual volume;
  • increased the maximum urinary flow, comparable with pharmacological intervention; and
  • decreased the voiding time.

This urodynamic profile is associated with a lower risk of urologic complications, such as cystitis and bladder stones.

Medications

The two main medication classes for BPH management are alpha blockers and 5α-reductase inhibitors.[64]

Alpha-blockers

Selective α1-blockers are the most common choice for initial therapy.[65][66][67] They include alfuzosin,[68][69] doxazosin,[70] silodosin, tamsulosin, terazosin, and naftopidil.[59] They have a small to moderate benefit at improving symptoms.[71][59][72] Selective alpha-1 blockers are similar in effectiveness but have slightly different side effect profiles.[71][59][72] Alpha blockers relax smooth muscle in the prostate and the bladder neck, thus decreasing the blockage of urine flow. Common side effects of alpha-blockers include orthostatic hypotension (a head rush or dizzy spell when standing up or stretching), ejaculation changes, erectile dysfunction,[73] headaches, nasal congestion, and weakness. For men with LUTS due to an enlarged prostate, the effects of naftopidil, tamsulosin, and silodosin on urinary symptoms and quality of life may be similar.[59] Naftopidil and tamsulosin may have similar levels of unwanted sexual side effects but fewer unwanted side effects than silodosin.[59]

Tamsulosin and silodosin are selective α1 receptor blockers that preferentially bind to the α1A receptor in the prostate instead of the α1B receptor in the blood vessels. Less-selective α1 receptor blockers such as terazosin and doxazosin may lower blood pressure. The older, less selective α1-adrenergic blocker prazosin is not a first-line choice for either high blood pressure or prostatic hyperplasia; it is a choice for patients who present with both problems at the same time. The older, broadly non-selective alpha-blocker medications such as phenoxybenzamine are not recommended for control of BPH.[74] Non-selective alpha-blockers such as terazosin and doxazosin may also require slow dose adjustments as they can lower blood pressure and cause syncope (fainting) if the response to the medication is too strong.

5α-reductase inhibitors

The 5α-reductase inhibitors finasteride and dutasteride may also be used in people with BPH.[75] These medications inhibit the 5α-reductase enzyme, which, in turn, inhibits the production of DHT, a hormone responsible for enlarging the prostate. Effects may take longer to appear than alpha blockers, but they persist for many years.[76] When used together with alpha-blockers, no benefit was reported in short-term trials, but in a longer-term study (3–4 years) there was a greater reduction in BPH progression to acute urinary retention and surgery than with either agent alone, especially in people with more severe symptoms and larger prostates.[77][78][79] Other trials have confirmed reductions in symptoms, within 6 months in one trial, an effect that was maintained after withdrawal of the alpha blocker.[78][80] Side effects include decreased libido and ejaculatory or erectile dysfunction.[81][82] The 5α-reductase inhibitors are contraindicated in pregnant women because of their teratogenicity due to interference with fetal testosterone metabolism, and as a precaution, pregnant women should not handle crushed or broken tablets.[83]

Phosphodiesterase inhibitors (PDE)

A 2018 Cochrane review of studies on men over 60 with moderate to severe lower urinary tract symptoms analyzed the impacts of phosphodiesterase inhibitors (PDE) in comparison to other drugs.[84] These drugs may improve urinary symptoms slightly and reduce urinary bother but may also cause more side effects than placebo. The evidence in this review found that there is probably no difference between PDE and alpha blockers, however when used in combination they may provide a greater improvement in symptoms (with more side effects). PDE also likely improves symptoms when used with 5-alpha reductase inhibitors.

Several phosphodiesterase-5 inhibitors are also effective but may require multiple doses daily to maintain adequate urine flow.[85][86] Tadalafil, a phosphodiesterase-5 inhibitor, was considered then rejected by NICE in the UK for the treatment of symptoms associated with BPH.[87] In 2011, the U.S. Food and Drug Administration approved tadalafil to treat the signs and symptoms of benign prostatic hyperplasia, and for the treatment of BPH and erectile dysfunction (ED), when the conditions occur simultaneously.[88]

Others

Antimuscarinics such as tolterodine may also be used, especially in combination with alpha-blockers.[89] They act by decreasing acetylcholine effects on the smooth muscle of the bladder, thus helping control symptoms of an overactive bladder.[90]

Self-catheterization

Intermittent urinary catheterization is used to relieve the bladder in people with urinary retention. Self-catheterization is an option in BPH when it is difficult or impossible to empty the bladder.[91] Urinary tract infection is the most common complication of intermittent catheterization.[92] Several techniques and types of catheter are available, including sterile (single-use) and clean (multiple use) catheters, but, based on current information, none is superior to others in reducing the incidence of urinary tract infection.[93]

Surgery

Main article: Surgery for benign prostatic hyperplasia

If medical treatment is not effective, surgery may be performed. Surgical techniques used include the following:

Minimally invasive procedures

In addition to traditional surgical approaches, several minimally invasive treatments are available for BPH, which may offer advantages depending on individual patient factors and prostate size.[96] These procedures are usually performed on an outpatient basis under local anesthesia or light sedation and allow quicker recovery with reduced risk of complications:[97]

Enucleation techniques:

  • Holmium laser enucleation of the prostate (HoLEP): performed using a Holmium:YAG laser[98]
  • Thulium laser enucleation of the prostate (ThuLEP): performed using a Thulium:YAG laser or, increasingly, a Thulium fiber laser (TFL)[99]

Both HoLEP and ThuLEP are endoscopic enucleation techniques in which prostatic adenoma tissue is dissected (“shelled out”) from the surgical capsule and subsequently removed. Studies have shown functional outcomes comparable or superior to transurethral resection of the prostate (TURP), with reduced bleeding, shorter catheterization time, and shorter hospital stay.[100] Current (2026) American Urological Association (AUA) guidelines list HoLEP and ThuLEP as treatment options for lower urinary tract symptoms (LUTS) associated with BPH, with procedure selection depending on surgeon experience and patient-specific factors.[101]

Ablation and vaporization techniques:

  • Holmium laser ablation of the prostate (HoLAP)
  • Photoselective vaporization of the prostate (PVP, 532 nm), using green light laser technology
  • Diode laser vaporization (980-1470 nm): Endoscopic removal of prostatic tissue with minimal bleeding (as the surrounding tissue is preserved), and good hemostatic properties; higher-power settings allow efficient tissue ablation, making the procedure particularly suitable for larger prostates[102]
  • Thulium laser transurethral vaporesection of the prostate (ThuVARP)

These procedures remove prostatic tissue through laser vaporization or coagulation rather than mechanical enucleation. They are associated with good hemostatic properties and minimal bleeding, making them particularly suitable for patients receiving anticoagulation therapy or those with increased bleeding risk.[103]

Non-ablative / mechanical implant procedures:

  • Prostatic urethral lift (marketed as UroLift): This intervention consists of a system of a device and an implant designed to pull the prostatic lobe away from the urethra.[104]
  • Temporary implantable nitinol device (TIND and ): is a device that is placed in the urethra that, when released, is expanded, reshaping the urethra and the bladder neck.[105]

Thermal energy-based therapies:

  • Water-vapor thermal therapy (marketed as Rezum): This is a newer office procedure for removing prostate tissue using steam aimed at preserving sexual function.

Endovascular / embolization techniques:

Novel / emerging or less established techniques:

Alternative medicine

While herbal remedies are commonly used, a 2016 review found the herbs studied to be no better than placebos.[108] Particularly, several reviews found that saw palmetto extract, while one of the most commonly used, is no better than a placebo both in symptom relief and in decreasing prostate size.[109][110][111]

Epidemiology

Globally, benign prostatic hyperplasia affects about 94 million males as of 2019.[3]

The prostate gets larger in most men as they get older. For a symptom-free man of 46 years, the risk of developing BPH over the next 30 years is 45%. Incidence rates increase from 3 cases per 1000 man-years at age 45–49 years, to 38 cases per 1000 man-years by the age of 75–79 years. While the prevalence rate is 2.7% for men aged 45–49, it increases to 24% by the age of 80 years.[112]

References

  1. ^ "Prostate Enlargement (Benign Prostatic Hyperplasia)". NIDDK. September 2014. Archived 4 October 2017 at the Wayback Machine. Retrieved 19 October 2017.
  2. ^ Kim EH, Larson JA, Andriole GL (2016). "Management of Benign Prostatic Hyperplasia" (Review). Annual Review of Medicine. 67: 137–151. doi:10.1146/annurev-med-063014-123902. PMID 26331999
  3. ^ Awedew AF, Han H, Abbasi B, Abbasi-Kangevari M, Ahmed MB, Almidani O, Amini E, Arabloo J, Argaw AM, Athari SS, Atlaw D, Banach M, Barrow A, Bhagavathula AS, Bhojaraja VS, Bikbov B, Bodicha BB, Butt NS, Caetano Dos Santos FL, Dadras O, Dai X, Doan LP, Eftekharzadeh S, Fatehizadeh A, Garg T, Gebremeskel TG, Getachew ME, Ghamari S, Gilani SA, Golechha M (November 2022). "The global, regional, and national burden of benign prostatic hyperplasia in 204 countries and territories from 2000 to 2019: a systematic analysis for the Global Burden of Disease Study 2019". The Lancet. Healthy Longevity. 3 (11): e754–e776. doi:10.1016/S2666-7568(22)00213-6. PMC 9640930. PMID 36273485
  4. ^ Silva V, Grande AJ, Peccin MS (April 2019). "Physical activity for lower urinary tract symptoms secondary to benign prostatic obstruction". The Cochrane Database of Systematic Reviews. 2019 (4). doi:10.1002/14651858.CD012044.pub2. PMC 6450803. PMID 30953341
  5. ^ Wilt TJ, Ishani A, Rutks I, MacDonald R (December 2000). "Phytotherapy for benign prostatic hyperplasia". Public Health Nutrition. 3 (4A): 459–472. doi:10.1017/S1368980000000549. PMID 11276294
  6. ^ Novara, Giacomo; Giannarini, Gianluca; Alcaraz, Antonio; Cózar-Olmo, José-M.; Descazeaud, Aurelien; Montorsi, Francesco; Ficarra, Vincenzo (2016-12-01). "Efficacy and Safety of Hexanic Lipidosterolic Extract of Serenoa repens (Permixon) in the Treatment of Lower Urinary Tract Symptoms Due to Benign Prostatic Hyperplasia: Systematic Review and Meta-analysis of Randomized Controlled Trials". European Urology Focus. 2 (5): 553–561. doi:10.1016/j.euf.2016.04.002. ISSN 2405-4569. PMID 28723522
  7. ^ Dhouibi, Raouia; Affes, Hanen; Ben Salem, Maryem; Hammami, Serria; Sahnoun, Zouheir; Zeghal, Khaled Mounir; Ksouda, Kamilia (2020-01-01). "Screening of pharmacological uses of Urtica dioica and others benefits". Progress in Biophysics and Molecular Biology. 150: 67–77. doi:10.1016/j.pbiomolbio.2019.05.008. ISSN 0079-6107
  8. ^ Wilt T, Ishani A, MacDonald R, Stark G, Mulrow C, Lau J (1999). "Beta-sitosterols for benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. 1999 (2). doi:10.1002/14651858.CD001043. PMC 8407049. PMID 10796740
  9. ^ Wilt T, Ishani A, Mac Donald R, Rutks I, Stark G (1998). "Pygeum africanum for benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. 1998 (1). doi:10.1002/14651858.CD001044. PMC 7032619. PMID 11869585
  10. ^ "Spotlight on Saw Palmetto: What the Science Says". NCCIH. Retrieved 2025-12-01.
  11. ^ Keehn, Aryeh; Taylor, Jacob; Lowe, Franklin C. (14 May 2016). "Phytotherapy for Benign Prostatic Hyperplasia". Current Urology Reports. 17 (7): 53. doi:10.1007/s11934-016-0609-z. ISSN 1534-6285. PMID 27180172
  12. ^ Chang RT, Kirby R, Challacombe BJ (April 2012). "Is there a link between BPH and prostate cancer?". The Practitioner. 256 (1750): 13–6, 2. PMID 22792684
  13. ^ "Lower urinary tract symptoms in men: management", NICE (National Institute for Health and Care Excellence)
  14. ^ "Urge incontinence". MedlinePlus. US National Library of Medicine. Archived 6 October 2015 at the Wayback Machine. Retrieved 26 October 2015.
  15. ^ White JR, O'Brien III DP, Walker HK, Hall WD, Hurst JW (1990). "Incontinence and Stream Abnormalities". Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd ed. Boston: Butterworths. ISBN 978-0-409-90077-4. PMID 21250138
  16. ^ Robinson J (11 February 2008). "Post-micturition dribble in men: causes and treatment". Nursing Standard. 22 (30): 43–46. doi:10.7748/ns2008.04.22.30.43.c6440. PMID 18459613
  17. ^ Sarma AV, Wei JT (July 2012). "Clinical practice. Benign prostatic hyperplasia and lower urinary tract symptoms". The New England Journal of Medicine. 367 (3): 248–257. doi:10.1056/nejmcp1106637. PMID 22808960
  18. ^ "Urination – difficulty with flow". MedlinePlus. US National Library of Medicine. Archived 6 October 2015 at the Wayback Machine. Retrieved 26 October 2015.
  19. ^ "Urination – painful". MedlinePlus. US National Library of Medicine. Archived 6 October 2015 at the Wayback Machine. Retrieved 26 October 2015.
  20. ^ "Bladder outlet obstruction". MedlinePlus. US National Library of Medicine. Archived 6 October 2015 at the Wayback Machine. Retrieved 26 October 2015.
  21. ^ "Benign Prostatic Hyperplasia". The Lecturio Medical Concept Library. Retrieved 5 July 2021.
  22. ^ Truzzi JC, Almeida FM, Nunes EC, Sadi MV (July 2008). "Residual urinary volume and urinary tract infection – when are they linked?". The Journal of Urology. 180 (1): 182–185. doi:10.1016/j.juro.2008.03.044. PMID 18499191
  23. ^ Wu CP, Gu FL (1991). "The prostate in eunuchs". Progress in Clinical and Biological Research. 370: 249–255. PMID 1924456
  24. ^ "Testosterone and Aging: Clinical Research Directions.". NCBI Bookshelf. Archived 5 November 2017 at the Wayback Machine. Retrieved 2 February 2015.
  25. ^ "Proscar (finasteride) Prescribing Information". FDA – Drug Documents. Merck and Company. Archived 3 March 2016 at the Wayback Machine. Retrieved 2 March 2015.
  26. ^ Bartsch G, Rittmaster RS, Klocker H (April 2002). "Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia". World Journal of Urology. 19 (6): 413–425. doi:10.1007/s00345-002-0248-5. PMID 12022710. S2CID 3257666
  27. ^ Feldman BJ, Feldman D (October 2001). "The development of androgen-independent prostate cancer". Nature Reviews. Cancer. 1 (1): 34–45. doi:10.1038/35094009. PMID 11900250. S2CID 205020623
  28. ^ Lagiou P, Mantzoros CS, Tzonou A, Signorello LB, Lipworth L, Trichopoulos D (1997). "Serum steroids in relation to benign prostatic hyperplasia". Oncology. 54 (6): 497–501. doi:10.1159/000227609. PMID 9394847
  29. ^ Roberts RO, Jacobson DJ, Rhodes T, Klee GG, Leiber MM, Jacobsen SJ (October 2004). "Serum sex hormones and measures of benign prostatic hyperplasia". The Prostate. 61 (2): 124–131. doi:10.1002/pros.20080. PMID 15305335. S2CID 24288565
  30. ^ Page ST, Lin DW, Mostaghel EA, Hess DL, True LD, Amory JK, Nelson PS, Matsumoto AM, Bremner WJ (October 2006). "Persistent intraprostatic androgen concentrations after medical castration in healthy men". The Journal of Clinical Endocrinology and Metabolism. 91 (10): 3850–3856. doi:10.1210/jc.2006-0968. PMID 16882745
  31. ^ Dimitrakov J, Joffe HV, Soldin SJ, Bolus R, Buffington CA, Nickel JC (February 2008). "Adrenocortical hormone abnormalities in men with chronic prostatitis/chronic pelvic pain syndrome". Urology. 71 (2): 261–266. doi:10.1016/j.urology.2007.09.025. PMC 2390769. PMID 18308097
  32. ^ du Toit T, Swart AC (February 2020). "The 11β-hydroxyandrostenedione pathway and C11-oxy C21 backdoor pathway are active in benign prostatic hyperplasia yielding 11keto-testosterone and 11keto-progesterone". The Journal of Steroid Biochemistry and Molecular Biology. 196. doi:10.1016/j.jsbmb.2019.105497. PMID 31626910. S2CID 204734045
  33. ^ Masiutin MG, Yadav MK (November 2022). ""Re: Adrenocortical Hormone Abnormalities in Men With Chronic Prostatitis/Chronic Pelvic Pain Syndrome"". Urology. 169: 273. doi:10.1016/j.urology.2022.07.051. PMID 35987379. S2CID 251657694
  34. ^ Dimitrakoff J, Nickel JC (November 2022). "Author Reply". Urology. 169: 273–274. doi:10.1016/j.urology.2022.07.049. PMID 35985522. S2CID 251658492
  35. ^ Ho CK, Nanda J, Chapman KE, Habib FK (June 2008). "Oestrogen and benign prostatic hyperplasia: effects on stromal cell proliferation and local formation from androgen". The Journal of Endocrinology. 197 (3): 483–491. doi:10.1677/JOE-07-0470. PMID 18492814
  36. ^ Niu YJ, Ma TX, Zhang J, Xu Y, Han RF, Sun G (March 2003). "Androgen and prostatic stroma". Asian Journal of Andrology. 5 (1): 19–26. PMID 12646998
  37. ^ Ansari MA, Begum D, Islam F (2008). "Serum sex steroids, gonadotrophins and sex hormone-binding globulin in prostatic hyperplasia". Annals of Saudi Medicine. 28 (3): 174–178. doi:10.4103/0256-4947.51727. PMC 6074428. PMID 18500180
  38. ^ Gat Y, Gornish M, Heiblum M, Joshua S (October 2008). "Reversal of benign prostate hyperplasia by selective occlusion of impaired venous drainage in the male reproductive system: novel mechanism, new treatment". Andrologia. 40 (5): 273–281. doi:10.1111/j.1439-0272.2008.00883.x. PMID 18811916. S2CID 205442245
  39. ^ Heber D (April 2002). "Prostate enlargement: the canary in the coal mine?". The American Journal of Clinical Nutrition. 75 (4): 605–606. doi:10.1093/ajcn/75.4.605. PMID 11916745
  40. ^ Zhang SX, Yu B, Guo SL, Wang YW, Yin CK (February 2003). "[Comparison of incidence of BPH and related factors between urban and rural inhabitants in district of Wannan]". Zhonghua Nan Ke Xue = National Journal of Andrology. 9 (1): 45–47. PMID 12680332
  41. ^ Gu F (March 1997). "Changes in the prevalence of benign prostatic hyperplasia in China". Chinese Medical Journal. 110 (3): 163–166. PMID 9594331
  42. ^ Chyou PH, Nomura AM, Stemmermann GN, Hankin JH (1993). "A prospective study of alcohol, diet, and other lifestyle factors in relation to obstructive uropathy". The Prostate. 22 (3): 253–264. doi:10.1002/pros.2990220308. PMID 7683816. S2CID 32639108
  43. ^ Suzuki S, Platz EA, Kawachi I, Willett WC, Giovannucci E (April 2002). "Intakes of energy and macronutrients and the risk of benign prostatic hyperplasia". The American Journal of Clinical Nutrition. 75 (4): 689–697. doi:10.1093/ajcn/75.4.689. PMID 11916755
  44. ^ Gacci M, Corona G, Vignozzi L, Salvi M, Serni S, De Nunzio C, Tubaro A, Oelke M, Carini M, Maggi M (January 2015). "Metabolic syndrome and benign prostatic enlargement: a systematic review and meta-analysis". BJU International. 115 (1): 24–31. doi:10.1111/bju.12728. hdl:2158/953282. PMID 24602293. S2CID 22937831
  45. ^ Wang J, Michelitsch T, Wunderlin A, Mahadeva R (March 2009). "Aging as a consequence of misrepair – A novel theory of aging.". Nature Precedings. arXiv:0904.0575. doi:10.1038/npre.2009.2988.1
  46. ^ Wang-Michelitsch J, Michelitsch T (2015). "Tissue fibrosis: a principal evidence for the central role of Misrepairs in aging". arXiv:1503.01376
  47. ^ Roehrborn CG (2005). "Benign prostatic hyperplasia: an overview". Reviews in Urology. 7 (Suppl 9): S3–S14. PMC 1477638. PMID 16985902
  48. ^ Wasserman NF (September 2006). "Benign prostatic hyperplasia: a review and ultrasound classification". Radiologic Clinics of North America. 44 (5): 689–710, viii. doi:10.1016/j.rcl.2006.07.005. PMID 17030221
  49. ^ Ojewola RW, Tijani KH, Fatuga AL, Onyeze CI, Okeke CJ (2020). "Management of a giant prostatic enlargement: Case report and review of the literature". The Nigerian Postgraduate Medical Journal. 27 (3): 242–247. Medknow. doi:10.4103/npmj.npmj_69_20. PMID 32687126. S2CID 220652018
  50. ^ Parsons JK (December 2010). "Benign Prostatic Hyperplasia and Male Lower Urinary Tract Symptoms: Epidemiology and Risk Factors". Current Bladder Dysfunction Reports. 5 (4): 212–218. doi:10.1007/s11884-010-0067-2. PMC 3061630. PMID 21475707
  51. ^ Eid K, Krughoff K, Stoimenova D, Smith D, Phillips J, O'Donnell C, Barqawi A (January 2014). "Validation of the Urgency, Weak stream, Incomplete emptying, and Nocturia (UWIN) score compared with the American Urological Association Symptoms Score in assessing lower urinary tract symptoms in the clinical setting". Urology. 83 (1): 181–185. doi:10.1016/j.urology.2013.08.039. PMID 24139351
  52. ^ Gammie A, Drake MJ (August 2018). "The fundamentals of uroflowmetry practice, based on International Continence Society good urodynamic practices recommendations". Neurourology and Urodynamics. 37 (S6): S44–S49. doi:10.1002/nau.23777. PMID 30614059. S2CID 58586667
  53. ^ Foo KT (June 2013). "The Role of Transabdominal Ultrasound in Office Urology". Proceedings of Singapore Healthcare. 22 (2): 125–130. doi:10.1177/201010581302200208. ISSN 2010-1058. S2CID 74205747
  54. ^ Aprikian S, Luz M, Brimo F, Scarlata E, Hamel L, Cury FL, Tanguay S, Aprikian AG, Kassouf W, Chevalier S (July 2019). "Improving ultrasound-based prostate volume estimation". BMC Urology. 19 (1). doi:10.1186/s12894-019-0492-2. PMC 6657110. PMID 31340802
  55. ^ Kitzing YX, Prando A, Varol C, Karczmar GS, Maclean F, Oto A (January 2016). "Benign Conditions That Mimic Prostate Carcinoma: MR Imaging Features with Histopathologic Correlation". Radiographics. 36 (1): 162–175. doi:10.1148/rg.2016150030. PMC 5496681. PMID 26587887
  56. ^ Singh S, Martin E, Tregidgo HF, Treeby B, Bandula S (October 2021). "Prostatic calcifications: Quantifying occurrence, radiodensity, and spatial distribution in prostate cancer patients". Urologic Oncology. 39 (10): 728.e1–728.e6. doi:10.1016/j.urolonc.2020.12.028. PMC 8492071. PMID 33485763
  57. ^ Mitterberger M, Horninger W, Aigner F, Pinggera GM, Steppan I, Rehder P, Frauscher F (March 2010). "Ultrasound of the prostate". Cancer Imaging. 10 (1): 40–48. doi:10.1102/1470-7330.2010.0004. PMC 2842183. PMID 20199941
  58. ^ Lee JS, Chung BH (2007). "Transrectal ultrasound versus magnetic resonance imaging in the estimation of prostate volume as compared with radical prostatectomy specimens". Urologia Internationalis. 78 (4): 323–327. doi:10.1159/000100836. PMID 17495490. S2CID 10731245
  59. ^ Hwang EC, Gandhi S, Jung JH, Imamura M, Kim MH, Pang R, Dahm P (October 2018). "Naftopidil for the treatment of lower urinary tract symptoms compatible with benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. 2018 (10). doi:10.1002/14651858.CD007360.pub3. PMC 6516835. PMID 30306544
  60. ^ "Benign prostatic hyperplasia". University of Maryland Medical Center. Archived 25 April 2017 at the Wayback Machine.
  61. ^ Silva V, Grande AJ, Peccin MS (April 2019). "Physical activity for lower urinary tract symptoms secondary to benign prostatic obstruction". The Cochrane Database of Systematic Reviews. 2019 (4). doi:10.1002/14651858.CD012044.pub2. PMC 6450803. PMID 30953341
  62. ^ De Jong Y, Pinckaers JH, Ten Brinck RM, Lycklama à Nijeholt AA. "Influence of voiding posture on urodynamic parameters in men: a literature review". Nederlands Tijdschrift voor urologie. Archived 14 July 2014 at the Wayback Machine. Retrieved 2 July 2014.
  63. ^ de Jong Y, Pinckaers JH, ten Brinck RM, Lycklama à Nijeholt AA, Dekkers OM (2014). "Urinating standing versus sitting: position is of influence in men with prostate enlargement. A systematic review and meta-analysis". PLOS ONE. 9 (7). Bibcode:2014PLoSO...9j1320D. doi:10.1371/journal.pone.0101320. PMC 4106761. PMID 25051345
  64. ^ Silva J, Silva CM, Cruz F (January 2014). "Current medical treatment of lower urinary tract symptoms/BPH: do we have a standard?". Current Opinion in Urology. 24 (1): 21–28. doi:10.1097/mou.0000000000000007. PMID 24231531. S2CID 40954757
  65. ^ Roehrborn CG, Nuckolls JG, Wei JT, Steers W (October 2007). "The benign prostatic hyperplasia registry and patient survey: study design, methods, and patient baseline characteristics". BJU International. 100 (4): 813–819. doi:10.1111/j.1464-410X.2007.07061.x. hdl:2027.42/73286. PMID 17822462. S2CID 21001077
  66. ^ Black L, Naslund MJ, Gilbert TD, Davis EA, Ollendorf DA (March 2006). "An examination of treatment patterns and costs of care among patients with benign prostatic hyperplasia". The American Journal of Managed Care. 12 (4 Suppl): S99–S110. PMID 16551208
  67. ^ Hutchison A, Farmer R, Verhamme K, Berges R, Navarrete RV (January 2007). "The efficacy of drugs for the treatment of LUTS/BPH, a study in 6 European countries". European Urology. 51 (1): 207–15; discussion 215–6. doi:10.1016/j.eururo.2006.06.012. PMID 16846678
  68. ^ MacDonald R, Wilt TJ (October 2005). "Alfuzosin for treatment of lower urinary tract symptoms compatible with benign prostatic hyperplasia: a systematic review of efficacy and adverse effects". Urology. 66 (4): 780–788. doi:10.1016/j.urology.2005.05.001. PMID 16230138
  69. ^ Roehrborn CG (December 2001). "Efficacy and safety of once-daily alfuzosin in the treatment of lower urinary tract symptoms and clinical benign prostatic hyperplasia: a randomized, placebo-controlled trial". Urology. 58 (6): 953–959. doi:10.1016/S0090-4295(01)01448-0. PMID 11744466
  70. ^ MacDonald R, Wilt TJ, Howe RW (December 2004). "Doxazosin for treating lower urinary tract symptoms compatible with benign prostatic obstruction: a systematic review of efficacy and adverse effects". BJU International. 94 (9): 1263–1270. doi:10.1111/j.1464-410X.2004.05154.x. PMID 15610102. S2CID 6640867
  71. ^ Wilt TJ, Mac Donald R, Rutks I (2003). "Tamsulosin for benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. ' (1). doi:10.1002/14651858.CD002081. PMID 12535426
  72. ^ Djavan B, Marberger M (1999). "A meta-analysis on the efficacy and tolerability of alpha1-adrenoceptor antagonists in patients with lower urinary tract symptoms suggestive of benign prostatic obstruction". European Urology. 36 (1): 1–13. doi:10.1159/000019919. PMID 10364649. S2CID 73366414
  73. ^ Santillo VM, Lowe FC (2006). "Treatment of benign prostatic hyperplasia in patients with cardiovascular disease". Drugs & Aging. 23 (10): 795–805. doi:10.2165/00002512-200623100-00003. PMID 17067183. S2CID 24428368
  74. ^ AUA Practice Guidelines Committee (August 2003). "AUA guideline on management of benign prostatic hyperplasia (2003). Chapter 1: Diagnosis and treatment recommendations". The Journal of Urology. 170 (2 Pt 1): 530–547. doi:10.1097/01.ju.0000078083.38675.79. PMID 12853821
  75. ^ Blankstein U, Van Asseldonk B, Elterman DS (February 2016). "BPH update: medical versus interventional management". The Canadian Journal of Urology. 23 (Suppl 1): 10–15. PMID 26924590. Archived 7 August 2016 at the Wayback Machine.
  76. ^ Roehrborn CG, Bruskewitz R, Nickel JC, McConnell JD, Saltzman B, Gittelman MC, Malek GH, Gottesman JE, Suryawanshi S, Drisko J, Meehan A, Waldstreicher J (March 2004). "Sustained decrease in incidence of acute urinary retention and surgery with finasteride for 6 years in men with benign prostatic hyperplasia". The Journal of Urology. 171 (3): 1194–1198. doi:10.1097/01.ju.0000112918.74410.94. PMID 14767299
  77. ^ Roehrborn CG, Barkin J, Tubaro A, Emberton M, Wilson TH, Brotherton BJ, Castro R (April 2014). "Influence of baseline variables on changes in International Prostate Symptom Score after combined therapy with dutasteride plus tamsulosin or either monotherapy in patients with benign prostatic hyperplasia and lower urinary tract symptoms: 4-year results of the CombAT study". BJU International. 113 (4): 623–635. doi:10.1111/bju.12500. PMID 24127818. S2CID 38243275
  78. ^ Greco KA, McVary KT (December 2008). "The role of combination medical therapy in benign prostatic hyperplasia". International Journal of Impotence Research. 20 (Suppl 3): S33–S43. doi:10.1038/ijir.2008.51. PMID 19002123
  79. ^ Kaplan SA, McConnell JD, Roehrborn CG, Meehan AG, Lee MW, Noble WR, Kusek JW, Nyberg LM (January 2006). "Combination therapy with doxazosin and finasteride for benign prostatic hyperplasia in patients with lower urinary tract symptoms and a baseline total prostate volume of 25 ml or greater". The Journal of Urology. 175 (1): 217–20; discussion 220–1. doi:10.1016/S0022-5347(05)00041-8. PMID 16406915
  80. ^ Barkin J, Guimarães M, Jacobi G, Pushkar D, Taylor S, van Vierssen Trip OB (October 2003). "Alpha-blocker therapy can be withdrawn in the majority of men following initial combination therapy with the dual 5alpha-reductase inhibitor dutasteride". European Urology. 44 (4): 461–466. doi:10.1016/s0302-2838(03)00367-1. PMID 14499682
  81. ^ Gormley GJ, Stoner E, Bruskewitz RC, Imperato-McGinley J, Walsh PC, McConnell JD, Andriole GL, Geller J, Bracken BR, Tenover JS (October 1992). "The effect of finasteride in men with benign prostatic hyperplasia. The Finasteride Study Group". The New England Journal of Medicine. 327 (17): 1185–1191. doi:10.1056/NEJM199210223271701. PMID 1383816
  82. ^ Gacci M, Ficarra V, Sebastianelli A, Corona G, Serni S, Shariat SF, Maggi M, Zattoni F, Carini M, Novara G (June 2014). "Impact of medical treatments for male lower urinary tract symptoms due to benign prostatic hyperplasia on ejaculatory function: a systematic review and meta-analysis". The Journal of Sexual Medicine. 11 (6): 1554–1566. doi:10.1111/jsm.12525. PMID 24708055
  83. ^ Deters L. "Benign Prostatic Hypertrophy Treatment & Management". Medscape. Archived 30 October 2015 at the Wayback Machine. Retrieved 14 November 2015.
  84. ^ Pattanaik S, Mavuduru RS, Panda A, Mathew JL, Agarwal MM, Hwang EC, Lyon JA, Singh SK, Mandal AK (November 2018). "Phosphodiesterase inhibitors for lower urinary tract symptoms consistent with benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. 2018 (11). doi:10.1002/14651858.CD010060.pub2. PMC 6517182. PMID 30480763
  85. ^ Wang Y, Bao Y, Liu J, Duan L, Cui Y (January 2018). "Tadalafil 5 mg Once Daily Improves Lower Urinary Tract Symptoms and Erectile Dysfunction: A Systematic Review and Meta-analysis". Lower Urinary Tract Symptoms. 10 (1): 84–92. doi:10.1111/luts.12144. PMID 29341503. S2CID 23929021
  86. ^ Pattanaik S, Mavuduru RS, Panda A, Mathew JL, Agarwal MM, Hwang EC, Lyon JA, Singh SK, Mandal AK (November 2018). "Phosphodiesterase inhibitors for lower urinary tract symptoms consistent with benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. 2018 (11). doi:10.1002/14651858.CD010060.pub2. PMC 6517182. PMID 30480763
  87. ^ "Hyperplasia (benign prostatic) – tadalafil (terminated appraisal) (TA273)". National Institute for Health and Clinical Excellence (NICE). 23 January 2013. Archived 24 February 2013 at the Wayback Machine. Retrieved 27 January 2013.
  88. ^ "FDA approves Cialis to treat benign prostatic hyperplasia". U.S. Food and Drug Administration (FDA). Archived 18 January 2017 at the Wayback Machine. Retrieved 7 May 2013.
  89. ^ Kaplan SA, Roehrborn CG, Rovner ES, Carlsson M, Bavendam T, Guan Z (November 2006). "Tolterodine and tamsulosin for treatment of men with lower urinary tract symptoms and overactive bladder: a randomized controlled trial". JAMA. 296 (19): 2319–2328. doi:10.1001/jama.296.19.2319. PMID 17105794
  90. ^ Abrams P, Andersson KE (November 2007). "Muscarinic receptor antagonists for overactive bladder". BJU International. 100 (5): 987–1006. doi:10.1111/j.1464-410x.2007.07205.x. PMID 17922784. S2CID 30983780
  91. ^ "Prostate enlargement (benign prostatic hyperplasia)". Harvard Health Content. Harvard Health Publications. Archived 3 April 2015 at the Wayback Machine. Retrieved 2 February 2015.
  92. ^ Wyndaele JJ (October 2002). "Complications of intermittent catheterization: their prevention and treatment". Spinal Cord. 40 (10): 536–541. doi:10.1038/sj.sc.3101348. PMID 12235537
  93. ^ Prieto JA, Murphy CL, Stewart F, Fader M (October 2021). "Intermittent catheter techniques, strategies and designs for managing long-term bladder conditions". The Cochrane Database of Systematic Reviews. 10 (10). doi:10.1002/14651858.CD006008.pub5. PMC 8547544. PMID 34699062
  94. ^ Franco JV, Garegnani L, Escobar Liquitay CM, Borofsky M, Dahm P (June 2021). "Transurethral microwave thermotherapy for the treatment of lower urinary tract symptoms in men with benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. 2021 (6). doi:10.1002/14651858.CD004135.pub4. PMC 8236484. PMID 34180047
  95. ^ "Transurethral resection of the prostate (TURP) - Risks". nhs.uk. 2017-10-24. Retrieved 2020-03-08.
  96. ^ "Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline (2026) - American Urological Association". www.auanet.org. Retrieved 2026-05-20.
  97. ^ "Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline (2026) - American Urological Association". www.auanet.org. Retrieved 2026-05-20.
  98. ^ Hartung, Friedrich O.; Kowalewski, Karl-Friedrich; von Hardenberg, Jost; Worst, Thomas S.; Kriegmair, Maximilian C.; Nuhn, Philipp; Herrmann, Thomas R. W.; Michel, Maurice S.; Herrmann, Jonas (April 2022). "Holmium Versus Thulium Laser Enucleation of the Prostate: A Systematic Review and Meta-analysis of Randomized Controlled Trials". European Urology Focus. 8 (2): 545–554. doi:10.1016/j.euf.2021.03.024. ISSN 2405-4569. PMID 33840611
  99. ^ Dhirubhai Tadha, Ajaykumar; Sarkar, Debansu; Kumar Pal, Dilip (January 2024). "A Prospective, Randomized Study Comparing the Outcome After Thulium Laser Enucleation of the Prostate with Conventional Monopolar TURP for the Treatment of Symptomatic Benign Prostatic Hyperplasia". Urology Research & Practice. 50 (1): 42–46. doi:10.5152/tud.2024.23128. ISSN 2980-1478. PMC 11059979. PMID 38451129
  100. ^ Yin, Lei; Teng, Jingfei; Huang, Chien-Jung; Zhang, Xiangmin; Xu, Danfeng (May 2013). "Holmium laser enucleation of the prostate versus transurethral resection of the prostate: a systematic review and meta-analysis of randomized controlled trials". Journal of Endourology. 27 (5): 604–611. doi:10.1089/end.2012.0505. ISSN 1557-900X. PMID 23167266
  101. ^ "Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia: AUA Guideline (2026) - American Urological Association". www.auanet.org. Retrieved 2026-05-20.
  102. ^ Shorbagy, Ahmed A.; Ismail, Mohammed; Kotb, Youssef M.; Desouki, Mohamed; Shabayek, Mohamed; Hanna, Peter (2025-05-23). "Laser vs. bipolar prostate vaporization in bleeding-prone patients: a randomized trial and cutting-edge analysis". World Journal of Urology. 43 (1): 322. doi:10.1007/s00345-025-05692-4. ISSN 1433-8726
  103. ^ Shorbagy, Ahmed A.; Ismail, Mohammed; Kotb, Youssef M.; Desouki, Mohamed; Shabayek, Mohamed; Hanna, Peter (2025-05-23). "Laser vs. bipolar prostate vaporization in bleeding-prone patients: a randomized trial and cutting-edge analysis". World Journal of Urology. 43 (1): 322. doi:10.1007/s00345-025-05692-4. ISSN 1433-8726
  104. ^ McNicholas TA (May 2016). "Benign prostatic hyperplasia and new treatment options - a critical appraisal of the UroLift system". Medical Devices: Evidence and Research. 9: 115–123. doi:10.2147/MDER.S60780. PMC 4876946. PMID 27274321
  105. ^ Porpiglia F, Fiori C, Bertolo R, Garrou D, Cattaneo G, Amparore D (August 2015). "Temporary implantable nitinol device (TIND): a novel, minimally invasive treatment for relief of lower urinary tract symptoms (LUTS) related to benign prostatic hyperplasia (BPH): feasibility, safety and functional results at 1 year of follow-up". BJU International. 116 (2): 278–287. doi:10.1111/bju.12982. hdl:2318/1623503. PMID 25382816. S2CID 5712711
  106. ^ Kuang M, Vu A, Athreya S (May 2017). "A Systematic Review of Prostatic Artery Embolization in the Treatment of Symptomatic Benign Prostatic Hyperplasia". CardioVascular and Interventional Radiology. 40 (5): 655–663. doi:10.1007/s00270-016-1539-3. PMID 28032133. S2CID 12154537
  107. ^ Pisco J, Bilhim T, Pinheiro LC, Fernandes L, Pereira J, Costa NV, Duarte M, Oliveira AG (May 2016). "Prostate Embolization as an Alternative to Open Surgery in Patients with Large Prostate and Moderate to Severe Lower Urinary Tract Symptoms". Journal of Vascular and Interventional Radiology. 27 (5): 700–708. doi:10.1016/j.jvir.2016.01.138. PMID 27019980
  108. ^ Keehn A, Taylor J, Lowe FC (July 2016). "Phytotherapy for Benign Prostatic Hyperplasia". Current Urology Reports. 17 (7). doi:10.1007/s11934-016-0609-z. PMID 27180172. S2CID 25609876
  109. ^ Bent S, Kane C, Shinohara K, Neuhaus J, Hudes ES, Goldberg H, Avins AL (February 2006). "Saw palmetto for benign prostatic hyperplasia". The New England Journal of Medicine. 354 (6): 557–566. doi:10.1056/NEJMoa053085. PMID 16467543. S2CID 13815057
  110. ^ Dedhia RC, McVary KT (June 2008). "Phytotherapy for lower urinary tract symptoms secondary to benign prostatic hyperplasia". The Journal of Urology. 179 (6): 2119–2125. doi:10.1016/j.juro.2008.01.094. PMID 18423748
  111. ^ Franco JV, Trivisonno L, Sgarbossa NJ, Alvez GA, Fieiras C, Escobar Liquitay CM, Jung JH (June 2023). "Serenoa repens for the treatment of lower urinary tract symptoms due to benign prostatic enlargement". The Cochrane Database of Systematic Reviews. 2023 (6). doi:10.1002/14651858.CD001423.pub4. PMC 10286776. PMID 37345871
  112. ^ Verhamme KM, Dieleman JP, Bleumink GS, van der Lei J, Sturkenboom MC, Artibani W, Begaud B, Berges R, Borkowski A, Chappel CR, Costello A, Dobronski P, Farmer RD, Jiménez Cruz F, Jonas U, MacRae K, Pientka L, Rutten FF, van Schayck CP, Speakman MJ, Sturkenboom MC, Tiellac P, Tubaro A, Vallencien G, Vela Navarrete R (October 2002). "Incidence and prevalence of lower urinary tract symptoms suggestive of benign prostatic hyperplasia in primary care – the Triumph project". European Urology. 42 (4): 323–328. doi:10.1016/S0302-2838(02)00354-8. PMID 12361895