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DOI: 10.1055/s-0044-1779513
Imaging of Non-malignant Conditions of the Prostate and Seminal Vesicles: A Comprehensive Review
- Abstract
- Introduction
- Benign Prostatic Hyperplasia
- Infections and Inflammatory Diseases
- Prostatic and Periprostatic Cysts and Their Mimics
- Benign Neoplasms of Prostate and Seminal Vesicles
- Conclusion
- References
Abstract
Non-malignant conditions of the prostate and seminal vesicles are much more common in imaging practice than prostate cancer. They include benign prostatic hyperplasia, infective and inflammatory prostatitis, prostatic and periprostatic cysts, and benign tumors. The advances in magnetic resonance imaging (MRI) of the prostate gland have dramatically improved the ability to identify these entities, many of them being identified incidentally in patients evaluated for other indications. Good knowledge of these conditions can aid in precise diagnosis and avoid interpretation pitfalls. In this article, we present non-malignant conditions of the prostate gland using several imaging modalities, including transrectal ultrasound, MRI, and computed tomography. We also present the pathological correlation for benign tumors.
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Introduction
Non-malignant conditions of the prostate and seminal vesicles (SVs) are common in clinical practice and often detected incidentally while reporting imaging studies. These include age-related changes such as benign prostatic hyperplasia, congenital and acquired prostatic and periprostatic cysts, infective and inflammatory changes in the prostate, and benign neoplasms. In multi-parametric MRI (mpMRI) of the prostate, many of these entities contribute significantly to pitfalls in image interpretation. This leads to both false positive and false negative diagnoses of clinically significant prostate cancer.[1] [2] [3] [4] Knowledge of their clinical presentation and imaging appearances can help accurate image interpretation and guide clinical referrers to optimal management. In this review, we present common non-malignant pathologies of the prostate and SVs and discuss the clinical presentation and their imaging appearances in different imaging modalities.
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Benign Prostatic Hyperplasia
Benign prostatic hyperplasia (BPH) refers to an increase in the number of prostatic stromal and epithelial cells in the transition zone (TZ) and periurethral glands that cause the formation of discrete nodules and prostate enlargement.[5] It develops in response to testosterone after it is converted to dihydrotestosterone.[6] Its prevalence increases with age and affects approximately 75% of men older than 70 years.[5] BPH can cause bladder outlet obstruction leading to lower urinary tract symptoms like urgency, frequency, weak stream, and nocturia.
Imaging modalities in BPH include transabdominal ultrasound, transrectal ultrasound (TRUS), and MRI. Computed tomography (CT) scan has limited value as it does not accurately define prostatic zonal anatomy. Transabdominal ultrasound is the standard first-line investigation for BPH and shows an increase in a prostate volume exceeding 25cc. The central gland is enlarged with hypoechoic or mixed echogenicity. There may be significant postvoid residual urine and associated bladder wall hypertrophy and trabeculations due to chronic bladder outflow obstruction.
On TRUS, BPH appears as a diffuse or nodular enlargement of the TZ, periurethral glandular tissue, or both.[7] Hyperplastic nodules are usually hypoechoic to peripheral zone (PZ) tissue but may be isoechoic or hyperechoic depending on the amount of fibrous, muscular, and glandular hyperplastic elements and are surrounded by fibrous envelopes that appear as hypoechoic rims ([Fig. 1]).[7] On MRI, BPH appears as band-like areas and/or encapsulated circumscribed round nodules in the TZ. While predominantly glandular nodules appear T2 hyperintense, stromal nodules may appear T2 hypointense and contribute to a substantial number of PIRADS 3 lesions in clinical practice.[6] The heterogeneous appearance of TZ on T2 due to both hyperintense and hypointense BPH nodules is likened to “organized chaos” ([Fig. 2]). BPH nodules showing complete T2 hypointense rim are categorized as typical BPH nodules (PIRADS 1), while those showing partial encapsulation are atypical nodules (PIRADS 2). Diffusion-weighted imaging (DWI) helps in differentiating BPH nodules from prostate cancer, as they do not show marked restricted diffusion on high b Value DWI (b≥ 1400) or marked hypointensity on apparent diffusion coefficient (ADC) images. On dynamic contrast-enhanced MRI (DCE-MRI), BPH nodules may show early enhancement, hence it is unreliable. Although BPH nodules typically occur in TZ, exophytic or extruded BPH nodules can be seen in the peripheral zone ([Fig. 3]) or central zone[3] and share a similar MRI appearance. [Table 1] shows the types of BPH based on ultrasound and MRI findings.
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Type 0 |
Normal prostate with volume <25cc |
Type 1 |
Bilateral TZ enlargement |
Type 2 |
Retro urethral enlargement also called median lobe hypertrophy |
Type 3 |
Bilateral TZ and retro urethral enlargement |
Type 4 |
Pedunculated intravesical prostatic protrusion, enlarged single or multiple nodules arising from intraluminal urethral submucosa |
Type 5 |
Bilateral TZ and/or retro urethral enlargement with pedunculated intravesical protrusion of prostate |
Type 6 |
Sub trigonal or ectopic enlargement |
Type 7 |
Other combination of enlargements |
Abbreviations: BPH, benign prostatic hyperplasia; MRI, magnetic resonance imaging; TZ, transition zone.
Early disease is managed conservatively with alpha-blockers and 5-alpha reductase inhibitors. Surgical management for symptomatic patients is achieved with transurethral resection of the prostate (TURP). Laser-based and thermal ablation procedures and prostatic artery embolization may also reduce periurethral prostatic volume and obstruction.[8] Any procedure that does not completely remove the TZ has the potential for recurrence and may result in the need for an additional procedure.
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Infections and Inflammatory Diseases
Prostatitis is inflammation or infection of the prostate and clinically presents with symptoms referable to the lower urogenital tract and perineum. Studies suggest the prevalence of prostatitis is 2 to 16%.[11] The National Institutes of Health classifies prostatitis into four categories—acute bacterial prostatitis, chronic bacterial prostatitis, chronic prostatitis or pelvic pain syndrome, and asymptomatic inflammatory prostatitis.[12]
Acute Prostatitis
Acute prostatitis has a bimodal age distribution affecting men of 20 to 40 years and over 60 years.[13] [14] The most common pathogen is Escherichia coli (in ∼60%), followed by Pseudomonas aeruginosa and Enterococcus species.[15] [16] The infection spreads as ascending urethral infection, direct seeding from prostatic biopsy, intraprostatic reflux of infected urine, or by hematogenous spread as in sepsis and tuberculosis. About 6% of acute bacterial prostatitis can progress to prostatic abscesses in whom imaging is indicated.[17] Patients with acute prostatitis who do not respond to treatment after 48 hours should be evaluated for a possible prostatic abscess.[18]
Prostatic abscess appears as a hypoechoic area with internal septae and thick well-defined walls on TRUS ([Fig. 4]); TRUS is also of value in ultrasound-guided drainage of abscess (at least 18G needle is preferred). Unroofing/transurethral drainage of the prostatic abscess is preferred in lesions too large to drain percutaneously or lesions that do not respond to percutaneous drainage.[19] Contrast-enhanced CT shows an edematous appearance of prostate and periprostatic stranding. Prostatic abscess appears as hypodense focus with peripheral enhancement and internal septations ([Fig. 5]).[20] Cross-sectional imaging also gives valuable information regarding extraprostatic spread. MRI offers better soft tissue resolution than CT and is more sensitive than TRUS in the early stages of abscess formation. Abscess shows a low signal on T1, high signal on T2-weighted MRI, central diffusion restriction and displays peripheral rim enhancement with gadolinium.[20]
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Prostate must be carefully reviewed in patients with cystitis with persistent fever in the absence of upper urinary tract infection (UTI), recurrent UTI in the absence of renal involvement/structural abnormalities of the urinary tract, secondary peritonitis, immunocompromised, diabetic patients, and those with sepsis ([Figs. 1] and [2]). Prostatic abscess carries high morbidity and mortality and needs a high index of suspicion, and imaging is critical for timely diagnosis and treatment.
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Chronic Prostatitis
It encompasses a spectrum of etiologies from a sequel to acute prostatitis, and recurrent UTIs to IgG4-related disease and tuberculous prostatitis. Chronic prostatitis appears as wedge-shaped T2 hypointense lesions with a linear pattern in the peripheral zone with or without capsular retraction and does not show diffusion restriction ([Fig. 6]). Granulomatous prostatitis (GP) is a nodular form of chronic prostatitis. It can be idiopathic, tuberculous, iatrogenic due to Bacille Calmette-Guerin (BCG) vaccine, intravesical BCG for bladder cancer, postradiotherapy or due to autoimmune aetiologies and systemic conditions like sarcoidosis.[21] GP demonstrates a tumor-like morphology, with nodular or diffuse hypoechogenic lesions on ultrasound, and has PIRADS 5 appearance on mpMRI.[22] On T2-weighted MRI, GP lesions appear hypointense like prostate cancer. GP and cancer lesions share high signal intensity on high b-value DWI and low signal intensity on the ADC map. On DCE-MRI, GP shows moderate persistent enhancement and prostate cancer shows early enhancement and rapid washout due to increased vascularity.[23] GP is more commonly diffuse when compared to prostate cancer. Unlike the diffuse forms of prostate cancer, in GP the prostatic capsule is usually intact ([Fig. 7]). Clinical profile combined with declining serial prostate-specific antigen (PSA) value in some cases may hint the radiologist to a diagnosis of GP over malignancy.
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Prostatic and Periprostatic Cysts and Their Mimics
Prostatic and periprostatic cysts are uncommon pathologies often encountered as incidental findings on imaging.[24] These are mostly asymptomatic but sometimes may present with lower urinary tract symptoms and infertility.[24] Knowledge of embryology and anatomical localization by high-resolution MRI helps in characterizing these lesions.
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i) Prostatic cysts
Prostatic Utricle and Müllerian Duct Cysts
The Müllerian duct is an embryonic structure that normally regresses in males, except for a part at its cephalic end that contributes to remnant structures such as the prostatic utricle and testicular appendix.[25] A prostatic utricle cyst is a cystic dilatation of the prostatic utricle. Müllerian duct cysts are cystic dilatations of segments of the Müllerian duct that failed to regress.
Ultrasonography, CT, and MRI can detect these cysts. The anatomic location, shape of the cyst, and relationship with the urethra can aid in distinguishing between prostatic utricle cyst and Müllerian duct cyst as summarized in [Table 2]. MRI has the advantage of superior soft tissue resolution and high-resolution images can assess relationships with adjacent structures better ([Fig. 8]).[26] [27]
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Management decisions are based on the size of the cyst, its location, and the symptoms of the patient. Cysts larger than 2.5 cm are usually symptomatic and may need urology referral and further management. These cysts can bleed or get secondary infection and very rarely can transform into malignancy.[26] Management options for Müllerian duct cysts include surveillance, TRUS-guided aspiration and injection of sclerosing agents, surgical excision, transurethral resection, and percutaneous aspiration. Laparoscopic excision has also been tried.[24] [27]
Ejaculatory duct cysts
Ejaculatory duct cysts usually develop secondary to ejaculatory duct obstruction[25] and can be congenital or acquired.[24] The ejaculatory duct is a short, approximately 2 cm long structure coursing through the central zone of the prostate gland and formed by the joining of duct from the SV and ductus deferens. On imaging, these are seen as paramedian cysts ([Fig. 9A, B]) in the central zone along the ejaculatory duct.[25] Larger lesions may extend above the prostate gland and appear as midline lesion.[25] [26] The obstructed ejaculatory duct causes proximal dilatation of the duct depending on the level of obstruction and extent of fibrosis. There can also be ipsilateral prominence of vas deferens, dilatation of SV ducts, and enlargement of SV. High-resolution MRI is helpful in localizing the level of obstruction.[25] Due to limited availability and cost factors, MRI is reserved for cases with inconclusive ultrasonography.[25] Aspirate shows spermatozoa, and fructose and may rarely contain calculi.[26] The treatment is usually surveillance and surgery is considered in symptomatic patients or those with infertility.
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Prostatic retention cysts (PRC) and cystic degeneration of BPH
These are usually seen in the region of glandular tissues of the prostate gland, mostly asymptomatic, and encountered during the 5th to 6th decades of life.[25] The exact etiology of PRC is unknown, but is seen frequently in patients with BPH[25] and could be the result of obstruction of the prostatic parenchymal ductules.[26] On imaging, these are round, smooth unilocular cysts and can occur in any prostatic zone, usually the peripheral zone with or without background changes of BPH ([Fig. 10A, B]). Cystic degeneration of BPH nodules results in irregularly shaped cysts commonly seen in the TZ of the prostate gland ([Fig. 10C]).
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Tumoral cysts
Some tumors like multilocular prostatic cystadenoma and adenocarcinoma also show cystic changes along with soft tissue components.[24] [28]
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ii) Periprostatic cysts
Periprostatic cysts include SV cysts, cyst of vas deferens, and Cowper's duct cysts.[24]
Seminal vesicle cysts
These can be congenital or acquired and may be associated with adult polycystic kidney disease.[26] [27] These are mostly detected incidentally unless they are large enough to cause obstructive urinary symptoms.[29] They occur commonly in sexually active males secondary to a malformed or stenosed duct system.[27] When congenital, they develop due to atresia of ejaculatory ducts and thereby, are associated with bulky distended SV. Congenital cysts are mostly unilateral and associated with anomalies like renal agenesis, ectopic ureteric insertion, and vas deferens agenesis. Zinner syndrome is a triad of unilateral renal agenesis, ipsilateral SV cyst, and ejaculatory duct obstruction[27] ([Fig. 11]). On imaging, they appear as well-defined round/oval/tubular cysts within the SV, posterior to the urinary bladder.[26] [29] In cases of hemorrhage and proteinaceous content, they appear hyperintense on T1-weighted imaging and hypointense to bladder contents on T2 weighted imaging ([Fig. 11]).[27] On TRUS, they are seen as anechoic cystic lesions within the SV with variable echogenicity in the presence of hemorrhage or proteinaceous content.[27] [29] These cysts are usually treated with conservative management. However, TRUS-guided cyst drainage can be done if symptomatic.[27]
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Cysts of the vas deferens
Ductus deferens, formerly called vas deferens, is a muscular tube that transports sperm from epididymis to ejaculatory ducts. These cysts are seen along the ductus deferens and cranial to the prostate gland and posterior to the urinary bladder.[27] [28] On MRI, these are seen as well-defined T1 hypointense, T2 hyperintense fluid signal thin-walled cysts and are not easily confused with other differentials[26] [27] due to their location along the course of the ductus deferens.
Cowper's (bulbourethral) duct cysts
Cowper's glands are paired structures located on either side of the urogenital diaphragm at the level of the membranous urethra.[30] Secretions from each gland drain into individual ducts that join to form a single duct that empties into the proximal bulbar urethra.[31] The dilatation of the duct called syringocele is very rare and develops due to duct obstruction. Based on its communication with the urethra, it is divided into open type and closed type.[30] These can be congenital or acquired, and encountered more often in pediatric population. The majority of them are asymptomatic. Symptoms if present include recurrent UTIs, voiding problems, dysuria, and palpable perineal mass.[32] On imaging, these are seen as well-defined midline or paramedian cysts that appear anechoic on ultrasound and hyperintense on T2-weighted MRI, located posterior to the posterior urethra and inferior to the prostatic apex[27] ([Fig. 12]). Asymptomatic or mildly symptomatic cases are kept under surveillance and patients with severe symptoms are managed by endoscopic deroofing of the cyst. Other options include endoscopic/ open trans-perineal excision or ligation of the cyst[33]
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iii) Mimics of prostatic and periprostatic cysts
Ureteroceles, dilatation of the prostatic urethra after TURP, bladder diverticula, hydroureter and ectopic insertion of the ureter ([Fig. 13]) are mimickers of prostatic and periprostatic cysts and the differentiating features[2] [4] have been tabulated in [Table 3].
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Benign Neoplasms of Prostate and Seminal Vesicles
A wide variety of neoplasms, both benign and malignant can occur in the prostate and SV.[34] Malignant neoplasms are much more common than benign neoplasms, with acinar adenocarcinoma being the most common neoplasm. Benign neoplasms are of mesenchymal origin and constitute less than 1% of all tumors.[35] They generally are large lesions that cause nonspecific and chronic lower urinary tract symptoms. PSA levels will usually be normal in these neoplasms because PSA is produced by epithelial cells of the prostate, which enter the bloodstream when the blood epithelial barrier is destroyed.
Stromal Tumors of Uncertain Malignant Potential
Prostatic stromal tumors of uncertain malignant potential (STUMPs) are rare stromal tumors with unpredictable biological behavior. They are reported to occur in adults of any age, with the highest prevalence in the 6th to 7th decades.[34] Based on the histologic appearance, there are five patterns of STUMPs.[34] The most common pattern is a lesion with hypercellular stroma with scattered atypical but degenerative-looking cells admixed with benign prostatic glands. A distinctive pattern of STUMP is the phyllodes subtype, with a leaf-like growth pattern. Stromal tumors are positive for CD34 and progesterone receptors and uncommonly express estrogen receptors.
STUMPs commonly arise from the peripheral zone rather than the TZ of the gland and appear as a solitary, sharply circumscribed, solid or solid-cystic mass with solid areas showing T1 hypointense and T2 hyperintense signal ([Fig. 14]) on MRI.[36] The cystic component can be clear fluid, mucinous, or blood. A rim-like hypointense “capsule” is characteristically seen on T2-weighted images ([Fig. 14]). The solid components of the lesion show gradual enhancement on DCE-MRI. Large tumors may invade adjacent organs such as the rectum and there are case reports of metastases to the lungs and bones.[37] The differential diagnosis includes BPH nodules, cystadenoma ([Fig. 18]), sarcomas, and other mesenchymal lesions. Treatment of STUMP is complete surgical resection; however, they frequently recur (up to 65%).[37]
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Benign Nonstromal Mesenchymal Tumors
Benign non-stromal mesenchymal tumors arise from smooth muscle elements in prostatic stroma or peri glandular tissue. Leiomyoma, schwannoma, solitary fibrous tumor (SFT), inflammatory myofibroblastic tumor (IMT), and paragangliomas are benign mesenchymal tumors reported to arise from prostate and are very rare.[36] Generally, they have non-specific imaging features and need a biopsy for a definitive diagnosis. The differentiation between benign and malignant mesenchymal tumors also may be difficult unless there is definite evidence of local invasion or metastasis.
Leiomyoma arising within the gland can resemble the stromal nodule of BPH if it is small, though most of them are very large at presentation.[38] Imaging shows a well-defined, solitary, solid mass with predominantly homogeneous enhancement. At MRI, T1 and T2-weighted images have low signal intensity and homogeneous enhancement when small, but large lesion can be heterogeneous on T2 and postcontrast images due to necrosis ([Fig. 15]). Expression of smooth muscle actin and desmin confirms the diagnosis, while CD34 is negative, distinguishing it from STUMP.[39]
Schwannomas typically arising in the 4th to 6th decades are commonly sporadic. A smaller proportion can be associated with hereditary syndromes like neurofibromatosis type 2 and schwannomatosis.[40] On CT, sporadic schwannomas are typically well-circumscribed solitary oval masses with cystic changes, calcifications, and variable enhancement. MRI usually shows low T1 signal intensity, heterogeneous high T2 signal, and variable post contrast enhancement.[41] [42]
SFT originating from prostate is rare and have been reported previously among different age group ranging from 21 to 75 years. They are generally large lesions over 5 cm and may induce paraneoplastic syndromes like hypoglycemia (Doege-Potter syndrome) due to tumor-secreted insulin-like growth factor-2.[43] [44] On MRI, SFT appears hypointense on T1-weighted images and displays mixed heterogeneous signal intensity on T2-weighted images, dependent on collagen or other components. Gradual post enhancement is seen owing to fibrous content. Diffusion restriction may indicate areas of high cellularity ([Fig. 16]).[45] Surgical removal remains the primary treatment; however, recurrence is reported in 10 to 30% of cases.[46]
Prostate IMT has been reported between ages 21 to 83 years.[38] [47] They appear hypointense on T1-weighted images and mixed heterogeneous on T2-weighted images depending on fibrosis and inflammation. Contrast-enhanced CT and MRI can display avid, homogeneous, or heterogeneous enhancement.[36]
Prostate paragangliomas are rare tumors derived from extra-adrenal chromaffin cells in sympathetic or parasympathetic paraganglia. They can have sporadic or familial occurrences (linked to syndromes like MEN 2A/B, von Hippel-Lindau, neurofibromatosis type 1, Carney complex, and familial paraganglioma syndromes). Functioning types may exhibit catecholamine-related symptoms.[48] [49] In contrast to CT and MRI, paraganglioma appears as hyper enhancing lesion reflecting the richly vascularized nature of these tumors. At MRI, paragangliomas typically show marked T2 hyperintensity with classic salt-and-pepper appearance due to multifocal signal voids. They tend to have high signal intensity at high b-value DWI, but the signal on the ADC map is not reduced or only mildly reduced. PET imaging with 68Ga DOTATATE will show marked avidity.[49]
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Ectopic Prostate Tissue
Ectopic prostatic tissue (EPT) is defined as the presence of prostatic tissue at sites other than the prostate. It is mostly reported in the urethra and bladder and less commonly reported in the genital tract involving SV, epididymis, and testis.[50] [51] There are case reports of EPT described in other locations, including the bowel,[52] pelvis,[53] [54] and spleen.[55] The origin of this around the lower urinary tract is believed to be vestigial remnants of developmental migration, while other sites may involve metaplasia or misplacement of prostate glands during development.[51] Clinical manifestations of EPT in the lower urinary tract include hematuria or urinary obstruction. EPT in the rest of the sites is either asymptomatic or has non-specific symptoms.[51] Prostate hyperplasia and neoplasms developing in EPT have been reported.[51] [52] MRI shows the typical signal intensity of the prostate gland with or without hyperplasia and [Fig. 17] is an example of EPT in the right distal ureter. The symptomatic patients are managed surgically.
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Cystadenoma of the Prostate and Seminal Vesicle
Cystadenoma of the prostate and SV are rare benign multi-locular cystic tumors. Though the same nomenclature is used for both prostate and SV lesions, they are classified separately in the World Health Organization classification with some differences in pathology.[34] These lesions are reported in patients between 16 and 80 years and are usually large lesions measuring over 7 cm.[36] They cause obstructive and irritative urinary symptoms due to their large size. The serum PSA level is often elevated in prostate cystadenoma while always normal in SV cystadenoma. Histological examination shows cysts lined by cuboidal cells without atypia in the background hypocellular stroma.[34] Immunohistochemical staining will be positive for PSA and prostate-specific acid phosphatase in prostate cystadenoma while they are negative in SV cystadenoma. Imaging helps in determining the epicenter of lesion (prostate or SV). Apart from the difference in the epicenter of the lesion, the imaging characteristics of both prostatic and SV cystadenomas are similar and are seen as large well-encapsulated multi-locular cystic masses that may have minimal solid areas ([Figs. 18] and [19]).[56] The cyst contents can range from simple fluid, to non-simple hemorrhagic or proteinaceous fluid, and imaging can show fluid-fluid levels. Enhancement of the septa and solid components may be observed. Surgical resection of the lesion is curative.
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Conclusion
Imaging diagnosis and differential diagnostic considerations for Non-malignant prostatic and SV lesions are broad. Along with the imaging findings, we must consider the clinical context, past medical history, treatment history, current symptoms, age of the patient, clinical examination findings, and serum PSA level to provide an accurate diagnosis and logical differential diagnosis. Knowledge of these conditions can help us identify or suspect entities that may mimic clinically significant prostate cancer on mpMRI in the appropriate clinical setting.
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Conflict of Interest
None declared.
Acknowledgement
We sincerely acknowledge Departments of Urology and Infectious disease and the Uro-Oncology multi-disciplinary team (MDT) of Christian Medical College Vellore, India.
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- 13 Krieger JN, Dobrindt U, Riley DE, Oswald E. Acute Escherichia coli prostatitis in previously health young men: bacterial virulence factors, antimicrobial resistance, and clinical outcomes. Urology 2011; 77 (06) 1420-1425
- 14 Roberts RO, Lieber MM, Rhodes T, Girman CJ, Bostwick DG, Jacobsen SJ. Prevalence of a physician-assigned diagnosis of prostatitis: the Olmsted County Study of Urinary Symptoms and Health Status Among Men. Urology 1998; 51 (04) 578-584
- 15 Etienne M, Chavanet P, Sibert L. et al. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infect Dis 2008; 8: 12
- 16 Shigehara K, Miyagi T, Nakashima T, Shimamura M. Acute bacterial prostatitis after transrectal prostate needle biopsy: clinical analysis. J Infect Chemother 2008; 14 (01) 40-43
- 17 Shakur A, Hames K, O'Shea A, Harisinghani MG. Prostatitis: imaging appearances and diagnostic considerations. Clin Radiol 2021; 76 (06) 416-426
- 18 Ha US, Kim ME, Kim CS. et al. Acute bacterial prostatitis in Korea: clinical outcome, including symptoms, management, microbiology and course of disease. Int J Antimicrob Agents 2008; 31 (Suppl. 01) S96-S101
- 19 Inflammatory and Pain Conditions of the Male Genitourinary Tract: Prostatitis and Related Pain Conditions, Orchitis, and Epididymitis - ClinicalKey [Internet]. [cited 2023 Dec 11]. Accessed January 17, 2023 at: https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323546423000562?scrollTo=%23hl0000225
- 20 Haaga JR, Dogra VS, Forsting M, Gilkeson RC, Ha HK, , and Sundaram M. , eds. Mosby Elsevier; 2008
- 21 Shukla P, Gulwani HV, Kaur S. Granulomatous prostatitis: clinical and histomorphologic survey of the disease in a tertiary care hospital. Prostate Int 2017; 5 (01) 29-34
- 22 Naik KS, Carey BM. The transrectal ultrasound and MRI appearances of granulomatous prostatitis and its differentiation from carcinoma. Clin Radiol 1999; 54 (03) 173-175
- 23 Bour L, Schull A, Delongchamps NB. et al. Multiparametric MRI features of granulomatous prostatitis and tubercular prostate abscess. Diagn Interv Imaging 2013; 94 (01) 84-90
- 24 Nghiem HT, Kellman GM, Sandberg SA, Craig BM. Cystic lesions of the prostate. Radiographics 1990; 10 (04) 635-650
- 25 Shebel HM, Farg HM, Kolokythas O, El-Diasty T. Cysts of the lower male genitourinary tract: embryologic and anatomic considerations and differential diagnosis. Radiographics 2013; 33 (04) 1125-1143
- 26 Curran S, Akin O, Agildere AM, Zhang J, Hricak H, Rademaker J. Endorectal MRI of prostatic and periprostatic cystic lesions and their mimics. AJR Am J Roentgenol 2007; 188 (05) 1373-1379
- 27 Trivedi J, Sutherland T, Page M. Incidental findings in and around the prostate on prostate MRI: a pictorial review. Insights Imaging 2021; 12 (01) 37
- 28 Nakamura Y, Shida D, Shibayama T. et al. Giant multilocular prostatic cystadenoma. World J Surg Oncol 2019; 17 (01) 42
- 29 McDermott VG, Meakem III TJ, Stolpen AH, Schnall MD. Prostatic and periprostatic cysts: findings on MR imaging. AJR Am J Roentgenol 1995; 164 (01) 123-127
- 30 Takahashi H, Potretzke TA, Kawashima A, Cheville JC, Masuoka S, Kim B. Imaging of the Bulbourethral (Cowper) gland: abnormalities and differential diagnosis. Radiographics 2022; 42 (07) 2037-2053
- 31 Surana S, Elshazly M, Allam A, Jayappa S, AlRefai D. A case of giant Cowper's gland syringocele in an adult male patient. Case Rep Urol 2015; 2015: 682042
- 32 Wagemans MEHM, Tsachouridis G, Kuijper CF, de Mooij KL, Klijn AJ, de Jong TPVM. Cowper's syringocele in the pediatric population: a retrospective study of 122 patients. J Pediatr Urol 2019; 15 (05) 546-551
- 33 Melquist J, Sharma V, Sciullo D, McCaffrey H, Ali Khan S. Current diagnosis and management of syringocele: a review. Int Braz J Urol 2010; 36: 3-9
- 34 Moch H, Humphrey PA, Ulbright TM, Reuter V. WHO Classification of Tumours of the Urinary System and Male Genital Organs. Lyon, France: International Agency for Research on Cancer; 2016
- 35 Grignon DJ. Unusual subtypes of prostate cancer. Mod Pathol 2004; 17 (03) 316-327
- 36 Marcal LP, Surabhi VR, Ramani NS, Katabathina VS, Paspulati RM, Prasad SR. Mesenchymal neoplasms of the prostate and seminal vesicles: spectrum of disease with radiologic-pathologic correlation. Radiographics 2022; 42 (02) 417-432
- 37 Johnson MH, Carter HB. Stromal tumor of uncertain malignant potential (STUMP) with PSA >500 ng/ml: a case report. Urol Case Rep 2015; 3 (05) 175-177
- 38 Hansel DE, Herawi M, Montgomery E, Epstein JI. Spindle cell lesions of the adult prostate | Modern Pathology [Internet]. Accessed January 17, 2023 at: https://www.nature.com/articles/3800676
- 39 Virarkar M, de Castro Faria S, Patnana M, Zhang M, Sagebiel T. Leiomyoma of the prostate: case report and review of the literature. Clin Genitourin Cancer 2018; 16 (04) e771-e776
- 40 Zhang Y, Zhao J, Xu P, Qi Q. Multiple schwannoma of the seminal vesicle: a case report. Medicine (Baltimore) 2020; 99 (33) e21603
- 41 Rha SE, Byun JY, Jung SE, Chun HJ, Lee HG, Lee JM. Neurogenic tumors in the abdomen: tumor types and imaging characteristics. Radiographics 2003; 23 (01) 29-43
- 42 Seminal vesicle schwannoma presenting with left hydroureteronephrosis - PMC [Internet]. [cited 2023 Dec 11]. Accessed January 17, 2023 at:: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4216547/
- 43 Solitary Fibrous Tumor of the Prostate. A Case Report and Literature Review - PMC [Internet]. [cited 2023 Dec 11]. Accessed January 17, 2023 at:: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8621876/
- 44 Herawi M, Epstein JI. Solitary fibrous tumor on needle biopsy and transurethral resection of the prostate: a clinicopathologic study of 13 cases. Am J Surg Pathol 2007; 31 (06) 870-876
- 45 Ronchi A, La Mantia E, Gigantino V. et al. A rare case of malignant solitary fibrous tumor in prostate with review of the literature. Diagn Pathol 2017; 12 (01) 50
- 46 Tanaka Y, Nakamoto A, Inada Y, Narumi Y, Hirose Y, Azuma H. A case of malignant solitary fibrous tumor of the prostatic urethra. BJR Case Rep 2018; 4 (04) 20180034
- 47 McKenney JK. Mesenchymal tumors of the prostate. Mod Pathol 2018; 31 (S1): S133-S142
- 48 Pernick N. Adrenal gland and paraganglia. In: Yang XJ, Zhou M. eds. Practical Genitourinary Pathology. Cham, Switzerland: Springer; 2021: 273-287
- 49 Padilla-Fernández B, Antúnez-Plaza P, Lorenzo-Gómez MF, Rodríguez-González M, Martín-Rodríguez A, Silva-Abuín JM. Paraganglioma of prostatic origin. Clin Med Insights Case Rep 2012; 5: 69-75
- 50 Halat S, Eble JN, Grignon DJ. et al. Ectopic prostatic tissue: histogenesis and histopathological characteristics. Histopathology 2011; 58 (05) 750-758
- 51 Yeager TS, Stroh BC, Youssef RE, Michaels PJ. Ectopic prostatic tissue involving the omentum and presenting with intussusception and small intestinal obstruction: a report of a rare case with a review of the literature. Human Pathology Reports 2022; 30: 300679
- 52 Dai S, Huang X, Mao W. A novel submucosa nodule of the rectum: A case of the ectopic prostatic tissue outside the urinary tract. Pak J Med Sci 2013; 29 (06) 1453-1455
- 53 Roy C, Guth S, Gasser B. et al. Benign hyperplasia in ectopic prostatic tissue: a rare cause of pelvic mass. Eur Radiol 1997; 7 (01) 35-37
- 54 Fulton RS, Rouse RV, Ranheim EA. Ectopic prostate: case report of a presacral mass presenting with obstructive symptoms. Arch Pathol Lab Med 2001; 125 (02) 286-288
- 55 Vogel U, Negri G, Bültmann B. Ectopic prostatic tissue in the spleen. Virchows Arch 1996; 427 (05) 543-545
- 56 Han C, Zhu L, Liu X, Ma S, Liu Y, Wang X. Differential diagnosis of uncommon prostate diseases: combining mpMRI and clinical information. Insights Imaging 2021; 12 (01) 79
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- 11 Cheah PY, Liong ML, Yuen KH. et al. Chronic prostatitis: symptom survey with follow-up clinical evaluation. Urology 2003; 61 (01) 60-64
- 12 Krieger JN, Nyberg Jr L, Nickel JC. NIH consensus definition and classification of prostatitis. JAMA 1999; 282 (03) 236-237
- 13 Krieger JN, Dobrindt U, Riley DE, Oswald E. Acute Escherichia coli prostatitis in previously health young men: bacterial virulence factors, antimicrobial resistance, and clinical outcomes. Urology 2011; 77 (06) 1420-1425
- 14 Roberts RO, Lieber MM, Rhodes T, Girman CJ, Bostwick DG, Jacobsen SJ. Prevalence of a physician-assigned diagnosis of prostatitis: the Olmsted County Study of Urinary Symptoms and Health Status Among Men. Urology 1998; 51 (04) 578-584
- 15 Etienne M, Chavanet P, Sibert L. et al. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infect Dis 2008; 8: 12
- 16 Shigehara K, Miyagi T, Nakashima T, Shimamura M. Acute bacterial prostatitis after transrectal prostate needle biopsy: clinical analysis. J Infect Chemother 2008; 14 (01) 40-43
- 17 Shakur A, Hames K, O'Shea A, Harisinghani MG. Prostatitis: imaging appearances and diagnostic considerations. Clin Radiol 2021; 76 (06) 416-426
- 18 Ha US, Kim ME, Kim CS. et al. Acute bacterial prostatitis in Korea: clinical outcome, including symptoms, management, microbiology and course of disease. Int J Antimicrob Agents 2008; 31 (Suppl. 01) S96-S101
- 19 Inflammatory and Pain Conditions of the Male Genitourinary Tract: Prostatitis and Related Pain Conditions, Orchitis, and Epididymitis - ClinicalKey [Internet]. [cited 2023 Dec 11]. Accessed January 17, 2023 at: https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323546423000562?scrollTo=%23hl0000225
- 20 Haaga JR, Dogra VS, Forsting M, Gilkeson RC, Ha HK, , and Sundaram M. , eds. Mosby Elsevier; 2008
- 21 Shukla P, Gulwani HV, Kaur S. Granulomatous prostatitis: clinical and histomorphologic survey of the disease in a tertiary care hospital. Prostate Int 2017; 5 (01) 29-34
- 22 Naik KS, Carey BM. The transrectal ultrasound and MRI appearances of granulomatous prostatitis and its differentiation from carcinoma. Clin Radiol 1999; 54 (03) 173-175
- 23 Bour L, Schull A, Delongchamps NB. et al. Multiparametric MRI features of granulomatous prostatitis and tubercular prostate abscess. Diagn Interv Imaging 2013; 94 (01) 84-90
- 24 Nghiem HT, Kellman GM, Sandberg SA, Craig BM. Cystic lesions of the prostate. Radiographics 1990; 10 (04) 635-650
- 25 Shebel HM, Farg HM, Kolokythas O, El-Diasty T. Cysts of the lower male genitourinary tract: embryologic and anatomic considerations and differential diagnosis. Radiographics 2013; 33 (04) 1125-1143
- 26 Curran S, Akin O, Agildere AM, Zhang J, Hricak H, Rademaker J. Endorectal MRI of prostatic and periprostatic cystic lesions and their mimics. AJR Am J Roentgenol 2007; 188 (05) 1373-1379
- 27 Trivedi J, Sutherland T, Page M. Incidental findings in and around the prostate on prostate MRI: a pictorial review. Insights Imaging 2021; 12 (01) 37
- 28 Nakamura Y, Shida D, Shibayama T. et al. Giant multilocular prostatic cystadenoma. World J Surg Oncol 2019; 17 (01) 42
- 29 McDermott VG, Meakem III TJ, Stolpen AH, Schnall MD. Prostatic and periprostatic cysts: findings on MR imaging. AJR Am J Roentgenol 1995; 164 (01) 123-127
- 30 Takahashi H, Potretzke TA, Kawashima A, Cheville JC, Masuoka S, Kim B. Imaging of the Bulbourethral (Cowper) gland: abnormalities and differential diagnosis. Radiographics 2022; 42 (07) 2037-2053
- 31 Surana S, Elshazly M, Allam A, Jayappa S, AlRefai D. A case of giant Cowper's gland syringocele in an adult male patient. Case Rep Urol 2015; 2015: 682042
- 32 Wagemans MEHM, Tsachouridis G, Kuijper CF, de Mooij KL, Klijn AJ, de Jong TPVM. Cowper's syringocele in the pediatric population: a retrospective study of 122 patients. J Pediatr Urol 2019; 15 (05) 546-551
- 33 Melquist J, Sharma V, Sciullo D, McCaffrey H, Ali Khan S. Current diagnosis and management of syringocele: a review. Int Braz J Urol 2010; 36: 3-9
- 34 Moch H, Humphrey PA, Ulbright TM, Reuter V. WHO Classification of Tumours of the Urinary System and Male Genital Organs. Lyon, France: International Agency for Research on Cancer; 2016
- 35 Grignon DJ. Unusual subtypes of prostate cancer. Mod Pathol 2004; 17 (03) 316-327
- 36 Marcal LP, Surabhi VR, Ramani NS, Katabathina VS, Paspulati RM, Prasad SR. Mesenchymal neoplasms of the prostate and seminal vesicles: spectrum of disease with radiologic-pathologic correlation. Radiographics 2022; 42 (02) 417-432
- 37 Johnson MH, Carter HB. Stromal tumor of uncertain malignant potential (STUMP) with PSA >500 ng/ml: a case report. Urol Case Rep 2015; 3 (05) 175-177
- 38 Hansel DE, Herawi M, Montgomery E, Epstein JI. Spindle cell lesions of the adult prostate | Modern Pathology [Internet]. Accessed January 17, 2023 at: https://www.nature.com/articles/3800676
- 39 Virarkar M, de Castro Faria S, Patnana M, Zhang M, Sagebiel T. Leiomyoma of the prostate: case report and review of the literature. Clin Genitourin Cancer 2018; 16 (04) e771-e776
- 40 Zhang Y, Zhao J, Xu P, Qi Q. Multiple schwannoma of the seminal vesicle: a case report. Medicine (Baltimore) 2020; 99 (33) e21603
- 41 Rha SE, Byun JY, Jung SE, Chun HJ, Lee HG, Lee JM. Neurogenic tumors in the abdomen: tumor types and imaging characteristics. Radiographics 2003; 23 (01) 29-43
- 42 Seminal vesicle schwannoma presenting with left hydroureteronephrosis - PMC [Internet]. [cited 2023 Dec 11]. Accessed January 17, 2023 at:: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4216547/
- 43 Solitary Fibrous Tumor of the Prostate. A Case Report and Literature Review - PMC [Internet]. [cited 2023 Dec 11]. Accessed January 17, 2023 at:: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8621876/
- 44 Herawi M, Epstein JI. Solitary fibrous tumor on needle biopsy and transurethral resection of the prostate: a clinicopathologic study of 13 cases. Am J Surg Pathol 2007; 31 (06) 870-876
- 45 Ronchi A, La Mantia E, Gigantino V. et al. A rare case of malignant solitary fibrous tumor in prostate with review of the literature. Diagn Pathol 2017; 12 (01) 50
- 46 Tanaka Y, Nakamoto A, Inada Y, Narumi Y, Hirose Y, Azuma H. A case of malignant solitary fibrous tumor of the prostatic urethra. BJR Case Rep 2018; 4 (04) 20180034
- 47 McKenney JK. Mesenchymal tumors of the prostate. Mod Pathol 2018; 31 (S1): S133-S142
- 48 Pernick N. Adrenal gland and paraganglia. In: Yang XJ, Zhou M. eds. Practical Genitourinary Pathology. Cham, Switzerland: Springer; 2021: 273-287
- 49 Padilla-Fernández B, Antúnez-Plaza P, Lorenzo-Gómez MF, Rodríguez-González M, Martín-Rodríguez A, Silva-Abuín JM. Paraganglioma of prostatic origin. Clin Med Insights Case Rep 2012; 5: 69-75
- 50 Halat S, Eble JN, Grignon DJ. et al. Ectopic prostatic tissue: histogenesis and histopathological characteristics. Histopathology 2011; 58 (05) 750-758
- 51 Yeager TS, Stroh BC, Youssef RE, Michaels PJ. Ectopic prostatic tissue involving the omentum and presenting with intussusception and small intestinal obstruction: a report of a rare case with a review of the literature. Human Pathology Reports 2022; 30: 300679
- 52 Dai S, Huang X, Mao W. A novel submucosa nodule of the rectum: A case of the ectopic prostatic tissue outside the urinary tract. Pak J Med Sci 2013; 29 (06) 1453-1455
- 53 Roy C, Guth S, Gasser B. et al. Benign hyperplasia in ectopic prostatic tissue: a rare cause of pelvic mass. Eur Radiol 1997; 7 (01) 35-37
- 54 Fulton RS, Rouse RV, Ranheim EA. Ectopic prostate: case report of a presacral mass presenting with obstructive symptoms. Arch Pathol Lab Med 2001; 125 (02) 286-288
- 55 Vogel U, Negri G, Bültmann B. Ectopic prostatic tissue in the spleen. Virchows Arch 1996; 427 (05) 543-545
- 56 Han C, Zhu L, Liu X, Ma S, Liu Y, Wang X. Differential diagnosis of uncommon prostate diseases: combining mpMRI and clinical information. Insights Imaging 2021; 12 (01) 79
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