Prostatic atrophy: clinicopathological significance

Billis, Athanase

doi:10.1590/s1677-55382010000400003

Cited by 23 publications

(10 citation statements)

References 30 publications

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“…The peak frequency was in the seventh decade of life. It has been observed that prostatic atrophy commences during the 5th decade, with continued progression of the process into the 8th decade [8,46]. It has been suggested that there is a possible link between prostatic atrophy, high-grade prostatic intraepithelial neoplasia (HGPIN) and/or carcinoma [9].…”

Section: Discussionmentioning

confidence: 99%

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Incidence of Sub-Clinical Prostatic Disease at Autopsy in the University College Hospital, Ibadan

Okani¹,

Akang²,

Ogunbiyi

2013

OJU

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This prospective study was undertaken to ascertain the incidence, histology and pathological features of different types of asymptomatic or sub clinical prostatic diseases. Prostate glands were obtained from 79 consecutive adult males aged 30 years and above who died from non-prostate related diseases at the University College Hospital Ibadan over an eighteen months period. The glands were weighed and fixed in 10% neutral buffered formalin. The sampling method of the prostate gland described by Vainer et al. (2011) was employed in this study. Paraffin-embedded sections were stained with haematoxylin and eosin and were systematically examined for focal prostate disease. The patients’ ages ranged from 30 to 86 years. The most common lesions were nodular hyperplasia (81%), followed by adenocarcinoma (6.3%). Three cases (3.8%) had schistosomiasis. Adenocarcinoma and nodular hyperplasia occurred in relatively older patients than those with normal glands or chronic prostatitis/schistosomiasis (p = 0.05). There was an increase in weight of the prostate with age (p < 0.001) and normal prostate glands weighed significantly less than diseased glands (p = 0.02). Focal prostatic atrophy was observed in 24.1% and metaplastic changes were observed in eight (10.1%) of the cases. Prostatic intraepithelial neoplasia (PIN) was not seen in any case, not even amongst the adenocarcinomas. The low frequency of prostatic adenocarcinoma and the absence of high grade prostatic intraepithelial neoplasia in this study despite the observation of increasing number of prostatic carcinoma required further investigation. Schistosomiasis was also found to be present in the adult male population.

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Section: Discussionmentioning

confidence: 99%

“…It has been suggested that there is a possible link between prostatic atrophy and high-grade prostatic intraepithelial neoplasia (HGPIN) and/or carcinoma. However, the association between partial atrophy and HGPIN and carcinoma remains controversial [8,9].…”

Section: Introductionmentioning

confidence: 99%

Incidence of Sub-Clinical Prostatic Disease at Autopsy in the University College Hospital, Ibadan

Okani¹,

Akang²,

Ogunbiyi

2013

OJU

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“…prostatic carcinoma or precursor lesions. 14,15 Atrophy is typically found incidentally in various prostatic specimens. Although atrophy is common in the peripheral zone, it may also be seen in the central zone and in the transitional zone.…”

Section: Adenosis (Aah) Chronic Inflammation Sclerosing Adenosismentioning

confidence: 99%

Benign mimics of prostatic adenocarcinoma

Trpkov

2018

Modern Pathology

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Benign mimics present either as common challenges in daily routine practice or may cause diagnostic dilemmas because some are less commonly seen and one may be less familiar in recognizing them. There are a multitude of mimics of prostatic adenocarcinoma, which may represent normal gland structures, benign proliferations, atrophic lesions, hyperplastic or metaplastic changes, and inflammatory processes. Some of them are preferentially found in certain anatomic areas of the prostate, either confined to the prostate, or outside of the gland. Various benign mimics of prostatic carcinoma may be also evaluated based on their morphologic similarity to Gleason patterns 3-5 of prostatic adenocarcinoma. Most of the mimics are easily recognizable in larger specimens, such as TUR of the prostate or radical prostatectomy specimens, but they may pose diagnostic problems when the evaluation is done on limited tissue, such as needle-core biopsies or if prostate specimens are infrequently encountered in practice. Therefore, before signing out a report with a diagnosis of prostatic carcinoma, pathologists should carefully consider and rule out the various benign lesions that may mimic carcinoma. This is particularly relevant in the current prostate biopsy practice which relies on using extended biopsy core templates. The awareness and familiarity with the characteristic features of the mimics and judicial use of additional ancillary tests, including immunohistochemistry can prevent overdiagnosis and false-positive interpretation. This review provides a contemporary update on the broad spectrum of the benign prostatic lesions that can mimic prostate adenocarcinoma, outlines their key morphologic and immunohistochemical diagnostic features, and provides a diagnostic, pattern-based approach in establishing a correct diagnosis and distinguishing them reliably from prostatic adenocarcinoma.

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“…Prostate gland atrophy is another commonly occurring phenomenon with increasing age in prostate biopsy specimens. Prostate atrophy associated with chronic inflammation, especially the phenotype of proliferative inflammatory atrophy (PIA), has been linked to high-grade prostatic intraepithelial neoplasia and/or prostate carcinoma [59]. On the other hand, there is some limited evidence that baseline prostate atrophy (PA) is independently associated with a lower risk of prostate cancer [60,61].…”

Section: Resultsmentioning

confidence: 99%

Monoamine Oxidase Deficiency Causes Prostate Atrophy and Reduces Prostate Progenitor Cell Activity

Liu

Liao

et al. 2018

Stem Cells

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Monoamine oxidases (MAOs) degrade a number of biogenic and dietary amines, including monoamine neurotransmitters, and play an essential role in many biological processes. Neurotransmitters and related neural events have been shown to participate in the development, differentiation, and maintenance of diverse tissues and organs by regulating the specialized cellular function and morphological structures of innervated organs such as the prostate. Here we show that mice lacking both MAO isoforms, MAOA and MAOB, exhibit smaller prostate mass and develop epithelial atrophy in the ventral and dorsolateral prostates. The cellular composition of prostate epithelium showed reduced CK5 or p63 basal cells, accompanied by lower Sca-1 expression in p63 basal cells, but intact differentiated CK8 luminal cells in MAOA/B-deficient mouse prostates. MAOA/B ablation also decreased epithelial cell proliferation without affecting cell apoptosis in mouse prostates. Using a human prostate epithelial cell line, we found that stable knockdown of MAOA and MAOB impaired the capacity of prostate stem cells to form spheres, coinciding with a reduced CD133 /CD44 /CD24 stem cell population and less expression of CK5 and select stem cell markers, including ALDH1A1, TROP2, and CD166. Alternative pharmacological inhibition of MAOs also repressed prostate cell stemness. In addition, we found elevated expression of MAOA and MAOB in epithelial and/or stromal components of human prostate hyperplasia samples compared with normal prostate tissues. Taken together, our findings reveal critical roles for MAOs in the regulation of prostate basal progenitor cells and prostate maintenance. Stem Cells 2018;36:1249-1258.

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Prostatic atrophy: clinicopathological significance

Cited by 23 publications

References 30 publications

Incidence of Sub-Clinical Prostatic Disease at Autopsy in the University College Hospital, Ibadan

Incidence of Sub-Clinical Prostatic Disease at Autopsy in the University College Hospital, Ibadan

Benign mimics of prostatic adenocarcinoma

Monoamine Oxidase Deficiency Causes Prostate Atrophy and Reduces Prostate Progenitor Cell Activity

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