Year : 2000 | Volume
: 17 | Issue : 1 | Page : 61--62
Basal cell hyperplasia of prostate - an entity a urologist must know
Suresh Bhat, Appu Thomas, M Nazar, George C Joseph, Dharmaraj
Department of Urology, Medical College, Kottayam, India
Deptartment of Urology, Medical College, Kottayam - 686 008
We report 2 cases of basal cell hyperplasia of prostate, which is an uncommon and elusive lesion. It is commonly associated with benign prostatic hyperplasia (BPH) and may sometimes be mistaken for malignancy. The knowledge about this disease helps in the correct diagnosis and avoidance of unnecessary or overtreatment.
|How to cite this article:|
Bhat S, Thomas A, Nazar M, Joseph GC, Dharmaraj. Basal cell hyperplasia of prostate - an entity a urologist must know.Indian J Urol 2000;17:61-62
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Bhat S, Thomas A, Nazar M, Joseph GC, Dharmaraj. Basal cell hyperplasia of prostate - an entity a urologist must know. Indian J Urol [serial online] 2000 [cited 2021 Sep 22 ];17:61-62
Available from: https://www.indianjurol.com/text.asp?2000/17/1/61/41024
A 25-year-old male presented with low back ache, suprapubic pain and mild dysuria of about 1-year's duration. His voiding was normal. Except for a similar episode about 3 years prior to this which was treated with a course of antibiotics, he had no significant past illness. Physicals were negative. Digital rectal examination showed a firm grade 1 enlargement of the prostate. Lab investigations were normal. Urine culture, urine AFB culture were normal. X-ray KUB and ultrasonography of upper urinary tract were normal. Prostatic biopsy revealed basal cell hyperplasia [Figure 1]. Patient was treated with a course of antibiotics for 1 month. Followed up at 3 years, he remained asymptomatic.
This 72-year-old man was referred following acute retention of urine. On digital rectal examination a firm nodular prostate was felt. Serum PSA was within normal limits. He underwent TURP. Histopathological examination of the specimen showed benign prostatic hyperplasia with basal cell hyperplasia.
The prostatic epithelium in the human is composed of 3 major cell types: epithelial cells, basal cells and neuroendocrine cells. The basal cells are small and round with a scanty cytoplasm but with dark nuclei. They are less differentiated and almost devoid of secretory products. They are rich in keratin (types 4,5,6) and constitute less than 10% of epithelial cell numbers. They are situated in between the secretory cells and rest on the basement membrane. The plasma membrane is rich in ATPase suggesting that these cells may be involved in active transport. They produce basemant membrane. Prostatic basal cells do not display myo-epithelial differentiation in contrast to basal cells in the breast, salivary glands, pancreas, etc. Its role in the production of the secretory cells is still controversial.  Basal cells are negative for prostate specific antigen (PSA) and prostatic acid phosphatase (PAP). Basal cell proliferation in the prostate gland exhibits a morphologic continuum ranging from focal basal cell hyperplasia (BCH) in the setting of nodular hyperplasia to florid adenoid basal cell tumor (ABCT). These diverse proliferations have been referred to by many names including fetalisation of prostate, embryonal hyperplasia, basal cell tumour, basal cell adenoma, basaloid carcinoma, adenoid cystic carcinoma etc.
BCH of the prostate may present as one of 2 types: small nests of basal cells or larger cellular aggregates which mimic more aggressive tumors.  Typical BCH consists of a proliferation of basal cells 2 or more cell layers thick at the periphery of prostate glands and acini. Frequently the proliferation may be more than 2-cell-layers thick protruding into the acinar lumen. The hyperplastic cells are larger than the usual cells. They are surrounded by a few concentric layers of compressed stroma, often associated with chronic inflammation. The nests vary from solid to cystically dilated glands. Small foci of BCH often occur within hyperplastic acini but are rarely noticed unless florid. Large areas of BCH occur as closely packed nests and often suggest the possibility of carcinoma especially, since basal cells commonly have recognizable nucleoli. This concern is enhanced when the lesion fails to react with PSA & PAP, atypical nuclei are present in its cells, or the margins of the hyperplastic nests are poorly demarcated in suboptimally preserved tissue. In contrast to most cases of transitional cell hyperplasia, BCH occurs in terminal ducts & acini of peripheral glands & its cells often exhibit a perpendicular orientation to the basement membrane. BCH frequently involves only part of the gland & occasionally protrudes into the lumen. In the largest series of BCH described by Cleary et al  all patients were above 60 years and had BPH in addition to BCH. 2 patients had concomitant carcinoma prostate foci. One of our cases is of interest in that the patient was young and had no voiding problems. The prostate felt firm on DRE. BCH is most often seen as a secondary change in benign prostatic hyperplasia (BPH). In BPH, the BCH is seen at the margin of the nodule and infarcts. Other associated lesions include chronic inflammation, calcification, clear cell changes and squamous metaplasia.  All the cells in BCH display intense cytoplasmic immunoreactivity with keratin 34 beta E 12.  As acini of prostatic adenocarcinoma lack basal cells, this staining is useful in confirming the diagnosis of Ca prostate. Normal prostatic basal cells do not display immunoreactivity for PSA, PAP or S-100 Protein. Young et al  and Jacobs et all have reported concomitant BCH and carcinoma prostate.
The differential diagnosis of BCH includes transitional cell hyperplasia, squamous metaplasia, transitional cell carcinoma of the prostate, adenocarcinoma of prostate and, adenoid cystic carcinoma of prostate. 
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