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 ::  Abstract
 ::  Introduction
 ::  Material and methods
 ::  Results
 ::  Discussion
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Year : 1989  |  Volume : 35  |  Issue : 3  |  Page : 157-61

Spectrum of histological lesions in 185 consecutive prostatic specimens.

Correspondence Address:
B V Mittal

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Source of Support: None, Conflict of Interest: None

PMID: 0002483935

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 :: Abstract 

One hundred and eighty five consecutive prostate specimens were studied. The predominant lesion noted was benign prostatic hyperplasia (B.P.H.) (92.97%). The incidence of carcinoma was low, (7.02%). Conditions which can mimic and should be considered in the differential diagnosis of carcinoma, like basal cell hyperplasia, atypical hyperplasia and atrophy associated hyperplasia were noted in 10, 4 and 3 cases of B.P.H. respectively. None of these cases showed evidence of carcinoma. Corpora amylacea were noted in 38.91% of the cases of B.P.H. and were conspicuously absent in cases of carcinoma. Chronic prostatitis was frequently encountered (58%) and metaplastic changes were seen in 11% of the cases.

Keywords: Adult, Aged, Aged, 80 and over, Carcinoma, Basal Cell, classification,complications,diagnosis,Diagnosis, Differential, Human, Male, Middle Age, Prostatic Hyperplasia, complications,diagnosis,Prostatic Neoplasms, complications,diagnosis,

How to cite this article:
Mittal B V, Amin M B, Kinare S G. Spectrum of histological lesions in 185 consecutive prostatic specimens. J Postgrad Med 1989;35:157

How to cite this URL:
Mittal B V, Amin M B, Kinare S G. Spectrum of histological lesions in 185 consecutive prostatic specimens. J Postgrad Med [serial online] 1989 [cited 2023 Oct 4];35:157. Available from:

 :: Introduction Top

Benign hyperplasia and carcinoma of the prostate are increasingly frequent with advancing age. Prostatic specimens thus constitute a good percentage of surgical pathology work load. This prompted us to investigate the spectrum of lesions in 185 consecutive prostatic specimens.

 :: Material and methods Top

One hundred and eighty five consecutive prostatic specimens were analysed. There were 86 prostatectomy specimens, 81 were trans-urethral resections and 18 needle biopsies. The clinical case histories were scrutinised. All the specimens were fixed in 10% buffered formalin and 5 sections were stained with haematoxylin and eosin. Toluidine blue stain was carried out whenever indicated.

Various histological lesions were listed and the carcinomas were classified according to the WHO classification and Gleason's grading system.[2]

The following patterns were recorded:

1. Benign prostatic hyperplasia (BPH):

(a) predominantly adenomatous

(b) predominantly fibromuscular

(c) both components equally present

2. Carcinoma (Ca) : The criteria are loss of normal architecture, cellular atypism and invasion of perineural spaces and blood vessels. When invasion of fibromuscular stroma is clearly evident, it is accepted as a criterion of malignancy.

3. Atypical glandular hyperplasia (AGH): i.e. prostate shows atypical glands with slight or moderate cellular atypia, but without conclusive evidence of invasive growth.

4. Atrophy associated hyperplasia (AAH): Epithelial proliferation associated with broad bands of sclerotic stroma and atrophic glands. Newly formed glands are elongated, distorted and are lined by a single layer.

5. Basal cell hyperplasia (BCH): Small nests of uniform cells with scanty cytoplasm forming solid nests and acinar structures with a strong affinity for toluidine blue.

 :: Results Top

Age distribution of the cases is depicted in[Table - 1].

BPH - Benign prostatic hyperplasia. Ca - Carcinoma.

BCH - Basal cell hyperplasia. AGH - Atypical glandular hyperplasia.

AAH - Atrophy associated hyperplasia.

BPH was the most frequent finding and was observed in 92.97% (172/185) of cases. Majority of the cases, 55.62% (103/185) showed adenomatous hyperplasia along with fibromuscular hyperplasia. These prostates were very firm. In one case leiomyomatous proliferation of smooth muscle fibres arranged in a whorling fashion was noted. Four cases revealed focal areas resembling fibroadenomatous pattern [Figure - 1].

Carcinoma of the prostate was observed in 13 cases (7.02%). None of these cases were below the age of 50 years. Two cases of carcinoma revealed BPH in the adjacent parenchyma. Associated chronic prostatitis was noted in one case.

Carcinomas were classified according i o the WHO classification.[11] There were 7 cases of small acinar carcinoma, one case of large acinar carcinoma and 5 cases had a solid or trabecular pattern.

Gleason's system of grading the carcinomas was employed. Most frequent grade in the primary pattern was the severe grade, i.e. grade V in 5 cases. Grade I [Figure - 2] was seen in only one case, while the remaining cases were grade II to III. Secondary pattern was usually of a lower grade. However, in 4 cases the material available was scanty (needle biopsy material) and hence only a single type of pattern was visualised.

Focal basal cell hyperplasia was noted in 10 cases of BPH [Figure - 3]. Small, uniform cells arranged in small nests and acinar pattern with an affinity for toluidine blue stain were noted in all these cases. There was no cellular atypia.

Atypical glandular hyperplasia (AGH) was noted along with BPH in 4 cases. These lesions were small and multifocal in 2 cases. All these cases were in the age group of 55-65 years. In 7 cases of BPH, atrophy associated hyperplasia (AAH) was present. Neither the cases of AGH nor AAH revealed presence of carcinoma.

Two cases of BPH revealed seminal vesicle inclusion and one case, Cowper's gland.

Metaplastic changes in the glandular lining epithelium was a common finding. Transitional metaplasia was the commonest, seen in 7.02% (13/185) cases; followed by squamous metaplasia, noted in 3.24% (6/185) of the cases. In 2 cases (1.08%), both squamous and transitional metaplasia were .noted. Care was taken to exclude the periurethral glands which can normally have a transitional lining. All the metaplastic changes were benign.

Corpora amylacea were noted in 38.91% (72/185) of the cases. Only 2 cases had abundant numbers of corporae, 14.59% showed a moderate number, while the majority of the cases (23.24%) showed an occasional corpora amylacea.

None of the cases with carcinoma revealed the presence of corpora amylacea. Prostatitis was observed in 107 cases (57.83%). Majority of the cases showed chronic non-specific inflammation characterised by lymphocytic infiltration (38.37%), but in 3 cases (1.6%) granulomatous inflammation was noted. Acute inflammation was noted in 13 cases (7.02%). In 20 cases (10.81%) it was accompanied by chronic inflammation.

Glandular secretions were noted in 74.05% (137/185) of the cases. Majority of the cases (45.5%, 84/185) showed scanty luminal secretions, while 23.78% (44/185) showed moderate amount of secretions, and 7 cases (3.78%) revealed excessive secretions. In the carcinoma group, of the 8 cases with small and large acinar carcinoma, 7 showed scanty secretions, and 1 showed moderate secretions.

 :: Discussion Top

Prostatism is a common malady in the geriatric age group. Benign hyperplasia and carcinoma of the prostate are increasingly frequent with advancing age and are uncommon before the age of 40.[4],[5] Harbitz and Haugen[7] noted benign hyperplasia in 80% of the men over 40 years of age. In our series of 185 cases, BPH was the predominant lesion, noted in 92.97% of the cases. This figure includes those cases in which BPH occurred together with any of the other lesions like carcinoma, atypical hyperplasia, atrophy associated hyperplasia or basal cell hyperplasia. BPH alone was noted in 74.59% of the cases. Majority of the cases were encountered in the 6th and 7th decade. The decline in the number of cases beyond the age of 80 years may reflect the average life span of people in our country which rarely exceeds beyond the 6th decade.[2] Majority of the cases of BPH showed hyperplasia involving both fibromuscular and adenomatous components. Amongst 19 cases showing a predominantly fibromuscular hyperplasia, one case showed a leiomyomatous nodular lesion. In 4 cases, focal areas showing fibroadenomatous pattern amidst nodular hyperplasia of prostatic glands were seen. Elbadawi[3] described a type of prostatic hyperplasia that he referred to as `fibro-adenoid'. He considered it to be an uncommon lesion that closely resembled fibro-adenoma of the breast. Kafandaris and Polyzonis[8] reported 12 lesions characterised by focal areas of stromal and glandular hyperplasia without cytologic atypia, reminiscent of the pericanalicular and intracanalicular configuration of the fibroadenomas of the breast, amidst benign nodular proliferation of the prostate. Our cases were very similar to these.

The incidence of carcinoma of the prostate was 7.02%. This is rather low compared to most reported series. The incidence of prostatic carcinoma increased with age. Harbitz and Haugen[7] noted that 50% of their 70 cases of carcinoma of the prostate were above the age of 80 years. It is pertinent to note that of the 185 cases that we studied, only 9 cases were above that age. This is due to the lower life expectancy of our population.[2] Direct comparison of total rates of prostatic carcinoma in different series may be misleading. There is a great discrepancy between the high frequency of prostatic carcinoma revealed at autopsy and the occurrence of carcinoma which has been clinically suspected (clinically manifest carcinoma). In clinically manifest carcinoma, the tumour is generally larger than in the latent one, but the histological features are essentially the same.

There were 13 cases of carcinoma of the prostate. Small acinar carcinoma pattern was found to be the most frequent (7 cases) followed by solid and trabecular pattern (5 cases).

We followed the Gleason's systems of grading prostatic carcinoma. In his experience this grading system revealed a very good correlation between the grades and the survival rates. It is essential to have a follow-up of the cases to correlate the grading with the survival rates. In our series follow-up was not available. Prostatectomy followed by orchidectomy was the mode of therapy and these cases were later lost to follow-up. However grading also predicts the biologic behaviour of the cases, hence we graded the tumours. Majority of our cases showed moderate to poor differentiation while only 1 case was well differentiated.

The relation between benign hyperplasia of the prostate and prostatic cancer has been controversial since the earliest description of these tumours. The finding at necropsy of prostates with carcinoma having a higher frequency of nodular hyperplasia than matched controls as well as reports of similar urine profiles of hormonal metabolites in patients with prostatic cancer and BPH compared with age matched controls might suggest that patients with BPH might be especially at risk for prostatic cancer.[10] However, of the 13 cases with carcinoma of the prostate in our series, only 2 cases showed BPH in the adjacent parenchyma.

Franks[4] had shown cancer to be arising from atrophic glands. None of our 13 cases with cancer showed presence of atrophy associated hyperplasia. Similarly, of the 7 cases of atrophy associated hyperplasia, none revealed any evidence of carcinoma.

Kastendick[9] had shown that 89.5% of the cases of well differentiated carcinoma had atypical hyperplasia. We had 4 cases of AGE associated with BPH. But none revealed any carcinoma.

Basal cell hyperplasia of the prostate is a rare, benign lesion that often has been misdiagnosed as adenocarcinoma. Two cell types are found within the glandular acini of human prostate. The basal and secretory cells can be distinguished at light microscopy by their different affinity for toluidine blue. Toluidine blue exhibits a strong affinity for basal cells, while secretory cells are poorly stained. In BPH, toluidine blue stained basal cells commonly form a single layer which rests on the basement membrane of glands. All the 13 reported cases by Cleary et al[1] were above the age of 60 years and all had BPH in addition to basal cell hyperplasia. Histologically small rests of uniform small cells with scant cytoplasm forming solid nests and acinar structures were noted. No evidence of nuclear atypia or pleomorphism has been reported. These cells had a strong affinity for toluidine blue. We had 10 cases of BCH, 8 cases were above the age of 60 years, with 2 cases in the 6th decade. There was no correlation between the cases of BCH and carcinoma.

Metaplastic transitional and squamous epithelium was noted in 11.35% of the cases. However all these changes were benign. These foci can at times be the source of transitional or squamous carcinomas in the prostate.

The prostatic epithelium enzymatically splits corpora amylacea from a Bence Jones like protein which it synthesizes. In the normal and benign prostatic enlargement, the enzyme machinery is functional resulting in the formation of corpora. In the neoplastic cells, the necessary enzyme machinery is lacking which can explain the rarity of corpora amylacea in the neoplastic prostatic glands. Corpora were noted in 72/172 of the cases of BPH. None of the cases of carcinoma of prostate showed presence of corpora amylacea.

Chronic prostatitis alone or complicating acute prostatitis was commonly found in association with BPH. Of particular interest were 3 cases of granulomatous prostatitis. Acute infection with or without abscess formation was noted in 12.14% of the cases.

Thus in conclusion, the commonest pathology encountered in the prostates studied was BPH (92.97%). Incidence of carcinoma was low (7.02%). Lesions like AGH, AAH and BCH were infrequent and had no correlation with the carcinomas. Prostatitis was encountered in a large number of cases and associated metaplastic change was seen in 11%.

 :: References Top

1.Cleary, K. R., Choi, H. Y. and Ayala, A. G.: Basal cell hyperplasia of the prostate. Amer. J. Clin. Pathol., 80: 850-854, 1983.  Back to cited text no. 1    
2.Directorate General of Health Services Ministry of Health and Family Welfare Government of India: Health Statistics of India. Ministry of Health and Family Welfare, New Delhi 1983.  Back to cited text no. 2    
3.Elbadawi, A.: Pathology: II. Proliferative lesions and neoplasms. In, "Male Accessary Sex Glands." Editors: E. Spring-Mills and E. S. E. Hafez, Elsevier Science Publishing Co. Inc. New York, 1980. Quoted by Manivel, C., Shenoy, V. Wick, H. R. and Dehner, L. P.: Cystosarcoma phyllodes of the prostate-a pathologic and immunohistochemical study. Arch. Patho. Lab. Med., 110: 534-538, 1986.  Back to cited text no. 3    
4.Franks, L. M.: Benign nodular hyperplasia of prostate: review. Ann. Roy. Coll. Surg. England, 14: 92-106, 1954.  Back to cited text no. 4    
5.Franks, L. M.: Latent carcinoma of prostate. J. Pathol. Bacteriol., 68: 603-616, 1954.  Back to cited text no. 5    
6.Gleason, D. F. and Mellinger, G. T.: Veterans Administration Cooperative Urological Research Group: Prediction of prognosis for prostatic adenocarcinoma by combined histological grading and clinical staging. J. Urol., 111: 58-64, 1974.  Back to cited text no. 6    
7.Harbitz, T. B. and Haugen, O. A.: Histology of the prostate in elderly men. A study in an autopsy series. Acta Pathol. Microbiol. Scand. Section A. 80: 756-768, 1972.  Back to cited text no. 7    
8.Kafandaris, P. M. and Polyzonis, M. B.: Fibroadenoma-like foci in human prostatic nodular hyperplasia. Prostate, 4: 33-36, 1983.  Back to cited text no. 8    
9.Kastendieck, H. and Altenahr, E.: Cytoand histomorphogenesis of the prostate carcinoma. A comparative light-and electron-microscopic study. Virchows Arch. Pathol. Anat., 370: 207-224, 1976.  Back to cited text no. 9    
10.Marmorston, J., Lombardo, L. J. Jr., Myers, S. M.. Gierson, H., Stern, E. and Hopkins, C. E.: Urinary excretion of neutral 17-Ketosteroids and pregnanediol by patients with prostatic cancer and benign prostatic hypertrophy. J. Urol., 93. 276-286, 1965.  Back to cited text no. 10    
11.Mostofi, F. K., Sesterhenn, I. and Sobin. L. H.: Histological typing of prostate tumours. In, "The International Histological Classification of Tumours". No. 22, World Health Organisation, Geneva, 1980.  Back to cited text no. 11    


[Figure - 1], [Figure - 2], [Figure - 3]


[Table - 1]

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2004 - Journal of Postgraduate Medicine
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