Differences in Pathological Features of Histological Inflammation Between Benign Prostatic Hyperplasia and Prostate Cancer

YANG Lu, ZHAO Kai, ZHANG Ao, LIU Liang-ren, LIU Zhen-hua, HAN Ping, WEI Qiang

Abstract

To study the pathologic features and differences of tissue inflammation in benign prostatic hyperplasia (BPH) and prostate cancer (PCa). Methods The HE stained slice obtained by prostate biopsy from 143 BPH and 106 PCa were reviewed to determine whether the tissue inflammation existed. According to the histological classification of prostatic tissue inflammation, the features of tissue inflammation and the differences of these features between the two groups were studied in detail. Results There were 142 cases found tissue inflammation in 143 BPH patients and 104 cases in 106 PCa patients, so the incidences of tissue inflammation in BPH and PCa were 99.3% and 98.1% respectively. The anatomical location of inflammation was significant difference between BPH and PCa group (P<0.05). The peri-glandular inflammation (56.3%) was primary in BPH, and interstitial inflammation (56.7%) was the main pattern in PCa. The inflammation range was also significant difference between the two groups (P<0.05). The inflammation was presented multifocally (60.6%) in BPH, and focal lesions (51.0%) was commonly found in PCa. Mild inflammation was most frequently observed in both groups (P>0.05). However, there were statistically significant differences between the two groups in the degree of moderate and severe inflammation (P<0.05). Conclusion The incidences of tissue inflammation were high in both BPH and PCa, but the pathological features of tissue inflammation were different between BPH and PCa.

 

Keywords: Prostatic hyperplasia, Prostate cancer, Tissue inflammation

 

Full Text:

PDF


References


Parsons JK. Benign prostatic hyperplasia and male lower urinary tract symptoms: epidemiology and risk factors. Curr Bladder Dysfunct Rep, 2010; 5 (4); 212-218.

Chughtai B, Lee R. Те A, et al. Inflammation and benign prostatic hyperplasia:clinical implications. Curr Urol Rep,2011; 12(4):274-277.

McLaren ID, Jerde TJ, Bushman W. Role of interleukins, IGF and stem cells in BPH. Differentiation,2011;82(4-5) :237-243.

Song L, Zhu Y, Han P, et al. A retrospective study correlation of histologic inflammation in biopsy specimens of Chinese men undergoing surgery for benign prostatic hyperplasia with serum prostate-specific antigen. Urology,2011;77(3);688-692.

Yi FX. Wei Q, Li H, et al. Risk factors for prostatic inflammation extent and infection in benign prostatic hyper¬plasia. Asian J Androl, 2006; 8(5); 621-627.

Liu L, Li Q. Han P, et al. Evaluation of interleukin-8 in expressed prostatic secretion as a reliablebiomarker of inflammation in benign prostatic hyperplasia. Urology, 2009; 74 (2):340-344.

De Nunzio C, Kramer G, Marberger M, et al. The controversial relationship between benign prostatic hyperplasia and prostate cancer:the role of inflammation. Eur Urol,2011; 60(1):106-117.

Nickel JC, True LD, Krieger JN, et al. Consensus development of a histopathological classification system for chronic prostatic inflammation. BJU International, 2001; 87 (9);797-805.

Parsons JK. Benign prostatic hyperplasia and male lower urinary tract symptoms; epidemiology and risk factors. Curr Bladder Dysfunct Rep, 2010; 5 (4): 212-218.

Cheng I, Witte JS, Jacobsen SJ, et al. Prostatitis, sexually transmitted diseases, and prostate cancer: the California Men’s Health Study. PLoS ONE,2010;5( 1):e8736.

Daniels NA, Ewing SK, Zmuda JM, et al. Correlates and prevalence of prostatitis in a large community-based cohort of older men. Urology ,2005; 66( 5); 964-970.

Gregory TM, Rosana E, Ranleigh LF, et al. The influence of chronic inflammation in prostatic carcinogenesis; a 5-year follow-up study. J Urol,2006; 176(3); 1012-1016.

Robert G, Descazeauda A, Allory Y, et al. Should we investigate prostatic inflammation for the management of benign prostatic hyperplasia? Eur Urol Suppl .2009;8(13):879- 886.

Cosimo DN, Gero K. Michael M. et al. The controversial relationship between benign prostatichyperplasia and prostate cancer: the role of inflammation. Eur Urol. 2011; 60 ( 1 ): 106- 117.

Alessandro S. Franco DS. Stefano S. et al. Inflammation and chronic prostatic diseases;evidence for a link, Eur Urol,2007; 52(4);964-972.

Martin NM.Dhillo WS, Banerjee A,et al. Comparison of the dexamethasone-suppressed corticotropin-releasing hormone test and low-dose dexamethasone suppression test in the diagnosis of Cushing’s syndrome. J Clin Endocrinol Metab,2006;91(7): 2582-2586.

Papanicolaou DA. Mullen N. Kyrou I. et al. Nighttime salivary cortisol; a useful test for the diagnosis of Cushing's syndrome. J Clin Endocrinol Metab,2002;87( 10);4515-4521.

Guaraldi F, Salvatori R. Cushing syndrome; maybe not so uncommon of an endocrine disease. J Am Board Fam Med. 2012;25(2):199-208.

Elamin MB. Murad MH, Mullan R, et al. Accuracy of diagnostic tests for Cushing syndrome; a systematic review and meta-analyses. J Clin Endocrinol Metab, 2008; 93 ( 5 ): 1553- 1562.

Reimondo G, Allasino B, Bovio S. et al. Evaluation of the effectiveness of midnight serum cortisol in the diagnostic procedures for Cushing’s syndrome. Eur J Endocrinol, 2005; 153(6);803-809.

Newell-Price J, Trainer P. Perry L, et al. A single sleeping midnight cortisol has 100% sensitivity for the diagnosis of Cushing’s syndrome. Clin Endocrinol, 1995;43(5) ;545-550.

Giraldi FP, Ambrogio AG, Martin M De, et al. Specificity of first-line tests for the diagnosis of Cushing ’ s syndrome; assessment in a large series. J Clin Endocrinol Metalb2007;92 (11);4123-4129.

Kyriazopoulou V, Vagenakis AG. Abnormal overnight dexamethasone suppression test in subjects receiving rifampicin therapy. J Clin Endocrinol Metab,1992;75( 1) ;315-317.

Nickelsen T, Lissner W, Schoffling K. The dexamethasone suppression test and long-term contraceptive treatment: measurement of ACTH or salivary cortisol does not improve the reliability of the test. Exp Clin Endocrinol, 1989; 94 ; 275- 280.

Meikle AW. Dexamethasone suppression tests; usefulness of simultaneous measurement of plasma cortisol and dexamethasone. Clin Endocrinol. 1982; 16( 4) ;401-408.

Chan КС, Lit LC, Law EL, et al. Diminished urinary free cortisol excretion in patients with moderate and severe renal impairment. Clin Chem,2004;50(4) :757-759.

Mericq MV, Cutler Jr GB. High fluid intake increases urine free cortisol excretion in normal subjects. J Clin Endocrinol Metab, 1998;83(2) ; 682-684.

DornLD.Lucke JF, LoucksTL, et al. Salivary cortisol reflects serum cortisol; analysis of circadian profiles. Ann Clin Biochem,2007;44(3) :281-284.

Poll EM, Kreitschmann-Andermahr I, Langejuergen Y,et al. Saliva collection method affects predictability of serum cortisol. Clin Chim Acta,2007;382( 1-2); 15-19.


Refbacks

  • There are currently no refbacks.