Miller et al. (1995) studied 20 men with prostatodynia/non-bacterial prostatitis and observed petechial haemorrhages on the bladder wall after hydrodistension under general anaesthesia. Signs of ”glomerulations” on the wall of the bladder after hydrodistension are thought to be diagnostic for interstitial cystitis (IC) (Elbadawi 1997). Miller et al. (1995) recommended that a diagnosis of interstitial cystitis should be considered for patients with a clinical diagnosis of non-bacterial prostatitis/prostatodynia if biopsies from the bladder mucosae showed increased numbers of mast cells. The role of mast cells in IC is unclear. In a recently published article, Berger et al. (1998) demonstrated bladder petechiae in 58% prostatitis cases, a much higher figure than expected.
Excessive numbers of mast cells have been demonstrated in TURP chips, and the similarities between interstitial cystitis in women and prostatitis in men have led investigators to conclude that many cases of prostatitis may be misdiagnosed as interstitial cystitis (Miller et al. 1995, Berger et al. 1998). On the other hand, it is also possible that some men with refractory non-bacterial prostatitis/prostatodynia indeed have interstitial cystitis (Berger et al. 1998, Meares 1998).
The exclusion criteria for CP/CPPS include the possibility of bladder cancer, and especially carcinoma in situ, with well-recognized irritative symptoms of bladder (frequency, urgency and dysuria). Involvement of the urothelium of the prostatic urethra can mimic the symptoms of chronic prostatitis, necessitating cystoscopy with proper biopsies (Schellhammer et al. 1995, Solsona et al. 1996, Montie et al. 1997, Luzzi & Cranston 2000).
Some speculations have been put forward concerning the possibility of prostatitis as a risk factor for prostate cancer. Serum PSA is the main diagnostic laboratory sign of a possible malignant process in the prostate gland (Polascik et al. 1999), but as an increase in PSA has been demonstrated in some cases of prostatitis, benign prostate hyperplasia and, of course, prostate cancer, they cannot be used as an absolute laboratory method for differentiating between these three main pathologies of the prostate gland (Nadler et al. 1995, Van Iersel et al. 1995, Pansadoro et al. 1996, Speights & Brawn 1996, Irani et al. 1997, Jung et al. 1998, Okada et al. 2000).
Prostatitis affects the more peripheral parts of the prostate (Blacklock 1974, Gardner and Bennet 1992, Bennet et al. 1993), and prostate cancer is also situated in the same area in most cases (Noldus & Stamey 1996). This problems was touched on by Hennenfent (1997), because there are many clinical cases suggesting a connection between prostatitis and prostate cancer, but what is missing is a population-based longitudinal survey concerning the possible higher prevalence of prostate cancer in prostatitis patients. Recently published PCR-based studies have raised speculations concerning the possible risk of prostate cancer developing out of a chronic inflammatory process (Riley et al. 1998, Keay et al. 1999, Hochreiter et al. 2000, Krieger et al. 2000c).
No prospective clinical studies are available to show any role of benign prostatic hyperplasia as an aetiological factor for the development of inflammation and prostatitis. The clinical knowledge available from the few published papers is based on retrospective studies and on histological findings based on prostate biopsies or surgically removed tissue (Kohnen & Drach 1974, Nickel et al. 1999a).
The true prevalence of histological prostatitis in the absence of other prostatic disease is very difficult to determine, for three reasons: firstly, most studies of prostatitis have used tissue from patients over 40 years old and the material has been obtained by surgery, secondly, the prostate tissue is altered by hyperplasia or the carcinoma process, which can contribute to the developement of inflammatory signs in it, and thirdly, the clinical definition of prostatitis is not uniform between investigators (Gardner & Bennett 1992, Bennett et al. 1993). The patients referred to had never been validated by clinical means to confirm or exclude the diagnosis of prostatitis, but they had always been investigated primarily by clinical means to find obstructive symptoms or to rule out possible malignancy in the prostate gland. With certain reservations, the prevalence of histologically confirmed prostatitis has been reported to be from 31% to 98% (Kohnen & Drach 1979, Melhorn 1987, Doble et al. 1989a, Nickel et al. 1999a) and even up to 100% (Schatteman et al. 2000).
Prostatic inflammation may exist in hyperplastic tissue of the prostate gland, and vice versa, and patients with obvious clinical symptoms of prostatitis and pain may have also signs of LUTS with or without BOO, as reported with frequencies from 11% (Mayo et al. 1998) to 54% (Kaplan et al. 1997), but the clinical relation between these two benign histological findings still has not been proved in a prospective study (Nickel et al. 1999a).