Tissue pressure measurement was used here for the first time to monitor the interstitial pressure of the prostate. It was postulated that pain, the leading symptom of patients with prostatitis, is caused by increased tissue pressure. In all three series, prostatic tissue pressures were significantly higher in the patients with prostatitis symptoms than in the controls.
This increased pressure may be due to local oedema in the prostate tissue, as the prostate is situated inside a compartmental system, surrounded by Denonvillier´s fascia, the endopelvic fascia and the anterior surface of the surgical capsule with puboprostatic ligaments (McNeal 1972, Blacklock 1974). The stroma of the prostate is rich in blood vessels, smooth muscle and sympathetic nerve fibres connected to baroreceptors and pain receptors (Dixon et al. 1999).
Similar findings of pathological processes associated with increased tissue pressure and pain are available in other parts and conditions of the human body, such as anterior tibial syndrome (Whitesides et al. 1975, Clayton et al. 1977, Mabee & Bostwick 1993, Witschger & Wegmüller 1994) and chronic pancreatitis (Ebbehøj et al. 1984, Ebbehøj et al. 1986). The compartmental syndrome represents a well-documented medical phenomenon, but it requires one obligatory physiological factor, namely increased tissue pressure. Despite the different aetiological backgrounds, the main symptom in all cases is pain, through local tissue damage, inflammation and oedema (Whitesides et al. 1975, Clayton et al. 1977, Ebbehøj et al. 1984, Ebbehøj et al. 1986, Mabee & Bostwick 1993, Witschger & Wegmüller 1994, Egan & Krieger 1997, Jaroma 2000).
The reason for pain, the increased tissue presure, can be evaluated by measuring the tissue pressure intracompartmentally, and there is consensus that if the interstitial tissue pressure reaches 40 mmHg some functional changes can be found and if it rises to 50–60 mmHg or 10–30 mmHg below the diastolic blood pressure and is present constantly over 6–12 hours, tissue damage is unvoidable (Whitesides et al. 1975, Gelberman et al. 1983, Ebbehøj et al. 1984, Ebbehøj et al. 1986, Witschger & Wegmüller 1994).
The present results showed that it is possible to measure intraprostatic tissue pressure with the Stryker® device without complications, and that the intraprostatic tissue pressure is high in patients with typical symptoms of chronic non-bacterial prostatitis. Pressure readings taken in the normal prostate tissue of men without symptoms 10 seconds after injection showed values below 40–50 mmHg and that for men with CP/CPPS over 60–70 mmHg. Meanwhile, the prostatic tissue end pressures after 120 seconds dropped to the physiological level (15–30 mmHg) in control men but remained higher than normal (over 40 mmHg) in the CPPS patients, thus pointing indirectly to microcirculation disturbances at some level in the capillary network of the prostatic tissue. The results showed that prostatitis patients belonging to clinical category IIIA developed a higher tissue pressure than patients belonging to category IIIB (p<0.001). This may reflect more severe inflammation, leading to disturbances in microcirculation and tissue damage, with a consequent scarring process (Guyton et al. 1971, Asthon 1975, Clayton et al. 1977, Mabee & Bostwick 1993, Jaroma 2000). Inflammation disturbs the regulatory mechanisms through the production of albumin-related products, and the osmotic pressure can temporaryly reach very high readings, causing oedema, with consequent pain in prostatitis patients (Krieger et al. 1996b, Egan & Krieger 1997). These results support the theory that reactions to microcirculation disturbances in closed compartmental spaces (including the prostate gland) can cause pain, as in other organs with a thick multilayer musculo-fibrotic capsule (Blacklock 1974, Patel & Rickards 1994, Cho et al. 2000). This provides an explanation for the physiological and histological changes to be found in the prostate tissue afterwards (Gardner & Bennett 1992, Bennet et al. 1993, Dixon et al. 1999).
No attempt has been made so far by others to verify the present findings of increased tissue pressure in patients with chronic prostatitis. Some indirect support can be derived from the work of Hegarty et al. (2000), however, who showed under cell culture conditions that increased prostate tissue pressure (over 80 mmHg) induced apoptosis of cells from BPH patients. There are also some critical points related to the PTPM approach. Proper placement of the needle in the prostate and careful setting and exact prefilling of the Stryker® device according to the manufacturer’s instructions are necessary for reliable measurements. The measurement procedure must also be carried out correctly in order to avoid failures and erroneous results. The time must be followed punctually, otherwise the results will not be comparable, and the needle position must be checked by TRUS if there is any suspicion of incorrect placement. The test PTPM procedure has proved slightly invasive, and spinal anaesthesia was used in all the examinations. There is a need to develop the test so that it would be more convenient and suitable for outpatient use.
The NIH-CPSI questionnaire (Litwin et al. 1999) has been developed to assess reliably the severity of symptoms in CP/CPPS patients when different investigators are involved and to follow-up the efficacy of treatment. It was translated into Finnish and validated in 1999 and the results of the first experiences with its use were reported by the author at the III International Chronic Prostatitis Workshop in Bethesda, Washington in October 2000 (Mehik et al. 2000). So far the results of only one survey, published by Shoskes et al. (1999), have been available for comparing the severity of prostatitis symptoms using this new tool. They reported total NIH-CPSI scores averaging 20.6 (range 12–39), while the average total score in the present study was 19.7 (range 17–22). Likewise, their pain score average was 8.9 (range 5–17) and the present figure 9.9 (range 8–11), their voiding score 3.0 (range 1–11) and the present score 3.3 (range 2–4), and their quality of life score averaged 7.9 (range 3–12), compared with the present 6.5 (range 5–7). We may preliminarily conclude that the patients in these two separate series had symptoms of the same subjective severities as measured in terms of their NIH-CPSI scores and could possibly be compared with each other despite their different surroundings (California, USA vs Oulu, Finland).
The present clinical-microbiological diagnosis of prostatitis by means of the Meares-Stamey four-glass test (Meares & Stamey 1968) or Nickel´s pre-massage and post-massage test (Nickel 1997, Nickel 1998b, Ludwig et al. 2000) can assess the severity of inflammation by microscopy of the expressed prostatic secretion and/or post-voided urine, but the tests are unfortunately not 100% reliable (Krieger et al. 2000b, Lacquaniti et al. 2000, Ludwig et al. 2000, Strohmaier & Bichler 2000), and therefore PTPM constitutes one extra valid tool for differential diagnosis in order to confirm the laboratory findings or categorize prostatitis patients (especially to distinguish between those of types IIIA and IIIB). When laboratory findings and PTPM are normal, the patient very probably has pain originating in some other site in the pelvis. All this can reduce the use of antibiotics, which is now the norm rather the exception even without any clinical reason or any evidence of bacteria in the prostatic fluid and/or urine (de la Rosette et al. 1992a, Moon 1997, Nickel et al. 1998).