I.9.2 Prostatitis Key Messages

217
I.9.2 Prostatitis
M.C. Bishop
Key Messages
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Acute prostatitis is a well-defined infective
condition caused by standard uropathogens.
Antibiotic treatment may need to be supplemented by surgery to deroof abscesses and
release calculi.
No more than 5 % of patients with chronic
prostatitis have unequivocal infection in the
urinary tract.
The majority of the remainder suffer from
chronic pelvic pain syndrome (CPPS; new
terminology NIH Category IIIA and B).
In a minority of CPPS cases, inflammatory
cells can be identified in expressed prostatic
secretion, postmassage urine, seminal fluid or
in prostate biopsy samples.
Prostatic localization tests are not recommended beyond the research clinic.
New molecular analytical techniques are likely
to clarify the link between infection, possibly
by fastidious or unusual organisms, inflammation and symptoms of chronic prostatitis.
Whatever the cause of CPPS, it is likely that
treatment aimed at pain management of
increasing sophistication will be required to
supplement or even replace conventional treatments (antibiotics, nonsteroidal anti-inflammatory agents, alpha-blocking drugs, etc.).
I.9.2.1
Introduction
The early classification of prostatitis described four
syndromes for which pelvic pain in the male was the
common factor (Drach et al. 1978) (Table I.9.1). The
occasional association of lower urinary tract symptoms
with the common sign of prostatic tenderness was reassuring, indicating that the condition generically was due
to inflammation in the prostate. Having established this
commonality, it was then possible to discern that chronic prostatitis was the commonest reason for specialist
urological referral in men under 50, with a prevalence in
males in the same age group of approximately 10 %
(Schaeffer 2003). Furthermore, its devastating effect on
the quality of life could be compared with unstable angina and Crohn’s disease (Wenninger et al. 1996; Pewitt
and Schaeffer 1997; McNaughton-Collins et al. 2000).
There was never any doubt about the diagnosis of
acute bacterial prostatitis. There was a little less certainty in the criteria for chronic bacterial prostatitis as a focus for recurrent acute urinary infection (Anderson
2002). Unfortunately, the commonest categories of
chronic abacterial prostatitis and prostatodynia were
very loosely defined according to the presence or absence of inflammatory cells and/or bacteria in expressed
prostatic secretion and/or urine passed immediately after massage or in seminal fluid. Unfortunately, the number of white blood cells and organisms diagnostic of
prostatitis was never validated. Opinion was markedly
divided. On the one hand, there were those who believed
in the “common wisdom” dictating that a significant
number of cases were caused by bacteria. However,
they could not be isolated either because of inadequate
bacteriological technique or as a result of the presence
of fastidious organisms which eluded conventional laboratory identification. The alternative view of the sceptics was that chronic prostatitis was not a distinct entity
at all (Lummus and Thompson 2001; Nickel 2000).
The later NIH classification went some way to providing a compromise and leaving the door open for further
research to settle the issue. This was to use the noncom-
Table I.9.1. Classification of prostatitis. (EPS Expressed prostatic secretion, PSA prostate-specific antigen, UTI urinary tract infection, WBC white blood cell count)
Category
Name
Defining features
Old classification
(Drach et al. 1978)
I
Acute bacterial prostatitis
Acute infection of prostate
Acute bacterial prostatitis
II
Chronic bacterial prostatitis
(CP)
Recurrent UTI WBC and +ve culture in EPS, etc.
when asymptomatic
Chronic bacterial prostatitis
IIIA
Chronic pelvic pain syndrome (CPPS) inflammatory
Symptoms of CPPS WBC in EPS/postmassage urine/ Chronic nonbacterial prostaseminal fluid
titis
IIIB
CPPS noninflammatory
Symptoms of CPPS, insignificant WBC in EPS, etc.
IV
Asymptomatic inflammatory
prostatitis
No symptoms Chance finding (e.g. ↑PSA) WBC ±
infection in postmassage specimens, inflammation
in prostatic histology or cytology
Prostatodynia
I.9
218
I.9 Problem: Diseases of the Prostate (Infection, Benign Prostatic Hyperplasia, Cancer)
mittal term “chronic pelvic pain syndrome” to cover
both inflammatory and noninflammatory abacterial
prostatitis. An interesting new category was also defined: asymptomatic inflammatory prostatitis (Krieger
et al. 1999).
It is possible that other perplexing chronic inflammatory states of the genitourinary tract having a welldefined acute phase should be considered as a continuum with prostatitis. Therefore, logically, a case could be
made for considering acute and chronic cystitis, epididymo-orchitis, urethritis and prostatitis together.
I.9.2.2
Diagnosis of Prostatitis
I.9.2.2.1
Categories
Acute Prostatitis (NIH Category I)
I.9
The diagnosis of acute bacterial prostatitis is invariably
straightforward. The background may be important.
Patients who have undergone urethral catheterization
and instrumentation or prostatic biopsy are at risk, and
particularly if they are immune-compromised. They
may present with pain in the lower abdomen, perineum, genitalia and lower back, a pyrexial illness and
symptoms of irritative or obstructive voiding. Rectally,
the prostate will be tender and even fluctuant due to abscess formation. The midstream urine specimen will
show a causative organism, which with few exceptions
will be a coliform with the frequency of pathogens reflecting the community from which the patient has acquired the organisms. These will invariably already
populate the bowel flora. Occasionally, prostatic infection will be associated with urethritis as part of a sexually transmitted infection. The organism will then be
Gonococcus or Chlamydia. Occasionally, and as in females with abacterial cystitis, several types of virus can
affect the urothelium and skin simultaneously, e.g. herpes zoster. Lower urinary tract inflammation may lead
to the development of systemic sepsis but rarely, generalized inflammatory symptoms may co-exist with lower urinary tract irritation as part of a named syndrome
(e.g. Reiter’s, Behçet’s).
Inflammation of the prostate may cause enlargement and acute retention. Serum inflammatory markers may be grossly elevated (ESR, CRP). PSA can rise to
levels of more than 100 ng/ml and it is important to understand that it may take up to 3 months after resolution of the acute prostatitis for baseline levels to be resumed (Tchetgen and Oesterling 1997).
Chronic Bacterial Prostatitis (NIH Category II)
A hallmark of a small minority of men with this condition is recurrent episodes of urinary tract infection
caused by one of the standard pathogens (commonly
Escherichia coli). There may be irritative or less often
obstructive lower urinary tract symptoms and patients
often complain of pain in the perineum, lower abdomen, genitalia, back and lower rectum. These men also
present with exacerbations of acute urinary infection
with worsening of symptoms of bladder irritation, occasionally pyrexia, abdominal and loin pain. As in
acute prostatitis, standard urinary pathogens can be
cultured from the midstream specimen during the episodes of UTI. Between these episodes, the prostatic origin of recurrent infection is apparently established by
the traditional Stamey-Meares four-glass test (Meares
and Stamey 1968). Here positive cultures are obtained
from material which is assumed to originate in the
prostate (expressed prostatic secretion, postprostatic
massage urine or specimens of ejaculate). The validity
of this test has always been questionable, as Koch’s postulates establishing a microbe as pathogenic are rarely
fulfilled. This is discussed in more detail below.
Chronic Pelvic Pain Syndrome (NIH Category III)
The majority of patients presenting with pelvic/perineal pain do not have a history of recent urinary tract infection. There may be a wide variety of additional
symptoms, much the same as are found in chronic bacterial prostatitis. In categories II–IIIB of prostatitis, the
prostate is variably tender on rectal examination.
In both categories IIIA and IIIB, midstream urine
specimens show normal white cell counts and insignificant bacterial colony counts on culture. The distinction
between the two is based on the presence of white
blood cells in expressed prostate-specific fluid and
urine after prostatic massage and/or in seminal fluid.
The methodology and significance of positive findings
in the Stamey-Mears test and its simpler alternative is
considered below.
Some enthusiastic investigators will perform transrectal ultrasound. A wide range of abnormalities may
be apparent, but their validity is questionable. The significance of multifocal calcification is not settled. Occasionally prostate cancer can be diagnosed in patients
presenting with pelvic pain, minimal or no elevation of
the serum PSA, a tender irregular prostate and focal
changes on transrectal ultrasound, which encourages
the operator to perform biopsies. Investigation of lower
urinary tract symptoms and haematuria will of course
dictate the need for flow studies, urodynamics, cystoscopy and upper tract imaging.
Rarely prostatic pain will be referred as part of a sacral
neuropathy and detailed investigation will then of course
be motivated by additional clinical signs. Included in this
category is the condition termed pudendal neuralgia.
The mere acquisition of a diagnostic label is, for some patients, important when no proof can be advanced.
I.9.2 Prostatitis
Category IV Asymptomatic Inflammatory Prostatitis
This is a relatively newly defined category in which
there is evidence of inflammation, infection or both in
prostate-specific specimens after massage and/or in cytological or histological investigations of prostatic biopsy specimens which have been obtained on account
of elevation of the serum PSA (Potts 2000).
I.9.2.2.2
The Stamey-Meares Test
The Stamey-Meares test has been the gold standard for
very many years for localizing inflammation and pathogenic organisms to the prostate. Arguably the test was
first described in 1930 (Nickel 1930). The protocol is
shown in Table I.9.2 and its interpretation in Table I.9.3.
Table I.9.2. Protocol for quantitative prostatic localization
(Stamey-Meares). (VB2 Premassage urine, VB3 postmassage
urine)
1. No voiding 3 h prior to test
2. Full bladder
3. Expose glans penis, clean with simple soap solution
4. Void urine
First 5 – 10 ml VB1
Mid stream
VB2
5. Vigorous prostatic massage for 1 min from periphery to
midline. Secretion at meatus – EPS
6. Immediately after massage void 5 – 10 mol
VB3
urine
7. VB1 – 3 and EPS immediate microscopy for WBC (N/HPF)
and culture
219
The test is difficult to perform. Often EPS is not obtained. False-negative findings are common. Virtually
all patients labelled as chronic prostatitis will have
been given antibiotics. It is quite possible that bacterial
growth will be suppressed even if medication is discontinued for a month before the test is performed. Organisms other than coliforms and of doubtful significance
may be cultured (e.g. Gram-positive organisms). A
grave drawback is that the results may not be predictive
of treatment response. Perhaps for one or more of these
reasons, the test is rarely performed. A simplified “poor
man’s test” describing the use of pre- and postmassage
urine has probably been in use unofficially as a substitute for some time (Nickel 1998) (Table I.9.2). Clearly
there should be no evidence of urethritis or cystitis,
which might easily co-exist with Category II prostatitis.
In these circumstances, there is no alternative to treatment with an antibiotic for at least 3 days. Ideally this
should not have great tissue penetration and nitrofurantoin is ideal. If chronic bacterial prostatitis is present there will still be an increase in inflammatory cells
and positive bacterial culture in the postmassage urine
specimen. Unfortunately, culture of the ejaculate is of
uncertain significance (Weidner et al. 1991).
I.9.2.2.3
Quantitation of Symptoms
There seems little doubt that the majority of primary
care physicians and possibly even urologists regard
chronic prostatitis as a diagnosis made on the basis of a
symptom complex and will offer standard treatment
without bothering with localization studies or, if they
I.9
Table I.9.3. Interpretation of Stamey-Meares test. (CC Colony count, WBC white blood cell count)
NIH
TEST
Category
VB1
Urethral
urine
VB2
Bladder
urine
VB3
Prostate
urine
EPS
Prostatic
fluid
Comments
I
CC
WBC
> 105/ml
+
> 105/ml
+
Prostatic
Prostatic
massage con- massage contraindicated traindicated
II
CC
WBC
Few
0
Few
±
> 104/ml
+
> 104/ml
+
+ recurrent UTI
IIIA
CC
WBC
0
0
0
0
0
+
0
+
Occasionally bacteria cultured in VB3, EPS.
No recurrent UTI
IIIB
CC
WBC
0
0
0
0
0
0
0
0
IV
CC
WBC
0
0
0
0
0
+
0
+
Occasionally bacteria cultured in EPS/VB3
Cystitis
CC
(Infective) WBC
> 105/ml
> 105/ml
> 105/ml
±> 105/ml
KASS count quoted but < 105/ml can be diagnostic
VB1 → EPS can all be +ve in presence of urethritis due to contamination; therefore treat with
nitrofurantoin then repeat
Urethritis CC
WBC
±> 105/ml 0
+
+
0
+
0
0
220
I.9 Problem: Diseases of the Prostate (Infection, Benign Prostatic Hyperplasia, Cancer)
do perform them they are not influenced by negative
results (McNaught-Collins et al. 2000). The situation is
perhaps akin to the official quantitation of lower urinary tract symptoms in the IPSS score. The name implies prostatic pathology and usually BPH. However,
this is by no means always the case and the score will
certainly not determine a diagnosis. Nevertheless, it is
immensely valuable for stratification of symptom severity and more particularly how much quality of life is
affected, for epidemiology and trials of treatment. A
multiplicity of questionnaires, tools, instruments and
indices have been devised (Brähler et al. 1997; Nickel
1998). The common factors in all are self-assessment by
the patient on the presence and degree of pain in the
genitalia, perineum, rectum and abdomen. Secondly,
voiding is assessed both from the point of view of obstructive and irritative symptoms. In some sexual function is assessed.
I.9.2.3
Aetiology of Chronic Prostatitis
I.9.2.3.1
An Infectious Disease?
I.9
Most prostatitis specialists feel that the majority of patients suffer from an infectious disease (Nickel 2000).
Failure by a urologist to culture an organism is therefore a matter of technical inadequacy. So-called cryptic, fastidious or even nonculturable microorganisms
are possible contenders (Weidner and Ludwig 2003)
(Table I.9.4). One contentious issue is how long prostate-specific fluid specimens should be cultured. One
group considers that EPS or semen should be cultured
for 5 days rather than the conventional 2 days (Shoskes
et al. 2000). In so doing, patients with white cells in EPS
may in fact be shown to have organisms, too. Such patients should perhaps be classified as Category II although officially they may not have had recurrent episodes of conventional urinary tract infection.
Table I.9.4. Causes of chronic pelvic pain syndrome
Conventional uropathogens
Autoimmune reaction (? Previous bacterial infection)
Dysfunctional high pressure voiding (+ intraprostatic duct
reflux)
Fastidious/nonculturable organisms/atypical bacteria
Bacterial fragments
Biofilm
Prostatic calculi
Viruses
Chemical irritation from instrumentation, catheterization,
etc.
Other diagnoses
Interstitial cystitis
Carcinoma in situ of bladder
Functional somatic syndrome
There is considerable scepticism that patients without objective evidence of inflammation, i.e. Type IIIB
do not have a microbial cause. The significance of inflammatory cells in EPS from patients with CPPS must
be questioned when the majority of patients have no
evidence of inflammation (IIIB). An important study
on the histopathology in 368 biopsies from 97 patients
with CPPS showed that inflammation was detectable in
only 33 % of patients and this was moderate or severe in
only 5 % of 97 patients who were evaluated (True et al.
1999). As asymptomatic men with positive white cells
in EPS are an entity, perhaps the relationship between
pain and white cells or other signs of inflammation is
not causal so that the distinction between IIIA and IIIB
is artificial. Even positive cultures may be questionable
whilst a normal flora of the prostate is still uncertain.
However, in a study of patients undergoing radical or
transvesical prostatectomy, the data were more reassuring in favour of the conventional view (Hochreiter et
al. 2000). Furthermore, a comprehensive analysis of
specific PCR (polymerase chain reaction) for all pathogens incriminated in chronic prostatitis and of broadspectrum PCR in prostate biopsies from men with
CPPS undergoing conventional testing showed correlation of EPS white cell concentration with the presence
of 16sr DNA (Krieger et al. 2003).
It is possible that the search for inflammatory cells
represents a rather crude approach and a more sensitive indication of inflammation might come through
the identification of cytokines and various measures of
oxidative stress in EPS (Shahed and Shoskes 2000). In
one such study, there was evidence of induced antioxidant enzymatic activity and of induction of the appropriate genes in symptomatic patients with positive EPS
culture. However, the organisms were predominantly
Gram-positive and their relevance would therefore
normally be questioned. In a small number of such
men, there was a detectable injury response, a favourable clinical response to antibiotics and a reduction of
oxidative stress.
A variety of constituents of prostatic fluid alter their
concentration rather typically in response to bacterial
infection (Table I.9.5) (Weidner et al. 1997). A rise in pH
can result from infection with an organism, producing
urease or a fall in citric acid concentration. Theoretically
this could lead to reduction in bioavailability of certain
antibiotics but in practical terms this is not an issue.
Another group investigated IL1 beta and tumour necrosis factor alpha (TNF [ ) in prostatic secretions
(Nadler et al. 2000). The levels appeared to be higher in
men with Category IIIA than IIIB and in healthy controls. There was a good correlation between the presence of IL1 q and TNF [ but none between either and
the presence of white blood cells.
It is possible that fungi might be implicated in some
cases of prostatitis even if patients are not immunosup-
I.9.2 Prostatitis
Table I.9.5. Changes in prostatic secretion in chronic bacterial
prostatitis (NIH II)
Rise
pH, IgA, IgG, IgM
LDH5/LDH1
Fall
Specific gravity
Prostate antibacterial factor (PAF)
Cations (zinc, magnesium, calcium)
Citric acid
Enzymes (lysozyme, acid phosphatase)
From Weidner et al. (1997)
pressed (Elert et al. 2000). Specialized culture media
and DNA analysis may be required to demonstrate
these elusive organisms.
The small numbers of men with Category I or II
prostatitis will mainly show coliform organisms of an
identical type in urine and EPS. In such patients, there
are a variety of potential routes of entry of bacteria into the prostate. Reflux of urine into the intraprostatic
ducts is certainly feasible and has been demonstrated
using appropriate imaging studies. Similarly, it is reasonable to suppose that heavy colonization of the male
urethra with coliforms such as from catheterization
instrumentation and anal intercourse can involve the
paraurethral glands and prostate. Heterosexual transmission has also been questioned. The presence of calculi within the prostate composed of substances found
in the urine but not the prostate (e.g. urate) are also
indicative of reflux. Such calculi very often harbour
bacteria and may be associated with biofilm, particularly if there is secondary infection from a Proteus.
The persistence of an inflammatory process initially
associated with proven bacterial infection is another
fascinating conundrum and is perhaps a common factor in a family of chronic inflammatory conditions
including prostatitis, epididymitis and interstitial cystitis.
I.9.2.3.2
Experimental Prostatitis
Rodent and animal models have been used to establish
coliform infection of the prostate (Nickel 1997). They
may provide important evidence for the origin of continuing chronic inflammation in sterile tissue from
acute infective prostatitis which apparently had resolved on appropriate antibiotic treatment. Abacterial
chronic prostatitis can also be induced by immunization with syngeneic prostatic tissue components. Another interesting observation in animal models is that
bacterial aggregates which adhere to the ductal epithelium become covered with glycocalyx matrix, rendering them relatively resistant to host defence mechanisms and antibiotics in normal tissue concentrations.
221
Animal models have also allowed another principle
to be established, namely that prostatic inflammation
may be a consequence of dysfunctional voiding caused
by obstruction combined with intraprostatic ductal reflux driving urine into the prostate gland. If the urine is
infected acute bacterial prostatitis will develop, but if
there has been previous infection a less severe form of
chronic bacterial inflammation occurs.
Experimental prostatitis with E. coli is well established but there is some evidence in large animal models that Chlamydia can also be pathogenic. These models, and in particular the dog, have been used to demonstrate prostate secretion of various antibiotics and to
study distribution and pharmacodynamics of the various agents. It was confirmed that several antibiotics,
e.g. trimethoprim and quinolones, were preferentially
concentrated in the duct systems. It was also shown
that the intraduct compartment was likely to be very
different in the inflamed gland compared with the normal uninfected gland. Infected ducts could be blocked
with debris, leading to unequal distribution of antibiotics apparently present in adequate concentration in the
normal gland.
There seems little doubt that animal models will offer great potential in studying the fundamental processes of bacterial invasion and adherence. It is likely
that the significance of bacterial DNA fragments detectable by molecular methodology will be clarified.
I.9.2.4
Treatment
I.9.2.4.1
Conventional
Acute Prostatitis
The treatment of acute prostatitis is usually straightforward, but there is a significant risk of endotoxaemia
and systemic sepsis. Initially a broad-spectrum antibiotic combination is given, if necessary intravenously,
together with supportive or resuscitative measures.
Blood and urine cultures should be taken and the antibiotic therapy adjusted according to the sensitivities
when they become available. If the clinical response is
unsatisfactory or not sustained the presence of a prostatic abscess should be considered and excluded by CT
scanning. Rectal manipulations should be avoided after
an initial very gentle diagnostic examination, as pressure on the inflamed gland may be extremely painful
and encourage systemic spread of infection. A prostatic
abscess may drain spontaneously into the urethra or
rectum but is quite likely to require deroofing by transurethral resection or preferably incision with the Collins knife. Although there is little guidance from the literature, it is probably wise to continue oral antibiotic
treatment for 3 weeks and to check MSU cultures
I.9
222
I.9 Problem: Diseases of the Prostate (Infection, Benign Prostatic Hyperplasia, Cancer)
monthly thereafter for 6 months. When the acute infection has settled, it is customary to investigate the urinary tract with some form of imaging. It is almost invariably normal.
Chronic Prostatitis
There is no high-quality evidence base on which to plan
treatment of any category of chronic prostatitis.
penetration. The presence of prostatic calculi may also
inhibit tissue penetration and bacterial clearance, but
again there is no hard evidence for this. Transurethral
resection may be effective in opening up the pockets of
calculi but tends to be used as a last resort, as of course
the procedure has to be very radical in removing as
much tissue as possible, particularly in the true glandular layer adjacent to the capsule.
Use of Alpha Blockers/Finasteride
Antibiotics
I.9
It is logical to give a long course of antibiotics in Category II disease, using the sensitivities from microbiological examination of the MSUs during the recurrent
episodes of acute urinary infection. If these results are
equivocal a clearer indication may be available from
culture of EPS or postmassage urine. In the very small
number of patients who hover between Category II and
IIIA, i.e. those without a history of recurrent urinary
infection but in whom there is clear evidence of bacterial infection in the prostate, treatment will logically be
based on sensitivities.
A fluoroquinolone is recommended with a presumed Gram-negative therapeutic target (Naber et al.
2000). The new evidence from molecular bacterial
analysis would suggest that tetracycline resistance is
common and interestingly it is a matter of clinical experience that any initial improvement with a tetracyclinebased antibiotic is not sustained (Krieger et al. 2003).
Similarly, it was found that the response to antibiotic
treatment in Category III patients would be predicted
from the presence of bacterial genomic fragments
demonstrated by 16 S recombinant real-time PCR
(RTPCR) reaction (Shoskes and Shahed 2000). In other
words, men with negative cultures and negative reaction could avoid prolonged courses of antibiotics and
the corresponding expense and the risk of side effects.
Many clinicians will, as an act of desperation, always
give antibiotics in CPPS. It is possible that in the future
this decision may be refined by use of these molecular
techniques.
Generally speaking, there is no evidence that there is
a difference in response between antibiotics with or
without the addition of anti-inflammatory agents between Category IIIA and IIIB disease. The point has
been well made that any benefit could be a placebo effect, particularly as it is short-lived (Weidner et al.
1999).
Prostatic Massage
Prostatic massage may be effective, particularly if undertaken under regional or general anaesthesia (Nickel
et al. 1999). The logic is to open blocked ducts and disperse sequestered bacteria, allowing better antibiotic
The use of alpha-blocker agents is also controversial.
Enthusiasts believe there is evidence of external urethral sphincter over-activity in patients with CP/CPPS
(Barbalias 2003). However, there is no correlation between response to treatment and the presence or extent
of urodynamically proven obstruction. It has even been
suggested that it may be responsible for prostatic inflammation and therefore the term “painful male urethral syndrome” may be appropriate. The evidence is
poor quality and therefore, as for every other agent or
combination used, the trial will be empirical. The evidence for efficacy of finasteride is more convincing and
perhaps underrated (Leskinen et al. 1999).
I.9.2.4.2
Alternative Treatments
The bioflavonoid quercetin was found to improve
symptoms in patients with CPPS Category IIIA and B
disease in a placebo-controlled trial (Shoskes et al.
1999). This naturally occurring substance has a variety
of actions, including inhibition of nitric oxide, tyrosine
kinase and inhibition of several inflammatory cytokines. Several studies have indicated that the levels of
IL1 and TNF [ in EPS and semen were higher in men
with Category IIIA than IIIB disease.
Interestingly, quercetin has been shown to cause a
decrease in levels of isoprostane, a marker of oxidative
stress in prostatic fluid.
There are many inconsistencies in relating symptoms to the presence of white blood cells and inflammatory markers in EPS, prostatic histopathology and
to the new molecular evidence for the presence of bacterial fragments. Most disturbing of all are the very
considerable number of patients who can be categorized as type IV chronic prostatitis. One subgroup concerned asymptomatic patients presenting to a urology
clinic for investigation of a raised PSA. Elevated white
cells were found in EPS in 42 % (Potts 2000). Clearly this
could represent a very large number of patients in a
population of middle-aged men and could be classified
as a control group in the study of inflammatory markers localized to the prostate in relation to chronic pain
and other symptoms which constitute the clinical diagnosis of CPPS. A recurring theme in this chapter is the
I.9.2 Prostatitis
lack of evidence that CPPS is a distinct entity. The point
has been well made that any benefit of any of the conventional treatments could be due to placebo effect,
particularly as it tends to be short-lived.
I.9.2.4.3
Psychosomatic Aspects
It is important that the clinician should not be permanently focussed upon the prostate as the source of
symptoms. Almost every specialty in medicine embodies a series of painful conditions for which no cause
can be found. There is undoubtedly a psychological
component for any patient in whom conventional testing shows negative results and a wide range of treatments is ultimately ineffective. This is compounded by
an unsympathetic, impatient approach by the clinician
who may imply to the patient that his symptoms are a
reflection of a weak personality or worse still malingering (Wessely et al. 1999).
In other allied specialties, gynaecology and coloproctology, very similar symptoms reflecting muscle
spasm within the pelvic floor are found. It may be helpful to view all of these syndromes as one family of conditions occurring in both sexes. In principle there may
be rather little difference between chronic epididymal
or penile pain syndromes and vulvodynia (Fall et al.
2004). There may be more specific conditions: pudendal nerve entrapment may after all be a real condition
but only if symptoms are restricted to unilateral burning sensation and lateral tenderness on rectal examination. There may be delayed pudendal nerve latency on
the appropriate side and local anaesthetic may be temporarily effective. MRI scanning may demonstrate the
course of pudendal and other pelvic nerves and spinal
roots affected by a variety of pathological conditions. A
high proportion of patients will respond, if only in the
short term, to physical therapy and internal massage to
effect a myofascial release of pelvic floor muscle trigger
points. This physiotherapeutic technique has been
shown to be effective in NIH category III patients (Potts
2003).
A whole range of allied conditions may co-exist, including irritable bowel syndrome, chronic fatigue syndrome, premenstrual pain and non-ulcer dyspepsia.
Disruptions in the serotonergic pathways have been
implicated. An entity termed the limbically augmented
pain syndromes implies an association between treatment of refractory pain and brain functions which may
be localized in the limbic system at the rostral end of
the brain stem, which links the hypothalamus, pineal
body, hippocampus and temporal lobe cortex. These
areas control sleep and arousal, libido, aspects of memory and tolerance to stress. The corollary is that all such
patients with functional somatic syndromes should be
considered together.
223
Appropriate medication, in particular tricyclic antidepressants, stress management and biofeedback techniques, can all be effective provided they are prescribed
as part of a programme planned in a specialized unit
and preferably administered by a single clinician with
well-developed counselling skills.
References
Anderson RU (2002) Management of chronic prostatitis –
chronic pelvic pain syndrome. Urol Clin North Am
29:235 – 239
Barbalias GA (2003) Why alphablockers in prostatitis? Eur Urol Suppl 2:27 – 29
Brähler E, Wurz J, Unger U et al (1997) The Giessen Prostatitis
Symptom Score. Standardisation of the questionnaire and
prevalence of symptoms. J Urol 157:239
Drach GW, Fair WR, Meares EM et al (1978) Classification of
benign disease as associated with prostatic pain: prostatitis
or prostatodynia? J Urol 120:266 – 269
Elert A, Von Knobloch R, Nusser R et al (2000) Isolated candidal prostatitis. J Urol 163:244
Fall M, Baranowski AP, Fowler CJ et al (2004) EAU guidelines
on chronic pelvic pain. Eur Urol 46:681 – 689
Hochreiter WW, Duncan JL, Schaeffer AJ (2000) Evaluation of
the bacterial flora of the prostate using a 16SrRNA gene
based polymerase chain reaction. J Urol 163:127 – 130
Krieger JN, Nyberg L, Nickel JC (1999) NIH consensus, definition and classification of prostatitis. JAMA 282:236 – 237
Krieger JN, Takahashi S, Riley DE (2003) Chronic prostatitis:
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