Showing posts with label introduction. Show all posts
Showing posts with label introduction. Show all posts

Sunday, September 6, 2009

Patient reported frequency and severity of urological symptoms

Presenting symptoms (described by patients and recorded by urologists) in 1074 patients with prostatitis.(1)

SymptomN (%)
Frequency689 (64.2)
Obstructive voiding675 (62.8)
Perineal pain or discomfort630 (58.7)
Suprapubic pain or discomfort492 (45.8)
Penile pain or discomfort360 (33.5)
Premature ejaculation305 (28.4)
Malaise229 (21.3)
Urethral discharge220 (20.5)
Inguinal pain or discomfort216 (20.1)
Erectile dysfunction205 (19.1)
Haematospermia169 (15.7)
Voiding difficulties162 (15.1)
Fever159 (14.8)
Purulent urine150 (14.0)
Abnormal seminal fluid 97 (9.0)
Myalgia 64 (6.0)
Abnormal urine (mucus) 61 (5.7)
Haematuria 46 (4.3)


Mean (sd) score
frequencyseverity
Penile pain or discomfort55.2 (386/699)1.3 (1.4)3.1 (2.7)
Perineal pain or discomfort81.6 (666/816)2.2 (1.3)4.5 (2.5)
Suprapubic pain or discomfort74.6 (561/779)2.0 (1.4)4.3 (2.5)
Ejaculatory pain or discomfort63.9 (461/721)1.4 (1.3)3.3 (2.4)
Testicular pain or discomfort43.9 (302/688)0.9 (1.2)2.5 (2.5)
Lumbar/inguinal/thigh pain35.4 (240/678)0.8 (1.3)2.3 (2.8)
or discomfort
Incomplete bladder emptying72.8 (541/743)1.8 (1.4)3.7 (2.7)
Burning during micturition81.7 (652/798)2.0 (1.3)4.2 (2.5)
Urgency72.4 (514/710)1.7 (1.4)3.9 (2.8)
Urinary frequency86.4 (717/830)2.4 (1.4)5.0 (2.7)

_____________
(1) Rizzo M, Marchetti F, Travaglini F, Trinchieri A, Nickel JC. Prevalence, diagnosis and treatment of prostatitis in Italy: a prospective urology outpatient practice study. BJU Int 92(9):955-959, 2003.

Saturday, February 7, 2009

Main view thoughts on causes

If NIH-I&II are excluded the answer is quite honestly simply: nobody knows for sure! But the following ideas and hypotheses on etiology and pathogenesis have been put forth (see Karlovsky (1), Pontari and Ruggieri (2), for a fuller review):

Popular ideas
  1. Undiscovered micro-organism causing "hidden" chronic infection (i.e. unhealed). The most popular vectors are bacteria. This has been pursued with pig-headed insistence despite no proof. But, remember Helicobacter pylori...
  2. Neuro-muscular or musculoskeletal disorders, e.g. myofascial pain.
  3. Persistent inflammation triggered by an inappropriate immunological response to a previous, and supposedly healed, infection.
Less popular ideas
  1. Auto-immune condition.
  2. Persistent neuropathy (damage to nerves controlling pain regulation/signaling) possibly caused by any of the above causes (or neurogenic inflammation and/or "idiopathic" mast cell activation). Pudendal neuropathy is popular, but oft unproven.
Other ideas
  1. Estrogen-similar substances, e.g. soy flavonoids.
  2. Endocrinological (hormonal) disorders.
  3. Psychological (when you do not know cause nor what to do blame the patient...).
Do notice that causes can be multiple. For example bacteria may trigger an inflammatory/neurological reaction that triggers a muscular reaction etc etc. Diet and life-style may in their turn exacerbate or skew symptoms, thus "confounding" the issue. Many of the above causes may also include some hitherto undiscovered genetic mechanism predisposing for the disease. Or some undiscovered pollutant.

Andra bloggar om , , ,
__________________
(1) Karlovsky ME, Pontari MA. Theories of prostatitis etiology. Curr Urol Rep 3(4):307-312, 2002.
(2) Pontari MA, Ruggeri MR Mechanisms in prostatitis/chronic pelvic pain syndrome. J Urol 172(3):839-845 2004

Prevalence

Prostatitis is thought to be the most common urological complaint for patients under 50 years of age. It is estimated to occur in 5-8% (and maybe up to 16%) of the male population (as lifetime prevalence). About 90-95% of these cases are attributable to CP/CPPS. Frequency increases with age and seemingly has a northward increase. The mean patient is a male between 38 and 48 years that has suffered from diffuse problems for up to, commonly, eight years. But onset can begin at as early an age as the upper teens.

Andra bloggar om , , ,

Wednesday, February 4, 2009

Historical notes

The below is mainly extracted from “Epidemiologic and diagnostic aspects of prostatitis" by A Mehik (1) and "A headache in the pelvis" by Wise and Anderson.

The first "modern" description of prostatitis was made by Verdies in 1838 and later confirmed by Young, Gereghty and Stevens in 1903. Some researchers focused on finding a bacterial cause, while the Freudian lot branded the patients as mentally ill and suffering of anal/rectal psychoses (Cumming and Chittenden, 1938), problems with the "male sexual identity" etc etc. (The usual crap. The unfortunate gut reaction of the medical establishments to not knowing things has a long history of attributing the messenger of bad tidings, i.e. the patient, with being possessed by the devil, although the modern version is usually that the sufferer must be a bed-wetting mental case with severe hypochondria.)

Kretschmer noted already in 1937 that the causes probably were multiple. The first detailed descriptions were presented by Ritter and Lippow in 1938 and by Grant also in 1938. During 1940s and 50ties it was generally believed that the cause was gonococcal infection. By 1957 Campbell noted that non-bacterial causes were common. New technology saw a rise in research during the 60ties and 70ties (especially Meares and Stamey), but the direction was still for bacterial or psychological causes.

The 90ties and the turn of the millennium saw a new flurry of research, especially in the USA and Canada, and interest also started to be directed at neuromuscular causes. The thought that neuromuscular causes may lie behind pelvic pain was not new. Thiele and Shapiro had as early as in the 30ties pointed at this possibility, but it went largely ignored, until Sinaki and Segura in 1979 drew attention to the possibility of pelvic floor tension causing prostatitis.

Most recently the question has been raised if the cause may be immune reaction / HPA axis dysfunction. Several lines of evidence (symptoms and signs) do in my opinion indicate that this is a real possibility, regardless if it is a cause or an effect.

Andra bloggar om , , ,
____________________
(1) Mehik A. Epidemiological and diagnostical aspects of prostatitis. Doctoral dissertation presented at the University of Oulu (Uleåborg), Oulu University Press 2001

Monday, February 2, 2009

Current definition and classification

Technically the term means inflammation of the prostate. An inflammation is caused by the reaction of the immune-system of your body against substances deemed foreign by said body. These may be parasites, pollen, dust, bacteria, viruses and others.
(To simplify: if the foreign body is external and “non-living” the reaction is called an allergy otherwise it is an infection. An auto-immune reaction is directed against your own bodily tissues. The immune reactions of your body are commonly classified in four hypersensitivity types.)

The current classification is according to the American National Institute of Health (NIH) consensus presented in 1995 and published for clinical use in 1999. It is the currently most common.

Bacterial prostatitis—NIH-I and NIH-II
Obviously pathogenic micro-organisms can only be identified as the promoters and cause of inflammation in very few cases, which also are pretty easily treated with antibiotics. This condition is called acute bacterial prostatitis (NIH-I) if onset is sudden and causing obvious illness. Prostate is also abnormal in NIH-I. If infection recurs – usually with milder symptoms than the acute form – it is called chronic bacterial prostatitis (NIH-II). This is more common in older (>50y) men. Only 5-10% of the prostatitis diagnosed patients are thought to suffer from bacterial prostatitis. Curiously only about 5% of IC patients also show “gross inflammatory disease” . (1)

Chronic prostatitis / chronic pelvic pain syndrome—NIH-IIIa and NIH-IIIb
If no obviously pathogenic or known micro-organism can be identified the condition is called chronic prostatitis/chronic pelvic pain syndrome (NIH-III, CP/CPPS; idiopathic or abacterial prostatitis). If markers of inflammation (white blood cells above a certain cut-off in semen, VB3-urine, first void after prostatic massage, and EPS) are found the condition is further sub-categorized as inflammatory CP/CPPS (NIH-IIIa), else non-inflammatory CP/CPPS (NIH-IIIb). The latter condition is also known as “pelvic myoneuropathy”, ”pelvic myofascial syndrome” or “prostatodynia” or “pelvic floor tension myalgia” depending on assumed cause. A study indicated that NIH-III patients can roughly be divided in 25% type ‘a’ and 75% type ‘b’ (2), while another found that only 33% had an inflamed prostate (with 5% having moderate or severe inflammation)(3) . It should be noted that the official leukocyte count is of questionable use, as correlation with symptoms is low (4) and as up to 20% of healthy controls have higher levels ! (5)

Do note that before the NIH system the term chronic prostatitis commonly encompassed NIH-II, NIH-IIIa and NIH-IIIb.

Asymptomatic inflammatory prostatitis—NIH-IV
Sometimes inflammation of the prostate is discovered incidentally or by biopsy, in patients not expressing any symptoms or concerns common to other prostatitis sufferers. This condition is called asymptomatic inflammatory prostatitis (NIH-IV).

Addendum feb 4
The current classification has hung around since the early forties in one way or another with various renamings of the four categories. It still does not take into account (obviously) the possibility of non-prostate related causes, and is essentially misleading by its focus on leukocytes and infection.


Andra bloggar om , , , ,
__________________
(1) Moldwin RM Similarities between IC and male CPPS. Curr Urol Rep 3:313-318
(2) Hosseini A, Ehrèn I, Peter Wiklund P. The use of intraprostatic nitric oxide measurements to differentiate between inflammatory and non-inflammatory abacterial chronic prostatitis.
(3) True LD, Berger RE, Rothman I, Ross SO, Krieger JN. Prostate histopathology and the chronic prostatitis/chronic pelvic pain syndrome: a prospective biopsy study. J Urol. 162(6):2014-2018, 1999.
(4) Schaeffer AJ, Datta NS, Fowler JE et al. Overview summary statement-diagnosis and management of CP/CPPS. Urology 60(6):1-4, 2002
(5) Nickel JC, Alexander RB, Schaeffer AJ et al. Leukocytes and bacteria in men with CP/CPPS compared to asymptomatic controls. J Urol 170(3):818-822, 2003.

Sunday, February 1, 2009

What is chronic prostatitis / chronic pelvic pain syndrome ?

That is the million-dollar question! It is possible that several different conditions, still to define/discover, are the underlying cause to CP/CPPS symptoms. It is also questionable if the prostate is involved. Research “is dominated by hypotheses, all of which lack a substantial evidential standing”. “Ethiogenic theories vary from the abstruse to the fashionable… and sadly often of confusion in medical thinking” (P. Hanno (1)). CPPS is most likely both under- and over-diagnosed.

“Patients with chronic pelvic pain syndrome (2) demonstrate no evidence of inflammation. They do not have urethritis, urogenital cancer, urethral stricture, or neurological disease involving the bladder. Indeed, they exhibit no overt renal tract disease.” What is known is that the men categorized with this label present with fairly similar symptoms and problems, that the condition is more common the more north you live and that it shows a relapsing (flare) and remitting (improvement) pattern superimposed on a seasonal pattern with wintertime exacerbations.

“If I knew how to really cure CPPS I would be world famous, make millions, afford an apartment over-looking Central Park, one in Aspen and one in Miami and only need to work three months a year” (Anonymous).
“We must break down the difference between the urologist, gynecologist and gastroenterologist and treat the pelvic floor as a single unit” (GR Sant).

Andra bloggar om , , ,
____________________
(1) IC Epidemiology Task Force Report of the Bethesda Oct 29, 2003 meeting. Draft 1/6/2004.
(2) A syndrome is, according to the Oxford Concise Medical Dictionary, “a combination of signs and/or symptoms that forms a distinct clinical picture indicative of a particular disorder” but is not necessarily of a related etiology. That is why the word “syndrome” is used in CPPS. Unfortunately in the case of CPPS it is rather a label to “a combination of signs and/or symptoms”. Period.

Saturday, January 31, 2009

“Being able to control the pain or to see a possible painless future is psychologically beneficial”

Introduction
It is easier to define what CP/CPPS is not than what it is. Despite many years of searching for obvious microbial causes to CP/CPPS none has been found. This does not mean that there are none, but the likelihood is very very small. The focus on the prostate and the visible micturition problems are likely misleading thought and effort. I would even venture to say that the dysuria is a secondaty phenomenon that obscures other more important symptoms. In a recent article doctor C Nickel asserts that “the biomedical model has failed” and that “our traditional etiologic model may not be correct” (1) it is more likely that medical science has been barking up the wrong tree altogether.

Why did I write this?
I got the diagnosis of chronic prostatitis/chronic pelvic pain syndrome, couple of years ago and was, well, quite frankly surprised that there was no known etiology, or known cure. So I just assumed the specialist was lazy and not up to date with the latest info. How wrong I realized I was about 400 medical papers later and a couple of web sites (that where not to useful) later. While reading I made notes that it occured to me I could edit and publish on a "blog". Maybe someone will find something of interest.

Topics
I aim to discuss the following topics (in no special order):
Current definition and history
Estimated prevalence
Current management and diagnosis
Healthy men and not
Symptom clusters and what those may indicate
Seasonality
General topics (sexual, mental health and comorbidities)
Current treatment and what it may indicate.
Microorganisms
Non-microbial inflammatory reactions
Neurology
Urodynamics
Muscoloskeletal
Th1/Th2 balance
Pain, brain and viscera
Psychology
Coping strategies
Visceral immunity and pain
Vitamin D, light and cold
HPA axis and vasopressin
HPG axis
Oral health, Th17 and mercury
Nutrition

Andra bloggar om , , ,
__________________
(1)Nickel C. CP/CPPS: the biomedical model has failed! So what’s next? Contemporary Urology, July 2006