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[Hawk]

This topic grew out of a very lengthy exchange that started somewhat off topic in the "Causes of Peyronies Disease" topic.    This will be the place to clearly state just what is and is not Peyronies Disease.  Here Peyronies Disease can be diferentiated from congenital curvature and any other conditions that exist that may cause deformity of the penis.

Please note that in order to effectively communicate we must speak the same language with the same definitions.  While it is ok to speculate on what does and does not comprise Peyronies Disease we need to label such as speculation or as private definition.

All readers should keep in mind that in most cases this is a discussion by lay people attempting to discuss some highly technical information and break it down in a form we can understand.  Much of it probably fails to stand up to sound scientific scrutiny on several levels. 

Caution, This is not a topic that new patients will find very helpful in treating Peyronies Disease.  If it gets to be a bit too much, move on to another topic. 

[Liam]

The fact of the matter is that the vast majority of men with Peyronies Disease have no other fibrotic diseases and the majority of men with other fibrotic diseases do not have Peyronies Disease.

Yes.  But, enough do to realize their is a relationship between these diseases/conditions.  It, also, implies Peyronies Disease is not just an injury.  It maybe the healing process gone haywire in response to an injury.

You can write your own definition (which happens to conform to your personal experience) and define every one that is not just like you as having a heretofore unidentified "Peyronies Disease like disease".

Definitions of peyronie's disease on the Web:

A plaque, or hard lump, that forms on the erection tissue of the penis. The plaque often begins as an inflammation that may develop into a fibrous tissue.
medicalcenter.osu.edu/patientcare/healthinformation/glossary/p.cfm

A deposit of scar tissue or plaque in the erectile tissue in the penis, sometimes causing painful and curved erections.
www.malehealth.com/HTML/B9_print.html

Curvature of the penis, usually during erection, caused by plaque (hardened or calcified tissues).
erection-disfunction.biz/glossary.html

I said:

I have also seen the description 100 times - plaque and pain and curve.

Its the same basic definition at every site including journal articles, studies, etc.

When asked about those that resolve, you say -> That was not Peyronies Disease.  It was Peyronies Disease-like.
When asked how you know, your answer is -> because it resolved

I have yet to see the elusive evidence of spontaneous resolution.  I hear about it like an urban myth.  There is no valid and reliable measure used.  So how can it be shown.  I would like to believe they happen and they may.  Until I see evidence, I will keep my working definition.  I admit they are assumptions.  But, they are based on observations.  Here is my thought process.  1) There is a very low reported spontaneous recovery rate (5-15%).  These are based on suspect observations.  Because there is no universally applied, objective diagnostic procedure used for identifying Peyronies Disease, there are some false positives.  There has to be some number. Five to Fifteen percent, I don't know.  False positives would spontaneously recover.   2) Other factors such as the skill of the physician, accuracy of the patient history, etc. would account for some percentage of false positives.  It has to happen.  I don't know the number.  Just these two factors put a serious dent in that 5-15% causing the 0% to be at least plausible. 

I would readily embrace such a radical unsupported position if it were not so radical and unsupported.

My feelings about the 5-15% number .

BTW, if someone told me they had Peyronies Disease and they cured it by putting peppermint oil on the area, I would probably try it.  I'm not THAT stubborn  .  No atheist in a fox hole or something like that.

I do believe there are varying degrees of Peyronies Disease, of course. 

One thing that bugs me about the issue of "plaque" is that there is no anatomic or physiologic definition of that term.

Tim, that is exactly my point.  There should be criteria.  But, there has to be something there to cause a bend.  And, the definition I used refers to the phenotypic expression of the disease/condition, naturally.  The histological differences point to (possibly) what most of us assumed;  There is a process/disease/condition going on that we can't see. 

The study raises the questions:
Did the histological changes cause the Peyronies Disease or vice versa?
Do some men without Peyronies Disease have these changes?
What were the changes?

Just something funny I noticed.  On the picture labeled "C", is the tissue on a toile coaster?

http://www.refertilisieren.de/literatur/penilecorporoplastik.pdf

One other fleeting thought.  A man receives a severe laceration to the penis (ala Bobbit ).  It heals and and forms inelastic scar tissue.  The penis bends.  Obviously not Peyronies Disease?  I bring this up to muddy the waters .  Are the traumas that cause Peyronies Disease only the ones that can't be seen?

[Hawk]

...I will keep my working definition.  I admit they are assumptions. 

I am pretty satisfied with that quote. While I largely disagree, I have no way of combating admitted assumptions.

Peace! 

[Liam]

While I largely disagree

Peace!   

Hawk,

If the world would learn this, think of all we could do.

Thanks for a good and spirited discussion!

Peace (to Tim and Old Man, too),

Liam

[Liam]

George, GMTA

George999

So what if Peyronies is to these underlying changes like a hip fracture is to osteoporosis?

Liam
   

Defining the Problem
« Reply #112 on: September 09, 2006, 09:13:54 AM » Quote Modify Remove Split Topic 

--------------------------------------------------------------------------------
For a while now, I have suggested different conditions that are often labeled as Peyronies Disease.  This is fine for a support group.  It is not proper, however, for the scientific community.

Although both may result in a bent penis, the cause and, thereby, the treatment are different.  Tim may correct my analogy.  A fall and osteoporosis may result in a broken bone.  Some of the treatments may be similar.  But, with osteoporosis, the underlying condition must be treated as well.   ****The break is analogous to the bend in the penis and the osteoporosis is the disease analogous to Peyronies Disease.****

This is nothing new.  We have known for a while some men spontaneously heal.  Maybe (probably?) its because the condition is not the same. 

We should not fear the truth.  We should welcome all men who have deformities of the penis.  We have more similarities than differences.  Just realize some may have a different condition.

Liam


This means sex is like a fall?  Somtimes I carry these things too far.   

It seems to fit so well

[Hawk]

Guys,

I am on the verge of making myself sick so I fear others are sick of this.  nevertheless, I want to make it clear that I don't question that Peyronies Disease has some connection with other fibrotic diseases.  I certainly agree to underlying factors.  My personal guess is that Peyronies Disease occurrs when a combination of several unknowns are present simultaneously and that these unknowns, like TGFb1, have more than one simple trigger.  This means they have more than one way to break the critical combination.  My disagreement is for laymen whose expertise consists of having the disease to assume to define or diagnose who has Peyronies Disease and who has a yet unnamed Peyronies Disease-like condition.  The truth is that It is a fact that no scientist has yet nailed down any data to determine that any such Peyronies Disease-like condition with a clearly different origin (etiology) than Peyronies Disease even exists.  Until we research, discover, and document such a non-existent condition we may be  unwittingly leading people on a *snipe hunt.

Could it be? - SURE
Is there any basis - NONE

I can come up with a working definition of Peyronies Disease that will define Liam or anyone else out of having Peyronies Disease based on my expertise as a cop, and my private definition, for whatever that is worth.  My concern is that our random speculation my be very confusing because it creeps into posts that are sometime actually directed to new members who post with questions.  Heaven forbid that they may actually think we know what the hell we are talking about because nothing could be further from the truth.  It may be fun to speculate about "what ifs" but I think we need to put more warning stickers on such speculation than are plastered on a step ladder if we are going to be responsible.

Within those confines the discussion is somewhat interesting but it is almost a candidate for the "off Topic" area or a new topic called "Total Speculation"

*PS: For the uninitiated, a snipe hunt is a practical joke played on unsuspecting victims as they try to catch non-existent snipe at night using totally ineffective methods.

[George999]

Hawk, I ALWAYS try to make sure that I stress to newcomers that they should be evaluated by a qualified physician.  And I really don't believe that anyone here has actively encouraged newcomers to try to diagnose themselves based on the posts on this site.  But having said this, you will have to admit that even physicians don't seem to agree on what constitutes Peyronies and what doesn't.  There have been more than one post where people have actually complained that they were told by one physician that they did NOT have Peyronies only to be told by another that they did.  I am not saying this as a put down.  In fact I appreciate your concern and your admonition.  But this IS the thread centered on causes of Peyronies and we really NEED to be able to brainstorm on this subject.  By your own confession even the pros don't known the answer to this.  If we are not free to speculate based on the meager trickle of information at hand, this thread would be pretty empty.  - George

PS - Perhaps there is a need for an official disclaimer on each thread to the effect that it is not the purpose of these discussions to attempt to diagnose Peyronies or any other affliction and that all enquirers should seek the counsel of a qualified medical professional.

[Liam]

Liam - Amateur Diagnostician

[Liam]

What I say is for discussion purposes only.  Discussion involves speculations just as the scientific process involves speculations.  Just look at all the treatments we discuss and try.  My goal is not to disuade someone who may have Peyronies Disease from getting it checked out.  I only want to open the thought processes of interested members to the possibilty of conditions which may lead to false positives for Peyronies Disease.

If there is some new guy who thinks he might have Peyronies Disease, get it checked out by a urologist.  I would never try to tell an individual whether he does or doesn't have it.  And, they should not try to diagnose themself.

I have on occasion told guys what they had didn't sound like Peyronies Disease.  I always follow or precede with the advice to see a doctor.  And, those guys lists of symptoms matched nobody's definition of Peyronies Disease.

I honestly don't question the popular definition.  I just believe men are being diagnosed with Peyronies Disease who don't have the symptoms that define the disease.


 

The truth is that It is a fact that no scientist has yet nailed down any data to determine that any such Peyronies Disease-like condition with a clearly different origin (etiology) than Peyronies Disease even exists.

  Here is something the authors of the paper called Atypical Peyronies Disease (yes, its a repost).  It kinda sort of has some of the syptoms but, not exactly.  Really its not even close.  Just dump it into the old catch-all called Peyronies Disease.  But, because it is really nothing like Peyronies Disease, just stick "atypical" in front of it.  Its like calling a sinus headache an atypical migrain.  They could have left it labeled ISS.  Thats a cool acronym.  But, noooooo! You know your in trouble after the introduction.

CASE REPORT
Nonpalpable Scarring of the Penile Septum As a Cause of Erectile Dysfunction: An Atypical Form of Peyronie's Disease
Anthony J. Bella, MD,**Department of Urology, University of California, San Francisco, CA;Anthony J. Bella, MD, Department of Urology, University of California, San Francisco, CA 94143–0738, USA. Tel: (415) 789–5109; Fax: (415) 476 8849; E-mail: [email protected] Alp Sener, MD,The Department of Surgery, Division of Urology, St. Joseph's Health Center, The University of Western Ontario, London, Canada Kirsten Foell, MD,The Department of Surgery, Division of Urology, St. Joseph's Health Center, The University of Western Ontario, London, Canada and Gerald B. Brock, MDThe Department of Surgery, Division of Urology, St. Joseph's Health Center, The University of Western Ontario, London, Canada *Department of Urology, University of California, San Francisco, CA; The Department of Surgery, Division of Urology, St. Joseph's Health Center, The University of Western Ontario, London, Canada
Anthony J. Bella, MD, Department of Urology, University of California, San Francisco, CA 94143–0738, USA. Tel: (415) 789–5109; Fax: (415) 476 8849; E-mail: [email protected]
ABSTRACT
 
Introduction. Men with nonpalpable isolated septal scars (ISS) identified with color duplex ultrasonography (CDU) comprise a group of previously unrecognized patients with wide-ranging sexual concerns.

Aim. We aim to identify the clinical characteristics of patients presenting with this atypical form of Peyronie's disease characterized by the absence of palpable deformity.

Materials and Methods. Of 482 consecutive patients who presented to a tertiary care erectile dysfunction (Erectile Dysfunction) clinic and underwent CDU after satisfying inclusion criteria, 27 (5.6%) men with nonpalpable ISS and no dorsal or ventral plaque were identified.

Main Outcome Measures. International Index of Erectile Function (IIEF), CDU, and clinical characteristics.

Results. The median age of the men with nonpalpable ISS was 49 years. The length of time from onset of symptoms to presentation was 22 months, and the pretreatment IIEF score was 14. The remaining 455 men who underwent CDU were of similar age (48 years) but had a markedly lower IIEF score of 9.5 (statistical median). ISS patients presented with decreased penile rigidity (20), penile shortening (13), chronic pain with erection (13; mean 33 months), and the inability to maintain an erection (7). Fourteen men had failed phosphodiesterase-5 inhibitor therapy, and four reported unsatisfactory results. Management options included retrial with oral agents, intracavernous pharmacotherapy, verapamil injections, and surgery.

Conclusions. The clinician should be suspicious for nonpalpable ISS in men with sexual concerns who present with decreased penile rigidity, length loss, and chronic pain with erection. Our findings support the use of CDU for this patient group, particularly when previous treatment has failed, because men with ISS had a greater likelihood of having no palpable deformity or curvature and ongoing penile pain. Bella AJ, Sener A, Foell K, and Brock GB. Nonpalpable scarring of the penile septum as a cause of erectile dysfunction: An atypical form of Peyronie's disease. J Sex Med 2007;4:226–230.

We aim to identify the clinical characteristics of patients presenting with this atypical form of Peyronie's disease characterized by the absence of palpable deformity

  characterized by no plaque and no bend or characterized by none of the primary characteristics of Peyronies Disease.


You be the judge.  Is this a form of Peyronies Disease or not?  And, regardless of your answer, how sure are you?

[Hawk]

Liam,

I hope i am not misrepresenting you.  I used your quotes to determine just what you are saying and i am ..... well..hmmm..at a loss.

I honestly don't question the popular definition.  I just believe men are being diagnosed with Peyronies Disease who don't have the symptoms that define the disease.

Should that have read: I just believe men are being diagnosed with Peyronies Disease who don't have the symptoms that define meet my private definition of the disease?

Here is something the authors of the paper called Atypical Peyronies Disease (yes, its a repost).  It kinda sort of has some of the symptoms but, not exactly.  Really its not even close.  Just dump it into the old catch-all called Peyronies Disease.  But, because it is really nothing like Peyronies Disease, just stick "atypical" in front of it.  Its like calling a sinus headache an atypical migrain.  They could have left it labeled ISS.  Thats a cool acronym.  But, noooooo! You know your in trouble after the introduction.

So do I understand you to mean that you feel more qualified to determine whether it fits the medical definition than these urologists at respected universities?

For instance could I boldly say, or even meekly say " After a thorough exam Anthony J. Bella, MD, Department of Urology, University of California, San Francisco;  Alp Sener, MD,The Department of Surgery, Division of Urology, St. Joseph's Health Center, The University of Western Ontario, London, Canada;   Kirsten Foell, MD,The Department of Surgery, Division of Urology, St. Joseph's Health Center, The University of Western Ontario, London, Canada; and Gerald B. Brock, MD The Department of Surgery, Division of Urology, St. Joseph's Health Center, The University of Western Ontario, London, Canada all agreed that I met the basic list of criteria to be diagnosed with Peyronies Disease but Liam, Peyronies Disease patient of 3 years, PDS contributor, and interpreter for the deaf has concludes otherwise?  I am glad Liam helped me find out that I really have a different disease that only shares a few characteristics with Peyronies Disease so i can be better informed"


Liam, I have to lovingly and laughingly say "Who the hell are you to presume with your experience and credentials that these men with their combined experience and credentials either just don't get it or are grossly and deliberately negligent in their diagnosis and classification of a group of characteristics resulting in penile deformity?

You be the judge.  Is this a form of Peyronies Disease or not?  And, regardless of your answer, how sure are you?

MY ANSWER: A lot more confident than I am in your determination and classification of what the disease is NOT, and I am very satisfied to let others decide based on the presentation.

Keep in mind that an atypical nose is called that because it is a nose, not because it is a tumor on someone's ass that doctors are not sure about.  Most diseases have atypical representations of that disease, thus the term.

[Liam]

My "private definition" is the same as any reputable definition on the internet.  Plaque leads to pain and curve.  I don't understand why this would be controversial.     Plaque is the defining characteristic.  It is what causes the curve and pain.  Maybe it is hard to find in some.  If something else that resembles Peyronies Disease is causing problems, why would we want to label it Peyronies Disease.

My speculation that Peyronies Disease does not "spontaneously resolve" is an entirely separate issue.  I have stated this is speculation.  I hope we all speculate, discuss, and come to a better understanding through the process.  BTW, we all agree the 50% spontaneous recovery they used to say (and some doctors still believe) is wrong.

Liam, I have to lovingly and laughingly say "Who the hell are you to presume with your experience and credentials that these men with their experience and credential either just don't get it or are grossly and deliberately negligent in their diagnosis and classification of a group of characteristics resulting in penile deformity?

My friend, I do not have the credentials and experience these researchers have.  What I have is the experience of reading.  Scars on the septum, without plaque is Peyronies Disease?   I guess they could be right and every definition of Peyronies Disease out there could be wrong. 

Here is another group discussing these lesions. 

 

Urol. 2007 Jan ;177 (1):179-83 17162033  [Select][Unselect] [Hide][Unhide] 
Isolated Septal Fibrosis or Hematoma-Atypical Peyronie's Disease? 
[My paper] William O Brant , Anthony J Bella , Maurice M Garcia , Kavirach Tantiwongse , Robert C Dean , Tom F Lue 
PURPOSE: Classically Peyronie's disease presents with penile curvature and/or pain, and is associated with a palpable penile plaque. We frequently examine patients with suspected Peyronie's disease ultrasonographically and have noted a subset of patients in whom we could identify only a circumscribed septal lesion. We identified characteristics of these patients. MATERIALS AND METHODS: Of our series of approximately 650 patients with Peyronie's disease 47 were identified with these lesions. RESULTS: Of the 47 patients 22 presented with penile curvature with or without accompanying or preceding pain. Of the 47 patients 17 had a significant history of trauma, although only had the classic stigmata of penile fracture. A total of 16 patients had no history of curvature, 7 presented with only penile shortening or focal lack of rigidity and 5 were incidentally found to have lesions during assessment for other complaints. Three patients presenting after trauma were noted to have septal liquefied hematomas, which we aspirated under ultrasound guidance. Followup ultrasound revealed minimal septal thickening. In 1 of these patients the hematoma was adjacent to more typical-appearing septal fibrosis. CONCLUSIONS: We theorize that these hematomas are due to septal fractures and may represent a forme fruste or possibly a precursor lesion of more typical septal fibrosis. Ultrasonographic evaluation may allow earlier identification and treatment of occult septal injuries or lesions and prevent subsequent fibrosis and its associated symptoms. 

I find their speculations theories  conform to the standard definition.  IMHO, they make a sound case.  In saying it may be a "precursor lesion" they are saying it is not Peyronies Disease.  It is the lesion (septal fracture) that may precede Peyronies Disease (typical-appearing septal fibrosis).


These patients do not have plaque.  Most of the guys here are painfully aware they have plaque.  Treatment must be different for these two groups.  This is the whole point of my soapbox.  I don't really care about the name they call it.  I just want scientist to be specific.  Words have meanings.

Having said that, I know definitions change as knowledge increases.  I don't think that is the case here.


ON A SEPARATE NOTE (A sharp I think)
After a quick search, I found three hits on conditions which could be mistaken (according to each report) for Peyronies Disease.  There were other references.  I post this as an FYI
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=7495125&dopt=Abstract[/quote]


http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8379702&ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum[/quote]

[
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=1569689&dopt=Citation[/quote]

[Liam]

Urethral manipulation syndrome. A new case][Article in Spanish]


Amat Cecilia M, Romero Pérez P.
Hospital Comarcal Marina Alta, Denia, Alicante, España.

The so-called "urethral manipulation syndrome" is distinct from the other andrological conditions of penile deviation. Unlike Peyronie's disease, the urethral manipulation syndrome is always secondary to any type of endourological instrumentation of the urethra. The deviation is always ventral and no tissue structural changes are demonstrable by ultrasound. Diagnosis is based on inspection and principally on a previous history of endoscopic exploration. If the condition does not resolve spontaneously, treatment is by surgical correction of the deviation.

PMID: 8379702 [PubMed - indexed for MEDLINE]

This seems to be at least one case of trauma to the penis causing a curve (ventral) that is not labeled Peyronies Disease.  Why?  No Plaque (structural changes).

[Hawk]

So do you think that these urologist that referred to atypical Peyronies Disease may have actually been looking at a condition that you found in your three hits?  If you do think that, you show no confidence in these urologists that have a specific interest in Peyronies Disease and were in fact interested enough to contribute to the Peyronies Disease research you think should be done.  Their entire point was to accurately identify the characteristics of atypical Peyronies Disease.  These were not some yaahoo family doctor looking at a urethral stricture for 10 seconds and shrugging his shoulders.

If you do not think they were looking at a condition covered by one of your hits then it only muddied our discussion and took it off track.

Do you also think that part of the problem with these urologists researching the characteristic of atypical Peyronies Disease is that they lack of reading of internet definitions of Peyronies Disease?

[Liam]

The three hits were FYI and not related to ISS study.  Sorry.  I guess I did not make that clear.  I will add "On a seperate note" before the three links.  I did say "I post this as an FYI.  That was my failed attempt to separate it from the rest of the discussion.  The symptoms from these are actually closer to Peyronies Disease than the ISS as desribed in the first paper I noted.


This is what the "atypical Peyronies Disease" researchers were studying.   The two groups were looking at the same thing.

Urol. 2007 Jan ;177 (1):179-83 17162033  [Select][Unselect] [Hide][Unhide] 
Isolated Septal Fibrosis or Hematoma-Atypical Peyronie's Disease? 
[My paper] William O Brant , Anthony J Bella , Maurice M Garcia , Kavirach Tantiwongse , Robert C Dean , Tom F Lue 
PURPOSE: Classically Peyronie's disease presents with penile curvature and/or pain, and is associated with a palpable penile plaque. We frequently examine patients with suspected Peyronie's disease ultrasonographically and have noted a subset of patients in whom we could identify only a circumscribed septal lesion. We identified characteristics of these patients. MATERIALS AND METHODS: Of our series of approximately 650 patients with Peyronie's disease 47 were identified with these lesions. RESULTS: Of the 47 patients 22 presented with penile curvature with or without accompanying or preceding pain. Of the 47 patients 17 had a significant history of trauma, although only had the classic stigmata of penile fracture. A total of 16 patients had no history of curvature, 7 presented with only penile shortening or focal lack of rigidity and 5 were incidentally found to have lesions during assessment for other complaints. Three patients presenting after trauma were noted to have septal liquefied hematomas, which we aspirated under ultrasound guidance. Followup ultrasound revealed minimal septal thickening. In 1 of these patients the hematoma was adjacent to more typical-appearing septal fibrosis. CONCLUSIONS: We theorize that these hematomas are due to septal fractures and may represent a forme fruste or possibly a precursor lesion of more typical septal fibrosis. Ultrasonographic evaluation may allow earlier identification and treatment of occult septal injuries or lesions and prevent subsequent fibrosis and its associated symptoms. 

Do you also think that part of the problem with these urologists researching the characteristic of atypical Peyronies Disease is that they lack of reading of internet definitions of Peyronies Disease?

I could speculate all day about the reasons the two groups reported differently.  But, instead, I'll explain the flaw I perceived.

The first group labeled their finding as a fact, "Nonpalpable Scarring of the Penile Septum As a Cause of Erectile Dysfunction: An Atypical Form of Peyronie's Disease" and "Aim. We aim to identify the clinical characteristics of patients presenting with this atypical form of Peyronie's disease characterized by the absence of palpable deformity."  They went in with the idea this was a form of Peyronies Disease.  A bias was introduced that flawed the study.

Their entire point was to accurately identify the characteristics of atypical Peyronies Disease.

Yes, that was the problem.  They should have identified the characteristics of septal scarring and left the speculation out.  It would have been entirely appropriate to include speculation in the "Discussion" portion of the paper.  For example, they could have said we believe this to be an atypical form of Peyronies Disease.

The second group stated their obsevation and stated theories.  Note the language used, "We frequently examine patients with suspected Peyronie's disease ultrasonographically and have noted a subset of patients in whom we could identify only a circumscribed septal lesion."  also "We theorize that these hematomas are due to septal fractures and may represent a forme fruste or possibly a precursor lesion of more typical septal fibrosis."


On a separate note:

Urethral Manipultion Syndrome only shows (in the context of these posts) it is possible for a trauma to cause curvature without causing Peyronies Disease.



BTW, IYO, What is the definition of Peyronies Disease that we should use?

[Hawk]

Liam,

I sent you a pm about moving these out of this topic.

Peyronies Disease is scar tissue formation that has hyertropic or keloid characteristics and forms in the tunica or carevernosal chambers of the penis.  This scaring, plaque, fibrosis, over-runs and replaces healthy elastic penile collagen with cross linked or non-elastic collagen resulting in the many manifestations we all know so well.  While the geneses, and etiology of the disease is not fully understood, when HEALTHY tissue is replaced with non-elastic scar tissue, that is Peyronies Disease.     

Injury and other unknown factors can trigger this replacement of healthy tissue.

In contrast, when scar tissue is confined to the limited boundaries of an injury, that is just normal healing. 

I have reason to think Peyronies Disease is very under-diagnosed, rather than contending that a large number of Peyronies Disease diagnoses are in fact some other diseases.  If Peyronies Disease were truly over diagnosed then it would have a very negligible impact in terms of numbers and we better come up with a cure here because no one else will care.

[Tim468]

Liam,

I think your problem is that you are being a bit rigid about how you define Peyronie's (and I think it is a problem, because you seem stuck on this point to the point of silliness, IMHO).

I think that this boils down to how physicians make diagnoses at all, ever. Typically, there are characteristics that help one make a diagnosis, and occasionally, there is a sine qua non that defines the disease. An example would be cystic fibrosis. This is a clinical disorder characterized by chronic lung disease and pancreatic insuffiency. The understanding of this disorder has grown by leaps and bounds (and FAR faster than the biologic understanding of Peyronies disease) because of the dedicated familes that keep pushing for a cure, and put their money where their mouth is.

But making a diagnosis is not so easy. That the seat test shows more chloride added to the testing repetoire - now we must see a seat test with a chloride over 60 to make the diagnosis.

Then we discovered the gene.

Then we discover more genes, and more, and more - now 2500 unique different genetic alterations that can lead to CF.

So how do we diagnose it? Well, the answer is by a gestalt assessment, with included data including the sweat test, and full genetic analysis. There are still patients that we see that have equivocal sweat tests, no identifiable genetic defect and we still follow them closely, perhaps saying "we think that you have CF, so we are going to pretend you do just to be on the safe side".

IOW, it is a clinical diagnosis. And as such, it has specific findings - but it is not required that all features be present.

For the sake of answering your argument, although I am not a urologist, I very much believe that any reputable urologist would identify the following men as having Peyronie's Disease:

1) a man with a 6 month history of painful erection, mild Erectile Dysfunction, a new deviation to the right at mid shaft with a palpable induration or nodule at the site of angulation.

2) a man with a 6 month history of painful erection, mild Erectile Dysfunction, a new deviation to the right at mid shaft without a palpable induration or nodule at the site of angulation.

3) a man with a 6 month history of painful erection, no Erectile Dysfunction, a new deviation to the right at mid shaft without a palpable induration or nodule at the site of angulation.

4) a man with a 1 year history of a (relatively) new deviation to the right at mid shaft with a palpable induration or nodule at the site of angulation.

5) a man with a 1 year history of a (relatively) new deviation to the right at mid shaft without a palpable induration or nodule at the site of angulation.

He would likely NOT make the diagnosis of Peyronies Disease with the following findings:

1) a man with a lifelong history of a deviation to the right at mid shaft with a palpable induration or nodule at the site of angulation (although he might strongly consider it, and wonder if the guy was too stupid to have noticed the change when it occured)(occasionally we see dumb patients).

2) a man with a 1 week history of a (relatively) new deviation to the right at mid shaft, painful erection without a palpable induration or nodule at the site of angulation (he might suspect that it will prove ultimately to be Peyronie's Disease, but hopeful that it a traumatic event that will heal completely).

3) a man with a history of taking vitamin E for two days and developing angulation that was severe, but had resolved by the time of clinic visit five days later.

4) a teenager with a "curve" to his erect penis (not sure when he got it) without any plaque palpable.

The point is that the diagnosis must make sense. It is rarely a requirement for a diagnosis to be made that all criteria must be present - only that no other diagnosis make sense.

To take care of a child with CF - a terrible disease with life-shortening implications - we never take the diagnosis lightly. We move heaven and earth to figure out if we are on the right or wrong track if we suspect it. Such is not the case for Peyronie's. General practioners ignore it, try to reassure, or make the diagnosis without thinking.

It is clear that as our understanding of Peyronies disease grows, we will grow in our understanding of how it works, and who is at risk. If a patient of mine has CF and no pancreatic insufficiency, I tell them they are lucky, not that they can't have CF (as one local PMD did).

I do not have any easily palpable plaque. But the new dent at the left base of my penis, which is painful on erection is due to Peyronie's Disease. Period. I am aware vaguely that it feels a bit thicker there when I palpate - but that is not so obvious as it is said to be in others. I also have a fine linear scar on my arm, and I cannot palpate any obvious scar tissue there with my eyes closed - but it's still there.

I would suggest not focusing so much on whether or not someone has plaque, because it is not useful. We hear planty of stories here that make no sense - a lack of plaque can hardly be used to filter out what we are hearing here or help us arnchair diagnosticians make any diagnoses at all.

Tim

[Liam]

What causes the bend if not plaque (palpable or otherwise)?

Also, when did this become MY definition?

General practioners ignore it, try to reassure, or make the diagnosis without thinking.

If you can say this, why am I being silly.  It makes my case.  As a matter of fact, as I reread your post, you say more to convince me of my view than you do to convice me I'm wrong.

I am at a loss (the people rejoice.....rah). 

[Hawk]

Liam,

I offered my definition of Peyronies Disease and you did not comment.

Just what do you see as the definition?

[Liam]

I like your definition.

From Merck Manual -Online Medical Library

Peyronie's disease is fibrosis of the cavernous sheaths leading to contracture of the investing fascia of the corpora, resulting in a deviated and sometimes painful erection.

They all include the same things: 1) Plaque/fibrosis 2) deviation/bend 3) Pain   
But, its the fibrosis (whether you can feel it or not) that causes the deviation and the pain.  If you can feel the plaque, you can be pretty sure of what you've got.  If you can't, just do imaging until you're sure no plaque/fibrosis is there.  At that point, start looking for the real problem. 

In contrast, when scar tissue is confined to the limited boundaries of an injury, that is just normal healing.

I suspect non-progressive scars from penile fracture are being labeled Peyronies Disease.

[Hawk]

I suspect non-progressive scars from penile fracture are being labeled Peyronies Disease.

I very much doubt that for a few reasons:

1. Unless your last name is Bobitt, the degree of likely damage to the penis is very UNLIKELY to be so large that normal healing would cause significant deformity. 

2. It certainly would not be progressive

3. It would occur in such close association with the injury that there would be little mystery that your penis was ripped half off and now it has a stable bend.  Who would call that Peyronies Disease?


PS:  I am not at all certain that all fibrosis can be imaged.  Certainly blood flow can be imaged but non-palpable, non-calcified, fibrosis

[Tim468]

The key factor is this: fibrosis may not be palpable, but present.

If one cannot feel it, or even image it, does not mean it is absent. For instance, one may not hear evidence of lung disease at all, an xray may be normal, and a pulmonary function test may be normal. Yet when one does a high resolution CT scan of the chest, it shows disease (see image).

The new ability to show disease does not meant that 5 years ago before ultrahigh resolution CT that such disease did not exist - we are just getting better at diagnosis.

My point is that no clinician would say "you don't have CF because I cannot SEE the proof of it", when we have other evidence that does show it is present.

I may not have PALPABLE plaque, but I have Peyronies.

Tim

[George999]

Tim, You are reminding me of the part about the practice of medicine being more of an art than a science.  It seems like that is still true even with all of our technological advances.  Trying to understand human affliction is, like discerning and iceberg, more about trying to understand what is going on under the surface than just taking at face value what we are seeing with our eyes.  And that is just one more reminder of how valuable doctors are in the process of diagnosis.  Thank you for once again bringing some valuable focus to this discussion.  - George

[Liam]

My point is that no clinician would say "you don't have CF because I cannot SEE the proof of it", when we have other evidence that does show it is present.

There are still patients that we see that have equivocal sweat tests, no identifiable genetic defect and we still follow them closely, perhaps saying "we think that you have CF, so we are going to pretend you do just to be on the safe side".

So the doctor should say something like, "We see no evidence of fibrosis but, due to your other symptoms, we are going to treat you for Peyronies Disease"  I could live with that.  Yeah, like thats going to happen.

I may not have PALPABLE plaque, but I have Peyronies.

I am aware vaguely that it feels a bit thicker there when I palpate

The plaque is there and in significant quantity to cause a curve.  Imaging would show it.  Imaging shows ISS.

Your point is well taken not to rule it out.  But, on the other hand, don't be too quick to rule it in when there is no fibrosis evident.
-----------------------------------------------------------------------------------------------------------------

*Related to other portions of our discussions*

While reading up on Penile fracture, I ran across this:

Résumé / Abstract
Purpose: This study was performed to determine whether patients with penile fracture or a long history of forcefully bending the erect penis (taqaandan), as models of acute and chronic penile trauma, had an increased rate of Peyronie's disease (Peyronies Disease). Materials and Methods: The study included 193 surgical cases of penile fracture (average followup 85 months), 150 cases of long history of taqaandan, and 50 cases of Peyronies Disease. All 3 groups of patients were interviewed and physically examined. Results: Signs of Peyronies Disease were found in only 1 case of long-term taqaandan and in no case of penile fracture. None of the 50 cases of Peyronies Disease had a history of penile fracture. Conclusions: Severe, acute trauma of penile fracture and moderate, chronic buckling injury of taqaandan are not associated with later development of Peyronies Disease. These findings question whether the hypothesis that trauma, trauma-induced smoldering inflammatory cascade and aberrant wound healing are the main causes of Peyronies Disease. Alternative, plausible, evidence based explanations should be sought for the etiology of Peyronies Disease. Any theory on the etiology of Peyronies Disease should provide an explanation for total lack of occurrence of Peyronies Disease following the trauma of penile fracture.

Source: http://cat.inist.fr/?aModele=afficheN&cpsidt=15855323

Woah! How did I miss this until now?

[Liam]

If one cannot feel it, or even image it, does not mean it is absent.

But, how likely is it that its present.  I can't help but ponder, if it is not a sufficient mass to show up on imaging, how likely is it to present with symptoms.  I don't know the answer.  I imagine not very.


George,

I do appreciate the skill of a diagnostician (especially Tim).  I just prefer a more objective process.  I like my art from the museum (Not really.  My taste in art is watching old Rocky and Bullwinkle cartoons.)
----------------------------------------------------------------------------------------------------------------

Not directly related to above discussion

Note "differential diagnosis" topic

Lue's book excerpt:

http://books.google.com/books?id=LW1fxcZmYyYC&pg=PA135&lpg=PA135&dq=differential+diagnosis+peyronie's&source=web&ots=ExlvH3NPqU&sig=4OeqNAs7ti0kt9yaJPw6J9HRZ_0#PPA135,M1

[George999]

I do appreciate the skill of a diagnostician (especially Tim).  I just prefer a more objective process.

But Liam, I think the above is actually a very subjective statement.  Objectivity means that the diagnostician is free from the limitations of hard evidence and can actually deduce from a given set of circumstantial signs a rather reliable tentative diagnosis.  If you limit the doctor to hard evidence, you will actually miss a lot of afflictions that will then go untreated until they finally present, at which point it will be too late for the patient.  - George

[Liam]

George,

I have been misdiagnosed three times (that I know of).  One of them could have had fatal consequences.
My former doc told me, "your prostate is a little large, nothing to worry about".  That was a subjective statement.  He should have biopsied (an objective test). 

My dad died from colorectal cancer.  The doctor (bone) told him he should learn to live (he could not lie down and had to sleep sitting up) with pain because he was getting older. This is another subjective statement.  My dad also presented with a change in bowel habits.  The doctor should have referred for a colonoscopy (objective).

In each case, the symptoms were there.  The tests were there.  If the doc had followed the road map in front of him instead of trying to fit my dad in a pigeon hole, my dad might have survived.

This was where I was coming from.  Now, I am all about running tests and ruling out. 

So, I think we are describing the same process after all.  In the immortal words of Gil Grissom (CSI), "follow the evidence"

[George999]

Liam, I couldn't agree more with you on this.  My point was rather in the other direction in the sense that just because the objective tests FAIL to indicate a specific health condition, that DOES NOT mean that that condition should be ruled out.  If the doctor has a gut feeling that something is going on, he or she should be acting appropriately on that gut feeling.  In this regard, I agree completely with Tim's guidelines on Peyronies.  When I said that medicine is more an art than a science, I was not meaning to infer that physicians should ignore the science, but rather apply the science to confirm the art.  But, in reality, the art, not the science is the leading edge.  If it were not, you would have doctors blindly running one test after another in order to detect abnormalities.  And that is simply not the way medicine is performed.

On the other hand, where there is a deformity in erections that appears suddenly out of nowhere, the lack of palpable plaque DOES not rule out Peyronies no matter what you might imagine.  And I think those are the kind of subjective, speculative statements some of us are taking issue with.  - George

[George999]

In defining Peyronies Disease, I think we also have to differentiate between frank Peyronies Disease and the apparently precipitating underlying histological issues that Tim touched on.  This is sort of like differentiating between in situ and cancer.  In reality,  for successful treatment to occur, both the histology AND the Peyronies Disease must be addressed together ALONG with whatever might be instigating the histological issues.

[Liam]

Palpable seems to be the word that is the sticking point.  Maybe the word "findable" would be more correct.  Why would any of the symptoms happen if there were not plaque/fibrosis (that could still be considered Peyronies Disease)?  So far nobody has addressed this question.

Does anyone have any thoughts on the "penile fracture not leading to Peyronies Disease" abstract in an earlier post?
 

Alternative, plausible, evidence based explanations should be sought for the etiology of Peyronies Disease. Any theory on the etiology of Peyronies Disease should provide an explanation for total lack of occurrence of Peyronies Disease following the trauma of penile fracture.

[Liam]

Excerpt:

Classical Peyronie's disease may be differentiated from localised cavernous fibrosis due to direct external trauma to the corpus, injury from a fractured penis, or damage to the cavernous tissue from intracavernous injections. Atypical areas in the crura are probably due to external trauma.

Source:  http://www.blackwell-synergy.com/links/doi/10.1111/j.1743-6109.2004.10116.x/full/

[George999]

Liam,  Once we come to the point where we understand that the Peyronies process begins with abnormal Tunica tissue in the first place, we then have to understand that any trauma, however minor or insignificant, can start the process of fibrosis.  In fact, the degree of susceptibility to Peyronies might well hinge on the degree of histological change in the tunica with more change causing one to be more susceptible to injury.  Thus, I think it might also be helpful to realize that that underlying histological 'change' or 'abnormality' is probably not like a '0'/'1' digital state, rather it is likely that is is more analog in its development, with small changes potentially proceeding larger ones.  And once you combine this with some sort of stress or trauma, the resulting fibrosis is likely not in '0'/'1' form either, but is likely to range from mild to severe.  And increasing fibrosis would make the tunica in the area of that fibrosis incrementally stiffer as the fibrosis progresses.  The definition of Peyronies, in my mind, would occur at the point where there becomes a definable deformity in erection that was not present previously that is attributable to the underlying fibrosis.  At some point that fibrosis might result in a progressive discernible thickening of the tunica.  But it is entirely possible if not likely that a mild fibrosis that is capable of instigating a deformity might well not cause any discernible/detectable/imagible thickening of the tunica.  Remember, it would merely require enough loss of elastin in the tissue to compromise its ability to stretch to its full size and that might not be a whole lot of change.  But at the other end of the spectrum, the tunica might become affected to the point of becoming downright leathery in its consistency, making Peyronies an easy diagnosis.  On the other hand, my observation has been that the fibrosis process can cause plaques that do not result in any noticeable deformity in erections.  They are simply abnormal accumulations of collagen that refuse to break down in normal manner and are very palpable but have little or no effect on the process of erection.  Is this condition Peyronies?  You tell me.  I suspect not, and yet the underlying problem is still the same and most physicians would immediately diagnose this as being Peyronies.  In short, I really suspect that a large part of this problem is that we are simply not dealing with black and white here, but rather with a huge range of grayscale that can be rather unsettling to those who are looking for simple answers.

As for Penile fracture causing Peyronies, I would suspect that that would be completely dependent on the underlying histological process that Tim referred to.  In the presence of those underlying histological changes, it would seem that penile fracture would indeed 'cause' Peyronies, whereas in their absence, Peyronies would be unlikely and completely healing would likely occur.  - George

[Liam]

I can mostly agree with you.  Some "grow" more fibrosis/plaque than others.  It is the fibrosis that differentiates Peyronies Disease from some other condition causing deformities of the penis.

I am intrigued by the numbers though.  I keep going back to this study.  I'm going to copy it again for convenience.

Urol. 2007 Jan ;177 (1):179-83 17162033  [Select][Unselect] [Hide][Unhide] 
Isolated Septal Fibrosis or Hematoma-Atypical Peyronie's Disease? 
[My paper] William O Brant , Anthony J Bella , Maurice M Garcia , Kavirach Tantiwongse , Robert C Dean , Tom F Lue 
PURPOSE: Classically Peyronie's disease presents with penile curvature and/or pain, and is associated with a palpable penile plaque. We frequently examine patients with suspected Peyronie's disease ultrasonographically and have noted a subset of patients in whom we could identify only a circumscribed septal lesion. We identified characteristics of these patients. MATERIALS AND METHODS: Of our series of approximately 650 patients with Peyronie's disease 47 were identified with these lesions. RESULTS: Of the 47 patients 22 presented with penile curvature with or without accompanying or preceding pain. Of the 47 patients 17 had a significant history of trauma, although only had the classic stigmata of penile fracture. A total of 16 patients had no history of curvature, 7 presented with only penile shortening or focal lack of rigidity and 5 were incidentally found to have lesions during assessment for other complaints. Three patients presenting after trauma were noted to have septal liquefied hematomas, which we aspirated under ultrasound guidance. Followup ultrasound revealed minimal septal thickening. In 1 of these patients the hematoma was adjacent to more typical-appearing septal fibrosis. CONCLUSIONS: We theorize that these hematomas are due to septal fractures and may represent a forme fruste or possibly a precursor lesion of more typical septal fibrosis. Ultrasonographic evaluation may allow earlier identification and treatment of occult septal injuries or lesions and prevent subsequent fibrosis and its associated symptoms. 

forme fruste - An incomplete or abortive form or manifestation of a condition or disease.
circumscribed - bounded or limited; confined to a limited space.
precursor In clinical medicine, a sign or symptom that heralds another

approx. 650 = number of men seen for Peyronies Disease
47/650 = 7.23% Total circumscribed septal lesion
22/650 = 3.38% Curve but no palpable plaque (my interpretation -verify for yourself)
16/650 = 2.26% No curve
07/650 = 1.07% Penile shortening or focal lack of rigidity
You can look at the other numbers.  I wish I could see how the numbers overlap.

Circumscribed septal lesion sure describes the group we've been discussing.  It seems to fit what everyone on this topic has been saying!  As silly as that might seem.

[Hawk]

Liam,

I may be getting old but if we were standing face to face having this conversation, this is where I would say, "so whats your point"?  It seems like you are grasping at straws to establish some very vague point.

From the literature I have read, even the "experts" disagree upon when a condition is or is not diagnosed as Peyronies Disease.  Does it really matter what percentage of fractures turn into Peyronies Disease?  Does it matter what percentage of DC patients get Peyronies Disease?  We know there is a connection.  That was never meant to imply they are inseparable.  It may matter from a standpoint of interest but certainly not from a standpoint of definition or who really has Peyronies Disease and who doesn't.

I was interested that the link you posted also made some other interesting (and questionable) points, many which run counter to the positions you have taken.  Here are a few:

The literature is devoid of robust epidemiologic studies ...

The data available suggest that the incidence of Peyronie's disease (as defined by a plaque) is higher than previously thought.

The prevalence... depends upon the definition and the means of detection. 

The pathophysiology of Peyronie's disease remains poorly understood and is considered to be multifactorial with the interplay of a genetic predisposition, trauma and tissue ischemia.

It is likely (but not certain)that the final common pathway involves fibrogenic cytokine induced fibrosis in the tunica albuginea. 

A history and examination are usually sufficient to make the diagnosis and further investigation is only necessary in selected patients.
 
There is a high chance of spontaneous improvement in men with untreated Peyronie's disease. ...a 10–82% improvement in angulation with time.

[Liam]

This whole discussion centers on my assertion there are men with symptoms similar to Peyronies Disease without actually having the disease.  Said a different way, there is a significant number of men who have been diagnosed with Peyronies Disease who really don't have it.  The several references I've posted make at least a prima facie case for this.

Does it really matter what percentage of fractures turn into Peyronies Disease?

 

Only that it shows trauma alone does not cause Peyronies Disease.  Not everyone believes this.

Does it matter what percentage of DC patients get Peyronies Disease?  We know there is a connection.

Thats how we know.

It may matter from a standpoint of interest but certainly not from a standpoint of definition or who really has Peyronies Disease and who doesn't.

If the two are related and if they are both fibrotic conditions, men without fibrosis could only be diagnosed with Peyronies Disease if people with non fibrotic constrictures of the hand could be diagnosed with Dupuytren's.  Also, if you have Dups and then you start getting a bend in the penis (or vice versa), you have a good indication of what the diagnosis is.  I read at least on article (seems like it was for ER docs) that said if the patient presented with Peyronies Disease symptoms, check the palms for Dups.  Other than these loosely related items, I don't maintain, nor have I ever maintained, there is any relevance to diagnosis.

The link  ( http://www.blackwell-synergy.com/links/doi/10.1111/j.1743-6109.2004.10116.x/full/ )
is interesting. 

A recent review of the literature [7] found that there was a 35–100% improvement in pain, 11–100% improvement in plaque size, and a 10–82% improvement in angulation with time

.

I agree, that is what the literature says.  Actually, I could claim improvement.  My "turtle effect" was eliminated. My condition, however, is worse.

A history and examination are usually sufficient to make the diagnosis and further investigation is only necessary in selected patients.

It seems to me, the selected patients to which they refer are the *subset of patients (47/650) that don't have identifiable plaque/fibrosis. (*see my previous post).

So far, I have presented several pieces of evidence for my point of view.  I would like to see any evidence, for Peyronies Disease without identifiable plaque, showing it is, indeed, Peyronies Disease.

Now let me say gain for the record.  As a support group (we are that of sorts and much, much more) I don't care about the reason for your problem other than for you to get proper help.  A man with a bent penis really just wants things better.  I do.

I care about this issue because I believe it is important to understand what a disease is.   OK, that sounded really obvious.  Why would we not question and theorize and ponder.  Why is it silliness?  Is it a "blasphemy", of sort, to ask if this small group of men who who don't have verifiable plaque/fibrosis might have something else.  Why would I even care?  Because you have to know what the problem is before you can fix it.  The two "atypical" studies have at lest recognized this group is out there and their needs are different.

[Hawk]

Liam,

I think I am losing interest in this point / discussion.  I have the following impression.  I think your question is relevant.  I just think you are presuming things that we are far from having answers to.

I conclude you are more convinced than the evidence warrants and you are running all evidence through a filter that supports your point.  If something supports it you weight that remark/study as very weighty.  If a scrap of evidence casts doubt, you zip by it on the way to another piece of supporting evidence.  Now, I could be wrong, but that is the impression I am left with.  I am unmoved by your argument since it appears to me like cherry picking.

I soundly agree that trauma absent all of the other factors that produce Peyronies Disease, would not produce Peyronies Disease.  I feel there has long been the acknowledgment here (with no contrary point of view) that several factors must be present to initiate Peyronies Disease.  I also think that no one in the research or medical community pretends to know all those factors much less all the switches that turn those factors on or off.  I think that many of the complex interactions of those factors with other body processes (both good and bad) are also a mystery.

As a result of the points in this last paragraph, I conclude it is presumptive to state either of the following False statements.

1.  All Peyronies Disease with clearly identifiable palpable plaque has the same etiology and therefore similar treatment.

2. Peyronies Disease-like symptoms with no detectable plaque (even with imaging) have their own unique etiology and can be clearly classified as NOT being Peyronies Disease.


While broken penis, DC, and other patient history may give clues, it does not establish the specific processes going on in that man's penis since we don't even know the process going on in the most classic case of Peyronies Disease.  It therefore seems very presumptive to me to declare such artificial divisions of Peyronies Disease /Peyronies Disease-like especially when it is declared by a person with no background in medicine or medical research.

Now, clearly a person with an extensive research background can choose to define Peyronies Disease as they prefer based on some subset of symptoms. Clearly, such a definition will move men in or out of that group but that does not mean the definition is anything but that person's artificial description.  It ignores issue such as common etiology and treatment.  Both etiology and treatment remain largely unknown or we would not be here.

I do think it is very safe to say athlete's foot, restless leg, and congenital curve are not Peyronies Disease because they are clearly understood conditions that exhibit none of the key processes common to Peyronies Disease. 
 

[Liam]

Hawk,

Your cherries are my plums   To my satisfaction, I have presented two cases indicating a subset referred to by some as "atypical" Peyronies Disease which by the authors assertion are devoid of the classical appearance of Peyronies Disease.  One of the papers suggest it may be a precursor and state the condition is "circumscribed". 

It therefore seems very presumptive to me to declare such artificial divisions of Peyronies Disease /Peyronies Disease-like especially when it is declared by a person with no background in any form of medicine or medical research.

   I posted these because they are medical researchers.

Now, clearly a person with an extensive research background can choose to define Peyronies Disease as they prefer based on some subset of symptoms. Clearly, such a definition will move men in or out of that group but that does not mean the definition is anything but that person's artificial description that ignores issue such as common etiology and treatment.

  This group did theorize on a common etiology by the terms "form fruste" and "precursor lesion".

BTW, What makes their description "artificial".  It seems they wrote what they observed.


I ammended the following trying to keep an open mind.


I conclude it is presumptive to state either of the following False statements.


1.  All Peyronies Disease with clearly identifiable palpable plaque has the same etiology and therefore similar treatment.

1b. All Peyronies Disease with clearly identifiable palpable plaque do not have the same etiology and therefore similar treatment.


2. Peyronies Disease-like symptoms with no detectable plaque (even with imaging) have their own unique etiology and can be clearly classified as NOT being Peyronies Disease.

2a. Peyronies Disease-like symptoms with no detectable plaque (even with imaging) do not have their own unique etiology.

I think I am losing interest in this point / discussion.  I have the following impression.  I think your question is relevant.  I just think you are presuming things that we are far from having answers to

.

I feel I have successfully presented and defended my case.  I will refrain from initiating any more discussion on the topic.  I will, however, respond to any posts as needed.

[whygodwhy]

im not sure if i have Peyronies Disease

I curve slightly under 15 degrees left and 20 degrees downward
there's redness along the underside of the shaft in the direction that it curves

but it is not hard or raised
I don't have any pain either

is this still considered a "plaque"?
its my understanding that to have Peyronies Disease you have to have a plaque

I had an ultrasound and they said there was no Calcified plaque (not sure if that means there was no plaque) but they said there was scar tissue
which makes sense since I used to have straight erections

is this peyronies?
what's the difference between plaque and scar tissue?
im not sure if i have plaque so im not completely sure if i have Peyronies Disease, but i think i do.  I want to be sure before i make efforts to try and dissolve a plaque that is actually just scar tissue, and so i can go about the best method of treatment

[George999]

whygod, sounds like you DO have Peyronies.  I would not get to concerned about how to differentiate 'plaque' from 'scar tissue' since even the docs don't seem to be able to agree on that one.  Suffice to say that not all scar tissue is created equal and Peyronies scar tissue probably displays some degrees of variation.  I wouldn't worry about that part.  Scar tissue or plaque, you should probably be more concerned about getting started with some appropriate treatment.  Topping the list:

1.  Make sure your diet and lifestyle are healthy - especially in terms of using non-inflammatory oils and fats instead of inflammatory ones.  Make sure your weight is healthy, avoid the kinds of things that trigger metabolic syndrome and insulin resistance.

2.  Full spectrum Vitamin E with all 8 tocos.

3.  Pentox if your doc will prescribe it for you.  Best Peyronies drug currently available and its generic and real cheep.

4.  Arginine.  SAN VasoFlow is just about the best out there in my opinion.

5.  Horny Goat Weed or Viagra or Cialis if you can get it.

6.  Last but not least, VED AFTER the inflammation is passed.

7.  Lots more on this forum that you can try, but the above list contains the heavy hitters in my perception.  Others will supply what I left out I am sure.  Your in a good spot right here to find the help you need.

- George

[Liam]

John Bobbit has scar tissue not Peyronies Disease.

You said you've had this for 10 years.  If there has been no change in 10 years, its probably NOT Peyronies Disease.  How old are you now?  I'm guessing early twenty-something?  It is SO rare to get Peyronies Disease at that young age.

BTW, Any response here, including mine, is speculation.

Liam

Also, George's recommendations are under the category "BETTER SAFE THAN SORRY".  THey can't hurt.  And, if you have Peyronies Disease, they may help.

[Hawk]

I really think that one thing that confuses a lot of people is the tossing around of terms like "plaque" and "scar tissue"....

Lumps occur when there is an almost tumor like process going on that results in an accumulation of collagen.  These lumps, in and of themselves, though abnormal and definitely not desirable, are not the cause of the deformities although they may or may not coexist with the deformities.  The deformities are actually caused by another process.  This is the process whereby collagen and fibrin displace elastin in the tissues.  Thus a person can have a significant sized "plaque" and exhibit little or no deformity as long as the localized tissue retains sufficient elastin.  On the other hand, there may be no lump at all, but if the tissue is depleted of elastin, there will be deformity.  In some cases, both conditions are concurrent.  When you treat such a condition with the objective of getting rid of collagen, the result will be that the lump will disappear, but since the remaining tissue is elastin deficient, it still refuses to stretch, which results in the deformity remaining.  This is one huge problem I see with the collagenase approach.  If whatever strategy proposed does not take into account the rejuvenation of elastin, it will be of no use in eliminating deformity.

- George

George,

I speak as a member whose personal nature is to always look for holes in bold absolute statements unless they are supported with facts on a point by point basis.  I have to wonder what a Peyronies Disease specialist or researcher might think when reading your explanation.   I suspect they may chuckle to themselves and that they may be able to shoot holes in many of the individual statements.  The problem is that you are intelligent and articulate enough to convince many people that your use of collagen vs elastin, or your dividing up the processes as two separate processes, are proper.  While this may be a working description to make a point, I doubt these are an accurate description of Peyronies Disease.  It is my opinion that if we strictly accepted some of these points we would find ourselves having to unexplain them down the road.  We of course have no way to research these ideas.  We can not even produce theories but are forced to speculate with fragmented evidence. 

Your posts are usually cautiously sprinkled with warnings of: "personal opinion" and other disclaimers but many people probably still suspect you may have more facts to support these theories that you do have.  It is clear that some take this information, ask not one question, and await further advice on how to act based on this information.  Speaking as one member, I certainly do not want to see such well thought out expression suppressed, but I do want to keep it from going unquestioned.  Your understanding certainly varies from mine.

Somewhat aside from this, you have the ability to work on an in-depth post about your understanding of Peyronies Disease complete with documenting the basis for your understanding.  If you ever decide to undertake such a project I am sure it would find a topic on the forum for full discussion.

[George999]

Hawk,

Feel free to shoot away at my posts as much as you see fit.  Don't worry, I don't take offense.  As for the collagen/elastin issue, I gather from the research I have seen that both elastin deprivation AND collagen accumulation are known characteristics of Peyronies.  Would you accept that statement?  From that, it becomes my speculation that these two characteristics are not hard linked because only that type of relationship could account for the type of behavior that I have personally observed in my own case.  I have seen palpable plaque which does not result in deformity during erection.  I have also seen deformity with NO palpable plaque but only a certain hardness in the localized area of the tunica during erections.  I would openly admit that I have no research to back up this speculation.  I would certainly like to see research in this direction, but I am not sure it would justify the investment since it probably would not contribute the kind of knowledge that would facilitate a cure.  But it certainly is helpful in understanding why elimination of palpable plaque is not the be all and end all of Peyronies treatment.  And even some doctors seem to think that the whole goal is to eliminate the palpable plaque.  Once they can't feel anything any more, you're cured, even if you do still have a 90 degree bend.  But if you have any research that disputes ANYTHING that I say, please point it out.  I have been wrong more times than I can count and you won't so much as ruin my day if you prove me a liar one more time.  I am very willing (in fact anxious) to learn and will be grateful for any contrary information you can provide.

Respectfully,

George

[Hawk]

"Why"

Well it looks like one thinks you fit the definition of Peyronies Disease and one thinks you do not.


Liam - I reject your criteria for Peyronies Disease.  You started by expressing the fact that if it gets better that it can be assumed it was not Peyronies Disease.  Now you seem to expand that to say that you think if it ever stabilizes that it was not Peyronies Disease.

Who in the medical community supports that view?  While that is a bit of a rhetorical question I know you will feel free to answer if you find someone that does. 

[Tim468]

Dogmatic thinking serves no purpose. Black and white is rarely an accurate description of the world.

For instance, elastin and collagen are simply two biologic materials formed via processes that individually and together affect the stretchability of a tissue. It makes sense to talk about them because they are important. I am sure a biologist or researcher who worked with either would find out discussions simplistic and silly.

However, what they might not be willing to think about is (in simple terms) how simple measures might lead to changes.

We talk about the effects of the VED on collagen - we have no clue. In fact, scarred tissue may not budge, but adjacent tissue may instead stretch out more than baseline, so that the overall tissue is more distensable and thus the penis goes straight.

The fun thing about speculating is that we can argue without facts as to what the benefits we see sometimes are due to.

Tim

[Hawk]

George,

while this discussion may take more energy and time than I have, here goes.

My understanding:

1. Almost every tissue in the body is made up of one of the many forms of collagen.  There are dozens of types of collagen.  We seemed to get away from specifying the type I, type II, type III (types of collagen worth discussing) when discussing collagen.  We over generalize and simplify the collagen issue to the point of being erroneous.  This for instance this why generally suppressing collagen would never work (as I know you understand).  I think it is correct to say elastic is only a component of collagen type II (I actually think type II is a componet of elastin).  This means to say that "lumps" are NOT the the accumulation of collagen as much as they are the replacement of one type of collagen with another.  They are most like "lumps" in the immature stage of inflammation and shrink as they mature.

2. Plaque when used in conjunction with Peyronies Disease (as opposed to arteries or teeth) is a term that is synonymous with hypertropic scar tissue.  In other words it is scar tissue (type III possibly changing to  type I) that over-runs healthy tissue which is made up of type II collagen.  Normal scar tissue stays within the bound of wounds.  This makes plaque/scar tissue VERY similar in many respects to keloids.  All of this is somehow driven by transforming growth factor 1 (TGF-B1) and prostaglandin E1.

3. Peyronies curve is caused only by plaque, ie. scar tissue.  If all plaque is eradicated, including non-palpable plaque, than all deformity is eradicated.  It is important to point out that curve is caused by plaque replacing healthy tissue in one side of the tunica.  If plaque is on opposing sides there will be a size reduction but possibly no curve since both sides of the tunica are shortened about equally.  A curve reduction can result from disease progression to the opposing side of the tunica.



PS: I see Tim posted while I was typing this and I concur that general absolute statements are simplistic and almost always impossible to defend which is one reason I always try to identify and challenge them.

[George999]

Hawk,

Allow me to make a few comments here.

  We over generalize and simplify the collagen issue to the point of being erroneous.  This for instance this why generally suppressing collagen would never work (as I know you understand).

I agree completely.  We can try to identify all of the components of "plaque" and try to eliminate them from our diet (if we were to ever be successful we would starve ourselves to death) until the cows come home, but *the problem is NOT COLLAGEN*.  *The problem is HOW THE BODY METABOLIZES COLLAGEN.*  Its not the components, its the process.  And only by fixing the process will the problem get solved, not by trying to do hocus pocus with the components.

I think it is correct to say elastic is only a component of collagen type II (I actually think type II is a componet of elastin).  This means to say that "lumps" are NOT the the accumulation of collagen as much as they are the replacement of one type of collagen with another.  They are most like "lumps" in the immature stage of inflammation and shrink as they mature.

From what I have read Elastin is quite distinct from Collagen.

See: http://grande.nal.usda.gov/ibids/index.php?mode2=detail&origin=ibids_references&therow=115435

(Don't get me going on Vitamin C here, that isn't my purpose.  Remember the problem is the process, not the components or trivial environmental factors.  My purpose in citing this reference is that it distinguishes collagen from elastin to the point of differentiation, in this case, pertaining to the effect of Vitamin C.)

And: http://en.wikipedia.org/wiki/Elastin

Note that the main components of Elastin are "the amino acids glycine, valine, alanine, and proline" while Collagen is much more complex, but I find no references that indicate that collagen contains elastin.

Peyronies curve is caused only by plaque, ie. scar tissue.  If all plaque is eradicated, including non-palpable plaque, than all deformity is eradicated.

I would not argue that elastin depleted tissue does not consist of plaque.  As I stated in my original post, doctors can not even agree on the what constitutes generic scar tissue as opposed to plaque.  The point is that abnormal tunica tissue, whatever you want to call it, can occur as lumps or be palpably invisible.  It takes different forms.  It is the accumulation of plaque that causes the lumps and it is the depletion of elastin (which is distinct from collagen) within the abnormal tunica tissue that causes the lack of elasticity that, in turn, causes the deformity.  AND various levels of elastin depletion can occur within plaque.

- George

Added note:  Collagen is what gives tissue strength, while elastin is what allows it to stretch.  In the case of abnormal tissue commonly referred to as scar tissue or plaque, the tissue tends to be depleted to some degree of elastin, in some cases becoming almost totally collagen.  While even normal Collagen is quite pliable, in the case of abnormal Collagen, it not only loses the elastin that normally accompanies it, but it itself becomes atrophied and inflexible.  So there are actually more than one underlying processes that contribute to the lack of flexibility in the affected tissue.

[George999]

We talk about the effects of the VED on collagen - we have no clue. In fact, scarred tissue may not budge, but adjacent tissue may instead stretch out more than baseline, so that the overall tissue is more distensable and thus the penis goes straight.

Tim, I think "no clue" is a little strong here.  I think there is plenty of evidence that physical forces on tissue can result in POSITIVE tissue remodeling.

Example:  Regular stretching exercises can cause tendons to become more flexible indicating improved elastin concentrations.

Example:  Regular exercise has now been shown to actually rejuvenate aging DNA in muscle tissue.  *PRETTY SPECTACULAR IN MY BOOK*

So there is significant evidence for such a process even though it is not proven in this case.

- George

[Hawk]

I think it is correct to say elastic is only a component of collagen type II (I actually think type II is a componet of elastin).  This means to say that "lumps" are NOT the the accumulation of collagen as much as they are the replacement of one type of collagen with another.  They are most like "lumps" in the immature stage of inflammation and shrink as they mature.

From what I have read Elastin is quite distinct from Collagen.

Added note:  Collagen is what gives tissue strength, while elastin is what allows it to stretch.  In the case of abnormal tissue commonly referred to as scar tissue or plaque, the tissue tends to be depleted to some degree of elastin, in some cases becoming almost totally collagen.  While even normal Collagen is quite pliable, in the case of abnormal Collagen, it not only loses the elastin that normally accompanies it, but it itself becomes atrophied and inflexible.  So there are actually more than one underlying processes that contribute to the lack of flexibility in the affected tissue.

George,

I agree that your explanation of elastin / collagen is more accurate than my statement that one is a component of the other.  It seems they are distinct and more accurately often elastin accompanies type II collagen.  I am skeptical of your statement that collagen is pliable.  We are 50 % collagen.  Bones and teeth are composed of collagen.  Type II collagen is a pliable helix found in cartilage and such pliable tissue (including a healthy tunica).  I am also skeptical of the statement "the problem is NOT COLLAGEN.  The problem is HOW THE BODY METABOLIZES COLLAGEN."  I think the problem is the collagen.  it is the type of collagen, type II vs. type III


Tons of interesting information exists on this topic.  one site of interest is http://www.sgul.ac.uk/depts/histopathology/ECMI.html

I especially find these statements interesting.

All proteins are continually degraded and resynthesised. This process allows tissues to grow and to undergo remodelling (e.g. involution of the uterus).

and

Elastin turnover is extremely slow with a half-life approaching the age of the organism. Elastin is mainly synthesised during development and any “damaged” elastin is either not replaced or replaced with non-functional fibres.  Excessive elastin degradation is observed in several disease, e.g. emphysema and atherosclerosis.

I fear this conversation is apt to branch off in so many directions that it will be difficult to keep track of exactly which branches to follow.  There is a vast amount of information on every point.  Every new post raises more questions than it answers.

[George999]

I am skeptical of your statement that collagen is pliable.  We are 50 % collagen.  Bones and teeth are composed of collagen.  Type II collagen is a pliable helix found in cartilage and such pliable tissue (including a healthy tunica).  I am also skeptical of the statement "the problem is NOT COLLAGEN.  The problem is HOW THE BODY METABOLIZES COLLAGEN."  I think the problem is the collagen.  it is the type of collagen, type II vs. type III

But what form the collagen takes IS dependent on how the body metabolizes collagen.  If the body metabolizes flexible collagen into inflexible collagen in a place where it doesn't belong, that process, excepting where it is transient, is the problem.

All proteins are continually degraded and resynthesised. This process allows tissues to grow and to undergo remodelling (e.g. involution of the uterus).

I would very much agree with this statement.

Elastin turnover is extremely slow with a half-life approaching the age of the organism. Elastin is mainly synthesised during development and any “damaged” elastin is either not replaced or replaced with non-functional fibres.  Excessive elastin degradation is observed in several disease, e.g. emphysema and atherosclerosis.

And I would very much disagree with this statement.  This is very old school.  They haven't observed it happening so they conclude it can't.  Note the comment I made to Tim regarding DNA remodeling.  DNA remodeling!  If I would have told someone five years ago that I could actually turn the clock back on my muscular DNA deterioration simply through exercise I would have been deemed to be crazy.  Now we know through research that that is exactly what happens.  When elastin gives up it is because whatever process in the body that is intended to replace it isn't working.  And that, in fact, may be the norm.  It may be simply part of the aging process.  But I am all but certain, that given the right stimulation, elastin can be produced.  There is already evidence of this.  There are cases of Peyronies on record where there is complete remission.  This can ONLY happen if elastin is able to infiltrate the tissue in question.  So I believe that they are simply wrong just like the 'experts' that put the statement that "most cases of Peyronies resolve themselves" on another infamous British website were wrong.  By the way, it is also now known that atherosclerosis CAN BE REVERSED given the right conditions AND I have personally seen keloids resolve over time.

- George

[Tim468]

I really think that this is all too simplistic, and therefore of little value as a discussion. I do not mean that as a slam, but simply to let you know how I think.

For instance, stretching may not affect elastin at all. It seems clear that in tissue expansion that the total numer of skin cells is unchanged, but simply stretched out and thinner. The density of skin hair follicles for instance, spreads out when the skin is stretched with tissue expanders.

So we can remodel tissue, but what is happening biochemically is little understood - nor is the effect of stretching on tendons very well understood either. Theories may make sense, but that does not mean they are correct.

Where this gets important IMHO is when we start to take action. With little rationale or data to guide one, someone started using the VED to help Peyronie's Disease. This practice has grown, and is being systematically studied or used by sirgeons now (as a routine part of post-operative care). A very important part of the progression of Peyronies Disease is that of fibrotic contration. This requires contractile elements (not just a lack of elastin, nor an excess of collagen).

I think of plaque as an ill-defined clinical description of the thickened tissue characterized by abnormal amounts of collagen, fibroblasts, contractile elements, and all of this heaped up and thickened. I may have some of this myself, but much more than that, I clearly have a non-thickened contractile problem with my tunica. It does not heap up, but it becomes transformed into less distensible tissue.

No one has learned to distinguish the differences between a lesion like mine, and a more "classic" lesion with a thickened area of plaque, or why they are different. Until we have a better way to describe these differences better, we will not be able to account for the biochemical individuality of different men with Peyronies Disease.

So for now, we are limited to discussions of Peyronie's that are hampered by little data, and a lack of individual data that can help the individual with his own problem. Sharing what we think helps us to understand this disease, IMO. Arguing about who is "right" seems futile, given the limits of the data we use to guide us.

That said, I am always impressed with the civility of the discussions here, and the willingness to learn from each other.

Tim

[j]

As an engineer it's painfully obvious to me that we're speculating on a basis of totally inadequate information and training, and a inability to actually see or measure the phenomenon in question. 

But, the bottom line is: I'm 55.  New drugs take maybe 15 years to hit the market; even if a research breakthrough occurred tomorrow, it's not going to help me unless it involves a new application of an already available drug.

There's an outside chance that some antifibrotic drug is found to be effective.  Maybe injectable Collagenase someday becomes available and turns out to work for Peyronies Disease.   I'm not holding my breath, waiting.

Urologists will go on gathering statistics, writing papers and giving talks at conventions, but none of that activity actually helps their patients; it just generates fees for office visits where patients are told "yes, you have Peyronie's - come back in 6 months".  The real money comes from surgeries. Thanks, but I'll pass on that.

As I see it, my only realistic chance for improvement is from a 'mechanical' procedure - like stretching with a VED, or perforation (Leriche), or hyperthermia.  Except for (maybe ) Dr. Levine in Chicago, the medical establishment has no interest in pursuing these treatment possibilities. 

That's why I've started using a VED.  If I'm careful, I won't damage anything further, and it might even help. 

Here we are again. Struggle to understand.

Started by Jack1909 General Discussion About Erectile Dysfunction

Do i even have Peyronies Disease?

Started by orriw Open Questions or General Comments (that won't fit under any other topics)