"Compelling evidence" that BXO is caused by urine
As those who have read a few of my posts will know, I'm a firm believer that BXO/LS is caused by urine. I've already cited a couple of medical studies or articles supporting this theory, and today I found another.
In the Journal of of the American Academy of Dermatology (Volume 66, Issue 4, Supplement 1, April 2012) there is a short article by Tang Ngee Shim and Christopher Bunker, of the Department of Dermatology, London suggesting "compelling evidence that male genital lichen sclerosus (MGLSc) is caused by exposure to urine".
Rather than select pieces of it, I will just reproduce the entire article:
"There is compelling evidence that male genital lichen sclerosus (MGLSc) is caused
by exposure to urine. MGLSc is an acquired cutaneous disease of uncertain etiology
that results in sexual dysfunction and urologic morbidity and carries a risk of
squamous cell carcinoma (SCC) of the penis (2-12.5%). Amongst prior postulated
pathogenic factors in GLSc are human papillomavirus (HPV) infection and autoim-
munity (autoantibodies to extracellular matrix protein 1 (ECM1) and HLA-DR and
DQ associations in female (F) GLSc. However, recent work of ours in MGLSc has
shown a lack of clinical correlation with HPV and ECM1 autoimmunity and a
transcriptosome unrelated to either. We argue chronic occluded exposure of
susceptible epithelium to urine is fundamental to the etiopathogensis of MGLSc.
It has been established beyond equivocation that the presence of foreskin is
essential to the development of MGLSc: the disease is exceedingly rare in the male
circumcised at birth (unless there is hypospadias). The idea has emerged that
naviculomeatal valve dysfunction and urinary dribbling are key factors. MGLSc is
associated with trauma, instrumentation, genital jewelry (piercing), and gross
anatomic abnormalities (eg, frank hypospadias). It never causes perianal disease: in
striking contraindication to women, the male perineum is never chronically
exposed to urinary irritation. Many men with MGLSc confess to postmicturition
dribbling, suggesting naviculomeatal valve dysfunction. Furthermore, meticulous
physical examination of these men often reveals an abnormal meatus or navicular
fossa, presumptively affecting the physiological performance of the naviculomeatal
apparatus as a low-pressure valve. In circumcised males, a tiny drop of urine
appearing at the meatus postmicturation will have negligible contact with a
keratinized glans before being absorbed by undergarments. In an uncircumcised
male with similarly dysfunctional terminal urethral arrangements, the situation is
very different. In these men, urine dribbling from the meatus after the prepuce has
been replaced following voiding will spread widely between the tightly opposed
mucosal surfaces of prepuce, glans, and distal shaft of the penis. Occlusion and the
phenomenon of koebnerization precipitate inflammation then scarring and then
cancer. Better insight into the pathogenesis of MGLSc is important to minimize
sexual morbidity, urologic dysfunction, and cancer risk it generates."
This sums up my condition to a tee. A small amount of dribbling of urine started, and because I have foreskin, this became trapped and contributed to the development of BXO.
So, you have to ask, when a medical doctor starts using phrases like 'compelling evidence' and 'proven beyond equivocation', why is a regular practice of removing this irritant apparently so hard to think of?
Circumcision solves BXO, because it prevents urine from staying on the glans and inner foreskin tissue long enough to do any harm. But don't you think it's a tad drastic, when simply wiping away the urine with a harmless piece of toilet paper also achieves the same result?
I've been racking my brains trying to contemplate why this might be. I will share my thoughts in a further subsequent post. In the meantime, I thought you would all be interested to know that this is now the third medical article I have found agreeing with my hypothesis. A quick web search found several other references to the strong relationship between BXO/LS and urine, in affected men.
This really is one extremely strange disease, both in how it behaves and in how the medical industry responds to it.
In the Journal of of the American Academy of Dermatology (Volume 66, Issue 4, Supplement 1, April 2012) there is a short article by Tang Ngee Shim and Christopher Bunker, of the Department of Dermatology, London suggesting "compelling evidence that male genital lichen sclerosus (MGLSc) is caused by exposure to urine".
Rather than select pieces of it, I will just reproduce the entire article:
"There is compelling evidence that male genital lichen sclerosus (MGLSc) is caused
by exposure to urine. MGLSc is an acquired cutaneous disease of uncertain etiology
that results in sexual dysfunction and urologic morbidity and carries a risk of
squamous cell carcinoma (SCC) of the penis (2-12.5%). Amongst prior postulated
pathogenic factors in GLSc are human papillomavirus (HPV) infection and autoim-
munity (autoantibodies to extracellular matrix protein 1 (ECM1) and HLA-DR and
DQ associations in female (F) GLSc. However, recent work of ours in MGLSc has
shown a lack of clinical correlation with HPV and ECM1 autoimmunity and a
transcriptosome unrelated to either. We argue chronic occluded exposure of
susceptible epithelium to urine is fundamental to the etiopathogensis of MGLSc.
It has been established beyond equivocation that the presence of foreskin is
essential to the development of MGLSc: the disease is exceedingly rare in the male
circumcised at birth (unless there is hypospadias). The idea has emerged that
naviculomeatal valve dysfunction and urinary dribbling are key factors. MGLSc is
associated with trauma, instrumentation, genital jewelry (piercing), and gross
anatomic abnormalities (eg, frank hypospadias). It never causes perianal disease: in
striking contraindication to women, the male perineum is never chronically
exposed to urinary irritation. Many men with MGLSc confess to postmicturition
dribbling, suggesting naviculomeatal valve dysfunction. Furthermore, meticulous
physical examination of these men often reveals an abnormal meatus or navicular
fossa, presumptively affecting the physiological performance of the naviculomeatal
apparatus as a low-pressure valve. In circumcised males, a tiny drop of urine
appearing at the meatus postmicturation will have negligible contact with a
keratinized glans before being absorbed by undergarments. In an uncircumcised
male with similarly dysfunctional terminal urethral arrangements, the situation is
very different. In these men, urine dribbling from the meatus after the prepuce has
been replaced following voiding will spread widely between the tightly opposed
mucosal surfaces of prepuce, glans, and distal shaft of the penis. Occlusion and the
phenomenon of koebnerization precipitate inflammation then scarring and then
cancer. Better insight into the pathogenesis of MGLSc is important to minimize
sexual morbidity, urologic dysfunction, and cancer risk it generates."
This sums up my condition to a tee. A small amount of dribbling of urine started, and because I have foreskin, this became trapped and contributed to the development of BXO.
So, you have to ask, when a medical doctor starts using phrases like 'compelling evidence' and 'proven beyond equivocation', why is a regular practice of removing this irritant apparently so hard to think of?
Circumcision solves BXO, because it prevents urine from staying on the glans and inner foreskin tissue long enough to do any harm. But don't you think it's a tad drastic, when simply wiping away the urine with a harmless piece of toilet paper also achieves the same result?
I've been racking my brains trying to contemplate why this might be. I will share my thoughts in a further subsequent post. In the meantime, I thought you would all be interested to know that this is now the third medical article I have found agreeing with my hypothesis. A quick web search found several other references to the strong relationship between BXO/LS and urine, in affected men.
This really is one extremely strange disease, both in how it behaves and in how the medical industry responds to it.
I would disagree with your statement that circumcision solves BXO. It was only after this operation that my condition developed. Admittedly I 'dribble' a lot but despite huge effort to ensure no urine stays around after the toliet, my condition has not improved (if anything things are still progressing to a worse state).
ReplyDeleteYou might be a rare exception. The vast majority of documented cases of BXO are solved by circumcision, and almost it almost never affects circumcised men to begin with. The only exception to this is with men who are obese and have what is known as a 'buried penis' whereby the penis becomes buried in the folds of skin due to excessive body fat. How long have you been keeping yourself dry for? Are you certain that what you have is indeed BXO?
DeleteYeah so I was circumcised aged 10 and noticed the development of this disease around 17. Diagnosed at 21. Been attempting to keep everything dry for about a year but not overly successful in doing so, I.e. lots of dribbling. But being circumcised would have thought underwear would absorb most of it anyway...
ReplyDeleteYou'd think underwear would work to absorb all moisture, but perhaps not. It would also depend on the type of underwear and the extent of your dribbling (eg is it dribbling long after you finish?). Do you ever find yourself damp to the touch despite having not urinated for a long time?
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