VVS and IC Connection??

[Guest guest]

I'm probably going over the four post limit - but I'm kind of catching

up for lost time here tonight. Hope nobody minds too much.

I wanted to comment on the connections that have been tentatively drawn

between vulvar vestibulitis and interstitial cystitis. I used to think

there was a good chance that the two were variations of the same type of

basic problem, and then I read a journal article that some of you with

IC and VVS may be interested in.

The title is " Parallel Pathologies? Vulvar Vestibulitis and Interstitial

Cystitis " and it was in the March 1997 issue of the Journal of

Reproductive Medicine. The authors are G. , MD and

Barry M. Berger, MD and it has some really interesting points in it.

This particular study is fairly technical and I don't completely

understand all the jargon in it, but from what I get - the basic gist is

that they still aren't really sure if IC and VVS are of 'parallel

pathologies'. It seems that there are specific epethelial defects found

in patients with IC when they do a type of staining of the bladder.

There is also positive immunofluorescence findings seen in patients with

IC. The study set out to see if patients with VVS had similar

epethelial defects and immunofluorescence findings.

Turned out that the vulvar epethelium of VVS patients did *not* show any

defects, but 9 of the 13 VVS patients did have positive

immunoflourescence findings. Sooooo - they end up saying that more

research into the immunoflourescence " stuff " needs to be explored and

that the positive findings in both VVS and IC could possibly be

associated with vascular injury and altered central neuronal processing.

The authors also discuss the possibility of viral etiologies - but seem

to lean toward the concept that the altered processing is a key.

I'm going to quote the last couple of paragraphs of the study for you

guys (I think that's okay with the copyright laws!) and I'd love to

discuss what you ladies make of it:

" In the search for greater understanding of VVS, exploration of classic

pain pathways and the mechanism of reflex sympathetic dystrophy has led

to the current focus on altered central neuronal processing.

Capsaicin-sensitive C-fibers are prolific in the lower genitourinary

tract. These fibers function by releasing predominately substance P,

which is thought to be responsible for the transmission and modulation

of pain responses. The release of substance P from nerve endings has

been shown to cause vasodilation and plasma extravasation in the rat and

guinea pig bladder. It would follow that damage to endothelial

integrity leads to leakage of fibrinogen, to antigenic stimulation of

IgM and to leakage of other products of tissue damage, activating the

complement cascade and resulting in positive immunofluorescence

studies. Linear C3 staining is frequently observed with concomitant

vascular injury. Leakage of fibrinogen and other inflammatory products

of tissue damage may also account for the angiogenesis seen in the

calssic tender, erythematous macules of VVS. For VVS, vestibulectomy

has probably been effective as a treatment because of excision of the

C-fibers as well as areas of neovascularization. A capsaicin analog to

deplete the fibers of substance P is a current research focus.

Altered central neuronal processing mediated by multifactorial insults

to the C-fibers of the urogenital tract could result in vascular injury,

as suggested by the IgM, fibrinogen and linear complement staining

found. Further study of immunofluorescence will yield information about

the possible pathophysiologic pathway. "

~Heidi