Hi,

I've looked at the older messages re VAIN and have more questions:

1. anything new from research since around 2008 when the last messages were dated (i think)?

2.i had a (cervical) leep abt 15 yrs ago after some low-grade squamus cell stuff showed up on paps/colposcopy etc. My understanding is that that was associated with HPV. For the past 15 yrs i've had perfect paps. This month my annual pap suggested high-grade dysplasia, and the colpo and biopsy confirmed this - for VAIN rather than cervical cell changes. i'm confused by comments from my doc, and i will follow up later with nurse and at the scheduled consult with the other doc who is expected to do laser treatment of the affected areas and whatever additional areas are warranted. But i would appreciate your input as well.

my doc was quite surprised by the VAIN, sees it only a couple of times a yr, and alluded to the old HPV presumably to explain it, but was quick to "assure" me not to worry abt the HPV as far as passing it on now, since 90% of sexually active poeple acc to him now have it, and it's a newsworthy event when someone doesn't have it . And he comes down on the side of not telling partners, because of that percentage. To me, that means i COULD be passing it on now -- just the fact the recipient may already have something too doesn't mean i'm not passing this on. That's the first thing i'd like to have clarified.

I also took what the doc said as meaning that the VAIN cells won't themselves be "shedding" virus during contact (unlike GW, for example) and for that reason intercourse before the treatment is undertaken won't affect the partner. Is this accurate or is my frazzled mind overinterpreting?

Finally, what about the timing of the appearance of these cells after 15 yrs? Is the sense that the old (or a new strain) of HPV may have popped up now causing these changes, or that they may have been developing for years? I know VAIN is supposed to develop quickly so i doubt it was developing for years, but still - within one year to catapult to high-grade dysplasia from nothing-- is that "standard"? A further wrinkle is that one nurse indicated that my HMO has changed labs this year, and they are picking up many more abnormalities than before... Would this suggest that the dysplasia's been around longer than the year, just not picked up by the original lab? aaaaarghhhh!! Does my having the VAIn cells now mean that HPV is active now, or could it have popped up, instigated the VAIN cells, and then gone inactive again, leaving the VAIN as a souvenir, as it were? Or should I assume this all means HPV is currently active?

many thanks - and sorry for the long-winded message!

franny

franny,

let me get some guidance on all this and I'll follow up soon. Sorry for the delay.

Thanks!
Fredo

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ASHA Moderator

Hi again Franny,

Thanks for being patient.

For those who might be new to the discussion, VaIN is when abnormal cells/lesions are found with the vagina, and it's similar to what can be found with the cervix during an abnormal Pap test.

It's true that almost all sexually active people have an HPV infection at some point in their lives. Many will have multiple HPV infections throughout their lifetime, which can make it hard to determine for sure if a current HPV diagnosis represents a new infection or if it's related to one from the past. Paps frequently miss cell changes/lesions; the reason Paps work so well in preventing major problems from developing is that having the tests consistently almost always means something will be detected before any real issues come about. So, the timing of the abnormal Pap isn't always a reliable indicator regarding when an underlying HPV infection was contracted.

It isn't the most common scenario for HPV to cause something to be detected again 15 years down the road, but it is possible. It's frustrating because there's no way to really sort that out.

There's also no way to know for certain if HPV can/will be transmitted to a partner. One would think it's possible if there are any lesions present that are caused by HPV, but you don't know for sure. Also, it's estimated that about 60%-70% of VaIN is related to "high risk" types of HPV, so the virus isn't even automatically assumed to be present. Don't be too alarmed by the "high risk" designation, as cancer is a very uncommon outcome here even when HPV is present.

I wish I had more specific answers to offer. I do hope this was helpful. Please post again anytime.

Best,
Fredo

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ASHA Moderator

Hi Fredo,

Many thanks. Intrigued by the comment about 60-70% of VaIN being related to high-risk HPV. Does that mean that 30-40% of VaIN may have other, possibly non-viral, origin? And while cancer may not be common with high-risk HPV, since i already have a diagnosis of high-grade dysplasia, that's more worrying i think. (??)

best,
franny

Here's an article on VaIN and VIN we ran in HPV News. Hopefully this will give some more insight.
Interview with Dr. Mark Einstein

Reprinted from the July 2006 HPV News. Copyright, 2007 - American Social Health Association. All Rights Reserved. To subscribe go to http://www.ashastd.org


The link between “high-risk” HPV types and cervical cancer has understandably been the focus of recent media attention due to the approval in June by the FDA of the first HPV/cervical cancer vaccine. Diseases related to HPV aren’t limited to the cervix, of course, and the News Desk section of this issue of HPV News has an article on the promise HPV vaccines have in preventing other diseases related to HPV, such as precancers of the vulva and vagina (known as vulvar intraepithelial neoplasia and vaginal intraepithelial neoplasia, or VIN and VAIN, respectively).

To learn more about how these diseases are diagnosed and managed, HPV News spoke with Mark Einstein, MD, assistant professor, Division of Gynecologic Oncology, Department of Obstetrics & Gynecology and Women’s Health at Albert Einstein College of Medicine and Montefiore Medical Center in New York. In addition to caring for patients, Dr. Einstein is a researcher who investigates potential therapies for gynecologic cancers.

HPV News: How common are VIN and VAIN?

Mark Einstein: The best estimates are about 1 to 2 cases per 100,000 for VIN and even less for VAIN. There seem to be some differences based on geography, what kind of patient population, etc. [editor’s note: the American Cancer Society estimates there are approximately 9,700 cases of cervical cancer annually in the U.S., and about 3,700 deaths]

Speaking of patient populations is there a specific demographic in which VIN or VAIN is more common?

Let’s split it up because there is some difference between the two. Certainly, “high-risk” HPV status is highly correlated with VIN and the disease is typically more common in older women; mean age is reported around 52. There seems to be an increased risk in patients with lichens sclerosis [LS, a condition where affected skin develops white spots that become shiny and smooth], and this could be because LS often “hides” the VIN, as these patients have very thick skin in this area.

With VAIN, it’s also found in older women and the average age seems to be somewhat higher than that of VIN. These patients also have a lot of the similar characteristics as patients with VIN; while they don’t get LS there is a high correlation with previous HPV infection. There also seems to be an increased risk of both VIN and VAIN related to smoking.

Is it safe to say VIN and VAIN are usually related to “high risk” HPV?

Absolutely. I think the relationship between HPV and VIN/VAIN is less than that of HPV and cervical precancers, but there certainly is a high relationship here - I’d say 60-70% of VIN/VAIN have “high risk” HPV status.

How are VIN and VAIN diagnosed clinically?

We’ll perform a vaginoscopy [using a special microscope called a colposcope] to look thoroughly at the vagina and vulva and then perform a biopsy on any lesions that are detected.

If there are no obvious lesions we often perform random biopsies; for VAIN, as an example, we most often perform those biopsies in the upper third of the vagina, which is the most common place where these types of lesions form.

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ASHA Moderator

Dr. Mark Einstein Interview Continued

What about clinical management? Does either disease tend to resolve without treatment?

I think it depends on the grade [extent] of the disease. Even with “high grade” disease like VIN-3, the incidence of progression to invasive cancer is only around 3%. In terms of the natural regression rate, though, most of us who treat a lot of these will be very uncomfortable allowing “high grade” disease like VIN-3 to regress for a couple of reasons: first of all it takes awhile, upwards of a few years and secondly even though we may have biopsied in one area there can be cancer in another area, so we’ll do a surgical procedure such as a wide local excision [removing the affected skin with a surgical blade] not only to treat, but also to get a tissue sample for diagnostic purposes.

In VAIN, while the risk of progression to invasive cancer is still fairly low, the rate at which this occurs is actually much higher compared to VIN; it’s been reported anywhere from 25-30%. Things can be missed with the vaginoscopy, though, so it’s important to biopsy to get a tissue sample for analysis. Similar to “high grade” VIN, I don’t feel comfortable depending on the immune response to resolve more extensive VAIN.

Now with lower grade lesions, we will often do what’s known as “active observation”. With VIN-1 or VIN-2, for example, we’ll have patients come in regularly, sometimes every 3 or 4 months, for vaginoscopies and potentially for biopsies.

What are treatment options for VIN and VAIN?

A lot of times with “low grade” lesions we’ll attempt medical management, such as using a topically applied cream like Efudex® [topical 5-fluorouracil, an anti-cancer agent] or Imiquimod [an immune response modifier sold as the brand Aldara™].

The steadfast and probably best treatment is often surgery, or removing affected tissue with a surgical blade [scalpel]. The benefit to that is we’ll have a tissue sample to send to the lab. For the higher grade lesions this is the preferred method and the data shows that recurrence rates seem to be less.

There are also tissue destructive techniques. Cryotherapy, or freezing the affected area, is not easy to do with either VIN or VAIN. Both involve very sensitive areas and it’s difficult to control the depth of tissue that’s impacted with this approach. The approaches we more often use are things we have full control over regarding the depth of the treatment, such as laser therapy.

Are recurrences pretty high with both conditions?

Recurrence rates of VAIN are reported at anywhere from 25-35%, and with VIN it’s estimated to be around 20-25%. Recurrence rates are higher in immunocompromised patients such as those with HIV.

Recurrence rates, then, are high and regardless of the therapy used, there’s aggressive active observation with follow-up exams.

Are there symptoms of VIN or VAIN a patient would likely notice?

With VIN, besides seeing a skin growth (lesion) or bump, patients often report they’ve had itching for a while. They also often haven’t seen a gynecologist or other health care provider in awhile to have the area examined; we’ve had patients say they’ve felt something there “for years” but have never had anybody see what was going on down there.

VAIN is relatively asymptomatic. Some patients may have increased vaginal discharge or may actually feel something, but most don’t feel anything and the skin lesions are usually picked up as an incidental finding on the gynecological exam.

Is there no basic screening for either beyond the standard gynecological exam?

Unfortunately there isn’t, which is why annual pelvic exams are still recommended even though Pap smear screening intervals have been extended in many cases.

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ASHA Moderator