Chronic Inflammation of v****a (possibly HPV related)?

Question

I have been struggling with this issue for 5+ years. Married 14 years, monogamous 18 years with husband. No infidelity ever. Maybe someone can help. My v****a is chronically inflammed in the bottom area. If you look the opening like a clock, it is between "5:00 and 7:00". I have been to 7 doctors. Checked for allergies at dermatologist - NONE. A Bartholin's Duct Cyst was removed 4 years ago. Inflammation persisted. 2 Biopsies taken (1 per year) 1st Results: Chronic Inflammatory cells and Squamous Cell Pappiloma. 2nd: Chronic Inflammatory cells and strong HPV possiblility. Was exposed to genital warts 18 years ago, never broke out. Gyne stated some HPV's cause cancer, some chronic inflammation. Treated with anti-viral gel (used for warts but Dr. hoped to make this go into remission). Was horrible, tissue worsened, peeled off, and felt like someone was extinguishing a cigarette on my v****a. Discontinued after 2 weeks of use (3 days on, 4 days off the gel) Do not want to surgically remove tissue for fear of making situation worse! Have "googled" this issue for several years, always leads to dead ends and Cervial issues, which I do not have YET. Don't smoke, NEVER did drugs, have 2 healthy children. Drink socially. Take multi-vitamins, and have dappled with "Acai" juice and other natural stuff. I am healthy, 38 years old, and lead a normal life. Desparate to try to find out what to do....current Gyne is great, but wants to "leave it alone" to observe....can't blame the guy, he is new to my case. Thought I'd reach out and see if anyone out there has experienced this, and has any advice.

Answer 1

If your new guy doesn't start to do something soon, I'd ask him to refer you to a university hospital gyn who specializes in cases like yours.  There are departments of GYN that specialize in vaginal pain issues, and you might be one of those patients.

Most of us have some form of HPV- there are only about 88 different HPV's out there, so you may have had a "sleeper" virus that is just now starting to cause issues.

Good luck.

Answer 2

yes you should be concerned if you were exposed to genital warts, they are almost always transferred on contact.  a friend of mine has genital warts and he uses wartrol. it stops the spread of the hpv virus and stops the growth and spread of genital warts. learn more at this link

http://www.homeoapthicremediesfor.com/wa...

Answer 3

I assume that the med you used was Aldara....it can really tear up the v***a...but it has saved some gals from having extensive v***a surgeries.  A couple of studies on VIN 2/3 are on line…some great info.

There are many things that can help with some of the side effects of Aldara…but I think I would get a good diagnosis before using Aldara…a few of the VIN gal I know also have used a cream called 5 FU.  

You can have HPV on the v***a but never develop a wart....

Are you googling v***a intrepeitheial neoplasia or VIN...from the pathology it does look like there is a strong possibility that the v***a issues are partly due to HPV...and maybe more is going on.  

I didn't do well with a GYN for my VIN...saw a great lady dermatologist....

I am not sure I agree with the GYN for the continued watch and wait

I wish you well...

VIN and v***a pathology from medical library . com

New Treatments for Vulvar Intraepithelial Neoplasia

______________________________________...

Helen L. Simpson, MD



  

Vulvar intraepithelial neoplasia is a relatively uncommon condition first alluded to when Bowen[7] described a vulvar skin condition called precancerous dermatosis in 1912. Thirty-one years later, Knight reported on VIN and described several cases in which the lesions were adjacent to invasive vulvar carcinoma, suggesting VIN as a precursor lesion. Currently, VIN is defined histologically as a disorientation of epithelial architecture that is limited by the basement membrane with no extension to the underlying dermis. Terminology is as follows:

  

--VIN 1--mild dysplasia

  

--VIN 2--moderate dysplasia

  

--VIN 3--severe dysplasia/carcinoma in situ

  

--Paget's disease



Vulvar intraepithelial neoplasia is most commonly seen in immunocompromised and postmenopausal women, but the incidence is increasing among healthy patients in younger age groups. Risk factors are similar to those observed for CIN. Race, parity, and comorbid medical conditions (except an immunocompromise status) seem to have no role in the development of VIN, whereas cigarette smoking is believed to be associated. An etiologic relationship exists between the development of VIN and human papillomavirus (HPV) infection, and HPV-16 is the most commonly isolated viral subtype. As many as 50% of patients are also found to have associated CIN or VAIN, providing additional support for a viral etiology.

Diagnosis

Patients may present with a variety of symptoms, including itching or burning and associated vulvar irritation, dyspareunia, labial erythema or swelling, or they may simply note the development of a lesion. Most patients are completely asymptomatic, and their lesions are identified during routine gynecologic examination.

Vulvar intraepithelial neoplasia may be unifocal or multifocal. Lesions are frequently white and raised, although they may also be gray or reddened macules. These lesions are most commonly found on the non-hair-bearing areas, such as the posterior v***a and periclitoral area, but may extend to involve the a**s, v****a, clitoris, or urethra.

The clinical diagnosis is suspected after direct visualization. There is no pathognomonic finding on physical examination. Application of acetic acid with colposcopic magnification may be helpful, but several minutes are required for the keratinized squamous epithelium to take up the solution. Abnormal vessel patterns are not commonly seen owing to the keratinization of vulvar skin. Toluidine blue staining may be helpful but lacks sensitivity or specificity. Liberal use of biopsy is recommended to make an accurate diagnosis and to rule out invasive disease. Occult invasion is more common with perianal lesions and in elderly patients.

Management

Management efforts are directed at relieving symptoms and preventing malignant conversion. These goals, combined with the increasing incidence in the younger population, have led to the adoption of treatment techniques that give optimal results but preserve normal tissue and function. Unfortunately, recurrence rates after treatment have been reported to range from 10% to 50% and are thought to be related to the grade of VIN and margin status along with the multifocal nature of the condition and its relationship with HPV.

As is true for CIN, VIN has the potential to progress to invasive carcinoma or to regress completely. VIN is found associated with invasive disease in 2% to 18% of patients. The precise biology is unknown because only rare cases of severe dysplasia are managed with observation alone. The risk of malignant transformation is low (3% to 12%), and the process is apparently slow. Some evidence suggests that regression is twice as likely as progression to cancer.

Once malignancy has been ruled out, the authors believe a brief period of observation is reasonable in young, compliant, asymptomatic women with only mild dysplasia. Observation is especially indicated for patients who have recently completed a