i was told by a doc. today that i have genital warts. i just had a pap 2 months ago and it was negative for everything. i have been diagnosed before with hpv-cervial cancer strand. i was told a year ago that it went away. the doc. today did no tests just looked and told me it was genital warts. i have also started getting them on my feet knees and hands. im not sure im convinced its genital warts at all. i will be going to the gyno to get an actual test but was wondering if there is anyone out there that might have any info or experience with this and could educate me more. i have done alot of reading and research on hpv and warts. this is just my last question. can hpv strand evolve into other strands? what i have down there looks more like a skin tag then a wart in my opinion. No, low risk HPV types can鈥檛 morph into high risk HPV types. Most visible warts are of a low risk HPV types. That said people that have a visible genital wart infection can also carry a co-infection with high risk HPV types. They are over 30 high and low risk HPV types that can affect the genital area. Many people carry multiple HPV types. Once you have an HPV type you can鈥檛 get it again but our acquired HPV type can reactivate years after the initial infection. We can also acquire new HPV types with a new sex partner.
Your past HPV test and Pap confirmed that you tested positive for abnormal cervical cell changes and high risk HPV types. The only FDA approved HPV test only screens for high risk HPV types of the cervix. Neither the Pap nor the HPV test includes cells of the vulva. Abnormal cells can take years to form or and they can regress. The HPV test looks at units of the virus per cell when the virus is in low viral load it will not show in any test.
Warts of the hand and feet are of the large family of HPV types but not of the types that affect the genital areas.
Skin tags of the penis and the vulva are often HPV. Skin tags are usually a result of some type of friction鈥?panties lines areas could be skin tags because of the friction of the fabric.
The skin tags or warts would be best examined by a dermatologist. Abnormal cervical cell change and your Pap smear are done with your GYN. A positive Pap with a positive HPV doesn鈥檛 always diagnosis a new HPV infection and a Pap may miss abnormal cell changes. It is important to always keep current with our Pap smears.
The dermatologist suggestion is based on my own personal experience. I had an abnormal spot on the vulva GYN dismissed it dermatologist felt it should be excised the spot pathology confirmed high risk HPV. I was on long term treatments of 5 FU after the spot was excised. I also have had two LEEP due to high risk progressive HPV of the vaginal cuff.
I wish you well.
Other skin growths that may look similar to a skin tag but are not tags include moles (dermal nevus), nerve and fiber-type moles (neurofibromas), warts, and "barnacles" or "Rice Krispies" (seborrheic keratosis).
Warts tend to be rougher, with a "warty" irregular surface whereas skin tags are usually smooth. Warts tend to be flat whereas tags are more like bumps hanging from thin stalk. While warts are almost entirely caused by human papilloma virus (HPV), tags are only sometimes associated with HPV.
Groin and genital lesions resembling skin tags may actually be genital warts or condyloma. A biopsy would help diagnose which of these growths are not skin tags. Very rarely, a basal cell skin or squamous cancer or melanoma may mimic a skin tag, but this is very uncommon.
http://www.medicinenet.com/skin_tag/page...
Genital warts
Condylomata bearing HPV-6 or -11 have identical clinical
manifestations and histology [2]. Recent studies have shown that about
100% of GWs are caused by either HPV-6 or -11 but that 20鈥?0% of
lesions also contain co-infections with HR HPV types [3] and [4]. GWs
do not usually result in major morbidity or mortality, but cause
significant psychological morbidity and very substantial healthcare
costs. Occasionally GWs persist for long periods of time and, rarely,
such long-standing lesions may progress to malignancy. GWs are highly
infectious, with a transmission rate of about 65% within sexual
partnerships from an infected to a susceptible sexual partner, and an
incubation period of between 3 weeks and 8 months, with the majority
developing warts at around 2鈥? months [3]. Once GWs have developed,
they may show minimal change over time, become more numerous or
larger, or regress spontaneously. The majority of placebo-controlled
GW therapy trials show low rates of regression (around 5% complete
clearance) in the short term, although in one study over 16 weeks 20%
of women and 5% of men using placebo completely cleared their warts,
and 38% of women and 22% of men using placebo cleared over 50% of
their baseline warts [3]. Regressing warts contain significantly more
CD4 positive T cells, both within the stroma underlying the lesions
and the condylomata themselves, and greater expression of activation
markers [3]. There is no report of the rate of spontaneous regression
that may occur in the longer term. Following GW clearance with
therapy, recurrence is common and is often seen within 3 months in 25%
of cases, although rates of up to 67% have been observed [3]. In
clinical practice recurrences are often seen at sites of previous
lesions, and in these cases HPV infection in stem cells or
slow-turnover cells at the site of previous clearance has persisted
and then reactivated. The proportion of HPV-6/11 infections that are
either completely cleared or persist in a latent form after clinical
resolution is unknown, and, indeed, animal models suggest that both
outcomes can occur [3].
HPV-6/11 as a cause of cervical neoplasia
HPV-6 and -11 are frequently associated with LSIL. A recent
meta-analysis of 55 studies reported HPV-6 to be present in 8.1% of
HPV-positive LSIL cases and HPV-11 in 3.2% of cases [25]. However, it
remains unclear in what proportion of these HPV-6/11-positive LSIL
cases there is concomitant co-infection with a HR type, and whether
such HR co-infections would be "minority passenger" infections as
described in GWs, or represent true multiple-morphology cervical lesions.
Costs of HPV-6/11 disease
The principal healthcare costs caused by HPV-6/11 are through GWs and
RRP. Recent UK- and USA-specific data on the costs of treatment of GWs
in routine clinical practice [38] and [39] estimated the cost of a
single successful episode of treatment of a case of GWs to be 拢216 ($
377) in the UK and $ 436 in the USA. Using the UK STI clinic 2004 GWs
prevalence data, this equates to around 拢31 million ($ 54 million) per
annum for the UK. One study from the USA estimated the annual direct
healthcare costs of GWs as $ 200 million [40]. In a report from the
Task Force on RRP, the annual cost for surgical procedures in the USA
was estimated to be $ 109 million for JORRP and $ 42 million for AORRP
[27]. In countries with cervical screening programmes there will also
be significant costs associated with HPV-6/11-associated abnormal
cytology and consequent procedures, although estimates of these costs
are not available.
http://www.elsevier.com/wps/find/journal...
VULVAR INTRAEPITHELIAL NEOPLASIA:
http://www.asccp.org/edu/practice/vulva/... No i believe that they are 2 different strands cause one is low risk and one is high risk. |
