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Vulvodynia: A Common and Under-Recognized Pain Disorder in Women and Female Adolescents -- Integrating Current Knowledge into Clinical Practice
Preliminary findings of research on factors associated with the risk of developing vulvodynia indicate that there may be multiple risk factors involved, but larger studies are needed to confirm these findings. Multiple studies suggest that vulvodynia patients experience more frequent vaginal infections, however, in most cases, prior vaginal infections were either self-reported or unconfirmed by the treating clinician. Research demonstrates that patients and clinicians are poor at accurately diagnosing vaginal infections (Ferris 1996, Ferris 2002, Ledger 2004, Schwiertz 2006). The only population-based case-control study to date, which compared the frequency of self-reported urogenital infections before the onset of vulvar pain, demonstrated that a history of genital warts (OR 3.4), trichomoniasis (OR 5.7), urinary tract infection (OR 2.0) or yeast infection (OR 2.1) was associated with increased risk of vulvodynia. The researchers also found that women with multiple infections prior to the onset of vulvar pain were at highest risk; a combination of urinary tract infection and STIs was associated with a 10-fold higher risk (Nguyen 2009). Recent pathophysiological studies have demonstrated a relationship between vulvodynia and Candida albicans (Babula 2004, Foster 2007, Ramirez De Knott 2005, Farmer 2011).
Research to date appears to implicate oral contraceptive (OC) use in the development and/or maintenance of vulvodynia in some subgroups. Some clinicians propose that the use of OCs, particularly at an early age, down-regulates estrogen receptors in the vulvovaginal tissue, causing the vestibular epithelium to become thin and fragile. In a study of women using Yasmin, Battaglia (2012) found decreased labial thickness, introital area, frequency of intercourse and orgasm during intercourse, as well as increased pain with intercourse and pulsatility index of the dorsal clitoral and posterior labial arteries. In another study, quantitative sensory testing of the vestibular mucosa in healthy women revealed significantly lower mechanical pain thresholds in the OC group, with the most sensitivity in the posterior vestibule. The investigators concluded that OCs may induce increased sensitivity in the vestibular mucosa in healthy women, possibly contributing to the development of vulvodynia (Bohm-Starke 2004). Heddini (2012) found that Provoked Vestibulodynia patients carrying a polymorphism in the guanosine triphosphate cyclohydrolase (GCH1) gene and using OCs had higher pain sensitivity compared to non-carriers. Several studies have demonstrated increased risk in this patient population (Sjoberg 1997, Greenstein 2007, Bazin 1994, Bouchard 2002), although a population-based study did not (Harlow 2008).
Other risk factors reported in the literature include a history of allergies (Harlow 2009); vulvar dermatoses (Coombs 2011); autoimmune disease (Driul 2011) and an altered immuno-inflammatory response (Breshears 2011); early age of menarche (Harlow 2001); dysmenorrhea (Granot 2004); difficulty or severe pain with first tampon use (Harlow 2003, Landry 2009, Legocki 2011); early age of first intercourse (Bazin 1994, Berglund 2002); pain with first intercourse (Legocki 2011); pain with/after sex (Reed 2012); nulliparity (Edgardh 2007); childhood nocturnal enuresis (Greenstein 2005); urinary burning (Reed 2012); nocturnal urination, pain with wiping, and bike riding (Legocki 2011); genetic variability (Babula 2008, Foster 2004, Gerber 2003, Jeremias 2000, Lev-Sagie 2009) and altered gene expression, particularly in genes implicated in osteoarthritis (Breshears 2011) and with an altered immuno-inflammatory response (Bornstein 2004, Bornstein 2008, Foster 1997, Foster 2007, Gerber 2002, Harlow 2009, Lev-Sagie 2009); and chronic pain in other areas of the body (Falik-Zaccai 2011, Arnold 2006, Heddini 2012). (See Section 6 Comorbidity references.)
Although one study supports some degree of association (Harlow 2005), several studies have refuted the notion that prior sexual and/or physical abuse is a risk factor for vulvodynia (Dalton 2002, Plante 2008, Edwards 1997, Reed 2000). Khandker (2011) is the only population-based epidemiological study to demonstrate antecedent depression and anxiety as risk factors for vulvodynia. Plante (2008) demonstrated that women with vulvodynia reported more adverse life experiences.
See Bohm-Starke 2010 for additional information.
According to the ISSVD (Bornstein 2016), known causes of chronic vulvar pain are: (1) infectious, (2) inflammatory, (3) neoplastic, (4) traumatic, (5) iatrogenic, (6) hormonal deficiencies, or (7) neurologic. If the cause is unknown, it is classified as vulvodynia. Conditions falling into the first seven categories must be ruled out prior to making a diagnosis of vulvodynia. Examples of some of these prevalent conditions follow, with references to journal articles that provide information on diagnosis and treatment. (This is beyond the scope of the current program.)
The image on the left is a vaginal smear identifying Candida albicans, using a gram stain technique. In-office diagnosis can be made with microscopy, using a potassium hydroxide prep, and vaginal culture can be used for speciation and sensitivity. Candida albicans is a component of the normal flora in many women. Under certain conditions, such as a hormone imbalance, antibiotic treatment, or transient localized immune suppression, C. albicans can multiply, resulting in a symptomatic condition known as vulvovaginal candidiasis. Recent studies have implicated recurrent or chronic vulvovaginal candidiasis as a causative factor in vulvodynia.
It should be noted that the microbiome of the vagina is very complex and many species of bacteria, which may be considered pathogens in other parts of the body, are not pathogens in the vagina. Bacterial species such as Group Beta Strep, Klebsiella, and e. coli are common in the vagina and should not be treated.