Women's Sexual Function and Dysfunction. Irwin Goldstein MD

Difficult cases: medical treatment of female sexual dysfunction

Edgardo F Becher, Andrea Salonia, Irwin Goldstein

According to the National Health and Social Life Survey,approximately 43% of American women suffer from sexual health concerns that, in some cases, cause significant personal and couple distress (see Chapter 2.1). Sexual dysfunction in women is a multifactorial syndrome with interrelated medical, psychologic, and interpersonal components.2-4 Thus, the best model to manage women with sexual problems would be a multidisciplinary setting staffed with sexual medicine psychologic- and biologic-focused health-care professionals. Management of women with sexual health concerns should be considered in a step care paradigm in which the selected therapies progress from least invasive to progressively more invasive, depending, in part, upon patient outcome2-4 (see Chapters 13.1-13.3, 14.1, 15.1, and 15.2).

In many cases, the female sexual dysfunction is based, in part, on an unrecognized medical condition.4-7 Possible medical problems include hormonal, neurologic, vascular, pharmacologic, inflammatory, infectious, and other nonpsychologic pathophysiologies.5-7 The aim of this chapter is to review difficult medical cases in women with sexual dysfunction. This chapter will review seven cases of women who presented for management of a sexual dysfunction in a multidisciplinary setting and ultimately required medical intervention as part of the care provided to manage the sexual complaint. This medical care was provided, in all cases, in addition to other interventions, including psychologic counseling and physical therapy as indicated. The purpose of the chapter is to illustrate some typical cases in which medical intervention strategies were utilized in the management of women with sexual health problems.

In this textbook on women’s sexual health, in which patient management is discussed, it is important to emphasize that evidence-based medical management in this field is still in its infancy.4 At the time of writing, there are no government agency-approved pharmaceutic agents indicated specifically for the treatment of a women’s sexual health disorder. Similarly, there are few recognized medical conditions that predictably interfere with women’s desire, arousal, or orgasm function. It is not the purpose of this chapter to illustrate anecdotal medical care. To the best of the authors’ abilities, each case is founded on peer review medical evidence.

As in other portions of this textbook relating to difficult case management, every effort has been made to protect the privacy of patients and to maintain the management strategies utilized in the case for teaching purposes.

Case 1

SR, aged 23, while inserting a tampon, noted something unusual “down there”. It felt like a series of clusters of small bumps on the left labium of her labia majora. She also felt a small “lump” near her clitoris. Once or twice a day, SR complained of itching in the area. SR tried to inspect this herself with a mirror but did not know what to look for.

SR is an au pair providing live-in child care for a family with three young children. She had limited sexual activity as a teenager and used condoms for contraception. For the last 2 years, she has used the combined oral contraceptive pill, in part, to control cramping and excessive menstrual bleeding. SR has little free time for dating and relationships, but she did meet someone at a party and they “hit it off”. SR was sexually active in this new relationship and they did not always use a condom. She did arouse and experience orgasm primarily through clitoral stimulation. SR believed that compared to the time when she was not using the combined oral contraceptive, her sexual responses were somewhat blunted.

SR was worried about the new “masses down there” and in particular was frightened about sexually transmitted diseases. As a result, she stopped sexual activity, including self-stimulation, until she could find out what was wrong. The decision to stop sexual activity caused stress in the relationship and caused her great personal anxiety and frustration. SR went to her primary care physician, but no abnormality was found during repeated internal pelvic examination. Pap smears were negative. SR was frustrated and determined to get a second opinion. After 6 months of abstinence and worry about the lumps, she self- referred herself to a multidisciplinary sexual medicine clinic.

She was evaluated by the psychologist as follows. SR is a 23- year-old single woman with a history of “finding something that feels different” on her genitals. The patient is very unhappy about this situation, feels guilty, and reports conflict in her relationship. The patient reports that this has been a frustrating issue for more than 6 months. There is no history of depression, substance abuse, or other mental health issues. There is no history of trauma or sexual abuse.

SR underwent physical examination under bright light with the examiner wearing magnifying surgical loupes. Upon clitoral hood retraction, a single 0.5 x 0.33 cm genital wart was noted on the left side of the prepuce (Fig. 14.2.1). In addition, within the hairs on the labia majora, a series of conylomata, 30-45 mm in size, some flat and some raised, were noted on the left labium of the labia majora and in the sulcus between the left labium of the labia majora and the labia minora.

SR agreed to undergo a minor surgical excision of the lesion on the frenulum under local anesthesia. A course of imiquamod was administered over 1 month for the lesions on the labia majora and in the sulcus. She received counseling on “safe sex” with condoms. She has stopped the combined oral contraceptive agents and has noted a restoration of the previous level of sexual desire, arousal, and orgasm that she experienced as a teenager. She has been advised to have annual Pap smears.

Comments

Genital warts, condylomata acuminata, caused by human papillomavirus infection are frequently encountered in sexual medicine care, as genital warts are one of the most common sexually transmitted diseases8 (see Chapter 7.7). Genital warts are caused, in part, by direct, skin-to-skin transmission of the human papillomavirus during sex with an infected person. Genital warts may be flesh-colored, painless, raised or flat, single or multiple, and small or large (often appearing cauliflowerlike), and may appear in and around the vulva, vestibule, vagina, or cervix. The various treatments for genital warts include topical chemicals (e.g. podofilox, imiquimod9), cryotherapy (liquid nitrogen), laser therapy, and surgical excision. The choice of therapy is based on multiple variables such as the quantity, dimension, and location of the lesions, as well as patient choice, cost, convenience, risks, and clinician experience. Human papillomavirus can cause genital warts and cervical cancer; thus, it is important that individuals with genital human papillomavirus be diagnosed and treated, and get annual follow-up, including Pap smears. Because the human papillomavirus remains dormant in the body, genital warts may reappear at any time after treatment. The goal of treatment is clearance of visible warts. Some evidence exists that treatment reduces infectivity, but there is no objective evidence yet that treatment reduces the incidence of cervical cancer.8,9

Figure 14.2.1. Physical examination was performed under bright light with the examiner wearing magnifying surgical loupes. Upon clitoral hood retraction, a single 0.5 x 0.33 cm genital wart was noted on the left side of the prepuce.

Case 2

FG, aged 57, complained of diminished arousal response for the last 4 years since entering menopause. She had “great sexual activity” from her teens to just before menopause. “I am interested in sex, I have always been and I maintain the drive. Sex is important for me and I love my husband very much.” Since starting menopause, “I’m dry as a bone” and “sex is most uncomfortable”. “I don’t even want to touch myself anymore.” “I am rarely able to achieve orgasm during intercourse.” “It just takes much more effort to have orgasm and the orgasms I achieve are very muffled.” FG tried eating soy supplements and a variety of herbals without success. She even tried sildenafil, obtained from a friend, but all this provided was a headache and facial flushing. The lubricants that she tried were messy and not very satisfactory.

FG was evaluated by her local gynecologist. She was referred to a sex therapist and started on low-dose, systemic estrogen and progesterone, and she was advised to purchase vibrators and lubricants. Since FG has a sister with breast cancer, FG discontinued the hormone treatment after several weeks after exposure to recent media discussion relating systemic estrogen use to increased breast cancer risk. FG referred herself to a multidisciplinary sexual medicine clinic.

FG was evaluated by the psychologist as follows. This 57- year-old married woman reports a chief complaint of diminished vaginal lubrication and discomfort during sexual intercourse for approximately 4 years. She states that she is unable to have a satisfying orgasm with her husband. Over recent years, this has become an increasing problem both for her and her husband. The patient does have some history of sexual abuse as a child, but she is reluctant to discuss this and feels that it is irrelevant. She denies that her past history has negatively affected her relationship with her husband. By nature, the patient is a positive, optimistic woman who appears pleased with the quality of her life. She has no history of depression or other psychologic issues. She drinks alcohol on social occasions and has no tobacco or illegal substance history.

FG underwent a history and physical examination. FG undergoes routine Pap smears and breast examination. She denies any history of sexually transmitted diseases, endometriosis, cervical dysplasia, or interstitial cystitis. Her last menstrual period was 4 years ago. There has been no history of breakthrough bleeding. She has occasional night sweats and hot flushes but is not disabled by them. Physical examination revealed a normal glans clitoris. Approximately two-thirds of the posterior aspect of the right and left labia minora were fused to the labia majora. The thickness of the upper third of the labia minora was several millimetres. The vagina lacked rugae and lubrication was absent on the vaginal walls (Fig. 14.2.2). There was positive Q-tip testing, grade 2-4/10, in multiple locations around the labial-hymenal junction. There was minimal vaginal wall bleeding with Q-tip contact. Biothesiometry studies revealed that the vibration perception threshold was 3 V in the right and left pulp index fingers, and 13-15 V in the labia, clitoris, frenulum, and urethral meatus. Hormone studies revealed the following values: thyroid-stimulating hormone 2.4 (0.4-5.50 µIU/ml), follicle-stimulating hormone 72 (23-116 mIU/ml), luteinizing hormone 33 (16-54 mIU/ml), prolactin 9.7 (1.8-20.3 ng/ml), dehydroepiandrosterone sulfate 93 (35-430 µg/ml), androstenedione 1.0 (0.2-3.1 ng/ml), total testosterone 33 (15-70 ng/dl), free testosterone 0.9 (0.3-1.9 ng/dl), sex hormone-binding globulin 49 (17-120 nmol/l), and estradiol <20 (11-526 pg/ml).

The patient was notified that her diagnoses were diminished arousal and orgasm, dyspareunia, diminished genital sensation, genital atrophy, atrophic vaginitis, and diminished estradiol. We discussed the various treatments of her atrophic vaginitis by estradiol administration. We suggested that as a safer alternative, especially as it concerns breast cancer risk, low-dose local estradiol was probably associated with less risk than systemic estradiol administration. FG began treatment with local estradiol to the vestibule and the vagina. Within weeks, FG noticed a real difference in lubrication and diminished discomfort. “I love this treatment.” She could not believe that it took her 4 years to get effective treatment for this problem, and she thinks that all postmenopausal women should be aware of local vaginal and vestibular low-dose estradiol therapy.

Figure 14.2.2. Physical examination revealed a normal glans clitoris. The right and left labia minora were fused to the labia majora for two-thirds of the posterior aspect. The thickness of the upper third of the labia minora was several millimetres. The vagina lacked rugae, and lubrication was absent on the vaginal walls.

Comments

Basic science research has shown that the sex steroid hormone, estradiol, is critical for vaginal structure and function, such as lubrication, blood flow, and sensitivity10 (see Chapters 5.5, 5.6, 6.3, 7.2, and 13.1-13.3). In postmenopausal women, vaginal atrophy is a frequent complaint with symptoms of vaginal dryness, itching, discomfort, and painful intercourse. Systemic estrogen treatment via oral or patch hormone therapy for symptoms of atrophic vaginitis is not necessary in all cases. A substitute strategy involves use of various local estradiol delivery systems, including low-dose estradiol creams, ointments, intravaginal tablets, suppositories, and silicone rubber rings. The low risk of systemic absorption of estradiol with local vaginal and vestibular low-dose estradiol administration has been assessed. In a recent study of 1472 women with histologically confirmed breast cancer, 69 had bothersome vaginal atrophy and were treated with topical vaginal estrogen. Topical estrogen usage did not appear to be associated with increased risk of recurrence of breast cancer.11 Most investigations show no major estrogen-related side effects or endometrial proliferation.12-14 In postmenopausal women, the efficacy of low-dose estradiol local vaginal and vestibular delivery systems for estrogen deficiency has been established. Local estradiol has been shown to alleviate numerous subjective symptoms (discomfort, dryness, and diminished sensitivity) and to have various objective outcomes, such as vaginal mucosal health, induction of a high maturation index of vaginal mucosal cells, and reduction of vaginal pH below 5.5. It may be necessary to try different delivery systems for some postmenopausal women, as individuals using topical estradiol can complain of uterine bleeding, breast pain, allergy to the vehicle, and perineal pain.11-14

Case 3

RH, aged 32, has been married for 10 years to her high-school sweetheart. RH is a teacher and during the summer, she works as a camp counselor. She has two children and always seems busy with community, education, and religious activities. She has had sexual activity only with her husband, and they waited until after they were married for sexual intercourse. She has never had orgasm during sexual intercourse, leading to frustration and anxiety concerning the couple’s sexual activities in general. As a result, she tends to avoid intimacy.

RH discussed the sexual problem with her gynecologist at a recent examination. Her physical examination was normal and she was advised to see a sex therapist. RH wanted to see the therapist with her husband, but he did not cooperate.

Over the next few years, the problem persisted and the frustration intensified. RH eventually sought help at a multidisciplinary sexual medicine clinic.

She was seen by the psychologist, who reported as follows. This is a 32-year-old woman who has been married for the past 10 years. She notes that she has a lifelong orgasm disorder. She continues to be sexually active but feels that any sexual contact is related to guilt and a sense of obligation. She reports that sex at this time feels like a task that needs to be completed. She has no sexual abuse history and no psychologic trauma. She has had some mild depression as an adult, but this seems insignificant for her sexual dysfunction. She feels pressure from her husband to be sexually active but describes him as minimally supportive. She drinks alcohol on a social basis, uses no illegal substances, and has not smoked since college.

On history taking, RH revealed that while she had limited interest in masturbation, she was able to have orgasmic release by herself. She was able to lubricate vaginally once she got involved in the sexual activity. There was some discomfort during penetration but there was no overt pain or tenderness. She had normal menses and never any sexually transmitted diseases. She never used oral contraceptive pills.

Physical examination revealed that the clitoris, frenulum, urethral meatus, labia minora, and hymenal tissues were unremarkable (Fig. 14.2.3). Biothesiometry studies revealed that the vibration perception threshold was 3 V in the right and left pulp index fingers and 7 V in the labia, clitoris, frenulum, and urethral meatus. Hormone studies revealed the following values: thyroid-stimulating hormone 1.1 (0.4-5.50 μIU/ml), follicle-stimulating hormone 2.5 (1.5-33.4 mIU/ml), luteinizing hormone 6.3 (0.5-76.3 mIU/ml), prolactin 11.3 (2.8-29.2 ng/ml), dehydroepiandrosterone sulfate 236 (35-430 μg/ml), androstenedione 2.5 (0.2-3.1 ng/ml), total testosterone 62 (15-70 ng/dl), free testosterone 1.3 (0.3-1.9 ng/dl), sex hormone-binding globulin 27 (17-120 nmol/l), and dihydrotestosterone 136 (50-250 pg/ml). The patient was notified that all hormonal testing was unremarkable.

Further history taking was performed in the presence of the husband. On careful questioning, it became apparent that he suffered from lifelong premature ejaculation. The estimated intravaginal ejaculatory latency time was consistently 1-2 min. The husband had a limited sexual repertoire and was completely unaware of the premature ejaculation, since this was how he always ejaculated.

Figure 14.2.3. Physical examination revealed that the clitoris, frenulum, urethral meatus, labia minora, and hymenal tissues were unremarkable.

Medical treatment in this case was directed to the husband and included selective serotonin reuptake inhibitors, topical anesthetics, and oral phosphodiesterase type 5 inhibitors. Medical treatment, in conjunction with the couple’s sex therapy was successful. The follow-up intravaginal ejaculatory latency time more than doubled to 4 min. He learned how to become more attentive to her sexual needs and broadened his foreplay repertoire. RH has, for the first time, experienced orgasm during sexual activity with her husband including sexual intercourse. The couple are more satisfied with their sexual activity and have increased the frequency to several times per week.

Comments

It is important to be aware that a sexual problem in one member of the couple may be caused by the partner (see Chapter 8.2). One classic example is dyspareunia resulting from severe penile curvature associated with Peyronie’s disease.15 Another standard example is anorgasmia in the woman secondary to premature ejaculation in the man.16 Premature ejaculation is one of the most common male sexual dysfunctions.17 The most important method of diagnosing premature ejaculation is by intravaginal ejaculatory latency time defined as the time, measured by stopwatch, between the start of vaginal intromission and the start of intravaginal ejaculation. An intravaginal ejaculatory latency time of 2 min or less is a common inclusion criterion for clinical studies in premature ejaculation. Premature ejaculation may also be assessed by subject assessment of ejaculatory control, satisfaction with ejaculatory control, sexual satisfaction, and partner sexual satisfaction. Most physicians do not inquire about the existence of premature ejaculation of the partner when the female patient has other sexual complaints (diminished interest, diminished arousal) or when the patient has orgasmic dysfunction. Since premature ejaculation in the male often adversely affects partner sexual satisfaction, partner distress is a common motivation for afflicted men to seek treatment. Treatment for premature ejaculation may include sex therapy, selective serotonin reuptake inhibitors, topical anesthetics, and phosphodiesterase type 5 inhibitors.18-21

Case 4

LA, a healthy, 38-year-old woman, married 5 years ago. She had an excellent previous sex life with good interest, arousal, and orgasmic function. She experienced no pain during sexual activity. The couple decided to have a child together, but, after several years of failure to achieve pregnancy, LA underwent evaluation for infertility. She took leuprolide acetate selfinjections for one and a half years during infertility treatment and in vitro fertilization cycles. Since the infertility treatment, LA claims to have lost her sexual desire. Compared to previous capabilities, she describes 10% desire, 10% arousal, and 10% orgasmic function. She also notes there is a moderate discomfort during initial penetration but this soon disappears. She states, “I want my sex life back, I want to have a family, but now I have to force myself to have sex.”

LA had sought advice from her gynecologist. She was told that all looked normal on physical examination and a serum testosterone blood test was “within normal limits”. Due to persistence of the sexual problem, LA was referred to a multidisciplinary sexual medicine clinic.

LA was initially evaluated by the psychologist, who reported as follows. This 38-year-old woman was seen today with her husband of 5 years. The patient is undergoing infertility evaluation. She reports that ever since the infertility treatment began, she experiences marked diminished desire, arousal, and orgasm and painful intercourse. As a result, the couple have been sexually active virtually exclusively to achieve pregnancy. Although this has been difficult and frustrating for them, they have remained close, open to communicating about the situation, and committed to finding a solution for both the infertility and sexual problems. The patient herself has a difficult early history with emotional and sexual abuse. Her mother died when she was 12 years old, and the patient began a difficult adolescence with alcohol and substance abuse. She then entered her first marriage, which lasted 4 years because of her abusive husband. She now seems stabilized, and denies any depression or other mental health-related issues. She has never been in psychotherapy. Some behavioral relaxation may be an important adjunct to her medical treatment.

LA underwent history taking and physical examination. There was no additional contributory medical or surgical history. Physical examination revealed a clitoris diminished in size and a partially phimotic prepuce. The urethral meatus was normal. The labia minora was fused to the labia majora bilaterally in the posterior 20%. There were multiple areas of erythema overlying ostia of minor vestibular glands (Fig. 14.2.4). Q-tip testing was positive in many of these locations. Biothesiometry studies revealed that the vibration perception threshold was 3 V in the right and left pulp index fingers and 15-18 V in the labia, clitoris, frenulum, and urethral meatus. Hormone studies revealed the following values: thyroid-stimulating hormone 1.6 (0.4-5.50 |jIU/ml), follicle-stimulating hormone < 1.5 (1.5-33.4 mIU/ml), luteinizing hormone <0.5 (0.5-76.3 mIU/ml), prolactin 8.8 (2.8-29.2 ng/ml), dehydroepiandrosterone sulfate 101 (35-430 µg/ml), androstenedione 1.2 (0.2-3.1 ng/ml), total testosterone 12 (15-70 ng/dl), free testosterone 0.3 (0.3-1.9 ng/dl), sex hormone-binding globulin 49 (17-120 nmol/l), and dihydrotestosterone 34 (50-250 pg/ml).

The overall impression was sexual dysfunction, including low desire, arousal, and orgasm; mild genital atrophy; diminished genital sensation; and dyspareunia with vestibular adenitis. The sex steroid blood tests revealed low gonadotropins, low total and free testosterone, and low dihydrotestosterone. Discussion ensued to communicate directly with the infertility specialists and consider the leuprolide acetate as a direct cause of the endocrine milieu disturbance. The patient sought second opinions concerning infertility management and presently is off leuprolide. Her testosterone values have remained abnormally low, as found at the 2-year follow-up. She has started to receive counseling from the sex therapist.

Figure 14.2.4. Physical examination revealed areas of erythema overlying ostia of minor vestibular glands.

Currently, the couple is considering an international adoption. The patient started systemic testosterone therapy with marked improvement in sexual function and diminished pain symptoms after 6 months of therapy. She has remained in psychologic therapy.

Comments

Androgens, like other sex steroids such as estrogens, are critical for sexual function and genital tissue structure10 (see Chapters 5.5, 6.1—6.3, and 13.1). Leuprolide acetate is approved for treatment of men with advanced prostate cancer.22 Leuprolide acetate is also used by gynecologists to treat women with endometriosis,23 uterine fibroids,24 and infertility.25 Leuprolide acetate is a gonadotropin-releasing hormone agonist that suppresses ovarian function, induces a “temporary” menopause state, and interrupts estrogen output. The use of leuprolide acetate for infertility is based on the observation that suppression of estrogen enables other hormonal preparations to induce multiple ovum development.25 Leuprolide acetate also significantly interferes with ovarian synthesis of testosterone.26 There are few well-controlled data on the long-term adverse effects of leuprolide acetate on androgen biosynthesis in women.

Case 5

GS, aged 43, consulted her primary care physician for increasingly disturbing and worsening localized itching and burning in the clitoris, a condition that she had had since 38 years of age. The clitoral pain symptoms have prevented her from wearing tight clothing. The itching and burning has increased significantly during the past year, adversely affecting her personal, social, and work life. She avoids relationships for fear that the interaction will lead to sexual activity. She has never had sexual intercourse. She performed clitoral masturbation on occasion as a young teenager but now avoids any clitoral contact. Her past medical history is negative for trauma or infections in the clitoral area.

GS was referred to several gynecologists and psychologists. She was managed with topical xylocaine and topical estrogen creams. She was also treated for yeast infections. Due to persistence of the clitoral pain, GS was referred to a multidisciplinary sexual medicine clinic.

GS was evaluated by the psychologist as follows. This 43- year-old, single woman presents with complaints of clitoral pain preventing her from engaging in sexual activity. The patient states that she is unable to achieve orgasm and doubts whether she has ever been orgasmic. She denies any significant psychologic history. She recently began taking a sleep medication since the symptoms interfered with sleep. The patient has never been abused or experienced any psychologic trauma. She has no history of substance or alcohol abuse. The patient is not currently in a relationship and reports that her clitoral pain is increasingly becoming an issue in possible relationships. She adds that men often perceive her clitoral pain as a personal failure. GS has seen therapists in the past, but no psychologic issues have been uncovered.

GS underwent a history and physical examination. She had normal menses, used no medications, and had no urinary tract symptoms. Physical examination revealed a white color patch and a pale, nonpigmented, skin-wrinkled area with scaling and cracking involving the entire clitoral hood, the left frenulum and the region between the posterior fourchette and the anus (Fig. 14.2.5). The rest of the vestibular examination revealed fusion of the labia minora onto the labia majora.

The diagnosis of lichen sclerosus was suspected. A biopsy of the clitoral hood was offered to define the disorder, but the patient refused. She was treated with twice daily topical clobe- tasol. After 8 weeks, she reported complete reversal of the itching, burning, and pain. Physical examination failed to identify any suspicious dermatitis lesions on the clitoral hood, clitoris or region between the posterior fourchette and anus. There was no obvious residual scarring of the clitoris, clitoral hood or region between the posterior fourchette and anus. She has noted improvement of her mood and general well-being, and feels ready to start new relationships. She was advised to continue counseling by the sex therapist.

Figure 14.2.5. Physical examination revealed a white-colored, pale, nonpigmented, skin-wrinkled area with scaling and cracking involving the region between the posterior fourchette and the anus.

Comments

Lichen sclerosus is a chronic genital dermatitis condition associated with visible signs of small white patches on the genitals27,28 and a wide variation in presentation symptoms, including, itching, burning, and pain with sex (see Chapters 9.5 and 12.2). In some women, the symptoms can interfere with sexual activity, routine activities, and sleep. The diagnosis of lichen sclerosus is suggested by physical examination showing white-colored genital, vulvar, and vestibular tissue with paleness, loss of pigmentation, and characteristic “cigarette paper” wrinkling. Diagnosis is conformed by biopsy. Genital lichen sclerosus is presently managed by the ultrapotent fluorinated steroid, clobetasol.28

Case 6

BC, a 37-year-old, single, Caucasian woman, complained primarily of severe pain localized to the genital region during heterosexual or self-masturbation, and during coital thrusting. This pain has affected her since age 26. BC described the genital sexual pain as starting as a localized discomfort at the anterior vaginal wall, and then becoming an actual pain at the clitoris, labia minora, urethral meatus, and region surrounding the urethral meatus. BC reported that the pain developed suddenly, without obvious cause. During the last several years, the genital sexual pain increased significantly, and she currently has diminished ability to have orgasm. BC has tried many over-the-counter analgesic agents without success. The overall condition has been very distressing and has adversely affected her sexual relationships.

Two to three months before the beginning of the genital sexual pain disorder at age 26, she complained of urinary urgency, frequency (10 times per day) and nocturia (three times per night), burning during voiding, and suprapubic discomfort during and after voiding. There was some relation between the genital sexual pain disorder and the irritative urinary symptoms, especially after coitus or just prior to menses. BC had multiple negative urine culture and sensitivity tests performed by her primary care physician.

BC was in a stable relationship with regular and satisfactory sexual intercourse for 5 years before the genital sexual pain disorder. BC has performed self-masturbation since she was 15 years old. Masturbation was never painful until she was 26 years of age. For the genital sexual pain disorder, BC had been treated with topical estrogen, local anesthetics, baclofen, alpha- blockers, and diazepam. BC reported that after having sex, significant amelioration of the local discomfort was achieved by bed rest in a face-down position.

BC was advised to seek a second opinion at a multidisciplinary sexual medicine clinic. BC was seen by the psychologist, who reported as follows. This 37-year-old, single woman has a chief complaint of genital sexual pain, urinary irritative and dysuria symptoms, and suprapubic discomfort. Over the last several years, this has become an increasing problem for both her and her partners. She is currently in a stable relationship. The patient has a history of sexual abuse as a child, but she is reluctant to discuss this. She denies that her past history has negatively affected her relationships or her ability to trust men. She does recall in her youth that her father and brother often looked at pornography, and she found this very embarrassing. By nature, the patient is a negative, pessimistic woman who is very cautious in decision making and in her relationships. She has no history of overt depression or other psychologic disorders. She consumes six alcohol drinks per week and used illegal substances during her teenage and early adult years.

Physical examination was negative for vaginitis, urethritis, or herpes. Bimanual examination revealed tenderness just under the posterior bladder wall and above the pubic bone. BC’s pelvic floor muscles were rigid. Because of suspicion of interstitial cystitis, BC underwent urodynamic testing. The first sensation of bladder filling occurred at 50 ml. The first strong desire to void occurred at 75 ml. BC’s irritative symptoms were reproduced during filling. Cystoscopy with hydrodistention was performed and verified the presence of Hunner’s ulcers, linear scarring, hypervascularity, and bloody effluent and glomerula- tions after hydrodistention. Potassium sensitivity testing showed increased epithelial permeability with the instillation of a mild potassium chloride solution, with exacerbation of the symptoms of urgency and pain.

BC underwent multimodal treatment for interstitial cystitis, including behavioral, pharmacologic, and surgical therapies. Behavioral therapies included dietary modification, bladder training, and pelvic floor physical therapy. Pharmacologic therapy involved pentsosan polysulfate, antihistamines, tricyclic antidepressants, anticholinergics, antiepileptics, muscle relaxants and anti-inflammatory agents, and narcotics for symptom relief. Surgical therapy included hydrodistention and intravesical instillations of dimethyl sulfoxide on a weekly basis.

After the first 4 weeks of interstitial cystitis treatment, BC reported a significant reduction of the sexual pain along with a major reduction of the “cystitis symptoms” previously described. BC also continued with the sexologic management.

Comments

Interstitial cystitis is a chronic, often severe, inflammation and hypersensitivity disorder of the bladder wall29-34 (see Chapters 7.3 and 17.4). Interstitial cystitis affects mainly middle-aged Caucasian women. It is estimated that there are 450,000 cases in the USA. Primary symptoms include urinary frequency and urgency, and lower abdominal or perineal pain. More than half of interstitial cystitis patients have pain while riding in car, and approximately two of three interstitial cystitis patients are unable to work full time because of the symptoms. Interstitial cystitis can produce pain that is perceived in any location in the pelvis in any combination with or without urinary frequency/ urgency and sexual pain disorders. Interstitial cystitis and vul- vodynia may coexist. The diagnosis of interstitial cystitis is based upon symptoms, excluding other conditions such as urinary tract infections, urethral diverticulum, or urethral stricture. Conclusive diagnosis of interstitial cystitis is made by cystoscopy during bladder distention that reveals small petechial hemorrhages or glomerulations) and/or larger Hunner’s ulcers, and by positive potassium testing. Treatment is multimodal, including behavioral, pharmacologic, and surgical interventions.29-34

Case 7

WA, a 33-year-old married woman, complained for 5 years of localized pain and burning in the introitus during penetration that persists after the sexual intercourse. WA noted that the pain was 10/10 on an analog visual pain scale, was present on every occasion, and caused her to stop the intercourse activity about half of the times. WA also noted a progressive decrease in sexual desire and arousal for the last 7 years. Compared to previous capabilities, WA has 20% desire, 20% arousal, and 80% orgasmic function. The sexual problem has generated considerable personal distress and interfered with the couple’s relationship. The husband believes that WA does not love him or find him sexually attractive. WA has had two normal pregnancies and vaginal deliveries. The last delivery at age 26 was followed by postpartum depression, for which she was treated with selective serotonin reuptake inhibitors for 2 years. She uses no medication at present other than combined oral contraceptives for the last 6 years.

WA was examined by various psychologists, primary care physicians, and her local gynecologist. No abnormalities were identified and no treatments have thus far proved effective. WA was referred to a multidisciplinary sexual medicine clinic.

WA’s psychologic evaluation was as follows. This is a 33- year-old woman who has been married for 11 years. The couple report a decline in sexual interest and satisfaction shortly after the birth of their second child 7 years ago. The couple are both very frustrated, and neither husband nor wife tend to initiate any sexual contact. The patient presents as having some mild agitated depression as well as chronic fatigue and stress secondary to her busy schedule and parenting duties. There is a past psychologic history of postpartum depression, but no history of sexual trauma or abuse. The couple have had marital counseling, although their communication is diminished due to lack of privacy and the inability to reach a resolution about the sexual issues.

WA underwent history taking and physical examination. She denied any past medical history, including high cholesterol, hypertension, diabetes mellitus, and cancer, as well as urinary tract infections, endometriosis, and interstitial cystitis. Physical examination revealed 30% clitoral phimosis, and normal labia and urethral meatus. At the labial-hymenal junction, there were regions of erythema overlying the ostia of the minor vestibular glands (Fig. 14.2.6). Q-tip testing was positive with an intensity of 4-8/10. The vagina had rugae and normal mucosa. Biothesiometry revealed vibration perception threshold testing of 3 V in the pulp index fingers and 10-13 V in the clitoris, frenulum, urethral meatus, and labia minora. Hormone studies revealed the following values: thyroid- stimulating hormone 2.1 (0.4-5.50 µIU/ml), follicle-stimulating hormone 1.5 (1.5-33.4 mIU/ml), luteinizing hormone 0.5 (0.5-76.3 mIU/ml), prolactin 12.3 (2.8-29.2 ng/ml), dehydroepiandrosterone sulfate 75 (35-430 µg/ml), androstenedione 0.9 (0.2-3.1 ng/ml), total testosterone 24 (15-70 ng/dl), free testosterone <0.3 (0.3-1.9 ng/dl), sex hormone-binding globulin 176 (17-120 nmol/l), and dihydrotestosterone 55 (50-250 pg/ml).

WA was diagnosed as having diminished desire and arousal, diminished genital sensation, vestibular adenitis, and androgen insufficiency. We advised WA to discontinue the oral contraceptives and initiate birth control by barrier method or encourage her husband to undergo vasectomy. We initiated a series of consultations for pelvic floor physical therapy and encouraged couple’s sex therapy. Gabapentin was administered to help diminish the sexual pain, and local anesthetics were prescribed to provide pain relief. Androgens were administered with dehydroepiandrosterone and local testosterone gel. At 3 months, laboratory results showed recovery of all hormonal parameters to the upper third of the reference values, with virtual complete elimination of the sexual pain and the beginning of sexual dreams, thoughts, and fantasies. All treatments continued, and hormonal blood tests evaluations were carried out every 3 months. At 9-month follow-up, the patient noted improvement of her mood and general well-being in addition to resolution of the genital symptoms. She has discontinued the gabapentin and no longer uses the topical xylocaine. She has noted some mild acne and increased facial hair that she refers to as “fuzzies” on her face cheeks.

 

Figure 14.2.6. At the labial-hymenal junction, regions of erythema overlay the ostia of the minor vestibular glands.

Comments

Vulvar vestibulitis syndrome was described by Friedrich35 in 1987 and is characterized by: 1) severe pain upon palpation in the vestibular area or in the introitus; 2) pain upon pressure localized in the vestibule; and 3) evident vestibular erythema of variable intensity for at least 6 months (see Chapters 12.1-12.6). Vulvar vestibulitis syndrome is associated with inflammatory involvement of the minor vestibular glands, revealing significant squamous metaplasia surrounded by inflammatory cells that form follicles of T lymphocytes and plasmatic cells.36,37 Eva et al. reported an abnormal expression of estrogenic receptors in vestibular tissue on patients with vulvar vestibulitis syndrome.38 Hodgins et al. found a significant decrease in the concentration of estrogenic receptors in biopsies of patients with vulvar vestibulitis when compared with a healthy control group.39 Sutherland found that women with vulvar vestibulitis syndrome and concomitant hypogonadism reveal a significant decrease in the concentration of androgenic receptors in the minor vestibular glands when compared with a control group.40 There is a relationship between use of oral contraceptives and vulvar vestibulitis syndrome, and it is probably related, in part, to the androgen insufficiency observed in women on the combined oral contraceptives.41-43 The treatment of vulvar vestibulitis syndrome includes: topical anesthetics, physical therapy, behavioral therapy, hormone therapy, and surgical excision.

Conclusion

Numerous psychologic and biologic pathophysiologies adversely affect women’s sexual health. This chapter focused on several biologic conditions, such as infection, partner sexual dysfunction, pain syndromes, hormonal aberrations, genital tissue atrophy, and adverse pharmacologic consequences. As the field of women’s sexual health matures and research investigations concerning biologic pathophysiologies become commonplace, it is hoped that evidence-based data will accumulate to support the safe and effective utilization of medical management alongside the traditional treatment by psychologic intervention.

Acknowledgments

Dr Edgardo Becher is grateful to Dr Sandra Ganna for her contribution. Dr Andrea Salonia is grateful to Dr Alberto Briganti, Dr Elena Longhi, Dr Giuseppe Zanni, Prof. Patrizio Rigatti, and Prof. Francesco Montorsi for their contributions.

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