Sex: Taboos, Assumptions, and Evidence

The population living with and beyond a cancer diagnosis continuously increases as a result of earlier detection and improvement in therapies, with an estimated 14.5 million people living with a history of cancer in the United States in 2014. As a result of this increasing survivorship population, health issues related to the persistent and late effects of cancer treatment are being highlighted as important, and their management is essential for long-term improvement in health. Changes in sexual health are one of the most common physical concerns, with 46% of post-treatment cancer survivors who responded to the 2006 LIVESTRONG survey reporting changes in sexual functioning; 71% of them did not receive post-treatment care for their sexual concern. Although the impact of cancer and its treatment on sexual health has been identified by survivors as important, it still seems to be a taboo subject and difficult for patients to bring forward to their health care team, in part because of their fear of not having their concerns addressed. Health care providers do not routinely incorporate sexual health inquiry into their practice for multiple reasons, including lack of comfort and knowledge with the subject as well as lack of resources and time. Health care providers often justify not asking about changes in sexual health in older, palliative, and nonpartnered patients because of the assumption that they are no longer interested in sex. The development of sexual difficulties in women from cancer treatment is multifactorial, and all treatment modalities can contribute to sexual morbidity as well as patient pretreatment psychosocial issues and sexual self-perception. Women with gynecologic or other pelvic cancers who are treated with surgery may have significant sexual dysfunction as a result of a decrease in estrogen from salpingooophorectomy, changes in body image, vaginal shortening, pelvic adhesions causing pelvic pain, and potential disruption of the pelvic nerves important in sexual arousal. Pelvic radiation induces vaginal fibrosis and narrowing that can lead to significant dyspareunia. However, cancer treatments that do not directly target the pelvis can also have a profound effect on sexual functioning in women. Reduction of circulating estrogen by administration of chemotherapy and endocrine therapies, such as aromatase inhibitors, can lead to accelerated atrophic vulvovaginitis in premenopausal women and worsen preexisting atrophy in postmenopausal women. Low levels of systemic estrogen result in decreased blood flow to the vulvar and vaginal tissue, decreased vaginal and cervical secretions, and decreased elasticity and thinning of the vaginal mucosa, resulting in penetrative dyspareunia and fear of pain with sexual activity. Current management focuses on improving overall vaginal health with nonhormonal therapies such as ongoing use of vaginal moisturizers and lubricants during sexual activity. Hormonal therapies, such as local estrogens, are effective in treating vaginal atrophy; however, the safety in women with hormone-responsive tumors such as estrogen receptor–positive breast cancers continues to be debated. Because of the uncertainty of the safety of local hormonal treatments, alternative novel nonhormonal therapies are appealing to patients and health care providers and are needed for the management of atrophic vulvovaginitis to improve quality of life for these women. However, research into these topics can challenge our assumptions, and indeed, the article by Goetsch et al that accompanies this editorial has done just that. Through their previous research, they have proposed that a component of penetrative dyspareunia may be a result of a pain disorder at the vaginal opening (vestibulodynia) secondary to neural hyperplasia and not related to vaginal dryness. Indeed, they and others have demonstrated reproducible tenderness of the vulvar vestibule in postmenopausal breast cancer survivors that can be alleviated with topical lidocaine, such that a subsequent speculum examination does not lead to pain. Animal studies seem to support this hypothesis, because low estrogen states are associated with an increase in vestibular neural hypertrophy. Goetsch et al have taken this observation further, in the form of a small, phase II, randomized, placebo-controlled study of 46 postmenopausal breast cancer survivors with high levels of pain and sexual distress who were randomly assigned to either saline or 4% aqueous lidocaine application just before intercourse. In the blinded portion of the study, patients using lidocaine experienced a much greater reduction in pain scores on intercourse and improvements in several domains of the validated Sexual Function Questionnaire. In the openlabel portion of the study that followed, 90% of the patients reported comfortable penetration, and remarkably, 17 of 20 previous abstainers resumed comfortable intercourse. Of course, any small randomized trial suffers from potential limitations and threats to its validity. In that regard, several questions arise in the interpretation of this study. How were the patients selected, and why were so few excluded as a result of alternative explanations for their dyspareunia? Were patients really blinded to the intervention when lidocaine likely has a different sensation impact than saline? Was that the reason why patients in the saline group also improved with time, or was it a result of the fact that baseline distress and pain were so high and a placebo effect was seen in both groups? Was follow-up long enough? Could there be a tachyphylaxis/rebound effect with prolonged use? There is no doubt that sexual distress is multifactorial and that these patients had high baseline scores but that, at the end of the study, they indeed were better and had resumed intercourse. The JOURNAL OF CLINICAL ONCOLOGY E D I T O R I A L VOLUME 33 NUMBER 30 OCTOBER 2

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