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Pharmacological Effects of Supportive Care Medications on Sexual Function

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    The long-term effects of reduced testosterone and amenorrhea are not well known. Sexuality is an important component of one's quality of life, especially for cancer survivors, but also for some people with advanced disease. Patients may report a history of changes in libido and sexual dysfunction. If these changes are distressing to the patient, serum total- and free-testosterone levels and prolactin levels may be obtained.[14] Should the patient seek improvement in libido and performance, treatment is often empirical, keeping in mind that there are many potential causes of changes in sexual function. Treatment options may include using nonopioids for pain, adding adjuvant analgesics in the hope that the opioid dose may be reduced, or replacing testosterone through injections, a patch, or gel if not contraindicated.[15] More research is needed to understand the relationship between opioids and sexual function, as well as the most effective treatment strategies.

    Selective Serotonin Reuptake Inhibitors

    Decreased sexual desire is a frequent symptom of depression, and sexual impairment in depressed patients has been consistently confirmed in controlled studies.[16,17][Level of evidence: II] Continued recognition of the difficulty in discerning the subjective complaints that are a part of the depressive syndrome, the consequences of treatment, a pre-existing sexual dysfunction, or a combination of these factors is needed. Approximately one-third of depressed patients without medication treatment report reduced sexual desire, anorgasmia, delayed ejaculation, or erectile dysfunction.[18] Selective serotonin reuptake inhibitors (SSRIs), tricyclics, monoamine oxidase inhibitors, and lithium have all been associated with sexual dysfunction.[19,20]

    Sexual desire is mediated through the central nervous system by the reception of sensory stimuli and the subsequent interpretation through the limbic system and prefrontal cortex.[21] Additionally, the hypothalamic and preoptic nuclei contribute to the mediation of this process. Serotonin inhibits hypothalamic arousal postsynaptic receptors resulting in the release of excitatory neurotransmitters. These neurotransmitters are responsible for the activation of the erectile centers of the spinal column. Upon activation of the erectile centers, subsequent erection, orgasm, and detumescence occur in males, whereas genital vasocongestion, vaginal lubrication, and clitoral enlargement occur in females.[22] Physiologically, serotonin is stored in synaptosomal vesicles awaiting another impulse for release. SSRIs inhibit this uptake mechanism, which results in the pooling of serotonin in the synaptic space.[21,23] The excess serotonin causes the postsynaptic receptors to down-regulate, resulting in decreased stimulation of the lower erectile centers. It is this action that is thought to be the principal mechanism for SSRI-induced sexual dysfunction.

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