BACKGROUND Profound hypogonadism has been noted in patients receiving intrathecal opioids. The purpose of the current study was to determine whether chronic consumption of oral opioids by male survivors of cancer also would lead to central hypogonadism and whether this hypogonadism was associated with symptoms of sexual dysfunction, fatigue, anxiety, and depression. METHODS A case–control study was conducted at The University of Texas M. D. Anderson Cancer Center (Houston, TX), in which 20 patients who were chronically consuming opioids were compared with 20 matched controls. Patients completed the Sexual Desire Inventory (SDI), the Hospital Anxiety and Depression Scale (HADS), the Functional Assessment of Chronic Illness Therapy with general and fatigue subscales (FACT‐G/FACIT‐F), and the Edmonton Symptom Assessment System (ESAS) questionnaires. Serum samples were collected for testosterone, follicle‐stimulating hormone (FSH), and luteinizing hormone (LH). RESULTS Comparing the opioid group with the control group, 18 of the 20 patients (90%; 95% confidence interval [CI], 65–98%) exhibited hypogonadism, compared with 8 of the 20 control patients (40%; 95% CI, 19–64%). The median testosterone level was 145 ng/dL versus 399.5 ng/dL (5.0 nmol/L vs. 13.9 nmol/L; P < 0.0001), the median FSH level was 2.85 milli–International Units (mIU)/mL versus 5.3 mIU/mL (P = 0.08), the median LH level was 1.8 mIU/mL versus 4.2 mIU/mL (P = 0.0014), the median SDI‐dyadic score was 18.5 versus 40 (P = 0.01), the median SDI‐solitary score was 0 versus 5 (P = 0.007), the HADS (anxiety) score was 8.5 versus 5.5 (P = 0.053), the HADS (depression) score was 7.5 versus 1.5 (P = 0.0002), the FACT‐G score was 64 versus 96.3 (P = 0.0001), and the FACIT‐F score was 24 versus 46 (P = 0.0003). CONCLUSIONS Survivors of cancer who chronically consumed opioids experienced symptomatic hypogonadism with significantly higher levels of depression, fatigue, and sexual dysfunction. With the increasing use of opioids among patients with cancer, further research in improving quality‐of‐life outcomes is warranted. Cancer 2004;100:851–8. © 2004 American Cancer Society.

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The use of neuraxial (intrathecal and epidural) analgesia has been suggested in treatment guidelines put forth for the treatment of refractory cancer pain. We review the literature and present our algorithm for using neuraxial analgesia. We also present our outcomes using this algorithm over a 28-month period. We used neuraxial analgesia in 87 of 4,107 patients, approximately 2% of those seen for pain consultation. Evaluation of those patients at an 8-week follow-up revealed improved pain control. After institution of neuraxial analgesia, there was a significant reduction in the proportion of patients with severe pain (defined as a "pain worst" score in the severe range of 7-10), from 86% to 17%, noted to be highly statistically significant. At follow-up, numerical pain scores decreased significantly from 7.9 +/- 1.6 to 4.1 +/- 2.3. No difference was noted between the intrathecal and epidural groups. Oral opioid intake after instituting neuraxial analgesia revealed a significant decrease from 588 mg/day oral morphine equivalents to 294 mg/day. At follow-up, self-reported drowsiness and mental clouding (0-10) also significantly decreased from 6.2 +/- 3.0 and 5.4 +/- 3.4 to 3.2 +/- 3.0 and 3.1 +/- 3.0, respectively. This retrospective review shows promising efficacy of neuraxial analgesia in the context of failing medical management.

The purpose of this study was to determine the prevalence of central hypogonadism and sexual dysfunction in male cancer survivors exposed to chronic high-dose oral opioid therapy. We studied 20 male patients with cancer-related chronic pain who were disease-free for at least one year. All patients consumed at least 200 mg-equivalent of morphine on a daily basis for at least one year. Participants completed the Sexual Desire Inventory questionnaire and serum levels of testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were assessed. Serum testosterone levels were reduced in these patients. The median value was 140 ng/dL (normal 241-827). There was no compensatory increase in FSH and LH. The median FSH level was 3.5 mIU/mL (normal 1.4-18.1). The median LH level was 2.1 mIU/mL (normal 1.5-9.3). The mean dyadic sexual desire score was 23.9+/-15.7 (normal value, 42.8+/-8.9). The mean solitary sexual desire score was 1.3+/-1.9 (normal value, 10.6+/-1.9). Our data suggest that chronic exposure to high-dose oral opioid therapy may result in marked central hypogonadism and sexual dysfunction. Given the increasing use of long-term opioid therapy for chronic pain syndromes, further investigation into these findings is warranted.