Our goal was to determine whether treatment of depressive symptoms with escitalopram during buprenorphine treatment for opioid dependence, would improve treatment retention compared to placebo in a 12-week, randomized, double-blind trial. Treatment drop-out was defined as missing seven consecutive buprenorphine dosing days. Participants were 76% male, 80% non-Hispanic Caucasian, and 64% heroin users. At baseline, the mean Beck Depression Inventory-II (BDI-II) score was 28.4 (±9.7). Sixty-one percent of participants completed the 12 week buprenorphine protocol. Dropout rates were 33.3% and 44.0% among those randomized to escitalopram or placebo respectively (p=.19). Relative to baseline, mean BDI-II scores were significantly lower at all follow-up assessments, but the treatment by time interaction effect was not statistically significant (p = .18). Participants randomized to escitalopram also did not have a significantly lower likelihood of testing positive for either opiates or other drugs during follow-up. Depressive symptoms often resolved with buprenorphine treatment and the immediate initiation of escitalopram does not improve treatment retention, depression outcomes, or illicit drug use. Clinicians should determine the need for antidepressant treatment later in buprenorphine care.
This study determined the frequency of reporting being introduced to opioids by a physician among opioid dependent patients. Cross-sectional analyses were performed using baseline data from a cohort of opioid addicts seeking treatment with buprenorphine. The primary outcome was response to the question: “Who introduced you to opiates?” Covariates included sociodemographics, depression, pain, current and prior substance use. Of 140 participants, 29% reported that they had been introduced to opioids by a physician. Of those who were introduced to opioids by a physician, all indicated that they had initially used opioids for pain, versus only 11% of those who did not report being introduced to opioids by a physician (p<0.01). There was no difference in current pain (78% vs. 85%, p=0.29), however participants who were introduced to opioids by a physician were more likely to have chronic pain (63% vs. 43%, p=0.04). A substantial proportion of individuals with opioid dependence seeking treatment may have been introduced to opioids by a physician.
It is unknown if infection with hepatitis C virus (HCV) is a risk factor for pain among persons who have used injection drugs (IDU). Multivariate regression was used to determine whether HCV was associated with greater likelihood of reporting significant chronic pain and discomfort intolerance in a cohort of 97 opioid dependent IDU. Study results suggest that participants with HCV may be more likely to suffer chronic pain (aOR=1.98; 95% CI: 0.76 to 5.12, p=0.16). Furthermore, HCV was found to be associated with a higher discomfort intolerance scale score, reflecting intolerance to physical discomfort (β=2.34; 95% CI: 0.06 to 4.62, p=0.04). Infection with HCV may be an overlooked cause for chronic pain and discomfort intolerance among opioid dependent IDU.
Pain is common among opioid dependent patients, yet pharmacologic strategies are limited. The aim of this study was to explore whether escitalopram, a selective serotonin reuptake inhibitor, was associated with reductions in pain. The study used longitudinal data from a randomized, controlled trial that evaluated the effects of escitalopram on treatment retention in patients with depressive symptoms who were initiating buprenorphine/naloxone for treatment of opioid dependence. Participants were randomized to take escitalopram 10mg or placebo daily. Changes in pain severity, pain interference and depression were assessed at 1, 2 and 3 months visits using the Visual Analog Scale, Brief Pain Inventory and the Beck Depression Inventory II, respectively. Fixed-effects estimator for panel regression models were used to assess the effects of intervention on changes in outcomes over time. Additional models were estimated to explore whether the intervention effect was mediated by within-person changes in depression. In this sample of 147 adults, we found that participants randomized to escitalopram had significantly larger reductions on both pain severity (b = −14.34, t = −2.66, p < .01) and pain interference (b = −1.20, t = −2.23, p < .05) between baseline and follow-up. After adjusting for within-subject changes in depression, the estimated effects of escitalopram on pain severity and pain interference were virtually identical to the unadjusted effects. In summary, this study of opioid-dependent patients with depressive symptoms found that treatment with escitalopram was associated with clinically meaningful reductions in pain severity and pain interference during the first three months of therapy.
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