Judith I Tsui1, Marlene C Lira2, Debbie M Cheng3, Michael R Winter4, Daniel P Alford5, Jane M Liebschutz5, Jianren Mao6, Robert R Edwards7, Jeffrey H Samet8. 1. Section of General Internal Medicine, Department of Medicine, University of Washington School of Medicine, 325 9th Avenue, Seattle, WA 98104, United States. Electronic address: tsuij@uw.edu. 2. Clinical Addiction Research and Education Unit, Section of General Internal Medicine, Department of Medicine, Boston Medical Center, 801 Massachusetts Ave., Second Floor, Boston, MA 02118, United States. 3. Department of Biostatistics, Boston University School of Public Health, 801 Massachusetts Ave., Third Floor, Boston, MA 02118, United States. 4. Data Coordinating Center, Boston University School of Public Health, 801 Massachusetts Ave., Third Floor, Boston, MA 02118, United States. 5. Clinical Addiction Research and Education Unit, Section of General Internal Medicine, Department of Medicine, Boston Medical Center, 801 Massachusetts Ave., Second Floor, Boston, MA 02118, United States; Section of General Internal Medicine, Department of Medicine, Boston University School of Medicine, 801 Massachusetts Ave., Second Floor, Boston, MA 02118, United States. 6. Department of Anesthesia, Massachusetts General Hospital, 101 Merrimac Street, Boston, MA 02110, United States. 7. Department of Anesthesia, Brigham and Women's Hospital, Pain Management Center, 850 Boylston Street, Chestnut Hill, MA 02467, United States. 8. Clinical Addiction Research and Education Unit, Section of General Internal Medicine, Department of Medicine, Boston Medical Center, 801 Massachusetts Ave., Second Floor, Boston, MA 02118, United States; Section of General Internal Medicine, Department of Medicine, Boston University School of Medicine, 801 Massachusetts Ave., Second Floor, Boston, MA 02118, United States; Department of Community Health Sciences, Boston University School of Public Health, 801 Massachusetts Ave., Second Floor, Boston, MA 02118, United States.
Abstract
BACKGROUND: Patients with opioid use disorders on opioid agonist therapy (OAT) have lower pain tolerance compared to controls. While chronic viral infections such as HCV and HIV have been associated with chronic pain in this population, no studies have examined their impact on pain sensitivity. METHODS: We recruited 106 adults (41 uninfected controls; 40 HCV mono-infected; and 25 HCV/HIV co-infected) on buprenorphine or methadone to assess whether HCV infection (with or without HIV) was associated with increased experimental pain sensitivity and self-reported pain. The primary outcome was cold pain tolerance assessed by cold-pressor test. Secondary outcomes were cold pain thresholds, wind-up ratios to repetitive mechanical stimulation (i.e., temporal summation) and acute and chronic pain. Multivariable regression models evaluated associations between viral infection status and outcomes, adjusting for other factors. RESULTS: No significant differences were detected across groups for primary or secondary outcomes. Adjusted mean cold pain tolerance was 25.7 (uninfected controls) vs. 26.8 (HCV mono-infection) vs. 25.3 (HCV/HIV co-infection) seconds (global p-value=0.93). Current pain appeared more prevalent among HCV mono-infected (93%) compared to HCV/HIV co-infected participants (76%) and uninfected controls (80%), as did chronic pain (77% vs. 64% vs. 61%, respectively). However, differences were not statistically significant in multivariable models. CONCLUSION: This study did not detect an association between HCV infection and increased sensitivity to pain among adults with and without HIV who were treated with buprenorphine or methadone for opioid use disorders. Results reinforce that pain and hyperalgesia are common problems in this population.
BACKGROUND:Patients with opioid use disorders on opioid agonist therapy (OAT) have lower pain tolerance compared to controls. While chronic viral infections such as HCV and HIV have been associated with chronic pain in this population, no studies have examined their impact on pain sensitivity. METHODS: We recruited 106 adults (41 uninfected controls; 40 HCV mono-infected; and 25 HCV/HIV co-infected) on buprenorphine or methadone to assess whether HCV infection (with or without HIV) was associated with increased experimental pain sensitivity and self-reported pain. The primary outcome was cold pain tolerance assessed by cold-pressor test. Secondary outcomes were cold pain thresholds, wind-up ratios to repetitive mechanical stimulation (i.e., temporal summation) and acute and chronic pain. Multivariable regression models evaluated associations between viral infection status and outcomes, adjusting for other factors. RESULTS: No significant differences were detected across groups for primary or secondary outcomes. Adjusted mean cold pain tolerance was 25.7 (uninfected controls) vs. 26.8 (HCV mono-infection) vs. 25.3 (HCV/HIV co-infection) seconds (global p-value=0.93). Current pain appeared more prevalent among HCV mono-infected (93%) compared to HCV/HIV co-infectedparticipants (76%) and uninfected controls (80%), as did chronic pain (77% vs. 64% vs. 61%, respectively). However, differences were not statistically significant in multivariable models. CONCLUSION: This study did not detect an association between HCV infection and increased sensitivity to pain among adults with and without HIV who were treated with buprenorphine or methadone for opioid use disorders. Results reinforce that pain and hyperalgesia are common problems in this population.
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