Chronic noncancer pain is a leading cause of sickness absence (SA) and disability pension (DP). The objectives of this study were to identify trajectories of SA/DP before and after strong and weak opioid initiation for noncancer pain and the factors associated with these trajectories. A longitudinal population-based study of 201,641 people (24-59 years) without cancer who initiated opioid analgesics in 2009 in Sweden was conducted. Trajectories of net annual SA/DP days in the 5 years before/after opioid initiation were estimated with group-based trajectory modelling. Multinomial logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for factors associated with trajectory groups. Among the 6.9% of people initiating strong opioids, 12.5% had persistent high SA/DP (estimated 320 days/year) before and after opioid initiation and 72.9% had persistent low/minimum SA/DP (estimated 30 days/year). Approximately 8.6% of people had increasing SA/DP, and 6.1% had decreasing SA/DP after opioid initiation, although this seemed to reflect continuation of preinitiation patterns. Trajectories were similar at lower SA/DP days/year among those initiating weak opioids. Persistent high SA/DP among strong opioid initiators were associated with ≥5 comorbidities (OR = 8.72, 95% CI 5.61-13.56), ≤9 years of education (OR = 5.83, 95% CI 4.84-7.03), and previous use of antidepressants (OR = 4.57, 95% CI 3.89-5.37) and antipsychotics (OR = 4.49, 95% CI 2.93-6.88). Three-quarters of people initiating opioids for noncancer pain had persistent low/minimum levels of SA/DP 5 years before and after initiation. Increasing and decreasing SA/DP after opioid initiation seemed to reflect a continuation of preinitiation patterns. Our findings highlight the complex range of sociodemographic and medication-related factors associated with persistent SA/DP.
More than three-quarters of people who initiate opioids for noncancer pain had persistent low/minimum levels of sickness absence/disability pension 5 years before and after opioid initiation.
aCentre for Medicine Use and Safety, Faculty of Pharmacy and Pharmaceutical Sciences, Monash University, Melbourne, Victoria, Australia
bDepartment of Pharmacy, Austin Health, Melbourne, Victoria, Australia
cDivision of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
dDepartment of Epidemiology and Preventive Medicine, Monash University, Melbourne, Victoria, Australia
eSchool of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia
fNational Drug and Alcohol Research Centre, UNSW Sydney, Sydney, New South Wales, Australia
Corresponding author. Address: Centre for Medicine Use and Safety, Faculty of Pharmacy and Pharmaceutical Sciences, Monash University, 381 Royal Parade, Parkville 3052, Melbourne, Victoria, Australia. Tel.: +61 3 9903 9533; fax: +61 3 9903 9629. E-mail address: samanta.Lalic@monash.edu (S. Lalic).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
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Received October 31, 2018
Received in revised form January 11, 2019
Accepted January 14, 2019