Samuelsen Per-Jostein, Nielsen Christopher Sivert, Wilsgaard Tom, Stubhaug Audun, Svendsen Kristian, Eggen Anne Elise
Regional Medicines Information and Pharmacovigilance Centre (RELIS), University Hospital of North Norway, P.O. Box 79, N-9038, Tromsø, Norway.
Department of Community Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
BMC Pharmacol Toxicol. 2017 Jun 9;18(1):45. doi: 10.1186/s40360-017-0149-2.
Increased pain sensitivity is a putative risk factor for chronic pain and consequently for analgesic use. Conversely, analgesic use may be a cause of increased pain sensitivity, e.g., through opioid-induced hyperalgesia. We aimed to study the association between pain sensitivity and analgesic use in a general population, and to test the hypothesis that increased baseline pain sensitivity is a risk factor for future persistent analgesic use.
The Tromsø Study (2007-08), a population-based health study, was linked with eight years of prescription data from the Norwegian Prescription Database. The cold pressor test was completed in 10,486 participants aged 30+ years, and we used cold pressor endurance time as a proxy measure of pain sensitivity. Cross-sectional associations with different measures of analgesic use were assessed. Furthermore, a cohort of 9,657 persons was followed for 4.5 years.
In the cross-sectional analysis, increased pain sensitivity was associated with analgesic use; regular users of opioids alone were more pain sensitive than regular users of non-opioid analgesics. Increased baseline pain sensitivity was a risk factor for persistent analgesic use, i.e., using non-steroidal anti-inflammatory drugs, paracetamol, or opioids for ≥ 90 days and proportion-of-days-covered ≥ 40% (HR = 1.22, 95% CI 1.06-1.40), although not statistical significant after confounder adjustment.
Increased pain sensitivity was associated with analgesic use in general, and reduced pain tolerance was found for both opioid and non-opioid analgesic users. The data suggest that hyperalgesia is an effect of analgesics, whereas pain tolerance has little impact on future analgesic use.
疼痛敏感性增加被认为是慢性疼痛以及由此导致使用镇痛药的一个风险因素。相反,使用镇痛药可能是疼痛敏感性增加的一个原因,例如通过阿片类药物引起的痛觉过敏。我们旨在研究普通人群中疼痛敏感性与镇痛药使用之间的关联,并检验基线疼痛敏感性增加是未来持续使用镇痛药的一个风险因素这一假设。
特罗姆瑟研究(2007 - 2008年),一项基于人群的健康研究,与来自挪威处方数据库的八年处方数据相关联。对10486名30岁及以上的参与者进行了冷加压试验,我们将冷加压耐受时间用作疼痛敏感性的替代指标。评估了与不同镇痛药使用指标的横断面关联。此外,对9657人进行了4.5年的随访。
在横断面分析中,疼痛敏感性增加与镇痛药使用相关;仅阿片类药物的常规使用者比非阿片类镇痛药的常规使用者对疼痛更敏感。基线疼痛敏感性增加是持续使用镇痛药的一个风险因素,即使用非甾体抗炎药、对乙酰氨基酚或阿片类药物≥90天且覆盖天数比例≥40%(风险比=1.22,95%置信区间1.06 - 1.40),尽管在进行混杂因素调整后无统计学意义。
一般而言,疼痛敏感性增加与镇痛药使用相关,并且发现阿片类和非阿片类镇痛药使用者的疼痛耐受性均降低。数据表明痛觉过敏是镇痛药的一种效应,而疼痛耐受性对未来镇痛药使用影响不大。