• Elina Iordanova Schistad, Audun Stubhaug, Anne-Sofie Furberg, Bo Lars Engdahl, and Christopher Sivert Nielsen.
• aDepartment of Physical Medicine and Rehabilitation, Division of Clinical Neuroscience, Oslo University Hospital, Ulleval, Oslo, Norway bDepartment of Pain Management and Research, Division of Emergencies and Intensive Care, Oslo University Hospital, Oslo, Norway cInstitute of Clinical Medicine, University of Oslo, Oslo, Norway dDepartment of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway eDepartment of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway fDivision of Ageing and Health, Norwegian Institute of Public Health, Oslo, Norway.
• Pain. 2017 Jul 1; 158 (7): 1280-1288.

AbstractThe aim of this study was to examine whether increases in severity of subclinical inflammation, measured by high-sensitivity C-reactive protein (hs-CRP), increased experimental pain sensitivity, measured by cold-pressor tolerance, and to test whether this relationship is independent of chronic pain. A large population-based study from 2007 to 2008, the sixth Tromsø Study, provided data from 12,981 participants. For the present analysis, complete data for 10,274 participants (age: median 58 years) were available. The main outcome measure was cold-pressor tolerance, tested by placing the dominant hand in circulating cold water (3°C) for a maximum of 106 seconds. Cox proportional hazard models, treating hand withdrawal during the cold-pressor test as the event and enduring the full test time as censored data, were used to investigate the relationship between hs-CRP levels (≤3 or >3 mg/L) and cold-pressure tolerance. The fully adjusted model was controlled for age, sex, education, body mass index, smoking status, alcohol consumption, emotional distress, statin usage, and self-reported presence of chronic pain. Additional analysis was performed in participants without chronic pain. Higher levels of hs-CRP were negatively related to cold-pressor tolerance (hazard ratio [HR] = 1.24, 95% confidence interval [CI], 1.12-1.37, P < 0.001), adjusted for age and sex. This relationship remained essentially unaltered after controlling for potential confounders (HR = 1.22, 95% CI, 1.09-1.36, P < 0.001), as well as for the presence of chronic pain (HR = 1.22, 95% CI, 1.09-1.36, P < 0.001). The present data show that subclinical inflammation is related to increased pain sensitivity, suggesting a potential role of inflammation in experimental pain which may be of importance for the development of clinical pain.

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