Human immunodeficiency virus (HIV) is a chronic infectious disease that causes inflammation. Antiretroviral therapy (ART) reduce inflammation, but not to normal levels. Inflammation can substantially exacerbate, if not cause, many types of chronic pain. The burden of chronic pain in PLWH is substantial, with prevalence estimates ranging from 39 to 85%. While chronic pain disorders are often heterogeneous (neuropathic, musculoskeletal) among PLWH, inflammation may represent a common contributor to poor chronic pain outcomes, yet this remains unknown. This study examined whether circulating pro-inflammatory cytokine levels were associated with experimental pain sensitivity and clinical pain severity in PLWH with chronic pain. Thus far, 28 PLWH with chronic pain (median CD4 + = 682.4; 11% detectable viral load > 200; 89% on ART) were recruited from an HIV clinic that provides comprehensive medical and social services. Blood samples were collected initially for the assay of circulating pro-inflammatory cytokine levels, specifically interleukin-6 (IL-6) and tumor necrosis factor—alpha (TNF-a). Participants then completed the Brief Pain Inventory before quantitative sensory testing of sensitivity to painful heat and mechanical stimuli. Analyses revealed that higher circulating IL-6 was significantly associated with greater temporal summation of heat pain at 440C (r = .627, p < .001) and 460C (r = .602, p = .001), greater temporal summation of mechanical pain at the trapezius (r = .558, p = .002), and greater self-reported clinical pain severity (r = .372, p = .05). Higher circulating TNF-a was significantly associated with temporal summation of mechanical pain at the hand (r = .457, p = .015) and trapezius (r = .440, p = .019). These results tentatively suggest that inflammation may represent a shared mechanism underlying heightened experimental pain sensitivity and greater clinical pain severity in PLWH with chronic pain, which may have implications for treatment of this important co-morbidity in HIV.
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