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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