Cross-sectional case-control study evaluates cAMP/EPACs markers in chronic low back pain, suggesting a pathophysiological mechanism without direct pain link.
Chronic low back pain represents a major public health issue, particularly in sub-Saharan Africa where it remains understudied. This cross-sectional case-control study, conducted in Dolisie (Congo), evaluated the involvement of cAMP/EPACs pathway markers (cyclic adenosine monophosphate and EPAC1/EPAC2 proteins) in low back pain. Seventy-five patients with chronic low back pain (pain duration ≥6 months, VAS score ≥30 mm) and 25 healthy controls were included. Intracellular concentrations of cAMP, EPAC1, and EPAC2 were measured in blood mononuclear cells (PBMCs) by ELISA, and pain intensity was measured using a visual analog scale (VAS). Analysis of our data showed a significant increase in cAMP (12.6 ± 2.1 for DL group against 3.2 ± 0.4 pmol/ml for TS group), EPAC1 (7.9 ± 1.2 for DL group against 2.1 ± 0.3 ng/ml for TS group) and EPAC2 (4.8 ± 0.7 for DL group against 1.5 ± 0.2 ng/ml for TS group) levels with a p-value < 0.0001 for the three markers compared. EPAC1 was more expressed than EPAC2, suggesting a predominant role in pain modulation. However, no significant correlation was observed between these biomarkers and VAS scores (p > 0.05), indicating that their activation reflects a pathophysiological mechanism without a direct link to subjective pain intensity. This study reveals dysregulation of the cAMP/EPACs pathway in chronic low back pain, opening up avenues for translational research targeting EPAC1 in a Congolese context. Limitations include the lack of clinical-biological correlation and the need for longitudinal studies to establish a causal link.
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Loubano-Voumbi et al. (2025) studied this question.
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