The association between the COMT rs4680 (G>A, Val-158-Met) polymorphism and the risk of fibromyalgia has been investigated in previous studies, but the results are controversial. Therefore, a meta-analysis has been performed to confirm the association between COMT rs4680 (G>A, Val-158-Met) polymorphism and the risk of fibromyalgia in this study. Our study includes eleven case-control studies with 2,909 individuals comprised of 1,365 fibromyalgia patients and 1,544 control subjects. The regression analysis was performed using the random effects model or the fixed effects model and OR with the corresponding 95 % CI was calculated for the allele, recessive, dominant, over-dominant, co-dominant 1, and co-dominant 2 model. No statistical significant associations were observed between COMT rs4680 (G>A, Val-158-Met) polymorphism and risk of fibromyalgia in allele model (P-value = 1.00), recessive model (P-value = 1.00), dominant model (P-value = 0.54), co-dominant 1 model (P-value = 1.00) and co-dominant 2 model (P-value = 1.00). In conclusion, our meta-analysis showed that the COMT rs4680(G>A, Val-158-Met) polymorphism might not be genetic risk factor for the fibromyalgia.

Background : This study aimed to identify the mechanisms of the antinociceptive effects of PG in the fibromyalgia (FM)-like animal model. Methods and Results : To assess the possible effect of PG on FM symptoms, we constructed a FM animal model induced by intermittent cold stress with slight modification. All mice underwent nociceptive assays using electronic von Frey anesthesiometer and Hargreaves equipment. To assess the relation between PG and the expression levels of brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), and phosphorylated CREB (p-CREB), western blotting and immunohistochemistry analyses were performed. In behavioral analysis, nociception tests showed that the pain threshold was significantly decreased in the FM group compared to control group. Western blot and immunohistochemical analyses of the medial prefrontal cortex and hippocampus showed downregulation of BDNF and p-CREB proteins in the FM group compared to control group. PG recovered these changes at behavioral tests and protein level. These results provide evidence that the effects of PG extract in the FM model may be related to its modulating effect on the BDNF signaling pathway in the hippocampus and medial prefrontal cortex. Conclusion : Our animal model may be involved in the mechanism by which PG extract is effective as a therapeutic agent for FM.