Genetic alteration predicts pain recovery after sexual assault

Previous studies have reported that sexual assault victims who report having severe pain across multiple body regions are experiencing stress-induced hyperalgesia, resulting from release of endogenous opioids. An initial period of analgesia is followed by delayed onset of persistent and widespread hyperalgesia. Gene variants have been associated with the u-opioid receptor and the most common variant is the single nucleotide polymorphism (SNP) A118G. Individuals with one or more copies of variant gene (allele) at the A118G have shown poor analgesic response to opioids.

A research team at the University of North Carolina hypothesized that activation of u-opioid receptors causes stress-induced hyperalgesia after a sexual assault and survivors with one or more copies of the variant gene at the A118G receptor would experience less receptor-mediated hyperalgesia and less pain in the initial weeks following the assault.

Women 18 years and older presenting for treatment by sexual assault nurse examiners working in ten different health systems were recruited for the study. The women were interviewed after one week and six weeks for evaluation of their pain symptoms. Genotyping was performed on all 52 study participants. The gene variant was found in 12 women (23%) and all were Caucasian.

The study results showed that the women with the gene variant resulting in reduced response to u-opioid receptor binding had clinically relevant reductions in pain severity. The findings suggest that women with one of more alleles at A118G may experience both a reduced analgesic response to endogenous opioids and a reduction in delayed-onset, more long-lasting opioid mediated hyperalgesia. The finding suggests that endogenous opioid-mediated hyperalgesia may contribute to pain symptoms after sexual assault.