Study identifies potential non-surgical treatment for inguinal hernias

Editor's Note

Researchers at Northwestern University successfully reversed hernias in male mice and restored normal anatomy without surgical intervention, according to a February 5 university announcement. The study also found that human hernia tissue shared the same molecular characteristics observed in the mouse model, suggesting a similar biological mechanism.

According to the article, the findings highlight estrogen receptor-alpha (ESR1) as a key factor in hernia formation. This receptor contributes to the activation of connective tissue cells and excessive fibrous tissue growth, ultimately leading to hernia development. Blocking ESR1 with the anti-estrogen drug fulvestrant, which is currently approved for treating certain types of breast cancer, reduced hernia size in the study’s mouse model and restored normal tissue structure.

To validate these findings in humans, researchers analyzed tissue samples from individuals undergoing hernia repair. They identified the same molecular markers present in the mouse model and found that estrogen and ESR1 activate genes associated with excessive tissue scarring. The study was published February 4 in the Journal of Clinical Investigation. 

According to the article, half of all men develop an inguinal hernia during their lifetimes. The underlying cause remains unclear, and the only existing treatment is surgical repair. More than one million inguinal hernia repairs are performed annually in the US, typically under general anesthesia. Even with surgery, recurrence rates range from 10% to 15%.