The clinical value of interleukins-8, -10, and -17 in idiopathic granulomatous mastitis.

Introduction: Idiopathic granulomatous mastitis (IGM) is a rare, chronic inflammatory benign breast disease. Although the etiology of this disease is unknown, it has been suggested that hormonal disorders, autoimmunity, smoking, and α1-antitrypsin deficiency may play a role in the etiopathogenesis. The aim is to investigate the changes in cytokine profiles including interleukin (IL)-4, -8, -10, -17, and tumor necrosis factor (TNF)-alpha in patients with IGM. Methods: Forty-seven patients with pathologically diagnosed IGM and 30 healthy women were included. The cytokines including IL-4, -8, 10, -17, and TNF-alpha were measured by human enzyme-linked immunosorbent assay. Results: The IL-8, IL-10, and IL-17 levels were higher in IGM patients than control group (p =.002; p =.008; and p =.018, respectively). The IL-8 levels of patients with active lesions and in remission were statistically higher than the control group (p =.027 and p =.015, respectively). IL-10 levels of patients in remission were higher than the control group (p =.024). There was no difference in IL-4 and TNF-ɑ levels between all groups. Conclusion: These results showed that proinflammatory cytokines including IL-8 and IL-17 have role in pathogenesis of IGM. However, the increased levels of IL-10 in especially patients in remission suggest that it reduces the release of proinflamatory cytokines as well as suppressing their function and activation for controlling IGM. Although IGM is thought to be a surgical disease, these cytokine changes indicate the presence of serious immune dysregulation. This suggests that in the treatment of IGM, treatment needs to evolve from surgery to medical treatment. Key points • The IL-8, IL-10, and IL-17 levels were higher in IGM patients than in control group. • The IL-8 levels of both patients with active lesions and in remission were high. • There was no difference in IL-4 and TNF-ɑ levels between all groups. [ABSTRACT FROM AUTHOR]