Activin A and Follistatin Serum Concentrations in Breast Augmentation Patients

Background: Capsular contracture is caused by an excessive fibrotic reaction similar as observed in other progressive fibrotic disorders. For their pathogenesis, several studies confirmed the importance of activins and follistatin. The aim of this study was to determine and analyze serum levels of Activin A and follistatin in patients with capsular contracture after aesthetic breast augmentation. Methods: The study included 361 female patients who underwent primary aesthetic breast augmentation, came for control examination after breast augmentation or for revision operation because of capsular contracture. Blood samples were taken and using a specific ELISA to determine the serum concentration levels of Activin A and Follistatin. Results: Ninety-six patients (n = 96), who developed a capsular contracture Baker ≥°III and underwent revision surgery were collected (capsular fibrosis group). One-hundred and fourteen patients (n = 114) were asymptomatic for capsular fibrosis Baker ≥°III after primary breast augmentation and 33 (n = 33) of them had developed no capsular fibrosis after more than 10 years (long-term group). For control group, blood samples were taken from 167 patients (n = 167) before primary aesthetic breast augmentation. Serum Activin A levels were significantly higher in the long-term Group compared with those in the capsular fibrosis- and the control groups. Follistatin levels were significantly lower in the capsular fibrosis group compared to the control- and the long-term groups. A small amount of control group patients (n = 16) developed a capsular fibrosis within 2 years after primary breast augmentation with significant lower follistatin levels. Retrospectively, they showed significantly lower serum follistatin levels than the control group even before the onset of capsular contracture. Conclusions: Capsular fibrosis has no effect on Activin A serum levels. In contrast, follistatin serum levels are lower in patients with capsular fibrosis. These results show that besides many other factors, a dysregulation of the Activin–follistatin axis may have importance on the pathogenesis of capsular contracture.