Capsular contracture - What are the risk factors? A 14 year series of 1400 consecutive augmentations.

The modern era of breast augmentation and reconstruction began in 1963, with the introduction of silicone implants by Cronin and Gerow. To date, the demand for cosmetic augmentation continues to increase exponentially. However, whilst the surgical techniques and quality of mammary prosthesis have improved dramatically in recent years, patients are still confronted with significant potential complications. We performed a retrospective study of 1400 consecutive primary breast augmentations performed between March 1995 and March 2009 by a single surgeon. We specifically examined the incidence of capsular contracture and the possible causative factors. Follow up ranged from 1 to 16 years. The mean age at the time of surgery was 32.8 years and fill volume was between 195 ml and 800 ml. Our capsular contracture rate was in the order of 26.9%. BMI >30, fill volumes >350 ml, smoking and alcohol consumption did not significantly increase capsular contracture rate. Implant type, pregnancy, infection and delayed haematoma significantly increased the risk of capsular contracture. Our series has given us a unique insight into the frequency of capsular contracture and identified several risk factors. To our knowledge, this is the first report of pregnancy having a significant effect on capsular contracture. We now counsel patients thoroughly into the detrimental effects of pregnancy on the implant.

Visfatin is regulated by rosiglitazone in type 2 diabetes mellitus and influenced by NFκB and JNK in human abdominal subcutaneous adipocytes.

Visfatin has been proposed as an insulin-mimicking adipocytokine, predominantly secreted from adipose tissue and correlated with obesity. However, recent studies suggest visfatin may act as a proinflammatory cytokine. Our studies sought to determine the significance of this adipocytokine and its potential role in the pathogenesis of T2DM. Firstly, we examined the effects of diabetic status on circulating visfatin levels, and several other adipocytokines, demonstrating that diabetic status increased visfatin*, TNF-α*** and IL-6*** compared with non-diabetic subjects (*p<0.05, **p<0.01, ***p<0.001, respectively). We then assessed the effects of an insulin sensitizer, rosiglitazone (RSG), in treatment naïve T2DM subjects, on circulating visfatin levels. Our findings showed that visfatin was reduced post-RSG treatment [vs. pre-treatment (*p<0.05)] accompanied by a reduction in HOMA-IR**, thus implicating a role for insulin in visfatin regulation. Further studies addressed the intracellular mechanisms by which visfatin may be regulated, and may exert pro-inflammatory effects, in human abdominal subcutaneous (Abd Sc) adipocytes. Following insulin (Ins) and RSG treatment, our in vitro findings highlighted that insulin (100 nM), alone, upregulated visfatin protein expression whereas, in combination with RSG (10 nM), it reduced visfatin*, IKKß** and p-JNK1/2*. Furthermore, inhibition of JNK protein exacted a significant reduction in visfatin expression (**p<0.01), whilst NF-κB blockade increased visfatin (*p<0.05), thus identifying JNK as the more influential factor in visfatin regulation. Additional in vitro analysis on adipokines regulating visfatin showed that only Abd Sc adipocytes treated with recombinant human (rh)IL-6 increased visfatin protein (*p<0.05), whilst rh visfatin treatment, itself, had no influence on TNF-α, IL-6 or resistin secretion from Sc adipocytes. These data highlight visfatin's regulation by insulin and RSG, potentially acting through NF-κB and JNK mechanisms, with only rh IL-6 modestly affecting visfatin regulation. Taken together, these findings suggest that visfatin may represent a pro-inflammatory cytokine that is influenced by insulin/insulin sensitivity via the NF-κB and JNK pathways.