The development of capsular contracture has been hypothesized to involve implant type, placement, seroma, hematoma, surgical technique, biofilm, and infection, all of which have some involvement in the overexpression of the inflammatory response which is suspected in the progression of capsular contracture.1 Previously analyzed contracted capsules show inflammatory cells consisting of myofibroblasts and leukotriene receptors.2 Montelukast (Singular; Merck & Co., Kenilworth, N.J.) a leukotriene receptor antagonist, inhibits one of the leukotriene receptors that leads to collagen production.3
Breast augmentation combined with an inverted T-point mastopexy further increases the inflammatory process compared with breast augmentation alone; therefore, montelukast may decrease the risk of capsular contracture. Previous investigators have reported the benefit of montelukast in relation to capsular contracture.4,5 The first author (S.L.) sought to determine whether prophylactically adding montelukast to the normative, postoperative management care in primary, breast augmentation/full mastopexy patients would reduce the incidence of capsular contracture. We evaluated 72 patients in a prospective, nonrandomized, voluntary trial who underwent primary breast augmentation/full mastopexy procedures performed by one surgeon from May of 2012 to August of 2015. All patients had smooth surface, saline implants placed retromuscularly and received a drain. Group A patients (n = 37) were started 1 week postoperatively with montelukast for a total of 3 months, and group B patients (n = 35) did not receive any montelukast during their routine postoperative course. Mean postoperative follow-up was 11 ± 4.5 months. We assessed whether differences in capsular contracture rates (Baker grade 3 and greater) between the two groups occurred.
Routine postoperative management with montelukast demonstrated a trend toward a statistically significant lower incidence of capsular contracture rates in cosmetic one-stage breast augmentation/full mastopexy patients compared with postoperative, non–montelukast-managed patients (group A, n = 37, 0 capsular contractures; group B, n = 35, four capsular contractures; p = 0.0509, Fisher’s exact test). A previous study published recently in the Journal evaluating a much larger patient demographic looked at two different leukotriene inhibitors. Montelukast, similar to our outcome review, was noted to be associated with a strong trend toward statistical significance.6 In the same study, however, zafirlukast (Accolate; AstraZeneca Pharmaceuticals, Cambridge, United Kingdom), which is a competitive antagonist to three leukotriene receptors, was found to have a definitive statistically significant reduction in capsular contracture and reduced encapsulation risk by over 50 percent. The potential of zafirlukast on the greater reduction in the capsular contracture rate compared to montelukast on our outcome review capsular contracture rate was not performed but may, similarly, have been duplicated in our study.
Although the sample size was small, our findings confirmed previous larger studies illustrating the potential benefit of prophylactically administering a leukotriene inhibitor in breast implant surgery. Additional studies, however, should be performed using multicenter trials to determine whether the addition of a leukotriene inhibitor should be included by plastic surgeons in the quest to reduce capsular contracture.
Neither of the authors has any commercial associations, financial disclosures, or conflicts of interest to declare in relation to the content of this article.
Sean Lille, M.D.Jason Jacoby, B.A.Private practiceScottsdale, Ariz.
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