Women with macromastia suffer from considerable musculoskeletal pain, physical limitation, and poor psychosocial well-being compared with their unaffected peers.1–26 Recent studies have found that reduction mammaplasty in adolescents and young women is a relatively safe procedure that can afford patients significant and sustained physical and psychosocial improvements.16–26
Despite the numerous documented benefits associated with reduction mammaplasty,2–26 some surgeons remain hesitant to operate on adolescents, in part because of a fear of postoperative glandular growth. Often, primary care providers will delay referral and surgeons will postpone surgery until the patient has reached chronologic adulthood. In addition, many third-party payors impose age restrictions when determining coverage for reduction mammaplasty without regard for the patient’s psychological and developmental maturity. As such, determining a young woman’s surgical readiness relies on insurance and anecdotal metrics, and disregards a potentially more comprehensive, patient-centric measure: biological maturity and, thereby, breast size stability.
The present study’s objective was to explore the relationship among the degree of breast hypertrophy, body mass index category, and age at first menses (menarche) in a single-surgeon cohort of young women undergoing bilateral reduction mammaplasty. We also aimed to measure the incidence of postoperative breast growth to present surgeons with a patient-centric method for timing reduction mammaplasty in adolescents to minimize the potential for postoperative breast growth.
PATIENTS AND METHODS
We obtained approval from the Boston Children’s Hospital Committee on Clinical Investigation (protocol number X08-10-0492) to both prospectively enroll patients and retrospectively review the medical records of women who underwent bilateral reduction mammaplasty at our institution from 2007 through 2019. All patients were between the ages of 12 and 21 years and nulliparous at the time of initial consultation. Written consent was obtained from patients and parents/guardians when appropriate. These prospectively enrolled patients (n = 417) were recruited during their initial consultation for reduction mammaplasty. We also retrospectively reviewed the charts of an additional 64 patients identified using the CPT code for reduction mammaplasty (19318). All patients in our final sample (n = 481) were evaluated and managed by a single pediatric plastic surgeon (B.I.L.). The diagnosis of macromastia was made using symptomatology, physical examination, two-dimensional photography, and modified Schnur criteria.27,28
Clinical Presentation and Demographics
Clinical staff completed standardized assessment forms for all subjects during the initial consultation that captured information concerning breast symptomatology, review of systems, and gynecologic and pubertal history. Patients’ baseline height and weight were measured. For adult subjects aged 20 years or older, body mass index category was determined using the Centers for Disease Control and Prevention Adult Body Mass Index Calculator and body mass index classifications.29 Body mass index–for-age percentiles and body mass index category were calculated for younger subjects (younger than 20 years) using the Centers for Disease Control and Prevention Child and Teen Body Mass Index Calculator and classifications, which account for both age and sex.30
Using patients’ height and weight measurements, body surface area (in meters squared) was calculated for each patient using the DuBois and DuBois formula.31,32 Intraoperatively, the amount of total resected breast tissue in grams was recorded by clinical staff. As the clinical significance of this amount varies by the overall size of the patient, a normalized breast tissue resected mass was calculated for each patient by dividing their total amount of tissue resected during surgery by their calculated body surface area. This normalized resection mass represents the “degree of breast hypertrophy” used in analyses. The duration of time (years) from first menses to reduction mammaplasty was calculated for each patient (referred to as “time since menarche”).
As part of their care, all patients are assessed for postoperative breast growth by the clinical team at every clinical encounter beginning at the first postoperative year using a combination of physical examination, two-dimensional photographic documentation, and bra fitting. Postoperative breast growth was deemed attributable to glandular proliferation when body mass index remained stable in the presence of a clinical assessment consistent with glandular hypertrophy. All other postoperative breast growth was attributed to adipose accumulation.
Data Management and Statistical Methods
Data were collected and stored using Research Electronic Data Capture, a secure Web-based application hosted at Boston Children’s Hospital with support through Harvard Catalyst.33 Statistical analyses were performed using IBM SPSS Version 24 (IBM Corp., Armonk, N.Y.). Subjects were included in analyses only if their baseline height and weight, menarche age, and amount of breast tissue resected were available. The associations between the following variables were assessed using analysis of variance and post hoc testing as appropriate: body mass index category, age at onset of pubertal breast development (thelarche) and menarche, and degree of breast hypertrophy.
Because of the cross-sectional nature of this study, the age at which breast growth stabilizes was approximated. Using menarche as a reference point for female puberty, the study’s primary hypothesis was that there would be a positive association between the number of years since menarche and breast size. As adolescent girls progress through puberty, their breasts will continue to grow. However, if adolescents are followed long enough, their breast size will eventually stabilize and the association will attenuate. In this context, the point at which this association attenuates is theoretically the optimal time to operate (Fig. 1). A linear regression model was fit to determine the effect of time since menarche on the degree of breast hypertrophy, stratified by body mass index category and years since menarche to pinpoint the time at which the association dissipates. A value of p < 0.05 was considered statistically significant for all analyses.
A total of 481 patients were included in analyses. The most commonly reported races in our sample included the following: white [n = 255 (53.0 percent)], unknown or other [n = 126 (26.2 percent)], black or African American [n = 67 (13.9 percent)], and Hispanic [n = 33 (6.9 percent)]. The majority of our sample were overweight or obese [n = 318 (66.1 percent)], with a mean body surface area of 1.8 ± 0.2 m2. On average, patients reached thelarche and menarche at 11.1 ± 1.9 years (range, 6 to 15 years) and 11.9 ± 1.5 years (range, 7 to 16 years), respectively. The mean total breast resection mass for the sample was 1395.3 ± 666.3 g, with a mean normalized tissue resected mass of 778.0 ± 317.5 g when accounting for patients’ body surface area (Table 1).
Table 1. -
|Mean age at thelarche ± SD, yr
||11.1 ± 1.9
|Mean age at menarche ± SD, yr
||11.9 ± 1.5
|Mean age at surgery ± SD, yr
||17.9 ± 1.9
|Mean amount of total tissue resected ± SD, g
||1395.3 ± 666.3
|Baseline BMI category
| Healthy weight
Effect of Body Mass Index Category
Age at thelarche and menarche and degree of breast hypertrophy significantly varied by body mass index category (p < 0.05, all). Post hoc testing revealed that although overweight and obese patients reached thelarche at similar ages (10.9 years versus 10.8 years; p = 0.68), thelarche occurred significantly later in healthy-weight patients (11.6 years; p < 0.05, both) (Fig. 2). Likewise, overweight and obese patients experienced first menses at comparable ages (11.7 years versus 11.4 years; p = 0.18), but were significantly younger than healthy-weight patients (12.5 years; p < 0.05, both). When normalizing the amount of tissue resected by each patient’s body surface area, obese patients had significantly more mean breast tissue removed (949.3 g) than their overweight (725.3 g) and healthy-weight peers (640.4 g; p < 0.001, both). When controlling for differences in body mass index category, age at menarche was a significant predictor of the degree of breast hypertrophy, with earlier menarche correlated with more severe hypertrophy (p = 0.002).
On average, our sample underwent reduction mammaplasty at 17.9 ± 1.9 years old, or 6.1 ± 2.1 years since menarche (range, <1 to 14 years). However, obese patients underwent surgery at a significantly younger age (17.7 years) than their healthy-weight (18.3 years) counterparts (p = 0.004). As hypothesized, time since menarche was a significant predictor of breast hypertrophy, such that a greater amount of time since menarche was correlated with more severe hypertrophy (p = 0.04). This model was then stratified by body mass index category. The association between time since menarche and degree of breast hypertrophy was no longer significant for healthy-weight and overweight patients (p > 0.05, all). However, this model remained significant for obese patients (p < 0.05) until they reached 9 years after menarche. Once the obese group reached this time point, the association was no longer significant (p > 0.05), indicating the point at which breast size stabilizes (Fig. 3).
Postoperative Breast Growth
At the time analyses were conducted, 446 subjects (92.7 percent) were at least 1 year postoperatively and were assessed for postoperative breast growth. These patients were followed clinically for a median of 20.2 months (range, 12.0 to 95.0 months; interquartile range, 13.4 months). Of these patients, 27 (6.1 percent) had some degree of postoperative breast growth. This growth resulted in a return of baseline breast-related musculoskeletal symptoms in half of affected patients [n = 14 of 27 (51.9 percent)]. A subset of patients who experienced regrowth indicated psychological distress attributable to their postoperative breast growth [n = 4 of 27 (14.8 percent)]. At the time of analyses, six patients (22.2 percent) had undergone a repeated reduction, and an additional six patients were interested in pursuing reoperation in the future.
Roughly half of all instances of postoperative breast growth were attributable to additional glandular proliferation [n = 14 of 27 (51.9 percent)] as opposed to weight gain [n = 13 of 27 (48.1 percent)]. Cause of regrowth (glandular versus weight gain) did not vary significantly by body mass index category (p = 0.36), and obese patients accounted for 35.7 percent (n = 5) of glandular regrowth cases. Of those experiencing regrowth because of glandular proliferation, obese patients underwent initial reduction mammaplasty at a median of 3.0 years (interquartile range, 5.5 years) after menarche (range, 1.2 to 7.7 years), whereas healthy-weight and overweight patients (n = 11) underwent surgery at a median of 6.0 years (interquartile range, 5.3 years) years after menarche (range, <1 to 11 years).
Operating on young obese women before the model-estimated 9-year postmenarche time point increased the likelihood of postoperative breast growth in general (OR, 1.19; 95 percent CI, 1.11 to 1.27) and regrowth attributable specifically to glandular proliferation (OR, 1.18; 95 percent CI, 1.11 to 1.26). In addition, when reduction mammaplasty was performed on healthy-weight and overweight women who were less than 3 years after menarche, the commonly regarded end of puberty,34 the likelihood of postoperative breast growth in general (OR, 5.23; 95 percent CI, 1.29 to 21.23) and growth caused by glandular proliferation increased (OR, 7.43; 95 percent CI, 1.37 to 40.41).
Reduction mammaplasty is a safe and effective means of alleviating the physical and psychosocial burden of adolescent macromastia.16–26 However, surgeons and third-party payors often impose arbitrary age cutoffs for surgery because of potential postoperative breast growth. This study is the first to derive a patient-centric method for assessing breast size stability in adolescents seeking reduction mammaplasty and to explore postoperative breast regrowth rates in young patients.
We sought to approximate the biological time point at which breast size stabilizes using linear regression modeling fit to determine the effect of time since menarche on the degree of breast hypertrophy. There was no demonstrable association between degree of breast hypertrophy and time since menarche in healthy-weight and overweight subjects, suggesting that breast growth ends relatively early in these patients. It is likely that breast size stabilization occurs within the commonly cited timeframe of 2 to 3 years after menarche,34 and thus was unable to be captured in our cross-sectional cohort (mean age, 17.9 years), as they largely completed breast growth before study participation. In contrast, breast size did not appear to stabilize in obese subjects until 9 years after menarche.
Overall, the occurrence of postoperative breast growth in our sample was low (6 percent). In addition, only half of regrowth cases were caused by continued glandular proliferation as opposed to weight gain. Cause of regrowth did not vary by body mass index category, with roughly one-third of glandular regrowth cases occurring in obese patients. In keeping with our model estimate, all obese patients who developed postoperative glandular breast growth underwent initial reduction mammaplasty before they had reached their ninth postmenarchal year. Operating on young obese women before the model-estimated 9-year postmenarche time point increased the likelihood of glandular breast regrowth by roughly 120 percent.
In addition, pursuing reduction mammaplasty in healthy-weight and overweight women less than 3 years after menarche increased the likelihood of postoperative glandular breast growth by over 700 percent. It must be noted, however, that seven healthy-weight and overweight patients experienced postoperative glandular growth after their third postmenarchal year. Interestingly, the majority of these seven patients were prescribed hormonal contraceptives to treat menstrual irregularities, indicative of potential endocrine disruption. Further research is needed concerning the role of hormonal dysregulation on abnormal breast development.
Special Considerations for Obese Patients
There are several considerations that must be made when treating obese adolescents with macromastia. Although obese patients’ breast size may take longer to stabilize than their healthy-weight peers, they may present for surgery at an earlier age because of undergoing puberty earlier and having greater breast hypertrophy. To obtain coverage from third-party payors, a greater amount of tissue must be resected from obese patients according to the Schnur criteria. In addition, to account for potential postoperative breast growth in younger obese patients, surgeons may elect to resect more liberally. However, removing too much breast tissue in these patients can cause the chest to become disproportionately small to the overall frame and lead to poorer aesthetic outcomes.
Regardless, the benefits of early surgical intervention may outweigh the risk of postoperative breast growth. Our group has previously demonstrated that adolescents and young women who experience postoperative breast growth still enjoy the same postoperative improvements in their physical and psychosocial as their unaffected peers.26 Rather than delay surgery outright in young obese or young symptomatic patients, such as those with considerable musculoskeletal pain, on the basis of biological and chronologic age, breast surgeons should consider the overall benefit of reduction mammaplasty. In addition, these patients in particular should be counseled regarding the potential risk of postoperative breast growth and be advised that repeated operation may be necessary later in life.
It is unclear from the current findings whether the longer duration of breast growth in obese patients is attributable to prolonged pubertal breast gland proliferation or weight gain during adolescence. It is commonly accepted that obese girls undergo both thelarche and menarche earlier than their healthy-weight counterparts, and this trend was observed in the present study.35–43 However, the role of adiposity on the duration of puberty remains understudied. During early puberty, follicle-stimulating hormone and luteinizing hormone work in concert to stimulate the production of estrogens and progesterone.44 Ovarian estrogen coupled with insulin-like growth factor 1 trigger the development and proliferation of breast tissue.45,46 Rising estrogen and progesterone levels promote continued breast development, increase body fat composition, and alter its distribution.47
Excess adipose during puberty can increase the bioavailability of estrogens by means of a cascade of amplified cortisol metabolism, insulin resistance, adrenal steroid production, and general endocrine disruption.46 Elevated local estrogen production because of excess aromatization in glandular tissue and adjacent, excess adipocytes may also explain the role obesity plays in the cause of adolescent macromastia.48 This theory accounts for the local proliferative effects of estrogen, and the lack of systemic signs of hyperestrogenism in patients with macromastia. Leptin, produced by adipocytes, has also been shown to increase aromatase activity in the breast tissue of men with gynecomastia, and can induce breast sensitivity to estrogen, thereby producing a synergistic proliferative effect.49,50 As such, it is plausible that adiposity may not only result in early puberty, but can also prolong puberty and its proliferative mechanisms by increasing the amount of circulating estrogen in surrounding breast tissue. This may help to explain why adolescent macromastia, which is by definition an overgrowth of breast gland rather than adipose tissue, is associated with obesity.
Study limitations must be addressed. As this study did not prospectively follow a cohort of patients from prepubescence to reduction mammaplasty, thelarche and menarche age are self-reported. In particular, thelarche age is subject to recall inaccuracies, as it is not a singular, salient event such as first menses. Likewise, as the age at which pubertal breast growth ends was not collected prospectively, this variable was estimated using statistical modeling. Results may not be generalizable, as the majority of subjects in the cohort were white and all subjects were recruited from a single institution. Black and Hispanic patients typically undergo puberty earlier than their white peers,51 as supported by the present study’s findings. As a result, it is possible that the duration of puberty may also vary by race. However, because of the relatively small number of minorities in our sample, analyses stratified by race would have been underpowered and were not performed.
The incidence of breast regrowth after reduction mammaplasty in teens and young women is relatively low. However, this occurrence may vary by patients’ body mass index category. Our findings demonstrate that readiness for reduction mammaplasty in young patients should not be determined using arbitrary age restrictions. Instead, surgical readiness is a complex decision that should be made by the surgeon on an individual basis incorporating the patient’s biological and psychological maturity, obesity status, potential for postoperative benefit, and risk tolerance for postoperative breast regrowth.
This work was supported in part by the Plastic Surgery Foundation (grant no. 192776; July of 2011). The Plastic Surgery Foundation had no involvement in the study design; collection, analysis, and interpretation of data; the writing of this manuscript; or the decision to submit the manuscript for publication.
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