Disparities in Breast Reconstruction: An Analysis of Treatment Choices.

BACKGROUND: Breast reconstruction methods vary based on factors such as medical history, breast size, and personal preferences. However, disparities in healthcare exist, and the role race plays in accessing to different reconstruction methods is unclear. This study aimed to investigate the influence of race and/or ethnicity on the type of breast reconstruction chosen. METHODS: This retrospective cohort study analyzed the University of Pittsburgh Medical Center Magee Women's Hospital database, including patients who underwent breast cancer surgery from 2011 to 2022. Multivariate analysis examined race, reconstruction, and reconstruction type (P < 0.05). RESULTS: The database included 13,260 women with breast cancer; of whom 1763 underwent breast reconstruction. We found that 91.8% of patients were White, 6.8% Black, and 1.24% were of other races (Asian, Chinese, Filipino, Vietnamese, unknown). Reconstruction types were 46.8% implant, 30.1% autologous, and 18.7% combined. Among Black patients, autologous 36.3%, implant 32.2%, and combined 26.4%. In White patients, autologous 29.5%, implant 48%, and combined 18.2%. Among other races, autologous 36.3%, implant 40.9%, and combined 22.7%. In patients who underwent breast reconstruction, 85.2% underwent unilateral and 14.7% of patients underwent bilateral. Among the patients who had bilateral reconstruction, 92.3% were White, 6.1% were Black, and 1.5% were of other ethnicities. CONCLUSIONS: Our analysis revealed differences in breast reconstruction methods. Autologous reconstruction was more common among Black patients, and implant-based reconstruction was more common among Whites and other races. Further research is needed to understand the cause of these variations.

DHT causes liver steatosis via transcriptional regulation of SCAP in normal weight female mice.

Hyperandrogenemia (HA) is a hallmark of polycystic ovary syndrome (PCOS) and is an integral element of non-alcoholic fatty liver disease (NALFD) in females. Administering low-dose dihydrotestosterone (DHT) induced a normal weight PCOS-like female mouse model displaying NAFLD. The molecular mechanism of HA-induced NAFLD has not been fully determined. We hypothesized that DHT would regulate hepatic lipid metabolism via increased SREBP1 expression leading to NAFLD. We extracted liver from control and low-dose DHT female mice; and performed histological and biochemical lipid profiles, Western blot, immunoprecipitation, chromatin immunoprecipitation, and real-time quantitative PCR analyses. DHT lowered the 65 kD form of cytosolic SREBP1 in the liver compared to controls. However, DHT did not alter the levels of SREBP2 in the liver. DHT mice displayed increased SCAP protein expression and SCAP-SREBP1 binding compared to controls. DHT mice exhibited increased AR binding to intron-8 of SCAP leading to increased SCAP mRNA compared to controls. FAS mRNA and protein expression was increased in the liver of DHT mice compared to controls. p-ACC levels were unaltered in the liver. Other lipid metabolism pathways were examined in the liver, but no changes were observed. Our findings support evidence that DHT increased de novo lipogenic proteins resulting in increased hepatic lipid content via regulation of SREBP1 in the liver. We show that in the presence of DHT, the SCAP-SREBP1 interaction was elevated leading to increased nuclear SREBP1 resulting in increased de novo lipogenesis. We propose that the mechanism of action may be increased AR binding to an ARE in SCAP intron-8.