Breaking Barriers to Breast Reconstruction among Socioeconomically Disadvantaged Patients at a Large Safety-net Hospital.

Socioeconomic disparities remain prevalent among those who undergo breast reconstruction. At our institution, patients must meet certain criteria to become eligible for breast reconstruction. The purpose of this study was to determine the impact of socioeconomic factors on breast reconstruction eligibility, enrollment, choice, and completion at our large safety-net institution. Methods: A retrospective chart review of patients who underwent partial or total mastectomy at a large safety-net hospital from 2016 to 2019 was completed. Surgical and demographic data were compared across varying socioeconomic factors. Results: A total of 645 patients were included in the study. More patients of a racial minority had government-based insurance than White patients (89% versus 81%; P = 0.01). Those with government-based insurance had higher average hemoglobin A1c values (6.26 versus 6.0; P = 0.03), proportion of American Society of Anesthesiologists scores greater than III (46% versus 40%; P = 0.01), and smokers (23% versus 9%; P = 0.02) than those with private insurance. Diabetic patients, patients with an American Society of Anesthesiologists greater than III, and active smokers were significantly less likely to receive a plastic surgery consult. Patients with government-based insurance underwent immediate tissue expander placement at mastectomy at rates lower than those with private insurance (57% versus 69%; P = 0.01). Conclusions: Barriers remain for socioeconomically disadvantaged patients to be eligible for, undergo, and complete breast reconstruction. Obesity, diabetes, smoking, and poor overall health were identified as the main barriers and were associated with racial minorities, government-based insurance, and lower incomes. Concerted effort through multidisciplinary teams is needed to maximize eligibility of socioeconomically disadvantaged breast cancer patients for reconstruction.

Expanding the Capacity of Otolaryngologists in Kenya through Mobile Technology.

OBJECTIVE: To determine if reliable, objective audiologic data can be obtained by nonotolaryngology and nonaudiology practitioners using novel mobile technology in an effort to expand the capacity for early identification and treatment of disabling hearing loss in the developing world. STUDY DESIGN: Cross-sectional, proof-of-concept pilot study. SETTING: Screenings took place during an annual 2-week otolaryngology surgical mission in October 2016 in semirural Malindi, Kenya. SUBJECT AND METHODS: Eighty-seven patients (174 total ears) were included from 2 deaf schools (n = 12 and 9), a nondeaf school (n = 9), a tuberculosis ward (n = 8), and a walk-in otology clinic at a local hospital (n = 49). An automated, tablet-based, language-independent, clinically validated, play audiometry system and wireless otoscopic endoscopy via an iPhone or laptop platform was administered by Kenyan community health workers (CHWs) and nursing staff. RESULTS: Various degrees of hearing loss and otologic pathology were identified, including 1 child presumed to be deaf who was found to have unilaterally normal hearing. Other pathology included 2 active perforations, 2 healed perforations, 2 middle ear effusions, and 1 cholesteatoma. CHWs and nursing staff demonstrated proficiency performing audiograms and endoscopy. Patients screened in a deaf school were more likely to complete an unreliable audiogram than patients screened in other settings (P < .01). CONCLUSION: This study demonstrates the feasibility of a non-otolaryngology-based hearing screening program. This may become an important tool in reducing the impact of hearing loss and otologic pathology in areas bereft of otolaryngologists and audiologists by allowing CHWs to gather important patient data prior to otolaryngologic evaluation.

Activin-dependent signaling in fibro/adipogenic progenitors causes fibrodysplasia ossificans progressiva.

Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal-dominant disorder characterized by progressive and profoundly disabling heterotopic ossification (HO). Here we show that fibro/adipogenic progenitors (FAPs) are a major cell-of-origin of HO in an accurate genetic mouse model of FOP (Acvr1 tnR206H ). Targeted expression of the disease-causing type I bone morphogenetic protein (BMP) receptor, ACVR1(R206H), to FAPs recapitulates the full spectrum of HO observed in FOP patients. ACVR1(R206H)-expressing FAPs, but not wild-type FAPs, activate osteogenic signaling in response to activin ligands. Conditional loss of the wild-type Acvr1 allele dramatically exacerbates FAP-directed HO, suggesting that mutant and wild-type ACVR1 receptor complexes compete for activin ligands or type II BMP receptor binding partners. Finally, systemic inhibition of activin A completely blocks HO and restores wild-type-like behavior to transplanted Acvr1 R206H/+ FAPs. Understanding the cells that drive HO may facilitate the development of cell-specific therapeutic approaches to inhibit catastrophic bone formation in FOP.