RESUMO
The COVID-19 pandemic had wide-reaching effects on healthcare delivery, including care for hip fractures, a common injury among older adults. This study characterized factors related to surgical timing and outcomes, length-of-stay, and discharge disposition among patients treated for operative hip fractures during the first wave of the COVID-19 pandemic, compared to historical controls. A retrospective, observational cohort study was conducted from 16 March-20 May 2020 with a consecutive series of 64 operative fragility hip fracture patients at three tertiary academic medical centers. Historical controls were matched based on sex, surgical procedure, age, and comorbidities. Primary outcomes included 30-day mortality and time-to-surgery. Secondary outcomes included 30-day postoperative complications, length-of-stay, discharge disposition, and time to obtain a COVID-19 test result. There was no difference in 30-day mortality, complication rates, length-of-stay, anesthesia type, or time-to-surgery, despite a mean time to obtain a final preoperative COVID-19 test result of 17.6 h in the study group. Notably, 23.8% of patients were discharged to home during the COVID-19 pandemic, compared to 4.8% among controls (p = 0.003). On average, patients received surgical care within 48 h of arrival during the COVID-19 pandemic. More patients were discharged to home rather than a facility with no change in complications, suggesting an opportunity for increased discharge to home.
RESUMO
Despite being an autosomal dominant disorder caused by a known coding mutation in the gene HTT, Huntington's disease (HD) patients with similar trinucleotide repeat mutations can have an age of onset that varies by decades. One likely contributing factor is the genetic heterogeneity of patients that might modify their vulnerability to disease. We report that although the heterozygous depletion of the autophagy adaptor protein Alfy/Wdfy3 has no consequence in control mice, it significantly accelerates age of onset and progression of HD pathogenesis. Alfy is required in the adult brain for the autophagy-dependent clearance of proteinaceous deposits, and its depletion in mice and neurons derived from patient fibroblasts accelerates the aberrant accumulation of this pathological hallmark shared across adult-onset neurodegenerative diseases. These findings indicate that selectively compromising the ability to eliminate aggregated proteins is a pathogenic driver, and the selective elimination of aggregates may confer disease resistance.
