ABSTRACT
Super-utilizers account for many emergency department visits (EDV) and hospitalizations. Among Medicare/Medicaid patients, 5% to 10% account for >50% of spending. Little is known about super-utilization in gynecologic oncology. Charts of 64 gynecologic oncology patients with ≥3 EDV and/or admissions over 12 months were reviewed retrospectively. Cancer type distribution was 47% ovarian, 23% cervical, 23% endometrial, and 6% vulvar. Treatment at index visit was 61% chemotherapy, 16% no treatment, 8% recent surgery, and 6% radiation. Mean visits was 5.7 (SD 3.9, range 3-28). Most common presenting complaints were gastrointestinal and pain. Patients near end of life were more likely to be admitted. EDV frequently occurred outside standard work hours (63%). EDV/admissions resulted in total variable expenses of $1 462 581 ($982 933 direct expense, $479 648 service expense). Interventions to decrease super-utilization could target symptom management, off-hour support, patients on chemotherapy, and end of life. Approaches could include multidisciplinary resources, palliative care teams, extending office hours, and earlier initiation of hospice.
Subject(s)
Genital Neoplasms, Female , Health Services Misuse , Adult , Aged , Aged, 80 and over , Emergency Service, Hospital/economics , Female , Humans , Medical Audit , Middle Aged , Palliative Care , Retrospective Studies , United StatesABSTRACT
The heat shock response, the cellular response to protein damaging stress, is critical in maintaining proteostasis. The heat shock response is regulated by the transcription factor HSF1, which is activated upon heat shock and other stresses to induce the expression of molecular chaperones. SIRT1 has previously been shown to activate HSF1 by deacetylating it, leading to increased DNA binding ability. We have investigated how the heat shock response may be controlled by factors influencing SIRT1 activity. We found that heat shock results in an increase in the cellular NAD(+)/NADH ratio and an increase in recruitment of SIRT1 to the hsp70 promoter. Furthermore, we found that the SIRT1 modulators AROS and DBC1 have an impact on hsp70 transcription, HSF1 acetylation status, and HSF1 recruitment to the hsp70 promoter. Therefore, AROS and DBC1 are now two new targets available for therapeutic regulation of the heat shock response.
