Triggers and Outcomes of Falls in Hematology Patients: Analysis of Electronic Health Records / 기본간호학회지

PURPOSE: The goal was to use electronic health records to identify factors and outcomes associated with falls among patients admitted to hematology units. METHODS: This retrospective case-control study included data from a tertiary university hospital. Analysis was done of records from 117 patients with a history of falls and 201 patients with no history of falls who were admitted to the hematology unit from January 1, 2013 to December 31, 2014. Risk factors were analyzed using hierarchical logistic regression; patient outcomes were analyzed using multiple logistic regression, Cox proportional hazards regression, and multiple linear regression. RESULTS: Clinical factors such as self-care nursing (OR=4.47, CI=1.64~12.11), leukopenia (OR=6.03; CI=2.51~14.50), and hypoalbuminemia (OR=2.79, CI=1.31~5.96); treatment factors such as use of narcotics (OR=2.06, CI=1.01~4.19), antipsychotics (OR=3.05, CI=1.20~7.75), and steroids (OR=4.51, CI=1.92~10.58); and patient factors such as low education (OR=3.16, CI=1.44~6.94) were significant risk factors. Falls were also associated with increased length of hospital stay to 21.58 days (p < .001), and healthcare costs of 17,052,784 Won (p < .001). CONCLUSION: These findings can be a resource for fall prevention education and to help develop fall risk assessment tools for adults admitted to hematology units.

Tumor Necrosis Factor and Regulatory T Cells

CD4⁺CD25⁺FoxP3⁺ regulatory T (Treg) cells play major roles in the maintenance of immune homeostasis. In this review, we comprehensively describe the relationship between tumor necrosis factor (TNF) and Treg cells, focusing on the effects of TNF on Treg cells and on TNF-producing Treg cells. Contradictory results have been reported for the effect of TNF on the suppressive activity of Treg cells. In patients with rheumatoid arthritis, TNF has been shown to reduce the suppressive activity of Treg cells. Meanwhile, however, TNF has also been reported to maintain the suppressive activity of Treg cells via a TNFR2-mediated mechanism. In addition, Treg cells have been found to acquire the ability to produce TNF under inflammatory conditions, such as acute viral hepatitis. These TNF-producing Treg cells exhibit T helper 17-like features and hold significance in various human diseases.

IL-17A-Producing Foxp3⁺ Regulatory T Cells and Human Diseases

CD4⁺Foxp3⁺ regulatory T (Treg) cells play major roles in immune homeostasis. While CD4⁺Foxp3⁺ Treg cells act to suppress other immune effector cells, there is growing evidence that they also produce pro-inflammatory cytokines, such as IL-17A, in inflammatory conditions. The pro-inflammatory cytokine milieu, toll-like receptor (TLR) signaling, and specific transcription factors are important for the production of IL-17A by CD4⁺Foxp3⁺ Treg cells. In particular, IL-17A-producing CD4⁺Foxp3⁺ Treg cells express RORγt, the T helper (Th) 17-specific transcription factor, in addition to Foxp3. IL-17A-producing CD4⁺Foxp3⁺ Treg cells are also involved in the pathogenesis of various diseases. Here we review the mechanisms underlying the induction of IL-17A-producing CD4⁺Foxp3⁺ Treg cells and the roles of these cells in human disease.

Regulatory T Cells in Hepatitis B and C Virus Infections

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are hepatotropic viruses that establish chronic persistent infection by effectively escaping the host immune response and can cause immune-mediated liver injury. It has recently become apparent that regulatory T (Treg) cells, specifically CD4⁺CD25⁺Foxp3⁺ Treg cells, modulate viral diseases by suppressing antiviral immune responses and regulating inflammatory host injury. The roles of Treg cells in HBV and HCV infections range from suppressing antiviral T cell responses to protecting the liver from immune-mediated damage. This review describes Treg cells and subpopulations and focuses on the roles of these cells in HBV and HCV infections.