Hospital-acquired pressure injury: our seven years of experience.

OBJECTIVE: A pressure injury (PI) happens on the skin and in deeper tissues. Generally, it occurs due to prolonged compression over bony structures. A PI, when occurring during a hospital stay, is regarded as a hospital-acquired pressure injury (HAPI), and is considered as a marker for patient care quality. It might cause medical, legal or economic problems, and could be a burden on health systems. In this study we evaluate the factors contributing to HAPI formation. METHOD: Between June 2014-June 2021, we retrospectively investigated the files of patients who were hospitalised with different medical conditions in Bayindir Sögütözü Hospital, Ankara, Turkey, for patients' age, sex, Waterlow scale score, mobilisation status, application of zinc-containing and/or barrier creams (ZnBC), airbed usage, hospitalisation period, and the day of wound opening. RESULTS: The study cohort comprised 2327 hospitalised patients: 303 (13%) developed Stage 2 and deeper PIs; 2024 patients were hospitalised and discharged without wound opening. We found an increased risk in male patients and a lack of efficacy of ZnBC in protection from HAPI in our study population. However, we observed that ZnBC helped to delay wound opening and that the most protective treatment was the use of airbeds. CONCLUSION: Health professionals should be more aware of HAPI formation with prolonged hospitalisation periods. Only the use of an airbed for a patient hospitalised for a long period appears to be protective against PI formation. On the other hand, use of ZnBC delays wound opening. However, further research is needed to demonstrate the protective effect of ZnBC, due to the lack of randomisation in our study and the lack of some nursing records.

Epigenetic silencing of the tumor suppressor genes SPI1, PRDX2, KLF4, DLEC1, and DAPK1 in childhood and adolescent lymphomas.

The aim of the study was to investigate the expression and methylation status of seven distinctive genes with tumor suppressing properties in childhood and adolescent lymphomas. A total of 96 patients with Hodgkin Lymphoma (HL, n = 41), Non-Hodgkin Lymphoma (NHL, n = 15), and reactive lymphoid hyperplasia (RLH, n = 40, as controls) are included in the research. The expression status of CDKN2A, SPI1, PRDX2, DLEC1, FOXO1, KLF4 and DAPK1 genes were measured with QPCR method after the RNA isolation from paraffin blocks of tumor tissue and cDNA conversion. DNA isolation was performed from samples with low gene expression followed by methylation PCR study specific to promoter regions of these genes. We found that SPI1, PRDX2, DLEC1, KLF4, and DAPK1 genes are significantly less expressed in patient than the control group (p = 0.0001). However, expression of CDKNA2 and FOXO1 genes in the patient and control groups were not statistically different. The methylation ratios of all genes excluding the CDKN2A and FOXO1 were significantly higher in the HL and NHL groups than the controls (p = 0.0001). We showed that SPI1, PRDX2, DLEC1, KLF4 and DAPK1 genes are epigenetically silenced via hypermethylation in the tumor tissues of children with HL and NHL. As CDKN2A gene was not expressed in both patient and control groups, we conclude that it is not specific to malignancy. As FOXO1 gene was similarly expressed in both groups, its relationship with malignancy could not be established. The epigenetically silenced genes may be candidates for biomarkers or therapeutic targets in childhood and adolescent lymphomas.