Factors associated with post-operative delirium in hip fracture patients: what should we care.

BACKGROUND: The postoperative delirium is a common yet serious complication in elderly patients with hip fracture. We aimed to evaluate the potential risk factors of delirium in patients with hip fracture, to provide reliable evidence to the clinical management of hip fracture. METHODS: This study was a retrospective design. Elderly patients who underwent hip fracture surgery in our hospital from June 1, 2019 to December 30, 2020 were selected. The characteristics and treatment data of delirium and no delirium patients were collected and compared. Multivariate logistic regression analysis was performed to analyze the influencing factors affecting postoperative delirium in elderly patients with hip fracture. RESULTS: A total of 245 patients with hip fracture were included, the incidence of postoperative delirium in patients with hip fracture was 13.06%. There were significant differences in the age, BMI, history of delirium, estimated blood loss and duration of surgery (all p < 0.05). There were significant differences in the albumin and TSH between delirium and no delirium group (all p < 0.05), Logistics analyses indicated that age ≥ 75 years (OR 3.112, 95% CI 1.527-5.742), BMI ≥ 24 kg/m2 (OR 2.127, 95% CI 1.144-3.598), history of delirium (OR 1.754, 95% CI 1.173-2.347), estimated blood loss ≥ 400 mL (OR 1.698, 95% CI 1.427-1.946), duration of surgery ≥ 120 min (OR 2.138, 95% CI 1.126-3.085), preoperative albumin ≤ 40 g/L (OR 1.845, 95% CI 1.102-2.835) and TSH ≤ 2 mU/L (OR 2.226, 95% CI 1.329-4.011) were the independent risk factors of postoperative delirium in patients with hip fracture(all p < 0.05). CONCLUSIONS: Postoperative delirium is very common in elderly patients with hip fracture, and it is associated with many risk factors, clinical preventions targeted on those risk factors are needed to reduce the postoperative delirium.

MicroRNA let-7i-3p affects osteoblast differentiation in ankylosing spondylitis via targeting PDK1.

Ankylosing spondylitis (AS) is a chronic autoimmune disease in which let-7i has been studied to involved. But, whether let-7i-3p could regulate osteoblast differentiation in AS remains unclear. This research targeted to decipher the impact of let-7i-3p on AS progression by modulating pyruvate dehydrogenase kinase 1 (PDK1). The bone mineral density of femur and lumbar vertebra and the maximum loading and bending elastic modulus of tibia, tumor necrosis factor-α (TNF-α), matrix metalloproteinase (MMP)-3, osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) in serum of AS mice, the pathological condition of synovial tissue were determined via let-7i-3p inhibitor and OE-PDK1 in animal experiment. Also, the cell viability and ALP activity were measured by let-7i-3p inhibitor and OE-PDK1 in cell experiments. let-7i-3p and PDK1 expression were detected. Let-7i-3p raised and PDK1 declined in AS mice. Depleted let-7i-3p and restored PDK1 increased bone mineral density and maximum loading and bending elastic modulus of tibia, reduced TNF-α, MMP-3 and RANKL contents, attenuated the pathological condition of synovial tissue and raised OPG content in AS mice. In cell experiments, up-regulating PDK1 and down-regulating let-7i-3p enhanced cell viability and ALP activity in AS mice. Low expression of let-7i-3p could enhance osteoblast differentiation in AS by up-regulating PDK1.Abbreviations: AS: Ankylosing spondylitis; PDK1: pyruvate dehydrogenase kinase 1; TNF-α: tumor necrosis factor-α MMP: matrix metalloproteinase; OPG: osteoprotegerin; RANKL: receptor activator of nuclear factor-κB ligand; miRNAs: MicroRNAs; BMD: bone mineral density; PFA: paraformaldehyde; NC: negative control; OE: overexpression; HE: Hematoxylin-eosin; PBS: phosphate-buffered saline; EDTA: ethylene diamine tetraacetic acid; DMEM: Dulbecco's Modified Eagle Medium; RT-qPCR: Reverse transcription quantitative polymerase chain reaction; GAPDH: glyceraldehyde phosphate dehydrogenase; UTR: untranslated region; WT: wild type; MUT: mutant type.