Outpatient Medication Use in Chinese Geriatric Patients Admitted for Falls: A Case-Control Study at an Acute Hospital in Hong Kong.

The study objective was to investigate the association of polypharmacy and medications with patient falls resulting in hip fractures among community-living geriatric patients. A case-control study was conducted at an acute public hospital in Hong Kong. The study population was community-living Chinese patients aged 65 years and above who were admitted for falls resulting in hip fractures during an 18-month study period. Each of these patients was matched to a control patient with the same age and sex, but without falls and fractures. Data were collected from electronic patient record. Data of 170 cases and 170 controls were eventually collected. The following variables associated with increased risk of falls resulting in hip fractures remained statistically significant after multivariate logistic regression, including benign prostatic hyperplasia [odds ratio (OR) = 2.654; 95% confidence interval (CI), 1.105-6.378; P = 0.029], first-generation antihistamines (OR = 3.176; 95% CI, 1.044-9.664; P = 0.042), antiparkinson medications (OR = 3.754; 95% CI, 1.158-12.169; P = 0.027), osteoporosis (OR = 3.159; 95% CI, 1.167-8.552; P = 0.024), and use of walking aids (OR = 2.543; 95% CI, 1.544-4.188; P < 0.001). In conclusion, this study identified various medications and comorbidities, rather than polypharmacy based on the number of medications, as predictors associated with increased risk of falls resulting in hip fractures for local geriatric patients. The findings provided insights into the potential medication-related fall prevention strategies, including clinical medication review, adverse drug event monitoring, and drug optimization.

Enhanced survival of melanopsin-expressing retinal ganglion cells after injury is associated with the PI3 K/Akt pathway.

In the present study, we studied the factors that contribute to the injury-resistant property of melanopsin-expressing retinal ganglion cells (mRGCs). Since phosphatidylinositol-3 kinase (PI3 K)/Akt signaling pathway is one of the well-known pathways for neuronal cell survival, we investigated the survival of mRGCs by applying the PI3 K/Akt specific inhibitors after injury. Two injury models, unilateral optic nerve transection and ocular hypertension, were adopted using Sprague-Dawley rats. Inhibitors of PI3 K/Akt were injected intravitreally following injuries to inhibit the PI3 K/Akt signaling pathway. Retinas were dissected after designated survival time, immunohistochemistry was carried out to visualize the mRGCs using melanopsin antibody and the number of mRGCs was counted. Co-expression of melanopsin and phospho-Akt (pAkt) was also examined. Compared to the survival of non-melanopsin-expressing RGCs, mRGCs showed a marked resistance to injury and co-expressed pAkt. Application of PI3 K/Akt inhibitors decreased the survival of mRGCs after injury. Our previous study has shown that mRGC are less susceptible to injury following the induction of ocular hypertension. In this study, we report that mRGCs were injury-resistant to a more severe type of injury, the optic nerve transection. More importantly, the PI3 K/Akt pathway was found to play a role in maintaining the survival of mRGCs after injury.

Up-regulated endogenous erythropoietin/erythropoietin receptor system and exogenous erythropoietin rescue retinal ganglion cells after chronic ocular hypertension.

AIMS: Recent studies have showed that erythropoietin (EPO) is a neuroprotectant for central nerve system neurons in addition to being a hematopoietic cytokine in response to hypoxia. In this study, we investigate the role of the EPO/EPO receptor (EPOR) system in the rat retina after ocular hypertension injury that mimics glaucoma. METHODS: Elevated intraocular pressure was induced by laser coagulation of the episcleral and limbal veins. Expression of EPO and EPOR in the normal and glaucomous retinas was investigated by immunohistochemistry and Western blot. To examine the effects of endogenous EPO on the survival of retinal ganglion cells (RGCs) subjected to hypertensive injury, soluble EPOR was directly injected into the vitreous body. Recombinant human EPO was both intravitreally and systemically administrated to study the effect of exogenous EPO on the survival of RGCs after ocular hypertension injury. RESULTS: Immunohistochemistry studies identified Müller cells as the main source of EPO in the normal retina. Expression of EPO and EPOR proteins was increased significantly 2 weeks after ocular hypertension. RGCs, amacrine and bipolar cells all demonstrated an increased expression of EPOR after ocular hypertension. Neutralization of endogenous EPO with soluble EPOR exacerbated ocular hypertensive injury, suggesting a role of the EPO/EPOR system in the survival of RGCs after injury. Similarly, topical and systemic administration of recombinant human EPO rescues RGCs after chronic ocular hypertension. CONCLUSIONS: These results indicate that an endogenous EPO/EPOR system participates in intrinsic recovery mechanisms after retina injury and RGCs might be rescued by exogenous administration of EPO.