Background/objectives: The purpose of this study was to identify demographic variables and systemic comorbidities that may increase risk of endogenous endophthalmitis (EE) development in patients with infective endocarditis (IE).
Subjects/methods: A retrospective database study was conducted using the 2002-2014 National Inpatient Sample (NIS). Patients with IE and EE were identified using ICD-9-CM codes. Descriptive chi-square and logistic regression analysis identified risk factors for EE in IE patients.
Results: Of 769,472 inpatients with a diagnosis of IE, 2248 had a diagnosis of EE. Women comprised 39.7% of IE patients without EE and 42.6% of those with EE (p = 0.005). The majority of IE cases with EE were in those 21-64-year-old (58.5%) age cohort and 67.4% of cases were Whites. Multivariate analysis revealed IE patients in the 21-64 (OR, 3.660) and 65+ age group (OR, 2.852) had increased risk of developing EE compared to the 0-20-year-old group. Hispanic (OR, 1.377) and Asian/Pacific Islander (OR, 1.620) patients had increased risk compared to White patients. Diabetes with (OR, 2.043) and without (OR, 1.433) chronic complications, alcohol use disorder (AUD; OR, 1.795), and cirrhosis (OR, 1.452) conferred an increased risk of developing EE, whereas, congestive heart failure (CHF; OR, 0.716), arrhythmia (OR, 0.678), and having a cardiac device (OR, 0.336) decreased risk of EE in IE subjects.
Conclusion: Older age (21+ years) and Hispanic and Asian/Pacific Islander background were associated with increased risk of developing EE in IE patients. Diabetes with and without chronic complications, AUD, or cirrhosis also conferred a 1.5-2 times increased risk. CHF, arrhythmia, or having a cardiac device were associated with decreased risk.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1038/s41433-024-03390-w | DOI Listing |
Alzheimers Dement
December 2024
GSK R&D, Stevenage, Hertfordshire, United Kingdom.
Background: Genetic variants in GRN, the gene encoding progranulin, are causal for or are associated with the risk of multiple neurodegenerative diseases. Modulating progranulin has been considered as a therapeutic strategy for neurodegenerative diseases including Frontotemporal Dementia (FTD) and Alzheimer's Disease (AD). Here, we integrated genetics with proteomic data to determine the causal human evidence for the therapeutic benefit of modulating progranulin in AD.
View Article and Find Full Text PDFBackground: Availability of amyloid modifying therapies will dramatically increase the need for disclosure of Alzheimer's disease (AD) related genetic and/or biomarker test results. The 21st Century Cares Act requires the immediate return of most medical test results, including AD biomarkers. A shortage of genetic counselors and dementia specialists already exists, thus driving the need for scalable methods to responsibly communicate test results.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Anesthesiology and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, U.S.A., Philadelphia, PA, USA.
Background: The vicious cycle between depression and dementia increases the risk of Alzheimer's Disease (AD) pathogenesis and pathology. This study investigates therapeutic effectiveness versus side effects and the underlying mechanisms of intranasal dantrolene nanoparticles (IDNs) to treat depression behavior and memory loss in 5XFAD mice.
Method: 5XFAD and wild-type B6SJLF1/J mice were treated with IDNs (IDN, 5 mg/kg) in Ryanodex formulation for a duration of 12 weeks.
Background: There is an urgent need for new therapeutic and diagnostic targets for Alzheimer's disease (AD). Dementia afflicts roughly 55 million individuals worldwide, and the prevalence is increasing with longer lifespans and the absence of preventive therapies. Given the demonstrated heterogeneity of Alzheimer's disease in biological and genetic components, it is critical to identify new therapeutic approaches.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Columbia University Irving Medical Center, New York, NY, USA.
Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!