Drug-Related Problems in Elderly Patients Attended to by Emergency Services.

The progressive aging and comorbidities of the population have led to an increase in the number of patients with polypharmacy attended to in the emergency department. Drug-related problems (DRPs) have become a major cause of admission to these units, as well as a high rate of short-term readmissions. Anticoagulants, antibiotics, antidiabetics, and opioids have been shown to be the most common drugs involved in this issue. Inappropriate polypharmacy has been pointed out as one of the major causes of these emergency visits. Different ways of conducting chronic medication reviews at discharge, primary care coordination, and phone contact with patients at discharge have been shown to reduce new hospitalizations and new emergency room visits due to DRPs, and they are key elements for improving the quality of care provided by emergency services.

YKL-40 (Chitinase 3-like I) is expressed in a subset of astrocytes in Alzheimer's disease and other tauopathies.

BACKGROUND: The innate immune system is known to be involved early in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders. The inflammatory response in the central nervous system can be measured postmortem or through a series of inflammatory mediator surrogates. YKL-40 (also named Chitinase-3-like I) has been frequently investigated in body fluids as a surrogate marker of neuroinflammation in AD and other neurological disorders. However, the expression pattern of YKL-40 in the human brain with neurodegenerative pathology remains poorly investigated. Our aim was to study the cellular expression pattern of YKL-40 in the brain of patients with clinical and neuropathological criteria for AD (n = 11); three non-AD tauopathies: Pick's disease (PiD; n = 8), corticobasal degeneration (CBD; n = 8) and progressive supranuclear palsy (PSP; n = 9) and a group of neurologically healthy controls (n = 6). METHODS: Semiquantitative neuropathological evaluation and quantitative confocal triple immunofluorescence studies were performed. An in-house algorithm was used to detect and quantify pathology burden of random regions of interest on a full tissue-section scan. Kruskal-Wallis and Dunn's multiple comparison tests were performed for colocalization and quantification analyses. RESULTS: We found that brain YKL-40 immunoreactivity was observed in a subset of astrocytes in all four diseases and in controls. There was a strong colocalization between YKL-40 and the astroglial marker GFAP but not with neuronal nor microglial markers. Intriguingly, YKL-40-positive astrocytes were tau-negative in PSP, CBD and PiD. The number of YKL-40-positive astrocytes was increased in tauopathies compared with that in controls. A positive correlation was found between YKL-40 and tau immunoreactivities. CONCLUSIONS: This study confirms that YKL-40 is expressed by a subset of astrocytes in AD and other tauopathies. YKL-40 expression is elevated in several neurodegenerative conditions and correlates with tau pathology.