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Donaldson Wilkins posted an update 6 months ago
To synthesize evidence on the association between human immunodeficiency virus (HIV) infection and cognitive impairment in older adults.
Meta-analysis.
Adults aged 50 years or older.
In this systematic literature review and meta-analysis, we searched PubMed, Scopus, Embase, and APA/PsycNet for studies published before July 21, 2020, that assessed the association between HIV-infection and cognitive impairment. We calculated pooled odds ratios (ORs) of cognitive impairment for people living with HIV (PLWH) and 95 % confidence intervals (CIs) using random-effect models and calculated pooled mean difference (MD) for major cognitive domains between PLWH and HIV-uninfected adults. We assessed risk of bias using the Newcastle-Ottawa scale.
Of the 4432 studies identified, 21 cross-sectional studies were eligible for the meta-analysis, including 15 examining global cognitive impairment. The meta-analysis showed that older PLWH were more likely to be cognitively impaired than HIV-uninfected controls (OR = 2.4or.
Our meta-analysis provides empirical evidence that HIV infection is associated with an increased risk of cognitive impairment among older adults, especially in cognitive domains of executive function, processing speed, verbal, recall, and motor/psychomotor.Patients with certain immune-mediated inflammatory diseases, such as rheumatoid arthritis (RA) and inflammatory bowel disease (IBD), have an increased risk of severe infectious diseases than the general population, which are mainly associated with the immunosuppressive treatments that they receive. These treatments act on the immune system through different mechanisms, causing different degrees of immunosuppression and a variable risk depending on whether the pathogen is a virus, bacteria or fungus. This article reviews the most relevant literature on the subject, which was selected and discussed by a panel of experts. The aim of this article is to review the risk of infections in patients with IBD and RA, and the potential preventive measures.
Spinal cord injury (SCI) patients may have intestinal dysmotility and digestive symptoms that are associated with small intestinal bacterial overgrowth (SIBO). The aim of this study is to describe the prevalence of SIBO in SCI patients and the risk factors of its development.
Twenty-nine consecutive SCI patients were studied (10 women/19 men; mean age 47 years), 16 with subacute injuries (<9 months) and 13 with chronic injuries (>1 year). Nine patients were affected by tetraplegia and 15 by paraplegia. Each patient underwent a glucose breath test according to the North American Consensus and the presence of abdominal symptoms was evaluated during the test. The results were compared with 15 non-neurological patients with SIBO.
Six patients tested positive for SIBO (21%), all of them affected by SCI in the subacute phase, 6/16 vs. 0/13 in the chronic phase (P<.05) and the majority with tetraplegia, 5/9 vs. 1/19 with paraplegia (P<.05). No statistically significant relationship was found with other clinical characteristics. All the tests were positive for methane or mixed (methane and hydrogen), while only 67% of the controls had methane-predominant production (P>.05).
SCI patients can develop SIBO, more frequently in the subacute phase and in tetraplegic patients, highlighting a high production of methane. This complication should be considered in neurogenic bowel management.
SCI patients can develop SIBO, more frequently in the subacute phase and in tetraplegic patients, highlighting a high production of methane. This complication should be considered in neurogenic bowel management.Five vascular endothelial growth factor receptor (VEGFR) ligands (VEGF-A, -B, -C, -D, and placental growth factor ) constitute the VEGF family. VEGF-A binds VEGF receptors 1 and 2 (VEGFR1/2), whereas VEGF-B and PlGF only bind VEGFR1. Although much research has been conducted on VEGFR2 to elucidate its key role in retinal diseases, recent efforts have shown the importance and involvement of VEGFR1 and its family of ligands in angiogenesis, vascular permeability, and microinflammatory cascades within the retina. Expression of VEGFR1 depends on the microenvironment, is differentially regulated under hypoxic and inflammatory conditions, and it has been detected in retinal and choroidal endothelial cells, pericytes, retinal and choroidal mononuclear phagocytes (including microglia), Müller cells, photoreceptor cells, and the retinal pigment epithelium. Whilst the VEGF-A decoy function of VEGFR1 is well established, consequences of its direct signaling are less clear. find more VEGFR1 activation can affect vascular permeability and induce macrophage and microglia production of proinflammatory and proangiogenic mediators. However the ability of the VEGFR1 ligands (VEGF-A, PlGF, and VEGF-B) to compete against each other for receptor binding and to heterodimerize complicates our understanding of the relative contribution of VEGFR1 signaling alone toward the pathologic processes seen in diabetic retinopathy, retinal vascular occlusions, retinopathy of prematurity, and age-related macular degeneration. Clinically, anti-VEGF drugs have proven transformational in these pathologies and their impact on modulation of VEGFR1 signaling is still an opportunity-rich field for further research.Glaucoma causes loss of vision through degeneration of the retinal ganglion cell (RGC) projection to the brain. The disease is characterized by sensitivity to intraocular pressure (IOP) conveyed at the optic nerve head, through which RGC axons pass unmyelinated to form the optic nerve. From this point, a pathogenic triumvirate comprising inflammatory, oxidative, and metabolic stress influence both proximal structures in the retina and distal structures in the optic projection. This review focuses on metabolic stress and how the optic projection may compensate through novel adaptive mechanisms to protect excitatory signaling to the brain. In the retina and proximal nerve head, the unmyelinated RGC axon segment is energy-inefficient, which leads to increased demand for adenosine-5′-triphosphate (ATP) at the risk of vulnerability to Ca2+-related metabolic and oxidative pressure. This vulnerability may underlie the bidirectional nature of progression. However, recent evidence highlights that the optic projection in glaucoma is not passive but rather demonstrates adaptive processes that may push back against neurodegeneration.