Ischemic stroke is a main complication of atrial fibrillation (cardiac arrhythmia). The aim of our study was to estimate the effects of citicoline (CDP-choline) therapy on the levels of circulating neurospecific protein markers in serum of the patients with ischemic stroke and atrial fibrillation. Fiftyfour patients (mean age 76 years) treated with citicoline in a dose of 2.0 g daily intravenously for 12 to 14 days in addition to basic treatment formed the examined group. Thirty-two patients (mean age 68.5 years) obtained only standard therapy and formed the control group. Serum levels of neuronal and glial protein markers, including glial fibrillary acidic protein (GFAP), a neurofilament light subunit (NF-L), myelin basic protein (MBP), and ionized calcium-binding adaptor molecule 1 (Iba1), were measured in patients of both groups before and after treatment; an immunoblotting technique followed by densitometry analysis were used. Supplementary citicoline treatment provided significant reductions of the levels of GFAP (33%, P = 0.034), NF-L (27%, P = 0.019), and MBP (32%, P = 0.018), as compared to the initial values, while there were no marked changes in the studied parameters in the control group. The results obtained allow us to hypothesize that therapeutic benefit of citicoline in patients with ischemic stroke and atrial fibrillation can be mediated through increasing neuronal viability, protecting against axonal injury, decreasing the level of reactive astrogliosis, preventing deficiencies in the blood-brain integrity, and reducing the intensity of demyelination. However, citicoline administration exerted no effect on the blood content of microglial marker Iba-1, thus possibly preserving an important functional significance of microglia, which is needed to resolve local inflammation and clear cellular debris, and also provide protective factors to reduce cell injury in the ischemic brain. The obtained results indicate that serum levels of neurospecific biomarkers are significant and clinically relevant indices of the efficiency of treatment of the above-mentioned pathologies and can be used for further investigations of the stroke pathophysiology and molecular mechanisms of nootropic-mediated neuroprotection.
Ischemic stroke is considered as one of the most frequent and severe complications of atrial fibrillation. The present study was undertaken to examine whether post-insult treatment with cytidine diphosphate-choline (CDP-choline, or citicoline) affects serum levels of the angiogenesis inhibitor angiostatin and neurospecific proteins as markers of brain damage in patients with cerebral ischemia associated with atrial fibrillation. Thirty-three patients with a diagnosis of acute ischemic stroke received citicoline sodium by intravenous infusions (1,000 mg daily for 14 days) in addition to the standard treatment (basic group). Twentyfive patients with the same pathologies, who received only standard therapy, were enrolled in the study as a control group. Serum content of angiostatin and neurospecific proteins, namely neurofilament heavy subunit (NF-H) and glial fibrillary acidic protein (GFAP), was measured by immunoblotting at the basal level and after the treatment. Citicoline treatment caused significant decreases in serum levels of angiostatin (by 40% vs. basal level, P < 0.05), GFAP (by 61%, P < 0.01), and the NF-H subunit (by 19%, P < 0.05) and had no effect on the serum albumin content. In contrast, there were no statistically significant differences between baseline levels of the studied protein markers and their content after the treatment period in the control group. These findings indicate for the first time that CDP-choline protects both astrocytes and neurons and improves angiogenic capacity through down-regulation of angiostatin in post-ischemic patients with atrial fibrillation after acute ischemic stroke. Further studies are needed to test associations between serum levels of these biomarkers, clinical outcomes, and treatment efficacy of stroke. K e y w o r d s: atrial fibrillation, ischemic stroke, citicoline, angiostatin, neurofilaments (NFs), glial fibrillary acidic protein (GFAP).I schemic stroke is a complex multifactorial and polygenic disease. It is generally accepted that one of the major risk factors for ischemic stroke is atrial fibrillation [1]. Past studies indicate that fibrillation of the atrium produces stasis of blood, which causes thrombus formation and embolism in the brain [2,3]. More recent investigations suggest that the pathogenesis of stroke in atrial fibrillation is more complicated and involves other factors in addition to the dysrhythmia [4,5]. It is well acknowled ged that atrial fibrillation is the most prevalent car-diac arrhythmia, affecting approximately 12% of the population worldwide. Being an independent risk factor for stroke, atrial fibrillation is associated with high mortality, morbidity, and socioeconomic burden [6]. Therefore, stroke prevention with appropriate prophylaxis remains central to management of both atrial fibrillation and its neurological complications. However, the search for effective neuroprotectors remains frustrating, and the current therapeutic protocols remain suboptimal. Ideally, sufficient protection must be provided to the ischemic brain a...
Background. Patients with chronic kidney disease (CKD) have increased all-cause mortality, especially cardiovascular. The majority of patients with CKD have stages 1-3 and are treated by primary care physicians and nephrologists. Arterial hypertension (HTN) is highly prevalent comorbidity among CKD population, but its control remains poor. Material and methods. This retrospective non-interventional cross-sectional study was conducted in the Centre of Nephrology Care in Dnipropetrovsk Mechnikov Regional Hospital, Dnipro, Ukraine. We aimed to select patients who are supposed to be followed-up by primary care practitioners but due to certain reasons required nephrologist's consultation. From 4540 patients who received medical care in the Centre of Nephrology Care 365 patients fulfilled inclusion criteria. They were subdivided by presence of HTN, CKD stage, presence of proteinuria and achieving blood pressure targets according to different standards. All patients were examined and followed-up according to local and European standards. Results. Forty-nine percent of patients had known HTN, and 21% had HTN de novo. Advance of CKD stage was significantly associated with increase in the most of laboratory findings, age and BP values. Non-proteinuric patients achieved BP goals significantly more often, than proteinuric ones. Females achieved BP targets more often, than males. Monotherapy was the most common treatment regimen. Conclusions. HTN occurs in 70% of patients with CKD and it is controlled in up to 34% of cases. HTN is important factor of CKD progression and it is closely connected with GFR and proteinuria.
Реферат. Уровень протеинурии и состояние эндотелиальной функции сосудов у больных хронической болезнью почек в сочетании с субклиническим гипотиреозом под влиянием комбинированной антигипертензивной терапии. Курята А.В., Гармиш И.П. Цель работы-оценить уровень протеинурии и изменения эндотелиальной функции сосудов у больных хронической болезнью почек (ХБП) в сочетании с субклиническим гипотиреозом (СГТ) под влиянием комбинированной антигипертензивной терапии (валсартан 160 мг и амлодипин 5 мг). Было обследовано 48 пациентов с ХБП I-II стадий и АГ 1 и 2 степени. В зависимости от функционального состояния щитовидной железы больные были разделены на 2 группы. В течение 12 недель пациенты принимали фиксированную комбинацию амлодипина 5 мг и валсартана 160 мг. За 12 недель наблюдения целевого уровня АД достигли 19 (86,3%) больных основной группы и 22 (84,6%) пациента из группы сравнения. Достоверно чаще нарушение эндотелийзависимой вазодилятации и более высокий уровень суточной протеинурии были зарегестрированы среди основной группы пациентов по сравнению с пациентами с сохраненной функцией щитовидной железы. В конце исследования уровень суточной протеинурии в основной группе уменьшился на 46,03% (p<0,01), а в группе сравнения-на 55,3% (p<0,01). СГТ может рассматриваться как дополнительный фактор, который влияет на течение ХБП и АГ путем ухудшения состояния эндотелиальной функции и увеличение уровня суточной протеинурии. Использование комбинированного антигипертензивного препарата (валсартан 160 мг и амлодипин 5 мг) обеспечило достижение целевых значений АД, улучшение эндотелиальной функции и снижение уровня суточной протеинурии у пациентов обеих групп.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.