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Inflammatory cytokines have been implicated as crucial contributors to the onset and progression of non-alcoholic fatty liver disease (NAFLD). The exact mechanisms by which interleukins (ILs) contribute to NAFLD may vary, and ongoing research is aimed at understanding the specific roles of different ILs in the pathogenesis of this condition. In addition, variations in environmental factors and genetics in each individual can influence the onset and/or progression of NAFLD. The lack of clinical studies related to the potential therapeutic properties of IL-1 inhibitors currently does not allow us to conclude their validity as a therapeutic option, although preclinical studies show promising results. Further studies are needed to elucidate their beneficial properties in NAFLD treatment.
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The existing literature highlights the presence of numerous coagulation factors and markers. Elevated levels of coagulation factors are associated with both existing and newly diagnosed cases of atrial fibrillation (AF). However, this article summarizes the role of coagulation in the pathogenesis of AF, which includes fibrinogen and fibrin, prothrombin, thrombomodulin, soluble urokinase plasminogen activator receptor, von Willebrand factor, P-selectin, D-dimer, plasminogen activator inhibitor-1, and platelet activation. Coagulation irregularities play a significant role in the pathogenesis of AF.
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INTRODUCTION: Plasma exchange (PE) is widely used in many immune-based neurological diseases. Our aim is to analyze characteristics of PE in neurological patients at the Clinical Center of Montenegro. METHODS: Our study involved neurological patients treated with PE between January 2020 and April 2022. RESULTS: In total, 246 PEs were performed in 43 patients. We divided patients into 4 groups according to indications. In 8/9 multiple sclerosis (MS) patients a decrease of Expanded Dysability Status Scale at least 0.5 was verified. In 14/20 Guillain Barre syndrome patients reduction of Hughes was observed. Four patients with myasthenia gravis (MG) were treated with PE. The most heterogeneous group (4) consisted of patients in whom the mechanism of disease development is assumed to be immune system dysregulation. Fourteen patients had any adverse event. CONCLUSION: Our results show that PE is widely used and safe in the treatment of neurological diseases.
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Síndrome de Guillain-Barré , Enfermedades del Sistema Nervioso , Neurología , Humanos , Intercambio Plasmático/métodos , Montenegro , Plasmaféresis , Síndrome de Guillain-Barré/terapia , Enfermedades del Sistema Nervioso/terapiaRESUMEN
Introduction: Myotonic dystrophy type 1 (DM1) and 2 (DM2) are genetically determined progressive muscular disorders with multisystemic affection, including brain involvement. Transcranial sonography (TCS) is a reliable diagnostic tool for the investigation of deep brain structures. We sought to evaluate TCS findings in genetically confirmed DM1 and DM2 patients, and further correlate these results with patients' clinical features. Methods: This cross-sectional study included 163 patients (102 DM1, 61 DM2). Echogenicity of the brainstem raphe (BR) and substantia nigra (SN) as well as the diameter of the third ventricle (DTV) were assessed by TCS. Patients were evaluated using the Hamilton Depression Rating Scale, Fatigue Severity Scale and Daytime Sleepiness Scale. Results: SN hyperechogenicity was observed in 40% of DM1 and 34% of DM2 patients. SN hypoechogenicity was detected in 17% of DM1 and 7% of DM2 patients. BR hypoechogenicity was found in 36% of DM1 and 47% of DM2 subjects. Enlarged DTV was noted in 19% of DM1 and 15% of DM2 patients. Older, weaker, depressive, and fatigued DM1 patients were more likely to have BR hypoechogenicity (p < 0.05). DTV correlated with age and disease duration in DM1 (p < 0.01). In DM2 patients SN hyperechogenicity correlated with fatigue. Excessive daytime sleepiness was associated with hypoechogenic BR (p < 0.05) and enlarged DVT (p < 0.01) in DM2 patients. Conclusions: TCS is an easy applicable and sensitive neuroimaging technique that could offer new information regarding several brainstem structures in DM1 and DM2. This may lead to better understanding of the pathogenesis of the brain involvement in DM with possible clinical implications.