Background and objectives. Stroke-induced mortality is the third most common cause of death in developed countries. Intense interest has focused on the recurrent ischemic stroke, which rate makes up 30% during first 5 years after first-ever stroke. This work aims to develop criteria for the prediction of acute recurrent cerebral ischemic hemispheric stroke (RCIHS) outcome on the basis of comprehensive baseline clinical, laboratory, and neuroimaging examinations. Materials and Methods. One hundred thirty-six patients (71 males and 65 females, median age 74 (65; 78)) with acute RCIHS were enrolled in the study. All patients underwent a detailed clinical and neurological examination using National Institutes of Health Stroke Scale (NIHSS), computed tomography of the brain, hematological, and biochemical investigations. In order to detect the dependent and independent risk factors of the lethal outcome of the acute period of RCIHS, univariable and multivariable regression analysis were conducted. A receiver operating characteristic (ROC) analysis with the calculation of sensitivity and specificity was performed to determine the prediction variables. Results. Twenty-five patients died. The independent predictors of the lethal outcome of acute RCIHS were: Baseline NIHSS score (OR 95% CІ 1.33 (1.08–1.64), p = 0.0003), septum pellucidum displacement (OR 95% CI 1.53 (1.17–2.00), p = 0.0021), glucose serum level (OR 95% CI 1.28 (1.09–1.50), p = 0.0022), neutrophil-to-lymphocyte ratio (OR 95% CI 1.11 (1.00–1.21), p = 0.0303). The mathematical model, which included these variables was developed and it could determine the prognosis of lethal outcome of the acute RCIHS with an accuracy of 86.8% (AUC = 0.88 ± 0.04 (0.88–0.93), p < 0.0001).
Helicobacter pylori is a unique microorganism capable of long-term colonization of the gastric mucosa, induction of the inflammatory process, antigenic mimicry and immune evasia. Flagella proteins, adhesins, invasive and aggressive enzymes, cytotoxin-associated protein, vacuolating cytotoxin can have a damaging effect on stomach epithelial cells. Recognition of molecular patterns of Helicobacter pylori by stomach cell receptors initiates activation of adapter proteins, protein kinases and transcription factors, leading to the production of proinflammatory cytokines, infiltration by neutrophilic granulocytes, absorption and killing of microorganisms by phagocytes with presentation of antigens to lymphocytes, while the activity and completeness of phagocytosis remain at a low level. Activation of CD8+-, CD16+- lymphocytes is accompanied by cytotoxic effect on both Helicobacter pylori and epithelial cells of the gastric mucosa. Weak immunogenicity of Helicobacter pylori antigens limits the production of anti-Helicobacter antibodies. Thus, activation of immune factors, in most cases, does not lead to complete elimination of the pathogen, but can aggravate the pathomorphological changes of the gastric epithelium.
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