Optic neuropathies constitute a group of conditions with various etiologies and might be caused by different factors; we can distinguish the genetic and acquired causes of optic neuropathies. Even though the symptoms are not highly specific, this condition is primarily characterized by unilateral or bilateral vision loss with worsening color detection. The loss may be acute or gradual depending on the causation. In this article, we included a specification of toxic optic neuropathy (TON) mainly triggered by alcohol abuse and also the usage of other substances, including drugs or methanol, as well as intoxication by metals, organic solvents, or carbon dioxide. Nutritional deficiencies, vitamin absorption disorder, and anemia, which usually appear during excessive alcohol intake, and their effect on the etiology of the optic neuropathy have been likewise discussed.

Hepatocellular carcinoma (HCC) is the most common liver cancer as well as the most prevalent cause of death in the adult patient population with cirrhosis. The occurrence of HCC is primarily caused by chronic liver inflammation that might occur because of a viral infection, non-alcoholic fatty liver disease (NAFLD), or various lifestyle-associated factors. The objective of this review was to summarize the current knowledge regarding the microenvironment of HCC, indicating how immune- and non-immune-cell stroma might affect the onset and progression of HCC. Therefore, in the following narrative review, we described the role of tumor-infiltrating neutrophils, bone-marrow-derived cells, tumor-associated mast cells, cancer-associated fibroblasts, tumor-associated macrophages, liver-sinusoidal endothelial cells, lymphocytes, and certain cytokines in liver inflammation and the further progression to HCC. A better understanding of the HCC microenvironment might be crucial to introducing novel treatment strategies or combined therapies that could lead to more effective clinical outcomes.

Irisin is a recently discovered hormone, synthesized mainly by the muscles. Expression of irisin and its precursor named FNDC5 was also found in the heart, kidneys, liver, pancreas, adipose tissue, and brain including cortical neurons, hippocampus, cerebellum, hypothalamus, and spinal cord. The purpose of this study is to review the latest research on the properties of the irisin and its cytoprotective effect against neuronal damage and to draw attention to its possible clinical use in the treatment of stroke. Notch pathway activity increases after ischemic damage, stimulating the repair of the affected brain area. Irisin activates the Notch pathway which inhibits the activity of microglia, secretion of inflammatory factors, and finally leads to reduction of the brain edema. Studies revealed that irisin increases levels of brain-derived neurotrophic factor (BDNF), leading to enhancement of survival and migration of the neurons, and protecting nerve cells from damage during the ischemic stroke. It was also found that irisin maintains mitochondrial integrity, reduces oxidative stress, and exerts a protective effect on the blood-brain barrier. Irisin entails a neuroprotective effect, reducing the extent of the infarcted area and the degree of brain damage. Stimulation of the irisin expression by physical activity or its exogenous administration remains the subject of research that raises hope for development of the new therapeutic options for diseases, especially ischemic stroke. Irisin is a recently discovered hormone, synthesized mainly by the muscles. Expression of irisin and its precursor named FNDC5 was also found in the heart, kidneys, liver, pancreas, adipose tissue, and brain including cortical neurons, hippocampus, cerebellum, hypothalamus, and spinal cord. The purpose of this study is to review the latest research on the properties of the irisin and its cytoprotective effect against neuronal damage and to draw attention to its possible clinical use in the treatment of stroke. Notch pathway activity increases after ischemic damage, stimulating the repair of the affected brain area. Irisin activates the Notch pathway which inhibits the activity of microglia, secretion of inflammatory factors, and finally leads to reduction of the brain edema. Studies revealed that irisin increases levels of brain-derived neurotrophic factor (BDNF), leading to enhancement of survival and migration of the neurons, and protecting nerve cells from damage during the ischemic stroke. It was also found that irisin maintains mitochondrial integrity, reduces oxidative stress, and exerts a protective effect on the blood-brain barrier. Irisin entails a neuroprotective effect, reducing the extent of the infarcted area and the degree of brain damage. Stimulation of the irisin expression by physical activity or its exogenous administration remains the subject of research that raises hope for development of the new therapeutic options for diseases, especially ischemic stroke.

Endovascular aneurysm repair (EVAR) is a minimally invasive technique widely used in abdominal aortic aneurysm treatment. The most common complications after EVAR are endoleaks, with type 2 endoleak (T2EL) being the most prevalent. T2EL detection and surveillance require imaging techniques such as computed tomography angiography (CTA), contrast-enhanced magnetic resonance angiography (CE-MRA), Doppler ultrasound, or digital subtraction angiography (DSA). However, these modalities are associated with numerous limitations, including exposure to ionizing radiation, contrast media administration, or operator dependency, as in the case of ultrasonography. A non-contrast-enhanced (NCE-MR) could be a substitute non-invasive method for endoleak monitoring. Our case report describes an 83-year-old female patient with type 2 endoleak and enlarging aneurysm sac detected on a CT scan. Despite the enormous aneurysm size, the patient underwent endovascular treatment owing to multiple comorbidities. Due to challenging feeding vessel anatomy, catheterization of the aneurysmal sac was impossible. Attempted polymerization of the aneurysmal sac with Glubran-2 partially sealed the sac and obliterated the feeders' inflow. Unfortunately, a non-targeted embolization resulted in the loss of patency of the right feeder and adjacent communicating branch. The patient underwent follow-up imaging that included non-contrast-enhanced as well as contrast-enhanced MRA. The examination revealed the presence of a small residual endoleak, a freshly formed thrombus, and areas of old thrombi. The NCE-MR appeared to be a valuable tool in endoleak detection and provided a de- tailed clot morphology.

Endovascular aneurysm repair (EVAR) is a minimally invasive technique alternative to conventional open surgical aneurysm repair. Nowadays, the majority of abdominal aortic aneurysms (AAAs) with suitable anatomy are primarily treated using EVAR; however, conventional EVAR procedure is associated with the necessity of contrast agent administration and exposure to ionizing radiation, which carries a risk not only for patients but also for the surgical team. Furthermore, the EVAR procedure may be unfeasible for patients with renal insufficiency and other contraindications to intravascular contrast agent administration, i.e. contrast allergy. An even less invasive guidance method for EVAR procedures seems to be intravascular ultrasound (IVUS), which may abolish the risk associated with contrast media usage and radiation exposure. The literature review concerns the latest research about IVUS guidance during EVAR to establish the current application of this imaging modality in daily clinical practice, its efficiency, advantages and drawbacks. Keywords: intravascular ultrasound aneurysm EVAR abdominal aortic aneurysm stent-graft

Statins are one of the key drugs in the treatment of cardiology patients. They lower LDL cholesterol levels, thereby reducing the risk of acute cardiovascular events. Statins are among the best studied drugs, and have been proven to be effective and safe in the treatment of dyslipidemia. Data presented in studies on the prevalence of statin intolerance (SI) varies widely, according to some studies, statin tolerance is the same as placebo, however, this is a common problem in clinical practice. The most common reported symptoms of SI include muscle pain. Patients are often afraid of starting satin treatment because of possible side effects. The appearance of myopathy in patients results in their discontinuation of therapy, which results in increased cardiovascular risk. In order to minimize the risk of SI, particularly statin-associated muscular pain (SI), a key role is played by discussion with the patient, exclusion of nocebo effects, identification of risk factors, dose modification and possible discontinuation of the drug. The purpose of this paper is to review the problem of the most common of the adverse effects of statins- myopathy, in terms of incidence, probable cause, and recommended treatment of patients.