Insulin resistance is documented in clamp studies in 75% of women with polycystic ovary syndrome (PCOS). Although it is not included in the diagnostic criteria of PCOS, there is a crucial role of this metabolic impairment, which along with hormonal abnormalities, increase each other in a vicious circle of PCOS pathogenesis. Insulin resistance in this group of patients results from defects at the molecular level, including impaired insulin receptor-related signaling pathways enhanced by obesity and its features: Excess visceral fat, chronic inflammation, and reactive oxygen species. While lifestyle intervention has a first-line role in the prevention and management of excess weight in PCOS, the role of anti-obesity pharmacological agents in achieving and maintaining weight loss is being increasingly recognized. Glucagon-like peptide-1 receptor agonists (GLP1-RAs) not only act by reducing body weight but also can affect the mechanisms involved in insulin resistance, like an increasing expression of glucose transporters in insulin-dependent tissues, decreasing inflammation, reducing oxidative stress, and modulating lipid metabolism. They also tend to improve fertility either by increasing LH surge in hypothalamus-pituitary inhibition due to estrogen excess connected with obesity or decreasing too high LH levels accompanying hyperinsulinemia. GLP1-RAs seem promising for effective treatment of obese PCOS patients, acting on one of the primary causes of PCOS at the molecular level.

Introduction. Type 2 Diabetes Mellitus is a metabolic disease the development of which depends on both environmental and genetic factors. The rapid increase in the number of cases observed in recent decades has been associated with the lifestyle predominant in the West, characterised by a high-calorie diet rich in carbohydrates and saturated fatty acids as well as little physical activity and chronic stress. Another disease with growing morbidity is Alzheimer’s Disease, a neurodegenerative disorder characterised by progressive dementia. State of the art. The results of numerous studies indicate many similarities between these two diseases in terms of their pathomechanisms, especially changes in the activity of enzymatic pathways, accumulation of peptides with altered structure, and chronic inflammation. Amyloid β, hyperphosphorylated tau protein, amylin, and apolipoprotein J are involved in both pathologies. The reasons for their excessive accumulation are not fully understood, but cellular metabolism disorders associated with insulin resistance and diabetes mellitus may play a key role in this process. It is highly probable that the changes observed at cellular level, which translate into the clinical state of patients, are caused by many abnormalities common to both diseases. Clinical implications. The discovery of pathophysiological similarities has resulted in attempts to use antidiabetic drugs in Alzheimer’s Disease therapy. While animal studies have revealed the potential benefits of oral antidiabetic drugs, studies on humans have not provided clear data regarding their effectiveness. Most clinical trial results are promising, but there have also been studies that have shown no significant, or even adverse, effects of these drugs on Alzheimer’s Disease course. Future directions. Undoubtedly, further research is needed to better understand the mechanisms by which the medications used in diabetes treatment affect the nervous system, and further clinical trials to compare the effectiveness of this therapy in patients presenting different clinical conditions at different stages of Alzheimer’s Disease. Introduction. Type 2 Diabetes Mellitus is a metabolic disease the development of which depends on both environmental and genetic factors. The rapid increase in the number of cases observed in recent decades has been associated with the lifestyle predominant in the West, characterised by a high-calorie diet rich in carbohydrates and saturated fatty acids as well as little physical activity and chronic stress. Another disease with growing morbidity is Alzheimer’s Disease, a neurodegenerative disorder characterised by progressive dementia. State of the art. The results of numerous studies indicate many similarities between these two diseases in terms of their pathomechanisms, especially changes in the activity of enzymatic pathways, accumulation of peptides with altered structure, and chronic inflammation. Amyloid β, hyperphosphorylated tau protein, amylin, and apolipoprotein J are involved in both pathologies. The reasons for their excessive accumulation are not fully understood, but cellular metabolism disorders associated with insulin resistance and diabetes mellitus may play a key role in this process. It is highly probable that the changes observed at cellular level, which translate into the clinical state of patients, are caused by many abnormalities common to both diseases. Clinical implications. The discovery of pathophysiological similarities has resulted in attempts to use antidiabetic drugs in Alzheimer’s Disease therapy. While animal studies have revealed the potential benefits of oral antidiabetic drugs, studies on humans have not provided clear data regarding their effectiveness. Most clinical trial results are promising, but there have also been studies that have shown no significant, or even adverse, effects of these drugs on Alzheimer’s Disease course. Future directions. Undoubtedly, further research is needed to better understand the mechanisms by which the medications used in diabetes treatment affect the nervous system, and further clinical trials to compare the effectiveness of this therapy in patients presenting different clinical conditions at different stages of Alzheimer’s Disease.

Since the beginning of the COVID-19 pandemic, there has been an urgent need to find effective treatment. It is widely known that virus attacks and damages mostly the lungs, but also infect vascular endothelial cells. Therefore, the protection of the endothelium is a promising target in the therapy of COVID-19 and its complications. In this review article, we focused on several groups of drugs with potential to protect the endothelium. The most promising ones are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, drugs targeting angiotensin-converting enzyme 2, heparins, sulodexide, acetylsalicylic acid, statins, tocilizumab, baricitinib, and defibrotide. Although the short period of trials and the lack of data necessitate further research, endothelial protection remains a promising target for COVID-19 therapy.

Introduction and purpose  The role of virtual reality (VR) is increasingly being discussed not only in the context of entertainment, but also in the medical field. Recently, there has been a growing number of literature analyzing its effect on reducing pain and anxiety, which are common problems of pediatric patients. These feelings can negatively affect their psyche, health recovery, but also doctor-patient cooperation and avoidance of treatment in the future.The purpose of this study is to analyze and summarize the potential of using virtual reality to reduce pain and anxiety in pediatric patients. Material and methods  A literature review of 2015-2022 based on PubMed and Google Scholar. Results  The literature reviewed shows the extensive use of virtual reality in the treatment of pain and anxiety in pediatric patients. VR is a good method for reducing perioperative anxiety, pain during wound care and pain as well as anxiety in invasive procedures. This method may not be beneficial in the treatment of acute pain and its role is uncertain during dental treatment. Disadvantages of this technique include the need for financial investment in equipment and trained staff. Patients may experience dizziness and motion sickness during its use. Another disadvantage is also that it does not provide a long-term analgesic effect. Conclusion There appears to be merit in using this technology as an adjunctive method to reduce pain and anxiety in pediatric patients. There is also a need for further research in this area and the development of appropriate therapeutic intervention for a specific age group and procedure in a well-defined process by a trained team.

Introduction and purpose Frostbite is a serious injury caused by cold, which is an inseparable element of human contact with nature. It can cause tissue damage and loss of function if not properly treated. It treatment consists of several stages that require the involvement of many people. The purpose of the article is to summarize information on epidemiology, pathophysiology, prehospital and hospital procedures and to draw attention to the complexity of patient care. Materials and methods A literature review based on PubMed and Google Scholar using the following keywords: frostbite, cold injury. Description of the state of knowledge: The literature review shows the breadth of the issue. The effectiveness of therapy depends on: knowledge of pathophysiology and risk factors, early diagnosis, discontinuation of exposure to cold, effective analgesic treatment, fluid therapy, transport of the victim to the appropriate center, rapid warming of frozen tissues, imaging diagnostics, initiation of thrombolytic treatment and, if necessary, surgery. It is also important to remember about long-term complications that worsen the quality of life of patients, such as chronic pain, hyperaesthesia or impairment or loss of limb functionality. Conclusions Frostbite is a relatively rare problem, but especially in winter, every medic will have to deal with it sooner or later. Considering the above information, the management of a patient with frostbite is a demanding and long-term process in which the cooperation and involvement of many medics is important, so it is worth having knowledge about them.

Clinical depression is a psychiatric disorder characterized by symptoms such as loss of interest and pleasure from typically enjoyable activities (anhedonia), pervasive low mood, and diminished energy leading to excessive fatigue and lower activity which have been present in a patient for at least two weeks. Available therapies consist primarily of pharmacological intervention. Indeed, some groups of medications such as SSRIs, SNRIs, TCA’s and tetracyclic antidepressants have been used to treat depression for decades, frequently in combinations. An example of such a combination is “California Rocket Fuel” composed of venlafaxine and mirtazapine Objective: To review the current literature on the efficacy of the combination of venlafaxine and mirtazapine in treating clinical depression both in drug-resistant depression and as a first-line option. To explore the risks and benefits of this choice of therapy and discuss its potential mechanism of action. Methods: Literature review of Pubmed, Google Scholar, Science Direct, and available medical textbooks. Conclusions: Treatment with venlafaxine and mirtazapine is safe, especially for drug-resistant depression. It is worth considering adding venlafaxine to already ongoing pharmacotherapy with mirtazapine when the patient experiences sleepiness and the symptoms of depression have not been sufficiently reduced. Augmenting venlafaxine treatment with mirtazapine also seems necessary when the patient complains of insomnia. One may consider implementing such therapy as a first-line treatment in patients who suffer from depression for a long time and experience insomnia in its course.