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Introduction Metformin is a widely used oral hypoglycemic agent for type 2 diabetes, with origins in medieval European medicine through the use of Galega officinalis. Subsequent centuries of research led to the development of synthetic biguanides, with metformin's approval as an antidiabetic agent in 1957. Since then, its therapeutic applications have broadened to address other metabolic and endocrine disorders, such as obesity, polycystic ovary syndrome (PCOS), and antipsychotic-induced weight gain. Purpose of the Study This study aims to review metformin's pharmacological properties, mechanisms of action, and its expanded clinical applications. Specifically, it focuses on metformin’s role in promoting weight loss and improving metabolic health across diverse patient populations, including those without diabetes. The study also addresses evidence gaps and proposes areas for further research on dose optimization and safety in non-diabetic populations. Materials and Methods A systematic literature review was conducted using databases such as PubMed and Google Scholar, focusing on studies examining metformin's effects on glycemic control, weight reduction, and metabolic stability. Conclusions Metformin's history underscores its evolution from traditional remedies to a versatile pharmacological agent for treating diabetes and other metabolic conditions. Ongoing research is essential to fully establish its optimal therapeutic parameters and long-term safety for diverse patient groups.

One of the essential elements of a visit to a pediatrician is a height measurement, which allows for the presentation of the child's growth tendency. Short stature is defined as a height that is lower than the average of a specific population, adjusted for age and sex, by at least 2 standard deviations, i.e., less than the 3rd percentile. Due to accompanying symptoms or their absence, the suspected etiology may vary. Genetic disorders are significant causes of short stature, especially among pediatric patients. The division distinguishes chromosomal, monogenic and polygenic disorders. Other possible causes of short stature may be the coexistence of chronic diseases or disorders of the endocrine system. In the case when the growth disorder is not a pathological condition, a variant of normal growth is diagnosed. In the diagnosis of short stature, in addition to a physical examination, it is sometimes necessary to perform laboratory or radiological tests, genetic tests, and specialist consultations.

Infliximab is a chimeric monoclonal antibody used in the treatment of chronic inflammatory diseases such as rheumatoid arthritis, Crohn's disease, ulcerative colitis, and psoriasis. It functions by inhibiting tumor necrosis factor-alpha (TNF-α), a cytokine central to the inflammatory processes of these conditions. Since its approval in 1998, infliximab has significantly improved the management of patients who do not respond well to conventional therapies. The article provides a comprehensive review of infliximab's pharmacological properties, its mechanism of action, FDA-approved uses, and its clinical benefits. It also discusses its safety profile, which includes potential risks like infections, infusion reactions, and long-term concerns such as an increased risk of malignancies. Regular monitoring of adverse effects is crucial for patient safety during treatment. Infliximab has demonstrated efficacy in reducing symptoms like pain, swelling, and skin lesions, and it helps in maintaining remission in conditions like Crohn's disease and psoriasis. The drug is typically administered via intravenous infusion, and its dosing varies depending on the disease and patient response. Additionally, the article highlights the role of therapeutic drug monitoring (TDM) to optimize treatment outcomes and reduce healthcare costs. In conclusion, infliximab remains an essential therapeutic option for managing severe chronic inflammatory diseases, though its use requires careful monitoring due to potential risks. Ongoing research is expected to refine its use and expand its indications, further enhancing its clinical application in inflammatory disease management.

Cannabinoids are chemical compounds that occur naturally in the cannabis plant. They have been known for thousands of years and have been used to treat conditions such as asthma, malaria, hypertension, and spasticity. The most common cannabinoids are tetrahydrocannabinol and cannabidiol. Due to their abundant type 1 and 2 cannabinoid receptors, they affect most systems in the human body. This review focuses on the effects of cannabis on the hypothalamic-pituitary-adrenal axis, the hypothalamic-pituitary-thyroid axis, growth hormone, food intake, glycemia regulation, reproductive system, prolactin, and oxytocin.

Introduction and purpose: Asthma is a chronic inflammatory disease of the airways. Its pathogenesis may be linked to the gut microbiome, which plays a key role in the immune system. This review analyzes current evidence regarding the influence of the gut microbiome on asthma development, particularly in the context of the gut-lung axis. The aim of this paper is to assess the current therapeutic possibilities for asthma based on the modulation of the gut microbiota. Materials and methods: The literature review includes articles from scientific databases (PubMed), selected for their citation impact and relevance to the topic under analysis. Results: The gut microbiota affects immune balance by producing short-chain fatty acids (SCFAs) and other metabolites that modulate the body’s inflammatory response. Gut dysbiosis may contribute to the development of asthma. The use of probiotics, prebiotics, and a fiber-rich diet has shown beneficial effects in reducing inflammation in asthma. Fecal microbiota transplantation (FMT) may represent a future therapeutic approach, though further clinical research is required. Conclusion: Modulation of the gut microbiota is a promising support in asthma therapy. A personalized treatment approach based on the patient's microbiota profile could potentially improve disease control and reduce the reliance on steroids in the future.

Introduction: Sarcoidosis is a multisystem inflammatory disease of unknown etiology. It is more common in women and in people suffering from obesity. A characteristic feature is the formation of non-sarcomatous granulomas, which could occure important organs. It could also present as an asymptomatic form, and its diagnosis may be made incidentally on a routine chest X-ray. Aim of the study: The aim of this study was to review the literature describing the disease sarcoidosis-its course, clinical forms, diagnosis and treatment. Methods and materials: : We reviewed the literature available in the PubMed database, using the key words: "sarcoidosis"; "granulomatosis’’; “cardiac sarcoidosis”; “neurosarcoidosis”; "pulmonary sarcoidosis''. Results: The most common form of sarcoidosis is pulmonary, with enlargement of hilar lymph nodes and parenchymal lesions. The disease could manifest itself in the form of skin lesions-specifically and non-specifically, ocular lesions, where nay most often appears as uveitis, usually bilateral, and could also involve the heart. Patients with neurosarcoidosis usually have involvement of the pituitary, hypothalamus, meninges and cranial nerves. Conclusion: The diagnosis of sarcoidosis is difficult because its symptoms are often nonspecific. Diagnosis is based on exclusion of other diseases and is confirmed through imaging, histopathological, and immunological tests. In most cases, the prognosis of sarcoidosis is positive, and the disease may resolve spontaneously or under treatment. Treatment of sarcoidosis depends on the severity of the disease and the involvement of specific organs, the most common treatment is glucocorticoids.

Introduction: Depressive disorders are among the most prevalent mental health conditions globally, affecting millions of people. Despite extensive research, the exact pathophysiology of depression remains unclear. Recent evidence suggests that neuroplasticity, particularly the role of brain-derived neurotrophic factor (BDNF), plays a crucial role in both the onset and treatment of depressive disorders. Aim of Study: This review explores the relationship between neuroplasticity and depression, focusing on BDNF as a central biomarker and potential therapeutic target. It also examines how antidepressant therapies and physical activity influence neuroplasticity and BDNF levels, offering insights into novel approaches for treating depressive disorders. Material and Methods: A literature review was conducted using PubMed and Google Scholar databases, focusing on peer-reviewed articles with the keywords: "neuroplasticity", "BDNF", "depression", "antidepressants" and "physical activity". Conclusions: Neuroplasticity, particularly through BDNF signaling, plays a critical role in the pathogenesis and treatment of depression. Elevated BDNF levels promote synaptic plasticity, neurogenesis, and recovery of brain function. Antidepressant treatments enhance neuroplasticity by increasing BDNF levels. Antidepressants and physical activity both influence neuroplastic processes, with BDNF serving as a key mediator.

Introduction and purpose: Contrast-induced nephropathy (CIN) is kidney damage that can occur after the administration of contrast agents used in medical imaging procedures like angiography and CT scans. The exact mechanism is not fully understood but is believed to involve direct toxic effects, changes in kidney blood flow, and inflammation. Diagnosis is based on increased serum creatinine levels after contrast exposure. CIN poses challenges due to the rising use of contrast imaging, an aging population, and the increasing prevalence of chronic conditions like diabetes and hypertension. The Aim of this article is to summarize information on how to prevent contrast-induced nephropathy. Review of medications and pre-procedural screening and monitoring helpful to lower risk of CIN. State of knowledge: Contrast-induced nephropathy (CIN) is a form of kidney damage that may occur following the administration of contrast agents used in medical imaging procedures. The exact mechanism of contrast-induced nephropathy is not fully understood, but it is believed to involve a combination of factors, including the direct toxic effects of the contrast agent on kidney cells, changes in blood flow to the kidneys, and the body's inflammatory response, direct effect of oxygen free radicals. The diagnosis of CIN is typically based on an increase in serum creatinine levels within a certain time frame after the administration of the contrast agent. According to European guidelines, the definition of CIN is increased creatinine level in serum by 25% from baseline or creatinine total level in serum increased by 0.5 mg/dL (44 µmol/L) 48-72h after contrast media administration. Material and methods. A review of the available literature of PubMed database from 1992 – 2024.