Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have transformed the management of obesity, demonstrating significant efficacy in inducing weight loss and improving metabolic parameters. However, emerging clinical and paraclinical evidence suggests that these agents may also contribute to an unintended reduction in skeletal muscle mass, potentially exacerbating or precipitating sarcopenic obesity, particularly in older or frail individuals with limited muscular reserves. This review critically examines current data on the effects of GLP-1 RAs on body composition, explores the underlying pathophysiological mechanisms of skeletal muscle wasting, and offers evidence-based strategies for attenuating these potential adverse outcomes. While GLP-1 RAs therapy remains central to obesity management, optimizing its use through early recognition and management of associated risks is essential to preserve muscular health, patient functional status and quality of life.

Electrocardiogram (ECG) still remains a very useful diagnostic method in modern cardiology. Its broad availability, noninvasiveness and good sensitivity explain why it plays a capital role in the very beginning of the process of diagnosis for every patient, with or without cardiac-related complaints. For the practitioner, good training in ECG interpretation is mandatory. Sometimes, the ECG trace reveals particular aspects that may cause confusion and complicate decision-making. In this article, we present several less common situations underlying the general context and ECG features. The syndromes studied have a high pathological significance and may range from acute emergencies that call for a rapid therapeutical response to chronic syndromes that require prolonged observation, monitoring and risk stratification.

Chronic obstructive pulmonary disease (COPD) is a global healthcare problem, characterized by a progressive and irreversible decline in lung function, primarily due to airflow limitation caused by inflammation and emphysema. While smoking is the main risk factor, systemic inflammation also plays a significant role in the development and progression of the disease, particularly in relation to autoimmune conditions. This literature review provides an overview of current evidence regarding the underlying pathophysiological mechanisms that link autoimmune inflammatory processes to COPD. It also examines the clinical relevance of these associations, with a focus on potential diagnostic and therapeutic implications. To ensure a comprehensive perspective, a broad literature search was conducted in PubMed and Embase in March 2025, using a wide range of search terms related to COPD and multiple autoimmune conditions. Relevant studies of any design were included if they provided valuable insights into the interplay between autoimmune processes and COPD, while non-English publications and commentaries were excluded. Studies suggest a potential association between COPD and autoimmune processes, with chronic systemic inflammation playing a central role. The evidence points to immune dysregulation as a contributing factor to both COPD progression and its connection to autoimmune conditions. The complex interactions between COPD and autoimmune diseases require further investigation. Gaining a better understanding of these interactions may provide new insights into managing patients with concurrent pulmonary and autoimmune conditions, emphasizing a growing area of clinical research.

Obesity represents a complex, multifactorial syndrome that represents a high burden for public health systems worldwide. Serotonin is an important factor in feeding behavior and weight regulation and their interplay implies multiple mechanisms that could explain the correlation with obesity, so understanding these interconnections is essential for developing targeted therapeutic strategies. A systematic review of the literature was conducted using PubMed and Scopus databases, using articles published between 1 January 2015 and 1 December 2024, based on predefined inclusion and exclusion criteria. After the selection process, 22 studies were selected for detailed analysis, focusing on the role of serotonin in obesity. Serotonin significantly influences appetite control and energy homeostasis through multiples pathways, including insulin resistance, high-fat diets, gut microbiota, low-grade inflammation, interferences with tryptophan metabolism, psychiatric modifications, genetic alterations of serotonin receptors, serotonin implications in eating behavior, and neurohormonal regulation of appetite. This review highlights the multidimensional characteristics of the serotonin–obesity association, along with its significance in metabolic and psychiatric pathologies. In order to develop more efficient methods for managing obesity, future studies should concentrate on serotonergic regulation and complex management strategies involving the neurohormonal axis.

Background: Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease predominantly affecting young individuals; however, its late-onset manifestation poses distinct clinical and diagnostic challenges. Methods: This report describes the case of a 93-year-old patient who presented in the Emergency Department with exertional dyspnea, lower limb edema, fatiguability, diffuse abdominal pain, predominantly in the hypogastric region, and loss of appetite. Results: Based on the clinical examination, laboratory tests, and imagistic investigations, we excluded the most common etiologies of edema (decompensated chronic heart failure, glomerular nephropathy/chronic kidney disease, decompensated vascular cirrhosis, hypothyroidism, and hypoproteinemia). Further diagnostic evaluation revealed elevated levels of anti-nuclear antibodies and anti-dsDNA antibodies, along with reduced complement levels, indicating active SLE as the underlying cause of the patient’s edema. During hospitalization, the patient received corticosteroid therapy and, after discharge, was referred to the Rheumatology Department for further treatment. Conclusions: In elderly patients, late-onset SLE exhibits distinct clinical manifestations compared to its early-onset counterpart, likely due to age-related alterations in immune system function.

Background and Objectives: Obesity, heart failure (HF), and atherosclerosis have common pathways, including chronic inflammation, immune cells activation, and metabolic disturbances. These pathways often coexist and overlap, increasing cardiometabolic risk. Growth differentiation factor 15 (GDF-15) is an emerging cytokine linked to inflammation, oxidative stress, and metabolic dysregulation, which are common pathways between heart failure, obesity and atherosclerosis. Beyond its established prognostic value in cardiovascular diseases (CVD) and HF, recent evidence suggests that GDF-15 may also reflect subclinical atherosclerosis, potentially improving early risk stratification in obese and HF populations. The aim of this review is to synthesize current evidence on the association between GDF-15 and markers of subclinical atherosclerosis, and to evaluate whether GDF-15 may serve as an integrative biomarker reflecting shared cardiometabolic pathways. Materials and Methods: We conducted a systematic review following PRISMA recommendations registered by CRD420251267457 number on PROSPERO. PubMed, Embase, Scopus, and Web of Science were searched for human studies evaluating the correlation between markers of subclinical atherosclerosis and GDF-15 concentration. We excluded the studies not published in English, not involving human participants, and not meeting the inclusion criteria. We assessed the risk of bias using the Joanna Briggs Institute appraisal tool. Due to the heterogeneity of studies, a narrative synthesis was performed. Result: The review included 18 studies, which evaluated the association between GDF-15 and subclinical atherosclerosis markers, such as intima media thickness, coronary artery calcium score, ankle-brachial index, and atherosclerotic plaques. Studies included patients with metabolic disorders, chronic inflammatory diseases, HIV cohorts, and general population samples. Most of the studies reported that GDF-15 levels were associated with greater atherosclerotic burden; however, results were frequently influenced by confounders. Methodological limitations, such as limited or highly specified samples, cross-sectional designs, variability in atherosclerotic-imaging technique, and inconsistent adjustment for confounders, restrict generalization of the results. Conclusions: Current evidence supports GDF-15 as a biomarker integrating inflammatory and metabolic stress signals, indirectly linking obesity, HF and subclinical atherosclerosis. While current data supports its prognostic relevance, further studies are needed to confirm its clinical utility in routine assessment and preventive cardiovascular care.