Raluca-Elena Alexa

Background: Obesity is commonly seen as a condition of overnutrition; however, it is paradoxically associated with micronutrient deficiencies. These deficiencies are clinically relevant and may contribute to the progression of obesity-related comorbidities through interconnected pathways, including chronic low-grade inflammation, oxidative stress, gut dysbiosis, and impaired nutrient absorption. Objectives: This narrative review aims to summarize current evidence regarding the prevalence, underlying mechanisms, and clinical consequences of micronutrient deficiencies in individuals with obesity, with particular emphasis on their metabolic implications and potential therapeutic strategies. Results: Among individuals with obesity, iron, zinc, magnesium, calcium, vitamin D, vitamin B12, and folate are the most frequently reported deficiencies. These deficiencies arise from multiple mechanisms, including poor diet quality, increased metabolic demands, and compromised gastrointestinal absorption. In addition, obesity-related alterations in pharmacokinetics may further interfere with micronutrient distribution and bioavailability. Together, these mechanisms may lead to various clinical outcomes, such as anemia, immune, metabolic, and cardiovascular dysfunctions, along with cognitive impairment. Although several studies suggest that correcting these deficiencies may improve clinical outcomes, findings remain inconsistent, highlighting the complex and multifactorial pathophysiology underlying micronutrient imbalance in obesity. Conclusions: Micronutrient deficiencies represent frequently overlooked contributors to metabolic dysregulation in obesity. Their identification and correction should be considered a central part of the obesity management strategy. A personalized supplementation approach, based on clinical, biological, and pathophysiological characteristics, may provide a complementary support for weight-management treatments.

Background and Objectives: Peripheral neuropathy (PNP) is a frequent and debilitating complication among patients with diabetes mellitus (DM) and other metabolic conditions, substantially affecting morbidity, functional status, and quality of life. Identifying predictors of PNP is essential for optimizing early diagnostic strategies and improving long-term management outcomes. The aim of this study was to determine the predictive factors of PNP in a cohort of patients with DM. Materials and Methods: A cross-sectional study including 117 patients diagnosed with DM assessed for PNP was conducted. All patients were evaluated clinically and biologically. PNP was clinically assessed using the Toronto Clinical Scoring System (TCSS) score and sudomotor function by Sudoscan. Results: The patients included were mostly males with type 2 DM and metabolic syndrome phenotypes. Moreover, the patients with PNP were much older than those without PNP (65 [57–69] vs. 59.50 [46–68] years, p = 0.008), with a longer duration of DM (10 [6–15.50] vs. 5.5 (2–14] years, p = 0.019), and associated autonomic diabetic neuropathy (χ² = 24.382, p < 0.001). Furthermore, TCSS and Sudoscan were correlated with a history of PNP, especially Sudoscan, which showed a very good discriminative ability for diabetic neuropathy diagnosis (AUC = 0.816). In a multivariable logistic regression including age, DM duration, and HbA1c, age was independently associated with PNP, with each additional year increasing the odds of neuropathy by approximately 6% (OR = 1.06, 95% CI 0.02–1.09, p = 0.002). When age was excluded, DM duration showed a borderline association with PNP (OR = 1.055, CI95% 0.997–1.117), suggesting potential overlap between these variables. Adding sudomotor assessment to the initial model improved the model performance (AUC 0.70–0.72). Conclusions: Age emerged as the main independent predictor of diabetic neuropathy, highlighting the role of cumulative metabolic exposure in the development of neural damage. Moreover, sudomotor assessment may have a complementary role in PNP assessment.

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.

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.

The renin–angiotensin–aldosterone system (RAAS) plays a central role in cardiovascular and renal homeostasis and is increasingly recognized for its broad immunomodulatory effects. Pharmacological RAAS inhibition, primarily via angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), has demonstrated therapeutic value beyond its use in hypertension and heart failure, extending to autoimmune, infectious, oncologic, and neurodegenerative conditions. ACEIs and ARBs modulate both innate and adaptive immune responses through Ang II-dependent and -independent mechanisms, influencing macrophage polarization, T-cell differentiation, cytokine expression, and antigen presentation. Notably, ACEIs exhibit Ang II-independent effects by enhancing antigen processing and regulating amyloid-β metabolism, offering potential neuroprotective benefits in Alzheimer’s disease. ARBs, particularly telmisartan and candesartan, provide additional anti-inflammatory effects via PPARγ activation. In cancer, RAAS inhibition affects tumor growth, angiogenesis, and immune surveillance, with ACEIs and ARBs showing distinct yet complementary impacts on tumor microenvironment modulation and chemotherapy cardioprotection. Moreover, ACEIs have shown promise in autoimmune myocarditis, colitis, and diabetic nephropathy by attenuating inflammatory cytokines. While clinical evidence supports the use of centrally acting ACEIs to treat early cognitive decline, further investigation is warranted to determine the long-term outcomes across disease contexts. These findings highlight the evolving role of RAAS inhibitors as immunomodulatory agents with promising implications across multiple systemic pathologies.

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.

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.

Heyde’s syndrome (HS) represents an association between aortic stenosis and intestinal angiodysplasias, and it has been demonstrated that acquired von Willebrand disease plays a pivotal role in the pathophysiology of this syndrome. In patients with HS, von Willebrand factor deficiency represents an additional risk factor, further contributing to the risk of bleeding and anemia. We present the case of an 86-year-old patient diagnosed with HS and von Willebrand deficiency in 2018. Four years prior, the patient underwent surgical aortic valve replacement. Since then, she has been receiving chronic oral anticoagulation therapy with a vitamin K antagonist. The patient was admitted to the Internal Medicine Clinic due to semi-solid dark stools, diffuse abdominal pain, and asthenia. Upon examination, the patient presented with an altered general status and clinical signs suggestive of anemia. Laboratory findings revealed anemia with elevated INR and aPTT values. Colonic angiodysplasias were identified during a colonoscopy, although no sources of active bleeding were detected. On the 9th day of hospitalization, the patient experienced an episode of lower gastrointestinal bleeding. The pharmacological management was adjusted, and argon plasma coagulation was recommended. Following treatment of the angiodysplastic lesions, the patient’s clinical evolution was favorable, with the correction of the anemia.