Background/Objectives: Complete blood count (CBC)-derived markers such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and lymphocyte-to-monocyte ratio (LMR) have gained increasing attention as accessible indicators of systemic inflammation. These parameters, calculated from routine blood tests, are widely available in clinical settings and are potentially relevant for a variety of chronic diseases. This review aims to explore current evidence and highlight potential future directions regarding the use of hematologic inflammatory biomarkers in chronic disease. Methods: We performed an extensive literature search on PubMed to identify full-text original studies published in the past five years, focused on investigating the clinical applications of hematologic inflammatory markers in chronic conditions. Results: CBC-derived inflammatory markers have been studied in a wide range of chronic diseases, including autoimmune diseases, metabolic disorders, chronic kidney disease, chronic infections, psychiatric diseases, and other conditions. These markers have been evaluated for multiple clinical purposes, such as aiding diagnosis, monitoring disease status, assessing disease activity, disease subtype characterization, predicting prognosis, and evaluating associations with disease outcomes. Conclusions: As chronic diseases affect millions of individuals globally, placing a burden for the healthcare system, patients, and their families, simple and cost-efficient tools like CBC-derived inflammatory markers have the potential to improve clinical case management.

The microbiota–gut–brain axis (MGBA) comprises a complex bidirectional communication network integrating neural, immune, metabolic, and endocrine pathways. Dopamine, traditionally viewed as a central neurotransmitter, also plays essential roles in the gastrointestinal (GI) tract, where it regulates motility, secretion, barrier homeostasis, and mucosal immunity. Growing evidence indicates that the gut microbiota significantly contributes to intestinal dopamine metabolism through specialized enzymatic pathways, particularly tyrosine decarboxylase in Enterococcus species and catechol dehydroxylase in Eggerthella species. These microbial reactions compete with host processes, alter dopaminergic tone, and degrade orally administered levodopa (L-DOPA), providing a mechanistic explanation for the variability in treatment response in Parkinson’s disease (PD). Beyond PD, microbially mediated alterations in dopaminergic signaling have been implicated in mood disorders, neurodevelopmental conditions, metabolic dysfunction, and immune-mediated diseases. This review synthesizes current mechanistic and translational evidence on the dopamine–microbiota interface, outlines microbial pathways shaping dopaminergic activity, and highlights therapeutic opportunities including microbiota modulation, dietary strategies, fecal microbiota transplantation, and targeted inhibitors of microbial dopamine metabolism. Understanding this interface offers a foundation for developing personalized approaches in neurogastroenterology and neuromodulatory therapies.

At the level of skin wounds, an electrical potential difference develops between the edges of the wound and the center of the wound, which favors the migration of cells in the process of their healing. Cells migrate in an electric field because they have a certain electrical membrane potential. This potential is due to differences in the transmembrane electrochemical gradient. The transmembrane electrochemical gradient is due to the migration of sodium, potassium, and calcium ions into the corresponding ion channels. If this is the case, the modification of the functionality of these ion channels should influence the membrane potential and, as a consequence, the wound healing process. In this experiment, we set out to investigate whether the chemical manipulation of ion channels by amiodarone influences the wound healing process. Amiodarone blocks several types of ion channels, but at different concentrations: at low concentrations, it blocks only potassium channels; at medium concentrations, potassium and calcium channels; and at high concentrations, it blocks potassium, calcium, and sodium channels. We worked on rats that were given experimental skin lesions and evaluated the influence of the healing of these lesions upon the topical administration of amiodarone in three concentrations, 200 nM, 2000 nM and 200,000 nM, compared to an untreated group and a group treated with benzyl alcohol, the amiodarone solvent. In our experimental conditions, low concentration amiodarone promoted wound healing both in terms of duration of healing and also in terms of speed of healing. This means that blocking some ions, possibly potassium channels, might promote wound healing.

Background/Objectives: Chronic wounds, including hidradenitis suppurativa (HS) and venous ulcers (VU), are commonly associated with complex microbial communities that may influence wound healing and treatment outcomes. Understanding microbial diversity and antibiotic resistance patterns is essential in order to optimize therapeutic strategies. This study aimed to investigate the microbial populations and antibiotic resistance profiles in HS and VU patients, comparing the prevalence of common pathogens and their antimicrobial resistance profiles. Methods: We conducted a cross-sectional analysis that included a total of 112 individuals (24 with the diagnosis of hidradenitis suppurativa and 88 diagnosed with venous ulcer). Wound swabs were cultured to identify bacterial species, and antibiotic resistance was assessed using a standard panel of antibiotics. Prevalence rates of key pathogens, such as Staphylococcus aureus, Pseudomonas aeruginosa, and Enterococcus faecalis, were compared between the two groups. Resistance patterns were analyzed using statistical methods to identify significant differences. Results: Staphylococcus aureus was the most common pathogen in both groups (45.8% in HS; 38.6% in VU), with a notable prevalence of methicillin-resistant S. aureus (MRSA). Pseudomonas aeruginosa was exclusively identified in VU patients (27.3%), while beta-hemolytic Streptococcus and Corynebacterium amycolatum were identified in HS cases only. Antibiotic resistance was moderate, notably in S. aureus and Proteus mirabilis, while one case of multidrug-resistant Pseudomonas aeruginosa was identified. Conclusions: This study highlights the distinctive microbial profiles and antibiotic resistance patterns in HS and VU chronic wounds. The predominance of S. aureus in both groups underscores the need for targeted therapies, while the absence of P. aeruginosa in HS wounds and the higher prevalence of other species emphasizes wound-specific microbial variations. These findings underscore the importance of personalized treatment strategies and continuous surveillance of antimicrobial resistance.

Opioid receptors are key modulators of pain, with both central and peripheral subtypes contributing to analgesia. While central opioid receptors have been extensively studied, peripheral opioid receptors, located on sensory nerve terminals and immune cells, have gained attention for their ability to provide localized analgesia and anti-inflammatory effects without central side effects such as respiratory depression and sedation. This narrative review explores the classification, localization, and activation of peripheral opioid receptors, emphasizing their role in inflammatory pain modulation. These receptors are upregulated in inflamed tissues, enhancing analgesic efficacy. Their activation modulates nociceptive signaling through inhibition of excitatory neurotransmitter release, potassium channel activation, and immune regulation. Peripherally acting opioid receptor agonists offer targeted pain relief, while selective antagonists mitigate opioid-induced constipation without affecting central analgesia. Preclinical studies, including carrageenaninduced inflammation models, have reinforced the potential of peripheral opioid receptor targeting in pain therapy. Future research should focus on optimizing these agents for clinical use, improving drug delivery systems, and integrating them into multimodal pain management strategies.