Background: In response to the goal of the World Health Organisation to eliminate hepatitis C virus infections by 2030, Romania is striving for national elimination. An already successful micro-elimination project was expanded to test-and-treat specific populations and at-risk groups. The aim of this project was to identify the individuals with HCV infection in disadvantaged regions who do not have proper medical care access. Materials and Methods: Our two-arm interventional cross-sectional study used rapid anti-HCV antibody testing on two population groups from the Romanian southwestern region of Oltenia, approached between September 2020 and May 2021. The first group consisted of predominantly over 40 years old individuals, recruited through five family doctors from two medium-sized towns (community lot—CL). We approached a second group, aged 18–65, through 11 medical offices of five large factories in the same region (industry lot, IL). A 12-items questionnaire was given to each participant, to determine risk factors and record demographic data. Eligible patients initiated antiviral therapy using direct-acting antivirals (DAAs). Results: We enrolled 15,383 individuals between all 16 locations. The overall prevalence by antibody testing was 0.77% (119 cases). Of these, 57 subsequently received treatment with DAAs. We identified blood transfusions as a risk factor within the CL. Participants in the IL reported a relatively high risk for the following situations: sharing of personal hygiene belongings with another person, performing previous blood transfusions, dental interventions and previous surgery. Conclusions: In this global context, the use of micro-elimination allows interventions to be faster and more efficient. This is possible by targeting smaller and specific HCV risk groups.

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by epidermal barrier dysfunction, immune dysregulation, and marked clinical heterogeneity. Growing evidence implicates the gut microbiome in AD-related pathways through microbial metabolites, intestinal barrier function, and systemic immune signaling. This narrative review synthesizes current evidence on gut microbial alterations in AD, with particular attention to short-chain fatty acids, tryptophan-derived aryl hydrocarbon receptor ligands, intestinal permeability, gut–skin microbiome interactions, and microbiota-targeted interventions. Human studies have reported associations between AD and altered abundance of selected microbial taxa, metabolite profiles, and markers of intestinal barrier dysfunction, whereas animal and in vitro studies provide complementary mechanistic evidence. However, findings remain heterogeneous across age groups, disease phenotypes, geographic populations, analytical platforms, and treatment exposures, and causality is incompletely established. Probiotic and synbiotic interventions have shown strain-specific and context-dependent effects, while postbiotics, fecal microbiota transplantation, washed microbiota transplantation, and metabolite-directed approaches remain investigational. AI-assisted multi-omics methods may improve biological stratification and hypothesis generation, but current applications are limited by small sample sizes, cohort heterogeneity, overfitting, insufficient external validation, and limited clinical implementation. Current evidence therefore supports the gut microbiome as a mechanistically plausible contributor, potential biomarker, and therapeutic target in AD while underscoring the need for longitudinal, phenotype-aware, and externally validated studies before routine clinical translation.

Background/Objectives: Atopic dermatitis (AD) has been associated with osteoporosis and fractures, but the magnitude, mechanisms, therapeutic implications, and clinical relevance of this relationship remain uncertain. This review critically evaluates the epidemiological and osteoimmunological evidence linking AD to skeletal fragility and proposes a lifespan-based, risk-adapted screening framework. Methods: A structured search of PubMed/MEDLINE and supplementary sources identified peer-reviewed publications from January 2020 through July 2026. Seventy-five studies, reviews, meta-analyses, guidelines, and consensus documents addressing AD, bone mineral density (BMD), osteoporosis, fractures, immune–bone pathways, treatment exposure, and skeletal assessment were included in a critical narrative synthesis. Results: A recent cohort-based meta-analysis associated AD with osteoporosis (odds ratio [OR], 1.56) and any fracture (OR, 1.08), although heterogeneity was substantial. Risk appeared greater in severe or long-standing disease and reflected the interaction among inflammatory, therapeutic, nutritional, behavioral, and age-related determinants. Systemic glucocorticoids constituted the clearest modifiable treatment-related risk, but did not fully explain the association. The RANK–RANKL–osteoprotegerin system and IL-4, IL-13, IL-31, and IL-33 provide biological plausibility, although their skeletal effects are context-dependent and predominantly supported by indirect or preclinical evidence. Available data do not demonstrate that dupilumab causes osteoporosis; emerging pediatric findings suggest improvements in growth and bone-related biomarkers, but do not demonstrate fracture prevention. Conclusions: AD alone does not justify universal DXA screening. Assessment should be individualized according to age, fragility-fracture history, disease severity and duration, cumulative systemic glucocorticoid exposure, nutritional status, physical activity, muscle function, and falls. Prospective studies combining standardized AD phenotyping with longitudinal imaging, biomarkers, and adjudicated fractures are required.

Background/Objectives: Osteoporosis is a major cause of skeletal fragility, yet occupational determinants of bone health remain comparatively underrecognized in clinical and occupational medicine. This review aimed to critically evaluate the relationships between occupational exposures and skeletal health, examine the biological mechanisms potentially linking workplace conditions to bone remodeling, and explore how occupational information could contribute to individualized osteoporosis risk assessment and prevention. Methods: A structured literature search was conducted focusing primarily on studies published between 2020 and June 2026, supplemented by relevant earlier landmark studies. Evidence concerning shift and night work, circadian and sleep disruption, indoor work and sunlight exposure, occupational physical activity and sedentary behavior, psychosocial stress, and selected chemical and environmental exposures was synthesized together with current approaches to osteoporosis diagnosis and fracture-risk assessment. Results: The available evidence suggests that night and rotating shift work, circadian disruption, limited daylight exposure, altered mechanical loading, and selected industrial exposures may be associated with changes in bone turnover, bone mineral density, osteoporosis, or skeletal fragility. Potential mechanisms converge on circadian and endocrine regulation, vitamin D–mineral homeostasis, inflammatory and oxidative pathways, RANK/RANKL/OPG signaling, and Wnt/β-catenin/sclerostin-mediated mechanotransduction. However, evidence remains heterogeneous, with limited prospective occupational cohorts and substantial variation in exposure assessment and skeletal endpoints. Occupational characteristics are not currently validated as independent criteria for diagnosing osteoporosis or as predictors of fracture risk. Based on the available evidence, we propose a Precision Occupational Medicine framework integrating cumulative occupational exposure, individual susceptibility, risk-enriched diagnostic assessment, personalized prevention, and longitudinal reassessment. Conclusions: Occupational factors may modify skeletal vulnerability, particularly when cumulative exposures interact with established osteoporosis risk factors. Current evidence supports risk-enriched assessment rather than universal occupational screening. Prospective studies are required to determine whether quantitative occupational exposure data improve prediction of longitudinal bone loss and fragility fractures beyond established clinical models and to validate the proposed framework for occupational practice.

Atopic dermatitis (AD) has been linked to osteoporosis and fractures, but the strength, mechanisms, treatment implications, and clinical significance of this relationship remain uncertain. This review critically assesses epidemiological and osteoimmunological evidence connecting AD with skeletal fragility and proposes a lifespan-based, risk-adapted screening framework. A recent cohort-based meta-analysis found associations between AD and osteoporosis (odds ratio [OR], 1.56) and any fracture (OR, 1.08), although heterogeneity was substantial. Risk appeared higher with severe or long-standing disease and reflected interactions among inflammatory, therapeutic, nutritional, behavioral, and age-related factors. Systemic glucocorticoids were the clearest modifiable treatment-related risk, but did not fully account for the association. The RANK–RANKL–osteoprotegerin system and IL-4, IL-13, IL-31, and IL-33 offer biological plausibility, although their skeletal effects are context-dependent and supported primarily by indirect or preclinical evidence. Available data do not show that dupilumab causes osteoporosis. Emerging pediatric findings suggest improvements in growth and bone-related biomarkers, but provide no evidence of fracture prevention. AD alone does not warrant universal DXA screening. Assessment should be individualized based on age, history of fragility fractures, disease severity and duration, cumulative systemic glucocorticoid exposure, nutritional status, physical activity, muscle function, and falls. Prospective studies combining standardized AD phenotyping with longitudinal imaging, biomarkers, and adjudicated fractures are needed.

Background/Objectives: Neural–tumor interactions are increasingly recognized in gastric cancer (GC), yet their relationship with circulating neuroactive mediators remains incompletely understood. This systematic review aimed to synthesize human evidence on circulating neurotransmitters, neuropeptides, and related mediators, assess their diagnostic, clinicopathological, treatment-associated, and prognostic relevance, and integrate clinical findings within a translational framework of neuro–tumor signaling. Methods: PubMed/MEDLINE, Scopus, and Web of Science Core Collection were systematically searched following PRISMA 2020 guidelines. Eligible studies assessed circulating neuroactive mediators in patients with GC. Clinical findings were synthesized by evidence domain and contextualized using complementary tumor-level receptor and signaling evidence. Results: Twenty-four publications representing 23 independent cohorts were included. Replicated circulating alterations were identified for galanin, motilin, and cholecystokinin, although gastrointestinal physiology and treatment-related changes complicated their interpretation. Progastrin-releasing peptide demonstrated diagnostic discrimination in a single study (AUC 0.713; sensitivity 85.9%; specificity 81.2%) and associations with clinicopathological characteristics. Dopaminergic and catecholamine-related alterations suggested systemic neuroendocrine involvement, while higher normetanephrine was associated with poorer survival in univariable analysis. Complementary mechanistic evidence implicated serotonergic, substance P/NK-1R, and neurotensin/NTSR1 pathways in tumor-associated signaling. The translational evidence map highlighted three overlapping biological dimensions: tumor-associated receptor-mediated signaling, systemic neuroendocrine and stress adaptations, and gastrointestinal physiological responses. However, small cohorts, heterogeneous biological matrices, historical assay variability, and limited independent validation restricted clinical interpretation. Conclusions: Circulating neuroactive mediators represent a biologically plausible but insufficiently validated biomarker domain in GC. Their clinical translation requires standardized prospective studies integrating circulating measurements with matched tumor biology, clinically relevant comparator populations, longitudinal outcomes, and independent validation. Pathway-oriented multimarker approaches may ultimately provide more informative neuroactive signatures than individual mediators.