Background and Objective: Copper (Cu) disturbances within humans have been associated with a wide range of disease states due to dysregulation of its essential physiological functions. The following article aims to aid the reader in diagnosing the cause of plasma Cu derangements in humans and discusses some of ways in which the biochemistry tests are performed and their limitations. By the end of the article, the reader will be able to order and interpret appropriate investigations when faced with a patient with low or high Cu concentration in plasma. Methods: A focused narrative literature review was performed using PubMed, OMIM and Google. Searches were conducted from September 2024 to September 2025 to identify relevant publications from database inception to September 2025. Key Content and Findings: Within this review are discussed key causes of low Cu, such as Menkes and zinc overload, and causes of high Cu plasma concentrations, such as dietary excess and cholestasis. From this, diagnostic flow charts have been created by the authors, providing a systematic approach for investigations. Conclusions: This article will help healthcare professionals with a practical framework to aid investigation into the cause of Cu concentration abnormalities in human plasma, where the cause is not immediately apparent. These algorithms have been presented and created within the limitations of the laboratory tests discussed within the paper, selected to be widely available.

Background: Despite isotope dilution mass spectrometry (IDMS) traceability, creatinine harmonization across platforms remains imperfect, particularly for Jaffe methods at physiological concentrations. Leveraging patient-like human serum pools measured across multiple routine platforms, we quantified method-dependent differences and their impact on derived estimated glomerular filtration rate (eGFR). Methods: Fifteen human serum pools were measured in triplicate across major vendors (Roche, Abbott, Beckman, Siemens; enzymatic and Jaffe; Werfen, Ortho enzymatic only). Triplicates were averaged per pool and platform. We summarized (I) cross-platform dispersion [per-pool coefficient of variation (CV)] within method families, (II) within-vendor relative bias (Jaffe vs. enzymatic), (III) concentration dependence, and (IV) eGFR impact using Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) 2021 (creatinine-only) in fixed scenarios (a 60-year-old female and a 60-year-old male). Results: Cross-platform dispersion was lower for enzymatic vs. Jaffe [median CV 3.21% (2.47–3.49%) vs. 5.05% (2.94–6.72%)]. Vendor-wise median relative bias (Jaffe vs. enzymatic) across pools: Roche +5.84%, Abbott +4.64%, Beckman −1.52%, Siemens +10.85%. Bias tended to be larger at low creatinine concentration. Depending on vendor and patient example (60-year-old female or male), method-dependent differences between Jaffe and enzymatic creatinine led to Kidney Disease: Improving Global Outcomes (KDIGO) G-stage reclassification in 7–40% of serum pools, with absolute ΔeGFR values up to 12–13 mL/min/1.73 m2 near decision thresholds. Conclusions: Enzymatic creatinine assays exhibit better inter-platform alignment and smaller method-dependent bias than Jaffe procedures, particularly in the low-concentration range, where small absolute differences may carry large clinical leverage thus reducing the risk of clinically meaningful eGFR shifts.

Background and Objective: Stress is associated with various responses depending on the kind and the intensity of exposure, the number of stressful events and the period of life (age of exposure). Stress modulates the epigenetic machinery, modulating gene expression and impacting health across life. The objective of this narrative review is to identify the impact of social stress on epigenetics and recognise the consequences on mental health. Methods: This narrative review was performed using PubMed, MEDLINE, Cochrane Library and Google Scholar from January 2015 to June 2025; search terms used to identify relevant publications were: “stress AND epigenetics”, “stress and DNA methylation”, “stress AND early-life”, “stress AND Covid-19”, “stress AND work”. Language was restricted to English. Key Content and Findings: This review aims to describe the impact of social stressors (i.e., trauma following abuse, crime, war, workplace stress) during early life, pregnancy and work-related stress on DNA methylation/demethylation at neonatal/child- and adult-age. Social stressors can perturb neuronal development, epigenetic age and adult health by modulation of DNA methylation at selected genes. Furthermore, maternal stress during pregnancy has been observed to perturb the child and mother epigenome, increasing the risk of epigenetic inheritance of these biomarkers in future generations. Work-related stress during coronavirus disease 2019 (COVID-19), with high working hours and reduced sleep time, represents an additional factor that contributes to the development of non-communicable diseases. Conclusions: Social stressors, in early life and in adulthood age can perturb mental health with long-term effects later in life; preventive strategies to promote epigenetic reversibility at a young age should be considered to avoid stress-induced intergenerational epigenetic inheritance. Actions to counterbalance stress-associated work include scheduling work hours with breaks to improve physical and emotional well-being. Guidelines for training and clinical practice with clear and precise instructions can be helpful to manage stress in healthcare personnel; furthermore, an educational program for people could represent a useful tool for social support.