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Background: Medication nonadherence of patients with chronic conditions is a complex phenomenon contributing to increased economic burden and decreased quality of life. Intervention development relies on accurately assessing adherence but no "gold standard" method currently exists.
Purpose: The present scoping review aimed to: (a) review and describe current methods of assessing medication adherence (MA) in patients with chronic conditions with the highest nonadherence rates (asthma, cancer, diabetes, epilepsy, HIV/AIDS, hypertension), (b) outline and compare the evidence on the quality indicators between assessment methods (e.g., sensitivity), and (c) provide evidence-based recommendations.
Methods: PubMed, PsycINFO and Scopus databases were screened, resulting in 62,592 studies of which 71 met criteria and were included.
Results: Twenty-seven self-report and 10 nonself-report measures were identified. The Medication Adherence Report Scale (MARS-5) was found to be the most accurate self-report, whereas electronic monitoring devices such as Medication Event Monitoring System (MEMS) corresponded to the most accurate nonself-report. Higher MA rates were reported when assessed using self-reports compared to nonself-reports, except from pill counts.
Conclusions: Professionals are advised to use a combination of self-report (like MARS-5) and nonself-report measures (like MEMS) as these were found to be the most accurate and reliable measures. This is the first review examining self and nonself-report methods for MA, across chronic conditions with the highest nonadherence rates and provides evidence-based recommendations. It highlights that MA assessment methods are understudied in certain conditions, like epilepsy. Before selecting a MA measure, professionals are advised to inspect its quality indicators. Feasibility of measures should be explored in future studies as there is presently a lack of evidence.
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http://dx.doi.org/10.1093/abm/kaab080 | DOI Listing |
ESC Heart Fail
September 2025
Department of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Heart failure (HF) is a multifactorial and pathophysiological complex syndrome, involving not only neurohormonal activation but also oxidative stress, chronic low-grade inflammation, and metabolic derangements. Central to the cellular defence against oxidative damage is nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that orchestrates antioxidant and cytoprotective responses. Preclinical in vitro and in vivo studies reveal that Nrf2 signalling is consistently impaired in HF, contributing to the progression of myocardial dysfunction.
View Article and Find Full Text PDFCurr Opin Lipidol
August 2025
Cardiometabolic Immunity Laboratory, Department of Physiology, Monash Biomedicine Discovery Institute (BDI) and Victorian Heart Institute (VHI), Monash University, Melbourne, Victoria, Australia.
Purpose Of Review: This review explores the evolving understanding of efferocytosis - the clearance of dead or dying cells by phagocytes - in the context of atherosclerosis. It highlights recent discovers in cell death modalities, impaired clearance mechanisms and emerging therapeutic strategies aimed at restoring efferocytosis to stabilize plaques and resolve inflammation.
Recent Findings: Recent studies have expanded the scope of efferocytosis beyond apoptotic cells to include other pro-inflammatory cell death modes, including pyroptosis, necroptosis and ferroptosis, revealing context-dependent clearance efficiency and immunological outcomes.
Curr Opin Neurol
October 2025
Neuromuscular Diseases Unit, Department of Neurology, IR SANT PAU, Hospital de la Santa Creu i Sant Pau, CIBERER, Barcelona, Spain.
Purpose Of Review: Autoimmune nodopathies (AN) are a recognized distinct group of immune-mediated peripheral neuropathies with unique immunopathological features and therapeutic implications. This review synthesizes recent advances in their pathogenesis, diagnosis, and management, which have refined their clinical classification and informed targeted treatment strategies.
Recent Findings: AN are characterized by autoantibodies targeting surface proteins in the nodal-paranodal area (anti-contactin-1, anti-contactin-associated protein 1, anti-neurofascin-155, anti-pan-neurofascin), predominantly of IgG4 subclass.
Macrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF's mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease.
View Article and Find Full Text PDFClin Exp Immunol
September 2025
Rheumatology Department, Université Paris-Saclay, Institut National de la Santé et de la Recherche Médicale (INSERM) UMR1184, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris (APHP), CEA , FHU CARE, Le Kremlin Bicêtre, France.
Introduction: Immunosenescence remodels immune functions and was first described with aging. It is present in 25% of cancer patients but has also been described in patients with Immune-mediated inflammatory diseases (IMIDs). This study aims at quantifying cells exhibiting a phenotype of senescence in CD4+ (T4sen) and CD8+ (T8sen) T cells, analyzing its potential drivers and the effect of anti-TNF treatment in a prospective cohort of patients with rheumatoid arthritis (RA), spondyloarthritis (SpA) and Sjögren disease (SjD).
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