Suzanne D van der Werff, Stephanie M van Rooden, Aron Henriksson, Michael Behnke, Seven J S Aghdassi, Maaike S M van Mourik, Pontus Nauclér
{"title":"The future of healthcare-associated infection surveillance: Automated surveillance and using the potential of artificial intelligence.","authors":"Suzanne D van der Werff, Stephanie M van Rooden, Aron Henriksson, Michael Behnke, Seven J S Aghdassi, Maaike S M van Mourik, Pontus Nauclér","doi":"10.1111/joim.20100","DOIUrl":"https://doi.org/10.1111/joim.20100","url":null,"abstract":"<p><p>Healthcare-associated infections (HAIs) are common adverse events, and surveillance is considered a core component of effective HAI reduction programmes. Recently, efforts have focused on automating the traditional manual surveillance process by utilizing data from electronic health record (EHR) systems. Using EHR data for automated surveillance, algorithms have been developed to identify patients with (ventilator-associated) pneumonia and (catheter-related) bloodstream, surgical site, (catheter-associated) urinary tract and Clostridioides difficile infections (sensitivity 54.2%-100%, specificity 63.5%-100%). Mostly methods based on natural language processing have been applied to extract information from unstructured clinical information. Further developments in artificial intelligence (AI), such as large language models, are expected to support and improve different aspects within the surveillance process; for example, more precise identification of patients with HAI. However, AI-based methods have been applied less frequently in automated surveillance and more frequently for (early) prediction, particularly for sepsis. Despite heterogeneity in settings, populations, definitions and model designs, AI-based models have shown promising results, with moderate to very good performance (accuracy 61%-99%) and predicted sepsis within 0-40 h before onset. AI-based prediction models detecting patients at risk of developing different HAIs should be explored further. The continuous evolution of AI and automation will transform HAI surveillance and prediction, offering more objective and timely infection rates and predictions. The implementation of (AI-supported) automated surveillance and prediction systems for HAI in daily practice remains scarce. Successful development and implementation of these systems demand meeting requirements related to technical capabilities, governance, practical and regulatory considerations and quality monitoring.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":" ","pages":""},"PeriodicalIF":9.0,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vincent Lak, Helen Sjöland, Martin Adiels, Christina E Lundberg, Josefina Robertson, Maria Åberg, Christian Alex, Martin Lindgren, Annika Rosengren
{"title":"Preexisting symptoms increase the risk of developing long COVID during the SARS-CoV-2 pandemic.","authors":"Vincent Lak, Helen Sjöland, Martin Adiels, Christina E Lundberg, Josefina Robertson, Maria Åberg, Christian Alex, Martin Lindgren, Annika Rosengren","doi":"10.1111/joim.20102","DOIUrl":"https://doi.org/10.1111/joim.20102","url":null,"abstract":"<p><strong>Background: </strong>Long COVID is defined as otherwise unexplained symptoms following a SARS-CoV-2 infection.</p><p><strong>Objective: </strong>To examine the prevalence of preexisting symptoms compatible with long COVID in individuals with a diagnosis of long COVID.</p><p><strong>Methods: </strong>This retrospective, observational study included the adult population (aged 18 years and older) in Region Västra Götaland, with at least one recorded healthcare contact between January 1, 2020, and November 30, 2023, from a regional database comprising all levels of healthcare contacts. Data on long COVID, relevant symptoms before and after the pandemic started (2016-2023), and SARS-CoV-2 infection status were extracted using the International Classification of Diseases version 10 (ICD-10) codes. Individuals who had been hospitalized due to a SARS-CoV-2 infection were considered separately.</p><p><strong>Results: </strong>Out of 1,415,885 individuals, 9202 (0.6%) had been diagnosed with long COVID. Among the non-hospitalized individuals, the record of at least one of the relevant symptoms was more common in those with long COVID compared to those without it (57.6% vs. 36.3% for men and 71.6% vs. 50.4% for women), already before January 1, 2020. Among individuals with any relevant symptom, the odds ratios (ORs) of having long COVID were OR = 2.28 (95% confidence interval [CI] = 2.10-2.48) for men and OR = 2.32 (95% CI = 2.18-2.48 for women) after adjusting for age group, obesity, asthma, and anxiety, compared with individuals without any relevant symptom.</p><p><strong>Conclusions: </strong>Individuals diagnosed with long COVID had more healthcare contacts for relevant symptoms even before the pandemic compared to individuals without long COVID.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":" ","pages":""},"PeriodicalIF":9.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144214410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shamila D. Alipoor, Parisa Norouzitallab, Anita Öst, Maria Lerm
{"title":"Dad's legacy: Epigenetic reprogramming and paternal inflammatory memory in offspring health","authors":"Shamila D. Alipoor, Parisa Norouzitallab, Anita Öst, Maria Lerm","doi":"10.1111/joim.20094","DOIUrl":"10.1111/joim.20094","url":null,"abstract":"<p>Over the past decade, numerous reports have highlighted intergenerational and even transgenerational epigenetic effects resulting from parental exposure to diets, toxins, and stress. In many cases, these parentally induced phenotypes do not seem to confer an obvious benefit, making it challenging to understand the evolutionary drivers behind them. In this perspective, we discuss recent observations in humans and rodents indicating that a parental infection or vaccination can enhance the offspring's ability to cope with infections. Such parental priming of their offspring's immune system and cellular defense would provide immediate protection to the newborn, offering a clear evolutionary advantage. Here, focusing mainly on paternal effects, we propose that a parentally induced inflammatory memory in the offspring could be the underlying mechanism for many of the reported inter- and transgenerational effects. Sperm-borne RNA could be a triggering signal to initiate inflammatory pathways in early embryogenesis. This gene-regulatory state would then be maintained via epigenetic mechanisms throughout each mitosis and last for the individual's lifetime. The accumulating understanding that diet, stress, toxins, and infections affect offspring health raises important questions about public health policies. There is an urgent need to understand what consequences different exposures during sensitive time windows have on future generations.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"298 1","pages":"16-30"},"PeriodicalIF":9.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.20094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nicole R. Fowler, Katherine A. Partrick, James Taylor, Michael Hornbecker, Kevin Kelleher, Malaz Boustani, Jeffrey L. Cummings, Tim MacLeod, Michelle M. Mielke, Jared R. Brosch, Janice Lee, Eli Shobin, James E. Galvin, Howard Fillit, Chinedu Udeh-Momoh, Deanna R. Willis
{"title":"Implementing early detection of cognitive impairment in primary care to improve care for older adults","authors":"Nicole R. Fowler, Katherine A. Partrick, James Taylor, Michael Hornbecker, Kevin Kelleher, Malaz Boustani, Jeffrey L. Cummings, Tim MacLeod, Michelle M. Mielke, Jared R. Brosch, Janice Lee, Eli Shobin, James E. Galvin, Howard Fillit, Chinedu Udeh-Momoh, Deanna R. Willis","doi":"10.1111/joim.20098","DOIUrl":"10.1111/joim.20098","url":null,"abstract":"<p>Primary care is the ideal setting for early detection of mild cognitive impairment (MCI) and Alzheimer's disease and related dementias (ADRD), as it serves as the primary point of care for most older adults. With the growing aging population, reliance on specialists for detection and diagnosis is unsustainable, highlighting the need for primary care-led assessment. Recent research findings on successful brain health prevention strategies, AD diagnostic tools, and anti-amyloid treatments empower primary care to play a central role in early detection and intervention. Primary care-focused resources are being developed, including tools for cognitive assessments and materials designed to educate patients about brain health and initiate discussions on lifestyle modifications, thereby making early detection more feasible and efficient. Identifying risk factors early enables providers to implement interventions that can slow cognitive decline and improve outcomes for patients and caregivers. If left undetected and unmanaged, MCI and ADRD can lead to worse outcomes, including increased falls, hospitalizations, financial vulnerability, and caregiver stress. Early detection enables the identification of reversible causes of cognitive impairment, supports the management of comorbidities worsened by cognitive decline, mitigates safety risks, and can preserve quality of life. Importantly, primary care is essential for addressing ADRD-related health disparities that disproportionately affect racial minorities, rural populations, and those of lower socioeconomic status. With a focus on the United States healthcare system, this perspective addresses how implementing early detection practices into primary care can improve outcomes for patients and caregivers, reduce societal burdens, and promote health equity in ADRD care.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"298 1","pages":"31-45"},"PeriodicalIF":9.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.20098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Adrian Post, Wendy A. Dam, Dion Groothof, Casper F. M. Franssen, Stephan J. L. Bakker, Robin P. F. Dullaart
{"title":"Higher circulating FGF21, lower protein intake, and lower muscle mass: Associations with a higher risk of mortality","authors":"Adrian Post, Wendy A. Dam, Dion Groothof, Casper F. M. Franssen, Stephan J. L. Bakker, Robin P. F. Dullaart","doi":"10.1111/joim.20099","DOIUrl":"10.1111/joim.20099","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Objectives</h3>\u0000 \u0000 <p>This population-based study explores associations of fibroblast growth factor 21 (FGF21), a key modulator of processes linked to protein metabolism, with protein intake and muscle mass, and their relationships with all-cause mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In 6395 participants (mean age 54 years; 50% women), circulating FGF21 (immunoassay), protein intake (Maroni equation using 24-h urinary urea excretion; low intake defined as <0.8 g/kg/day), and muscle mass (24-h creatinine excretion rate indexed to height squared (CERI)) were documented.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>FGF21 concentration was 896 (540–1384) pg/mL, protein intake was 1.01 (0.85–1.19) g/kg/day, and CERI was 4.1 ± 0.9 mmol/day/m<sup>2</sup>. Higher FGF21 was associated with higher odds of low protein intake (odds ratio per doubling: 1.48; 95% confidence interval [CI]: 1.38–1.58; <i>p</i> < 0.0001) and lower muscle mass (standardized beta: −0.08; 95% CI: −0.10; −0.06; <i>p</i> < 0.001). Over 10.4 years of follow-up, 955 deaths were registered. Higher FGF21 was associated with increased mortality (hazard ratio (HR) per doubling: 1.09; 95% CI: 1.02–1.16; <i>p</i> = 0.009). Conversely, higher protein intake (HR per doubling: 0.67; 95% CI: 0.56–0.81; <i>p</i> < 0.0001) and higher CERI (HR per standard deviation increase: 0.83; 95% CI: 0.76–0.90; <i>p</i> < 0.0001) were associated with a lower risk of mortality, independent of potential confounders. However, the FGF21-mortality association became non-significant after adjusting for protein intake.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Higher FGF21 was associated with higher odds of low protein intake. The observed association of higher FGF21 concentrations and risk mortality was predominantly attributable to lower protein intake. In contrast, both higher protein intake and higher muscle mass were independently associated with lower mortality risk, highlighting the potential relevance of protein intake and maintenance of muscle mass in long-term health.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"298 1","pages":"2-15"},"PeriodicalIF":9.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.20099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alfonso Giaquinto, Veronica Abate, Anita Vergatti, Riccardo Muscariello, Adelaide Iervolino, Martina Pucci, Guido Cavati, Filippo Pirrotta, Gianpaolo De Filippo, Roberta Esposito, Lanfranco D'Elia, Daniela Merlotti, Luigi Gennari, Domenico Rendina
{"title":"Standard and advanced echocardiographic study of patients with Paget's disease of bone: Evidence of a pagetic heart disease?","authors":"Alfonso Giaquinto, Veronica Abate, Anita Vergatti, Riccardo Muscariello, Adelaide Iervolino, Martina Pucci, Guido Cavati, Filippo Pirrotta, Gianpaolo De Filippo, Roberta Esposito, Lanfranco D'Elia, Daniela Merlotti, Luigi Gennari, Domenico Rendina","doi":"10.1111/joim.20069","DOIUrl":"10.1111/joim.20069","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Paget's disease of the bone (PDB) is a metabolic bone disorder involving one or more skeletal sites. Cardiovascular diseases (CVDs) have been described in patients with PDB but have not been systematically analysed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This study aimed to compare standard and advanced (speckle-tracking) echocardiographic parameters measured in patients with PDB and controls matched for age, weight, height and history of hypertension but without metabolic bone disorders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This multicentre case–control study included all patients with PDB referred to the Federico II and Siena Universities, Italy, from March 2019 to October 2022. During the same time, we enrolled at least one control for each patient, matched for age, sex, body mass index (BMI) and history of hypertension.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Sixty-nine patients with PDB and 115 healthy controls were enrolled in this study. All patients with PDB were treated with zoledronic acid at the time of diagnosis. Compared with controls, on standard echocardiography, patients with PDB showed a high prevalence of aortic and mitral valve calcifications and/or sclerosis, reduced left ventricular (LV) ejection fraction, stroke volume, cardiac output, increased interventricular septum thickness, posterior wall thickness, LV mass index, relative wall thickness, relative diastolic wall thickness, <i>E</i>/<i>e</i>′ ratio and systemic vascular resistance. Using speckle-tracking echocardiography, patients with PDB showed a lower global longitudinal strain and global myocardial work efficiency than controls. There was no relationship between the PDB activity and extent and severity of cardiac abnormalities.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Overall, the myocardial function and structure were impaired in patients with PDB. Additionally, PDB was associated with early subclinical myocardial damage.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"297 6","pages":"630-641"},"PeriodicalIF":9.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.20069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The yin–yang between clonal hematopoiesis of indeterminate potential and autoimmune diseases","authors":"Zachary Brady, Valeria Visconte","doi":"10.1111/joim.20091","DOIUrl":"10.1111/joim.20091","url":null,"abstract":"<p>The article by Wu et al. [<span>1</span>] in the <i>Journal of Internal Medicine</i> investigates the relation between clonal hematopoiesis of indeterminate potential (CHIP) and autoimmune diseases. The reason behind such relation might be attributed to changes in the immune system occurring with advanced age.</p><p>Indeed, CHIP is common in the elderly and asymptomatic. Individuals with CHIP have an increased risk of hematologic malignancies and chronic inflammatory diseases, such as cardiovascular disease [<span>2, 3</span>]. The latter has been associated to enhanced production of proinflammatory cytokines and accelerated atherosclerosis. More recently, studies have found associations between CHIP and multiple autoimmune diseases; specifically, large CHIP clones (>10% or >15%) were associated with an increased risk of seropositive rheumatoid arthritis (RA) and, to a lesser extent, RA [<span>4</span>]. Of note is that 60% of patients with the notable hemato-immunoinflammatory VEXAS syndrome have CHIP [<span>5</span>]. Observations from studies of Behçet's disease, a chronic inflammatory immune-mediated disorder, indicate that some extent of inflammation is associated with CHIP emergence [<span>6</span>].</p><p>Wu et al. [<span>1</span>] set out to address the interplay between CHIP and autoimmune diseases. To do so, the authors analyzed data collected from whole blood-derived exome sequencing (WES) of 456,692 UK Biobank participants after exclusion of (a) individuals with hematologic malignancies, (b) individuals with more than 10 third-degree relatives, (c) heterozygous outliers, and (d) participants with a baseline autoimmune disease. Overall, 19 immune-mediated inflammatory diseases were selected (Addison's disease, ankylosing spondylitis, coeliac disease, type 1 diabetes, Graves’ disease, Crohn's disease, ulcerative colitis, multiple sclerosis, myasthenia gravis, pernicious anemia, polymyalgia rheumatica, primary biliary cholangitis, psoriasis, RA, Sjögren's syndrome, systemic lupus erythematosus, systemic sclerosis, vasculitis, and vitiligo). Association between CHIP (with a variant allele frequency [VAF] more than (a) 2%, (b) 10%, and (c) specific CHIP mutation) was analyzed. In total, 58 CHIP genes were included.</p><p>Overall, 17,433 (3.82%) individuals had any CHIP (<i>DNMT3A</i> [2.40%] with p.R882H being the most common mutation, <i>TET2</i> [0.47%], <i>ASXL1</i> variants [0.25%], spliceosomal genes [0.11%], and <i>PPM1D</i> [0.11%] variants). More than one CHIP mutation was detected in 6.10% of individuals. Specific CHIP mutations were associated with different autoimmune diseases. A large part of the study focuses on making inflammation the central node between CHIP and autoimmune disorders. However, as per today, this connection is still very vague and rather inconclusive due to the high number of inflammatory markers possibly involved in the process and the inability to assess all of them.</p><p>A point of discussion rem","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"297 6","pages":"558-559"},"PeriodicalIF":9.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.20091","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}