Kamal Awad, Ahmed K. Mahmoud, Hesham Sheashaa, Mohammed Tiseer Abbas, Milagros Pereyra Pietri, Isabel G. Scalia, Fatmaelzahraa Abdelfattah, Mahshad Razaghi, Hana Mousa, Ramzi Ibrahim, Juan M. Farina, Steven J. Lester, Chadi Ayoub, Reza Arsanjani
{"title":"Risk of rhabdomyolysis with concomitant use of statins and SGLT2 inhibitors: A population-based cohort study","authors":"Kamal Awad, Ahmed K. Mahmoud, Hesham Sheashaa, Mohammed Tiseer Abbas, Milagros Pereyra Pietri, Isabel G. Scalia, Fatmaelzahraa Abdelfattah, Mahshad Razaghi, Hana Mousa, Ramzi Ibrahim, Juan M. Farina, Steven J. Lester, Chadi Ayoub, Reza Arsanjani","doi":"10.1111/joim.70062","DOIUrl":"10.1111/joim.70062","url":null,"abstract":"","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 3","pages":"417-419"},"PeriodicalIF":9.2,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802822","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}
Susanne Lundin, Rui Liu, Markus Idvall, Samuel Lundgren, Annika Tibell, Gabriel C. Oniscu
{"title":"The complexity of public attitudes towards xenotransplantation: A web survey among the Swedish population","authors":"Susanne Lundin, Rui Liu, Markus Idvall, Samuel Lundgren, Annika Tibell, Gabriel C. Oniscu","doi":"10.1111/joim.70054","DOIUrl":"10.1111/joim.70054","url":null,"abstract":"","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 3","pages":"414-416"},"PeriodicalIF":9.2,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145766686","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}
Maxime Billotte, Thomas Moulinet, Alain Meyer, Houda Camara, Loïs Bolko, Kévin Didier, Sandra Dury, Bernard Bonnotte, Hervé Devilliers, Philippe Bonniaud, Guillaume Beltramo, Julien Campagne, Nadine Magy-Bertrand, Aurore Chaudier, Simon Valentin, Roland Jaussaud, Paul Decker
Objectives
To assess factors associated with rapidly progressive interstitial lung disease (ILD) (RP-ILD) at time of ILD diagnosis in a multicentric retrospective cohort study of antisynthetase syndrome (ASyS). We used a complementary unsupervised approach, hierarchical clustering, to delineate distinct phenotypes among ASyS patients with ILD.
Methods
A total of 132 patients with ASyS, defined according to the 2024 ACR/European Alliance of Associations for Rheumatology (EULAR) ASyS classification criteria, and ILD, diagnosed by CT scan, were included. RP-ILD was defined by the presence of respiratory failure at ILD diagnosis or rapid ILD progression during the first 3 months.
Results
In our study, 39% of patients had RP-ILD at ILD diagnosis. Multivariate logistic regression analysis with cluster-robust SE identified the factors associated with RP-ILD at ILD diagnosis as male sex (aOR = 9.7 [1.6–59.5], p = 0.006), fever (aOR = 128 [12.6–1300], p < 0.001), organizing pneumonia (OP) pattern (aOR = 66.8 [3.4–1316], p = 0.006), and pleural effusion (aOR = 20.2 [1.1–373], p = 0.04), whereas RP-ILD was associated with lower likelihood of severe muscle disease (aOR = 0.004 [0.0001–0.13], p = 0.002). Clustering analysis identified four distinct groups: Cluster 1 (n = 62) included patients with systemic presentation, non-RP-ILD at ILD diagnosis, and anti-Jo-1 antibodies with good prognosis; Cluster 2 (n = 40) included older age patients with more RP-ILD at ILD diagnosis, pleuropericarditis, and a higher mortality rate.
Conclusion
Fever, pleural effusion, and OP pattern were independently associated with RP-ILD in ASyS patients. Unsupervised cluster analysis identified a severe inflammatory phenotype in ASyS patients with ILD.
{"title":"Clinical profiles associated with rapidly progressive interstitial lung disease in antisynthetase syndrome: A multicentric cohort study (TYPASS study)","authors":"Maxime Billotte, Thomas Moulinet, Alain Meyer, Houda Camara, Loïs Bolko, Kévin Didier, Sandra Dury, Bernard Bonnotte, Hervé Devilliers, Philippe Bonniaud, Guillaume Beltramo, Julien Campagne, Nadine Magy-Bertrand, Aurore Chaudier, Simon Valentin, Roland Jaussaud, Paul Decker","doi":"10.1111/joim.70058","DOIUrl":"10.1111/joim.70058","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>To assess factors associated with rapidly progressive interstitial lung disease (ILD) (RP-ILD) at time of ILD diagnosis in a multicentric retrospective cohort study of antisynthetase syndrome (ASyS). We used a complementary unsupervised approach, hierarchical clustering, to delineate distinct phenotypes among ASyS patients with ILD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 132 patients with ASyS, defined according to the 2024 ACR/European Alliance of Associations for Rheumatology (EULAR) ASyS classification criteria, and ILD, diagnosed by CT scan, were included. RP-ILD was defined by the presence of respiratory failure at ILD diagnosis or rapid ILD progression during the first 3 months.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In our study, 39% of patients had RP-ILD at ILD diagnosis. Multivariate logistic regression analysis with cluster-robust SE identified the factors associated with RP-ILD at ILD diagnosis as male sex (aOR = 9.7 [1.6–59.5], <i>p</i> = 0.006), fever (aOR = 128 [12.6–1300], <i>p</i> < 0.001), organizing pneumonia (OP) pattern (aOR = 66.8 [3.4–1316], <i>p</i> = 0.006), and pleural effusion (aOR = 20.2 [1.1–373], <i>p</i> = 0.04), whereas RP-ILD was associated with lower likelihood of severe muscle disease (aOR = 0.004 [0.0001–0.13], <i>p</i> = 0.002). Clustering analysis identified four distinct groups: Cluster 1 (<i>n</i> = 62) included patients with systemic presentation, non-RP-ILD at ILD diagnosis, and anti-Jo-1 antibodies with good prognosis; Cluster 2 (<i>n</i> = 40) included older age patients with more RP-ILD at ILD diagnosis, pleuropericarditis, and a higher mortality rate.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Fever, pleural effusion, and OP pattern were independently associated with RP-ILD in ASyS patients. Unsupervised cluster analysis identified a severe inflammatory phenotype in ASyS patients with ILD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 3","pages":"365-380"},"PeriodicalIF":9.2,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12869006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720212","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}
Gene therapy is emerging as a groundbreaking strategy for treating epilepsy, offering new hope to patients who do not respond to conventional medications. Despite advancements in anti-seizure treatments, nearly 30%–40% of individuals with epilepsy continue to experience uncontrolled seizures, highlighting the urgent need for more effective and long-lasting solutions. By addressing the underlying causes of epilepsy at the genetic level, gene therapy represents a paradigm shift in treatment. Two key approaches are being explored: (1) activating or supplementing beneficial genes to suppress seizures and (2) silencing harmful genes or pathways that contribute to epilepsy. To achieve these objectives, viral vectors, such as adeno-associated viruses and lentiviruses, have shown promise in delivering targeted genetic interventions. In parallel, cutting-edge techniques such as optogenetics, chemogenetics, and clustered regularly interspaced short palindromic repeat-based gene editing are enhancing the precision of these therapies, enabling greater control over neuronal activity. However, significant challenges exist, including ensuring safe and efficient gene delivery, maintaining long-term therapeutic effects, and mitigating potential side effects. This review examines recent developments in gene therapy for epilepsy, assessing its potential to deliver targeted, long-lasting treatments for drug-resistant epilepsy. By examining current strategies, therapeutic targets, and emerging technologies, it provides insights into the promising future of gene therapy as a transformative tool in epilepsy treatment and summarizes current clinical trials utilizing gene and cell therapy technologies for epilepsy.
{"title":"Gene therapy for epilepsy: An emerging, promising approach for a serious neurological disorder","authors":"Marco Ledri, Merab Kokaia","doi":"10.1111/joim.70059","DOIUrl":"10.1111/joim.70059","url":null,"abstract":"<p>Gene therapy is emerging as a groundbreaking strategy for treating epilepsy, offering new hope to patients who do not respond to conventional medications. Despite advancements in anti-seizure treatments, nearly 30%–40% of individuals with epilepsy continue to experience uncontrolled seizures, highlighting the urgent need for more effective and long-lasting solutions. By addressing the underlying causes of epilepsy at the genetic level, gene therapy represents a paradigm shift in treatment. Two key approaches are being explored: (1) activating or supplementing beneficial genes to suppress seizures and (2) silencing harmful genes or pathways that contribute to epilepsy. To achieve these objectives, viral vectors, such as adeno-associated viruses and lentiviruses, have shown promise in delivering targeted genetic interventions. In parallel, cutting-edge techniques such as optogenetics, chemogenetics, and clustered regularly interspaced short palindromic repeat-based gene editing are enhancing the precision of these therapies, enabling greater control over neuronal activity. However, significant challenges exist, including ensuring safe and efficient gene delivery, maintaining long-term therapeutic effects, and mitigating potential side effects. This review examines recent developments in gene therapy for epilepsy, assessing its potential to deliver targeted, long-lasting treatments for drug-resistant epilepsy. By examining current strategies, therapeutic targets, and emerging technologies, it provides insights into the promising future of gene therapy as a transformative tool in epilepsy treatment and summarizes current clinical trials utilizing gene and cell therapy technologies for epilepsy.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 3","pages":"302-327"},"PeriodicalIF":9.2,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12869011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712876","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}
Federica Pallotti, Camille Mettler, Matthias Papo, Michele Iudici, Roberto Padoan, Boris Sorin, Francesca Regola, Franco Franceschini, Sergey Moiseev, Pavel Novikov, Mario Andrea Piga, Gianluca Moroncini, Silke R. Brix, Abdul Hadi Kafagi, Samuel Deshayes, Achille Aouba, Julien Campagne, Paolo Delvino, Jan Willem Cohen Tervaert, Luisa Brussino, Martin Michaud, Nils Venhoff, Federico Alberici, Claudia Iannone, Sophie Rosenstingl, Marin Moutel, Jean-Marc Galempoix, Vincent Cottin, Clara Jaccard, Diane Riehl, Paul Legendre, Anne Claire Billet, Paola Parronchi, Luca Quartuccio, Vitor Teixeira, Allyson Egan, David Jayne, Enrico Tombetti, Marco Caminati, Christian Pagnoux, Alexis Regent, Marc Ruivard, Loïc Guillevin, Xavier Puéchal, Benjamin Terrier, the French Vasculitis Study Group (FVSG)
Background
Granulomatosis with polyangiitis (GPA) and eosinophilic granulomatosis with polyangiitis (EGPA) are distinct forms of antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV). Increasing evidence suggests overlapping features, particularly in proteinase 3 (PR3)-ANCA-positive EGPA and GPA with eosinophilia. This study aimed to characterize overlapping EGPA/GPA forms and assess their clinical and therapeutic implications.
Methods
We conducted a European, multicenter, observational study, including 135 patients with overlapping EGPA/GPA features. Definitions were based on ACR/EULAR classification criteria and other clinical and biological findings. Clinical, biological, and histological characteristics were analyzed using unsupervised hierarchical clustering approach. Comparisons were made with established EGPA and GPA control cohorts.
Results
Three clusters emerged: Cluster 1, a hybrid phenotype (pulmonary nodules, PR3-ANCA positivity, high relapse rate); Cluster 2, a systemic inflammatory phenotype (constitutional symptoms, PR3-ANCA positivity, moderate renal involvement); and Cluster 3, a severe vasculitis form (severe renal disease, alveolar hemorrhage). Including typical EGPA and GPA control cohorts revealed two main clusters a posteriori: an EGPA cluster and a GPA cluster. Cluster 1 overlapped with both EGPA and GPA clusters, whereas Clusters 2 and 3 predominantly aligned with GPA. Kaplan–Meier analysis revealed that Cluster 1 and the typical EGPA cohort had the best overall survival, whereas Cluster 3 had the poorest survival. Relapse-free survival was highest in typical EGPA and poorest in Cluster 3 and typical GPA.
Conclusion
This study delineates the heterogeneity of EGPA/GPA overlap and underscores the need for personalized treatment approaches. Future prospective studies should explore targeted therapies, including rituximab and IL-5 blockade, in these overlapping AAV subtypes.
{"title":"Overlapping forms of granulomatosis with polyangiitis and eosinophilic granulomatosis with polyangiitis: Insights from a European multicenter study","authors":"Federica Pallotti, Camille Mettler, Matthias Papo, Michele Iudici, Roberto Padoan, Boris Sorin, Francesca Regola, Franco Franceschini, Sergey Moiseev, Pavel Novikov, Mario Andrea Piga, Gianluca Moroncini, Silke R. Brix, Abdul Hadi Kafagi, Samuel Deshayes, Achille Aouba, Julien Campagne, Paolo Delvino, Jan Willem Cohen Tervaert, Luisa Brussino, Martin Michaud, Nils Venhoff, Federico Alberici, Claudia Iannone, Sophie Rosenstingl, Marin Moutel, Jean-Marc Galempoix, Vincent Cottin, Clara Jaccard, Diane Riehl, Paul Legendre, Anne Claire Billet, Paola Parronchi, Luca Quartuccio, Vitor Teixeira, Allyson Egan, David Jayne, Enrico Tombetti, Marco Caminati, Christian Pagnoux, Alexis Regent, Marc Ruivard, Loïc Guillevin, Xavier Puéchal, Benjamin Terrier, the French Vasculitis Study Group (FVSG)","doi":"10.1111/joim.70056","DOIUrl":"10.1111/joim.70056","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Granulomatosis with polyangiitis (GPA) and eosinophilic granulomatosis with polyangiitis (EGPA) are distinct forms of antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV). Increasing evidence suggests overlapping features, particularly in proteinase 3 (PR3)-ANCA-positive EGPA and GPA with eosinophilia. This study aimed to characterize overlapping EGPA/GPA forms and assess their clinical and therapeutic implications.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a European, multicenter, observational study, including 135 patients with overlapping EGPA/GPA features. Definitions were based on ACR/EULAR classification criteria and other clinical and biological findings. Clinical, biological, and histological characteristics were analyzed using unsupervised hierarchical clustering approach. Comparisons were made with established EGPA and GPA control cohorts.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Three clusters emerged: Cluster 1, a hybrid phenotype (pulmonary nodules, PR3-ANCA positivity, high relapse rate); Cluster 2, a systemic inflammatory phenotype (constitutional symptoms, PR3-ANCA positivity, moderate renal involvement); and Cluster 3, a severe vasculitis form (severe renal disease, alveolar hemorrhage). Including typical EGPA and GPA control cohorts revealed two main clusters a posteriori: an EGPA cluster and a GPA cluster. Cluster 1 overlapped with both EGPA and GPA clusters, whereas Clusters 2 and 3 predominantly aligned with GPA. Kaplan–Meier analysis revealed that Cluster 1 and the typical EGPA cohort had the best overall survival, whereas Cluster 3 had the poorest survival. Relapse-free survival was highest in typical EGPA and poorest in Cluster 3 and typical GPA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study delineates the heterogeneity of EGPA/GPA overlap and underscores the need for personalized treatment approaches. Future prospective studies should explore targeted therapies, including rituximab and IL-5 blockade, in these overlapping AAV subtypes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 3","pages":"349-364"},"PeriodicalIF":9.2,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12869015/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712860","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}
Håkon Bøås, Paz Lopez-Doriga Ruiz, Jesper Dahl, Hanne L. Gulseth, German Tapia
Background
Studies suggest an increase in autoimmune diseases following SARS-CoV-2 infection and/or COVID-19-vaccination. We aimed to describe possible associations in Norway.
Methods
We used information from the emergency preparedness register for COVID-19, BeredtC19, for all residents aged 18–64 (N = 3,450,080). BeredtC19 includes data from mandatory nationwide registers on demographics, SARS-CoV-2 tests, deaths, vaccinations, and hospitalizations. Cox regression was used to estimate adjusted hazard ratios (aHRs) for 30-day and 30–180 day risk windows.
Findings
SARS-CoV-2 infection was associated with an increased risk of purpura, thrombocytopenia, and agranulocytosis within 30 days and 30–180 days. In the first 30 days, Bell's palsy and inflammatory arthritis were associated with infection, whereas 30–180 days postinfection showed an association with polyneuropathy. Vaccination was associated with an increased risk of inflammatory bowel disease (IBD) and celiac disease, both in the first 30 days and 30–180 days postvaccination. Additionally, in the first 30 days postvaccination, we found associations with inflammatory arthritis and erythema nodosum, and between 30 and 180 days with arthralgia, agranulocytosis, and acute disseminated encephalomyelitis (ADEM). There was also a reduced risk of dermatopolymyositis 30–180 days postvaccination.
Interpretation
Most autoimmune disorders showed no significant association with SARS-CoV-2 infection or COVID-19 vaccination. Associations between vaccination and IBD and ADEM warrant further investigations, as these observations reflect associations and do not establish causality.
{"title":"New-onset autoimmune disease following SARS-CoV-2 infection and mRNA vaccination in Norway: A retrospective cohort study","authors":"Håkon Bøås, Paz Lopez-Doriga Ruiz, Jesper Dahl, Hanne L. Gulseth, German Tapia","doi":"10.1111/joim.70052","DOIUrl":"10.1111/joim.70052","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Studies suggest an increase in autoimmune diseases following SARS-CoV-2 infection and/or COVID-19-vaccination. We aimed to describe possible associations in Norway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used information from the emergency preparedness register for COVID-19, BeredtC19, for all residents aged 18–64 (<i>N</i> = 3,450,080). BeredtC19 includes data from mandatory nationwide registers on demographics, SARS-CoV-2 tests, deaths, vaccinations, and hospitalizations. Cox regression was used to estimate adjusted hazard ratios (aHRs) for 30-day and 30–180 day risk windows.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Findings</h3>\u0000 \u0000 <p>SARS-CoV-2 infection was associated with an increased risk of purpura, thrombocytopenia, and agranulocytosis within 30 days and 30–180 days. In the first 30 days, Bell's palsy and inflammatory arthritis were associated with infection, whereas 30–180 days postinfection showed an association with polyneuropathy. Vaccination was associated with an increased risk of inflammatory bowel disease (IBD) and celiac disease, both in the first 30 days and 30–180 days postvaccination. Additionally, in the first 30 days postvaccination, we found associations with inflammatory arthritis and erythema nodosum, and between 30 and 180 days with arthralgia, agranulocytosis, and acute disseminated encephalomyelitis (ADEM). There was also a reduced risk of dermatopolymyositis 30–180 days postvaccination.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Interpretation</h3>\u0000 \u0000 <p>Most autoimmune disorders showed no significant association with SARS-CoV-2 infection or COVID-19 vaccination. Associations between vaccination and IBD and ADEM warrant further investigations, as these observations reflect associations and do not establish causality.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 2","pages":"271-282"},"PeriodicalIF":9.2,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12789287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660047","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}
Maria Dons, Charlotte Näslund-Koch, Morten Sengeløv, Sofie Bøgh-Sørensen, Kristoffer Grundtvig Skaarup, Marianne Bengtson Løvendorf, Filip Soeskov Davidovski, Anne Marie Reimer Jensen, Brittany N. Weber, Lise Lotte Gluud, Claus Zachariae, Lone Skov, Tor Biering-Sørensen
Background
Individuals with psoriasis have a high prevalence of metabolic dysfunction–associated steatotic liver disease (MASLD), yet the association between MASLD as a cardiometabolic risk factor and cardiac manifestations in this population remains unclear.
Objectives
We aimed to evaluate associations between MASLD, cardiometabolic risk factors, and cardiac structure and function in adults with psoriasis.
Methods
We performed a cross-sectional analysis of 255 adults with psoriasis prospectively enrolled. Participants underwent transthoracic echocardiography and transient elastography. MASLD was defined by hepatic steatosis with a controlled attenuation parameter of ≥250 dB/m and the presence of ≥1 cardiometabolic risk factor(s), excluding other liver disease causes. Cardiac structure and function were compared between individuals with psoriasis and MASLD and those without MASLD. Associations between MASLD and myocardial dysfunction were assessed in uni- and multivariable regression models.
Results
MASLD was present in 92 participants (36.1%), of whom 5 (5.4%) had evidence of increased liver stiffness. Those with MASLD exhibited higher blood pressure, body mass index (BMI), and more adverse cardiometabolic profiles. MASLD was associated with cardiac structural changes and worse diastolic and systolic function. After adjusting for age, sex, and BMI, most associations were attenuated. In fully adjusted models, higher BMI and diabetes, but not MASLD, were independently associated with myocardial dysfunction.
Conclusions
In adults with psoriasis, the association between MASLD and cardiac structural and functional changes was attenuated after adjusting for BMI and cardiometabolic risk factors, underscoring the importance of cardiometabolic risk factor control, in particular of obesity and diabetes, in psoriasis with concomitant MASLD.
{"title":"Metabolic dysfunction-associated steatotic liver disease, cardiometabolic risk factors, and cardiac manifestations in psoriasis: A cross-sectional study of 255 patients","authors":"Maria Dons, Charlotte Näslund-Koch, Morten Sengeløv, Sofie Bøgh-Sørensen, Kristoffer Grundtvig Skaarup, Marianne Bengtson Løvendorf, Filip Soeskov Davidovski, Anne Marie Reimer Jensen, Brittany N. Weber, Lise Lotte Gluud, Claus Zachariae, Lone Skov, Tor Biering-Sørensen","doi":"10.1111/joim.70053","DOIUrl":"10.1111/joim.70053","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Individuals with psoriasis have a high prevalence of metabolic dysfunction–associated steatotic liver disease (MASLD), yet the association between MASLD as a cardiometabolic risk factor and cardiac manifestations in this population remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>We aimed to evaluate associations between MASLD, cardiometabolic risk factors, and cardiac structure and function in adults with psoriasis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We performed a cross-sectional analysis of 255 adults with psoriasis prospectively enrolled. Participants underwent transthoracic echocardiography and transient elastography. MASLD was defined by hepatic steatosis with a controlled attenuation parameter of ≥250 dB/m and the presence of ≥1 cardiometabolic risk factor(s), excluding other liver disease causes. Cardiac structure and function were compared between individuals with psoriasis and MASLD and those without MASLD. Associations between MASLD and myocardial dysfunction were assessed in uni- and multivariable regression models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>MASLD was present in 92 participants (36.1%), of whom 5 (5.4%) had evidence of increased liver stiffness. Those with MASLD exhibited higher blood pressure, body mass index (BMI), and more adverse cardiometabolic profiles. MASLD was associated with cardiac structural changes and worse diastolic and systolic function. After adjusting for age, sex, and BMI, most associations were attenuated. In fully adjusted models, higher BMI and diabetes, but not MASLD, were independently associated with myocardial dysfunction.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In adults with psoriasis, the association between MASLD and cardiac structural and functional changes was attenuated after adjusting for BMI and cardiometabolic risk factors, underscoring the importance of cardiometabolic risk factor control, in particular of obesity and diabetes, in psoriasis with concomitant MASLD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 2","pages":"283-299"},"PeriodicalIF":9.2,"publicationDate":"2025-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627392","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}
Martin Lindgren, Helen Sjöland, Demir Djekic, Josefina Robertson, Maria Åberg, Erik Thunström, Zacharias Mandalenakis, Jon Edqvist, Christina E. Lundberg, Martin Adiels, Annika Rosengren
Background
The long-term risk across severity strata of people infected with SARS-CoV-2 has not yet been comprehensively described.
Methods
Using nationwide registries, all COVID-19 cases in Sweden with <2 vaccine doses, with and without initial hospitalization (February 1, 2020 to June 30, 2022), were identified and matched with non-COVID comparators. Participants were followed during the early, intermediate, long-term, and extended phases (365+ days) regarding death, acute myocardial infarction (AMI), ischemic stroke (IS), or heart failure (HF), and a composite of major adverse cardiovascular events (MACEs). Hazard ratios (HRs) were estimated using Cox proportional hazard regression adjusted for age, sex, obesity, hypertension, need of assisted living, Nordic origin, education, and Charlson Comorbidity Index.
Results
We identified 1,024,623 nonhospitalized (mean age: 40.4 years, 48.1% men) and 49,855 hospitalized (mean age: 58.8 years, 58.9% men) COVID-19 cases who were matched with 1,022,266 and 249,142 non-COVID comparators, respectively. Overall, nonhospitalized cases had no remaining risk of MACE past the early phase following COVID-19 infection. Among hospitalized cases, the risk of MACE remained elevated into the long-term and extended follow-up period (HRs 1.70 [confidence interval (CI) = 1.56–1.86] and 1.62 [CI = 1.51–1.72]) compared with comparators. After 365 days, they had a persistently increased risk of death (HR = 1.75, CI = 1.62–1.89), IS (HR = 1.40, CI = 1.18–1.67), HF (HR = 2.07, CI = 1.74–2.45), and AMI (HR = 1.28, CI = 1.07–1.53), compared with non-COVID comparators.
Conclusions
Hospitalized COVID-19 cases continued to have a nearly doubled risk of cardiovascular events and death after the first year of follow-up, whereas nonhospitalized cases had risks comparable to population comparators.
背景：SARS-CoV-2感染人群不同严重程度的长期风险尚未得到全面描述。结果：我们确定了1,024,623例未住院（平均年龄：40.4岁，男性48.1%）和49,855例住院（平均年龄：58.8岁，男性58.9%）的COVID-19病例，他们分别与1,022266例和249,142例非covid比较者匹配。总体而言，未住院的病例在COVID-19感染后的早期阶段没有剩余的MACE风险。在住院病例中，与比较组相比，MACE的风险在长期随访和延长随访期间仍然升高（hr为1.70[置信区间(CI) = 1.56-1.86]和1.62 [CI = 1.51-1.72]）。365天后，与非covid比较者相比，他们的死亡风险持续增加（HR = 1.75, CI = 1.62-1.89）、IS （HR = 1.40, CI = 1.18-1.67）、HF （HR = 2.07, CI = 1.74-2.45）和AMI （HR = 1.28, CI = 1.07-1.53）。结论：住院的COVID-19病例在随访一年后心血管事件和死亡的风险几乎翻了一番，而非住院病例的风险与人群比较者相当。
{"title":"Long-term risk of cardiovascular events after COVID-19 in the Swedish adult population—A matched cohort study","authors":"Martin Lindgren, Helen Sjöland, Demir Djekic, Josefina Robertson, Maria Åberg, Erik Thunström, Zacharias Mandalenakis, Jon Edqvist, Christina E. Lundberg, Martin Adiels, Annika Rosengren","doi":"10.1111/joim.70048","DOIUrl":"10.1111/joim.70048","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The long-term risk across severity strata of people infected with SARS-CoV-2 has not yet been comprehensively described.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using nationwide registries, all COVID-19 cases in Sweden with <2 vaccine doses, with and without initial hospitalization (February 1, 2020 to June 30, 2022), were identified and matched with non-COVID comparators. Participants were followed during the early, intermediate, long-term, and extended phases (365+ days) regarding death, acute myocardial infarction (AMI), ischemic stroke (IS), or heart failure (HF), and a composite of major adverse cardiovascular events (MACEs). Hazard ratios (HRs) were estimated using Cox proportional hazard regression adjusted for age, sex, obesity, hypertension, need of assisted living, Nordic origin, education, and Charlson Comorbidity Index.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We identified 1,024,623 nonhospitalized (mean age: 40.4 years, 48.1% men) and 49,855 hospitalized (mean age: 58.8 years, 58.9% men) COVID-19 cases who were matched with 1,022,266 and 249,142 non-COVID comparators, respectively. Overall, nonhospitalized cases had no remaining risk of MACE past the early phase following COVID-19 infection. Among hospitalized cases, the risk of MACE remained elevated into the long-term and extended follow-up period (HRs 1.70 [confidence interval (CI) = 1.56–1.86] and 1.62 [CI = 1.51–1.72]) compared with comparators. After 365 days, they had a persistently increased risk of death (HR = 1.75, CI = 1.62–1.89), IS (HR = 1.40, CI = 1.18–1.67), HF (HR = 2.07, CI = 1.74–2.45), and AMI (HR = 1.28, CI = 1.07–1.53), compared with non-COVID comparators.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Hospitalized COVID-19 cases continued to have a nearly doubled risk of cardiovascular events and death after the first year of follow-up, whereas nonhospitalized cases had risks comparable to population comparators.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 2","pages":"241-254"},"PeriodicalIF":9.2,"publicationDate":"2025-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12789278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627351","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}
Maria Bygdell, Erik Bülow, Simon B. Larsson, Robert Sigström, Huiqi Li, Jari Martikainen, Ailiana Santosa, Lisa Lundberg-Morris, Susannah Leach, Magnus Gisslén, Carl Bonander, Jörgen Månsson, Kristoffer Strålin, Fredrik Nyberg
Background and objective
Post-infectious sequelae can increase burden on healthcare systems. We aimed to assess the long-term effect of COVID-19 on healthcare utilization across all levels of care.
Methods
In this register-based cohort study, we included all adult (≥18 years) residents in Sweden's two largest counties with a registered COVID-19 index date between 31 January 2020 and 9 February 2022. Each exposed individual was matched 1:1 to a control without registered COVID-19 on index date based on gender, birth year, vaccination status and the change in number of healthcare contacts between 2018 and 2019. We counted the number of healthcare contacts across all levels of care during the pre-index (13–1 months) and post-index (4–15 months) full-year periods. A difference-in-difference (DID) analysis was used to assess changes in the number of healthcare contacts and specific diagnoses, between each individual's pre- and post-periods, as well as comparing individuals with and without COVID-19.
Results
The study included 753,905 matched pairs, comprising 1,415,432 unique individuals. Trends in healthcare contacts were parallel between the matched groups prior to the index date. The DID analysis revealed a mean increase of 0.33 (95%CI 0.30–0.36) healthcare contacts following COVID-19, mainly observed from a smaller proportion of the population (5%) and by contacts with primary healthcare. The largest diagnosis-specific difference was observed for reactions to severe stress (0.02, 0.01–0.03). The estimate varied across gender, acute COVID-19 severity, virus variant period and vaccination status.
Conclusion
This study demonstrates increased healthcare utilization after COVID-19 in a smaller proportion of the population.
{"title":"Change in healthcare utilization before and after COVID-19 using data from 1.5 million individuals","authors":"Maria Bygdell, Erik Bülow, Simon B. Larsson, Robert Sigström, Huiqi Li, Jari Martikainen, Ailiana Santosa, Lisa Lundberg-Morris, Susannah Leach, Magnus Gisslén, Carl Bonander, Jörgen Månsson, Kristoffer Strålin, Fredrik Nyberg","doi":"10.1111/joim.70051","DOIUrl":"10.1111/joim.70051","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and objective</h3>\u0000 \u0000 <p>Post-infectious sequelae can increase burden on healthcare systems. We aimed to assess the long-term effect of COVID-19 on healthcare utilization across all levels of care.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this register-based cohort study, we included all adult (≥18 years) residents in Sweden's two largest counties with a registered COVID-19 index date between 31 January 2020 and 9 February 2022. Each exposed individual was matched 1:1 to a control without registered COVID-19 on index date based on gender, birth year, vaccination status and the change in number of healthcare contacts between 2018 and 2019. We counted the number of healthcare contacts across all levels of care during the pre-index (13–1 months) and post-index (4–15 months) full-year periods. A difference-in-difference (DID) analysis was used to assess changes in the number of healthcare contacts and specific diagnoses, between each individual's pre- and post-periods, as well as comparing individuals with and without COVID-19.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study included 753,905 matched pairs, comprising 1,415,432 unique individuals. Trends in healthcare contacts were parallel between the matched groups prior to the index date. The DID analysis revealed a mean increase of 0.33 (95%CI 0.30–0.36) healthcare contacts following COVID-19, mainly observed from a smaller proportion of the population (5%) and by contacts with primary healthcare. The largest diagnosis-specific difference was observed for reactions to severe stress (0.02, 0.01–0.03). The estimate varied across gender, acute COVID-19 severity, virus variant period and vaccination status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study demonstrates increased healthcare utilization after COVID-19 in a smaller proportion of the population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 2","pages":"255-270"},"PeriodicalIF":9.2,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12789290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627334","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}
Xiaoying Kang, David Bergman, Jiangwei Sun, Karin Wirdefeldt, Jonas F. Ludvigsson
Background
The microbiota–gut–brain axis has been implicated in dementia. Yet whether dementia is associated with microscopic colitis (MC), an age-related inflammatory colonic disease involving gut dysbiosis, remains unknown.
Methods
Using the nationwide ESPRESSO cohort in Sweden, we compared MC patients histologically diagnosed 1990–2017 and aged ≥30 years to their population-based comparators and siblings, separately. MC association with incident and prevalent dementia diagnosis, respectively, was investigated in a matched cohort and a matched case-control design.
Findings
Following 13,037 MC patients and 61,710 population comparators for a median of ∼10 years, we observed 4674 incident dementia cases (46% were Alzheimer's disease [AD]). During the first 5 years since biopsy, MC was associated with a 19% higher dementia risk (adjusted hazard ratio [aHR]: 1.19; 95% confidence interval [CI]: 1.07–1.32). This short-term association applied to both AD and vascular dementia and appeared stronger as compared to siblings (aHR: 1.55; 95% CI: 1.22–1.97). After 5 years, it attenuated to null in both comparisons, regardless of dementia subtype. Prior dementia was less prevalent in MC (adjusted odds ratio [aOR]: 0.73; 95% CI: 0.65–0.82). This inverse association was independent from medications commonly prescribed in MC but was not supported by sibling findings (aOR: 1.11; 95% CI: 0.81–1.51).
Conclusions
MC patients may be more vulnerable to dementia diagnosis in early disease course. The intriguing inverse association between MC and preexisting dementia implies a possible underdiagnosis of MC in demented population and warrants further investigation.
{"title":"Microscopic colitis is associated with an increased risk of dementia in a Swedish population","authors":"Xiaoying Kang, David Bergman, Jiangwei Sun, Karin Wirdefeldt, Jonas F. Ludvigsson","doi":"10.1111/joim.70046","DOIUrl":"10.1111/joim.70046","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The microbiota–gut–brain axis has been implicated in dementia. Yet whether dementia is associated with microscopic colitis (MC), an age-related inflammatory colonic disease involving gut dysbiosis, remains unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using the nationwide ESPRESSO cohort in Sweden, we compared MC patients histologically diagnosed 1990–2017 and aged ≥30 years to their population-based comparators and siblings, separately. MC association with incident and prevalent dementia diagnosis, respectively, was investigated in a matched cohort and a matched case-control design.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Findings</h3>\u0000 \u0000 <p>Following 13,037 MC patients and 61,710 population comparators for a median of ∼10 years, we observed 4674 incident dementia cases (46% were Alzheimer's disease [AD]). During the first 5 years since biopsy, MC was associated with a 19% higher dementia risk (adjusted hazard ratio [aHR]: 1.19; 95% confidence interval [CI]: 1.07–1.32). This short-term association applied to both AD and vascular dementia and appeared stronger as compared to siblings (aHR: 1.55; 95% CI: 1.22–1.97). After 5 years, it attenuated to null in both comparisons, regardless of dementia subtype. Prior dementia was less prevalent in MC (adjusted odds ratio [aOR]: 0.73; 95% CI: 0.65–0.82). This inverse association was independent from medications commonly prescribed in MC but was not supported by sibling findings (aOR: 1.11; 95% CI: 0.81–1.51).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>MC patients may be more vulnerable to dementia diagnosis in early disease course. The intriguing inverse association between MC and preexisting dementia implies a possible underdiagnosis of MC in demented population and warrants further investigation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"299 2","pages":"216-227"},"PeriodicalIF":9.2,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12789275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145601605","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}
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