Journal of Internal Medicine最新文献

{"title":"The changing epidemiology of human type 2 diabetes–associated atherosclerosis: Pathophysiological mechanisms and emerging treatment possibilities","authors":"Dania Al-Sharify,&nbsp;Jiangming Sun,&nbsp;Andreas Edsfeldt","doi":"10.1111/joim.70118","DOIUrl":"10.1111/joim.70118","url":null,"abstract":"<p>Type 2 diabetes (T2D) is a major global health concern strongly associated with atherosclerosis and subsequent macrovascular complications. These complications are the leading cause of death among T2D patients. Despite a decline in cardiovascular events over the last decade, individuals with T2D still have an approximately doubled risk compared to those without diabetes. This shows an urgent need for therapies targeting biological processes specific to T2D-associated atherosclerosis. Nevertheless, more research is needed to identify exactly which processes can be targeted therapeutically. Current therapies either target lipid metabolism or inflammation, two processes commonly considered important in T2D-associated atherosclerosis. However, more recent human plaque tissue studies show no differences in plaque levels of lipids nor inflammatory markers, possibly reflecting improved clinical treatment strategies. Other distinct differences in plaque tissue composition in T2D have been put forward, including thin fibrous caps and large necrotic cores. Moreover, T2D may influence several biological processes affecting both plaque formation and progression (such as oxidative stress and efferocytosis). These mechanisms could potentially also be targeted to prevent atherosclerotic cardiovascular complications. This review focuses on the shifting epidemiology of T2D-associated cardiovascular complications, as well as biological changes in T2D plaques, and how these changes can guide future clinical approaches to further reduce atherosclerotic complications.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 2","pages":"131-152"},"PeriodicalIF":7.6,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148238650","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":"Persistent and emerging cancer risks after migration: Evidence from North and South Korean cohorts","authors":"Junshik Hong,&nbsp;Kyeong Jin Kim,&nbsp;Jimi Choi,&nbsp;Jung A. Kim,&nbsp;Kyoung Jin Kim,&nbsp;Yo Han Lee,&nbsp;Sang Min Park,&nbsp;Sung In Jang,&nbsp;Jung Myun Lee,&nbsp;Ju Hyang Lee,&nbsp;Mun Jeong Choi,&nbsp;Young-Hoon Kim,&nbsp;Sin Gon Kim","doi":"10.1111/joim.70082","DOIUrl":"10.1111/joim.70082","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>North Korean defectors in South Korea offer a rare natural model to trace cancer risk evolution after rapid environmental transition, given shared genetics but markedly contrasting early life exposures with South Korean residents.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using the Korean National Health Insurance database, we constructed a nationwide matched cohort of 25,798 North Korean defectors and 1,276,601 South Korean residents (1:50 frequency matching by sex, age, and index year). We compared overall and site-specific cancer risks and examined time-varying hazard ratios (HRs) since resettlement.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Overall cancer risk was higher among defectors (HR 1.13; 95% confidence interval, 1.07–1.18), particularly in men (HR 1.31). Liver (HR 2.53), uterine cervical (HR 2.10), and lung cancer (HR 1.69) were markedly elevated, reflecting infection- and deprivation-related legacies. In contrast, cancers more prevalent in developed countries, notably breast (HR 0.48) and colorectal (HR 0.71), were initially lower. However, HRs began to rise over time, especially for breast cancer, indicating a trend toward convergence with host-population patterns.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The cancer profile of North Korean defectors demonstrates a dual burden: persistent risks from infection-related cancers rooted in pre-defection exposures and growing vulnerability to lifestyle-related cancers after resettlement. These findings highlight the importance of dual-track prevention strategies that address both legacy and emerging cancer risks in rapidly transitioning populations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 2","pages":"164-178"},"PeriodicalIF":7.6,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70082","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147429473","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":"Hospital at Home in 10 years—Here, borrow my binoculars","authors":"Michael Montalto","doi":"10.1111/joim.70112","DOIUrl":"10.1111/joim.70112","url":null,"abstract":"<p>Hospital in the Home (HAH) refers to the delivery of acute hospital care to patients at home, or in their usual place of care, including nursing homes. HAH is an acute hospital substitution service—it delivers medical, nursing and allied health staff, skills, interventions and treatments, technologies and supervision usually found in hospitals to sick patients at home. The mission of HAH is to improve the lives of sick people who need hospitals. Patients consistently express a preference for the HAH model of care. HAH has developed an evidence base for safety and effectiveness over the last 30 years, but its role has become prominent since the COVID-19 pandemic. In most health systems where HAH is successful, it is organised and funded as an acute hospital inpatient service. Progress continues to broaden the clinical applications of HAH and narrow the operational definition and processes. It is likely that in 10 years, HAH will form an essential part of the scope of an acute hospital, taking its place alongside the Emergency Department and Intensive Care.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 2","pages":"153-163"},"PeriodicalIF":7.6,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147969182","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":"Potassium binders as enablers of guideline-directed renin–angiotensin–aldosterone system inhibitor therapy","authors":"Carmine Zoccali,&nbsp;Francesca Mallamaci","doi":"10.1111/joim.70100","DOIUrl":"10.1111/joim.70100","url":null,"abstract":"&lt;p&gt;Hyperkalemia sits at the heart of a paradox in cardiorenal medicine. The very drugs that best protect patients with chronic kidney disease (CKD) and heart failure (HF)—renin–angiotensin–aldosterone system inhibitor (RAASi)—are also a major driver of elevated serum potassium and the clinical anxiety that leads to their down-titration or withdrawal. Contemporary guidance has shifted decisively toward the view that hyperkalemia should prompt &lt;i&gt;management&lt;/i&gt;, not abandonment, of RAASi therapy, especially in patients at high cardiovascular and renal risk [&lt;span&gt;1-3&lt;/span&gt;] (Fig. 1). Yet across health systems, the journey from this principle to stable, long-term prescriptions remains incomplete.&lt;/p&gt;&lt;p&gt;Epidemiologic work from large populations has clarified both the scale and the consequences of dyskalemia. In a major North American health system, hyperkalemia clustered in individuals exposed to intensive antihypertensive regimens, particularly those incorporating RAASi, and was tightly linked to underlying cardiorenal burden [&lt;span&gt;2&lt;/span&gt;]. Scandinavian data from routine care have shown that both hyperkalemia and hypokalemia are common and independently associated with adverse outcomes, underscoring that “normal” potassium is a narrow and fragile target in unselected clinical populations [&lt;span&gt;3&lt;/span&gt;]. In HF, modest elevations of potassium are associated not only with excess mortality but also with clinicians’ reluctance to initiate or maintain full neurohormonal blockade [&lt;span&gt;4&lt;/span&gt;]. Against this backdrop, potassium becomes more than a number; it is a recurrent barrier to the implementation of evidence-based therapy.&lt;/p&gt;&lt;p&gt;The therapeutic ambitions of nephrology and cardiology make the stakes even higher. The KDIGO 2024 CKD guideline places RAAS blockade at the core of reno-protection across albuminuric phenotypes, with explicit recommendations to up-titrate to maximally tolerated doses and to avoid unnecessary interruption [&lt;span&gt;5&lt;/span&gt;]. In parallel, the 2021 ESC HF guideline envisions comprehensive neurohormonal blockade—ACEi/ARB/ARNi, beta-blockers, MRAs, and SGLT2 inhibitors—as standard care in HF with reduced ejection fraction to be maintained chronically whenever feasible [&lt;span&gt;6&lt;/span&gt;]. Within this framework, recurrent hyperkalemia is no longer a marginal side-effect; it is a central determinant of whether patients ever reach and remain on the therapies that underpin modern gains in survival.&lt;/p&gt;&lt;p&gt;For decades, our options for resolving this tension have been unsatisfactory. Dietary potassium restriction and diuretic intensification are variably effective and can compromise nutritional and volume status. Sodium polystyrene sulfonate, the traditional cation-exchange resin, has been used widely despite a troublesome gastrointestinal profile [&lt;span&gt;7&lt;/span&gt;]. Not surprisingly, clinicians have often responded to rising potassium by attenuating or discontinuing RAASi. Yet observational data increasingly reveal the cost of this re","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 2","pages":"106-109"},"PeriodicalIF":7.6,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70100","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147969138","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":"Sclerosing cholangitis and microscopic colitis—In search of the lost cause","authors":"Per M. Hellström","doi":"10.1111/joim.70099","DOIUrl":"10.1111/joim.70099","url":null,"abstract":"&lt;p&gt;Primary sclerosing cholangitis (PSC) and microscopic colitis (MC) are two separate conditions with distinctly different symptoms, where epidemiological data now show growing evidence that these two entities can co-occur more than expected by chance.&lt;/p&gt;&lt;p&gt;In the current issue of Journal of Internal Medicine, Bergman and collaborators [&lt;span&gt;1&lt;/span&gt;] describe a bidirectional epidemiological analysis employing first a cohort study showing an incidence rate of PSC and MC of 11.9 (confidence interval, 7.8–18.3, compared with controls 1.7; CI: 1.0–2.8). Then, an added case-control study showed PSC to be more common in MC patients with a frequency of 0.08% as compared to controls with 0.01%, yielding an odds ratio of 7.26; CI: 3.5–15.1. Taken together and based on background epidemiological data of more than 22,000 cases of MC versus more than 108,000 healthy people, the results show a possible association between the two diseases. This is in line with a previous systematic review of twelve cases [&lt;span&gt;2&lt;/span&gt;]. Even though the absolute risks of co-occurrence are low, MC may have a diagnostic relevance for symptoms and signs of PSC.&lt;/p&gt;&lt;p&gt;The Bergman paper [&lt;span&gt;1&lt;/span&gt;] in this issue explores the co-occurrence of PSC and MC and forwards the question of what—if anything—connects the two conditions. It reviews proposed mechanisms, be it due to genetic susceptibility through linkage of HLA alleles between PSC and MC or changes of the microbiome with increased bacterial translocation across the intestinal mucosa, immune dysregulation or enterohepatic bile acid circulation as possible common disease mechanisms. Hence, this framework opens a possibility for clinicians and researchers to move from association to explanation.&lt;/p&gt;&lt;p&gt;So, why is this pairing intriguing? Both conditions are uncommon, possibly immune-mediated and often chronic, making repeated co-occurrence clinically noticeable. PSC is strongly linked to inflammatory bowel disease (IBD) (classically ulcerative colitis), but MC sits outside the ‘classic IBD’ category, raising questions about shared pathways. Understanding possible shared drivers for MC and PSC could clarify risk stratification, surveillance strategies and treatment choices.&lt;/p&gt;&lt;p&gt;MC is characterized by chronic, watery, non-bloody diarrhoea with macroscopically normal colonoscopy and characteristic histology; it includes &lt;i&gt;lymphocytic colitis&lt;/i&gt; and &lt;i&gt;collagenous colitis&lt;/i&gt;. It occurs mainly in postmenopausal women, but there are exceptions to this rule. The symptoms are usually managed with budesonide at a low dosage, along with removal of non-steroid anti-inflammatory drugs, proton pump inhibitors and sertraline, but may require additional treatment with cholestyramine, 5-aminosalicylic acid or immunomodulators. The clinically recognized association between active coeliac disease and MC, as well as activation of the immune responses by rectal instillation of Fraser's gluten fraction, speaks in favour of a general immu","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 1","pages":"2-4"},"PeriodicalIF":9.2,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147969197","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":"Microscopic colitis and primary sclerosing cholangitis are bidirectionally associated: A nationwide matched cohort and case–control study","authors":"David Bergman,&nbsp;Anders Forss,&nbsp;Jiangwei Sun,&nbsp;Fahim Ebrahimi,&nbsp;Björn Lindkvist,&nbsp;Charlotte Hedin,&nbsp;Hannes Hagström,&nbsp;Annika Bergquist,&nbsp;Jialu Yao,&nbsp;Jonas F. Ludvigsson","doi":"10.1111/joim.70084","DOIUrl":"10.1111/joim.70084","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Microscopic colitis (MC) is an inflammatory disease of the colon. Although there is a known association between inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC), evidence linking MC and PSC remains scarce. We aimed to investigate the bidirectional association between MC and PSC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Leveraging the nationwide Swedish histopathology cohort Epidemiology Strengthened by histoPathology Reports in Sweden, we conducted a matched cohort study (2002–2023, follow-up until 2024) and a case–control study (1987–2023). Patients with IBD were excluded. Adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs) were estimated using Cox regression and adjusted odds ratios (aORs) using conditional logistic regression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The cohort study included 21,340 patients with biopsy-confirmed MC and 101,707 matched reference individuals (matched by age, sex, birth year and county). Over a median follow-up of 7 years, PSC was diagnosed in 21 patients with MC and 15 reference individuals, corresponding to incidence rates of 11.9 (95% CI = 7.8–18.3) and 1.7 (95% CI = 1.0–2.8) per 100,000 person-years, yielding an aHR of 7.17 (95% CI = 3.69–13.9). The case–control study included 22,729 MC cases and 108,467 matched controls. Prior PSC was more frequent among MC cases (19/22,729; 0.08%) than controls (12/108,467; 0.01%), yielding an aOR of 7.26 (95% CI = 3.50–15.1). Our findings remained robust across multiple sensitivity analyses, including sibling-controlled analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This nationwide study reveals a bidirectional association between MC and PSC. Although absolute risks are low, these findings suggest that MC may have diagnostic relevance in suspected PSC cases, and vice versa. Physicians treating MC patients should be alert to signs and symptoms of PSC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 1","pages":"78-92"},"PeriodicalIF":9.2,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497072","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":"Global kidney health: Are we failing the silent pandemic?","authors":"Taewon Yi,&nbsp;Daniel V. O'Hara,&nbsp;Adeera Levin","doi":"10.1111/joim.70088","DOIUrl":"10.1111/joim.70088","url":null,"abstract":"<p>Chronic kidney disease (CKD), although not infectious, has a sharply rising global incidence, alarming rates of death and disability, and the potential to disrupt health systems and economies. Thus, it demands the urgency and global attention of past pandemics. Over 850 million people are affected, disproportionately impacting people in low- and middle-income countries. Although CKD can be detected with simple and cost-effective testing, it is a silent condition, often remaining asymptomatic until it has progressed to advanced stages where effective treatment options are limited. Early detection relies on systematic population-level screening, especially among individuals with comorbidities. The global response to CKD has remained largely silent: There is limited evidence of prioritization within health agendas and inadequate infrastructure for screening, surveillance, and treatment. Coordinated global action is required to halt this silent “pandemic,” especially given advances in care and policy: New effective disease modifying therapies may lead to remission of CKD for many individuals, and the 2025 World Health Organization's adoption of the Kidney Health Resolution at the 78th World Health Assembly prioritizes kidney health to reduce the burden of noncommunicable diseases through promoting early screening, strengthening disease prevention, and improving access to care. In this review, we examine the failure to address the escalating CKD “pandemic” and explore how the use of low-cost and cost-effective screening tools, such as simple urine dipstick testing, and applying lessons learned from the COVID-19 pandemic are critical to further reframing CKD as a public health emergency and prioritizing kidney health on the global agenda.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 1","pages":"26-38"},"PeriodicalIF":9.2,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70088","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607651","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":"Regarding: Poor long-term cardiovascular risk factor management after acute coronary syndrome: An observational cohort study","authors":"Laurent Fauchier,&nbsp;Thibaud Genet,&nbsp;Mickael Guglieri","doi":"10.1111/joim.70105","DOIUrl":"10.1111/joim.70105","url":null,"abstract":"&lt;p&gt;Dear Editor,&lt;/p&gt;&lt;p&gt;We read with interest the study by Schubert et al. reporting suboptimal long-term cardiovascular risk factor monitoring and control after acute coronary syndrome (ACS). The authors should be commended for leveraging comprehensive electronic health records to characterize real-world care beyond the first year [&lt;span&gt;1&lt;/span&gt;]. The findings of declining measurement rates and persistently low attainment of LDL-C and blood pressure targets are clinically relevant. However, several aspects warrant further consideration. In particular, ignoring myocardial infarction (MI) subtype (STEMI vs. NSTEMI), age, and the underlying sex distribution may introduce substantial confounding when evaluating sex differences in post-ACS management, potentially generating spurious associations or misleadingly attenuating true disparities.&lt;/p&gt;&lt;p&gt;Confounding by MI phenotype is critical in this setting. STEMI and NSTEMI represent distinct populations with markedly different epidemiological profiles. STEMI predominantly affects men (≈70%), whereas NSTEMI shows a more balanced sex distribution, with women being disproportionately represented among NSTEMI presentations. Importantly, NSTEMI patients are consistently less likely to receive intensive secondary prevention and achieve optimal adherence compared with STEMI [&lt;span&gt;2&lt;/span&gt;]. As a result, analyses that pool both entities may artificially exaggerate apparent treatment gaps in women, simply reflecting their overrepresentation in a population that is globally undertreated [&lt;span&gt;3&lt;/span&gt;]. Conversely, if sex disparities are more pronounced within NSTEMI itself, aggregation may dilute the true magnitude of within-group differences, masking clinically relevant inequities.&lt;/p&gt;&lt;p&gt;Age also represents a potential effect modifier. Women present with MI at substantially older ages than men across both STEMI and NSTEMI. This has several implications. Older patients are less likely to receive intensive therapies irrespective of sex, introducing treatment-intensity bias [&lt;span&gt;4&lt;/span&gt;]. In addition, age is closely associated with a higher burden of comorbidities—such as chronic kidney disease or heart failure—that influence both therapeutic decisions and outcomes. Finally, the effect of sex on prognosis varies across age strata: younger women exhibit worse outcomes compared with men, whereas this difference attenuates or reverses in the elderly [&lt;span&gt;5&lt;/span&gt;]. Failure to account for these interactions may therefore obscure meaningful sex-specific effects.&lt;/p&gt;&lt;p&gt;These combined mechanisms create a high risk of Simpson's paradox, whereby pooled analyses yield associations that differ from—or even contradict—those observed within clinically relevant subgroups [&lt;span&gt;6&lt;/span&gt;]. For example, even if women receive less optimal care within both STEMI and NSTEMI, aggregation may suggest smaller or absent differences due to the unequal distribution of MI subtypes. Overall, failure to account for MI type and age is li","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 1","pages":"97-98"},"PeriodicalIF":9.2,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147758448","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":"Trends in celiac disease autoimmunity before and after the COVID-19 pandemic","authors":"James A. King,&nbsp;Stephanie Coward,&nbsp;Jenny Godley,&nbsp;Amy Metcalfe,&nbsp;Paul E. Ronksley,&nbsp;Tyler Williamson,&nbsp;Gilaad G. Kaplan","doi":"10.1111/joim.70101","DOIUrl":"10.1111/joim.70101","url":null,"abstract":"&lt;p&gt;In Alberta, Canada, rates of testing for celiac disease (CeD) based on tissue transglutaminase antibodies (tTG-IgA) remained stable from 2012 to 2019; however, incidence of CeD autoimmunity increased by 6% per year from 31.5 per 100,000 person-years in 2015 to 40.3 per 100,000 person-years in 2019 [&lt;span&gt;1&lt;/span&gt;]. As healthcare systems shifted resources to prioritizing the COVID-19 pandemic, delivery of primary care including nonurgent laboratory testing was reduced. It is therefore important to understand if and how trends in the incidence of CeD autoimmunity since 2019 may have been affected by delays in testing for chronic diseases.&lt;/p&gt;&lt;p&gt;We developed a retrospective, population-based cohort using health administrative data from Alberta, which is a province in Canada with approximately 4.4 million residents. There is universal healthcare coverage for &gt;99% of residents, including laboratory testing, primary care, emergency visits, and hospital admissions. Accordingly, this data source is essentially comprehensive of healthcare interactions in a publicly funded system.&lt;/p&gt;&lt;p&gt;All records for tTG-IgA were identified in Alberta between April 2012 and March 2025 from a province-wide laboratory database. Incident cases of CeD autoimmunity were defined as unique individuals newly positive for tTG-IgA between April 2015 and March 2025. Rates of CeD autoimmunity were analyzed by quarter to capture variation within years while balancing stability of estimates. Trends for two time periods—April 2015 to December 2019 (pre-pandemic) and January 2021 to March 2025 (post-pandemic)—were modeled using negative binomial regression while incorporating the population at-risk as an offset term. Given the different trends in prior incidence of CeD autoimmunity in Alberta [&lt;span&gt;1&lt;/span&gt;], analyses were stratified into pediatrics and adults. Average percentage changes across quarters in the two time periods were estimated from the model. Statistical analyses were performed in RStudio using the &lt;i&gt;MASS&lt;/i&gt; package [&lt;span&gt;2&lt;/span&gt;]. Further details on the methods are provided in the Supplement.&lt;/p&gt;&lt;p&gt;Observed incidence of CeD autoimmunity in children ranged between 27.5 (April–June 2020) and 110.2 (January–March 2023) per 100,000 person-years (Fig. 1a). Although incidence rates were notably higher in the post-pandemic period, there was no significant difference between the two trends (&lt;i&gt;p &lt;/i&gt;= 0.796). On average, pediatric incidence increased per quarter by 1.22% (95% CI: 0.08, 2.37) prior to the pandemic versus 1.45% (95% CI: −0.61, 3.55) in the post-pandemic period. Similar findings were observed when restricted to those with a tTG-IgA value ≥10 times the ULN (Table S1); however, a potential trend of decreasing incidence may be occurring in the last year (Fig. S1).&lt;/p&gt;&lt;p&gt;Incidence of CeD autoimmunity in adults ranged from 20.4 (April–June 2020) to 47.8 (April–June 2024) per 100,000 person-years (Fig. 1b). There was a statistically significant change in the t","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 1","pages":"93-96"},"PeriodicalIF":9.2,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147758438","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":"Contrast-enhanced CT—Nephrotoxic or not? A critical review of propensity-score-adjusted studies","authors":"Ulf Nyman,&nbsp;Jonas Björk,&nbsp;Mikael Hellström,&nbsp;Peter Leander,&nbsp;Per Liss,&nbsp;Gunnar Sterner,&nbsp;Torkel B. Brismar","doi":"10.1111/joim.70095","DOIUrl":"10.1111/joim.70095","url":null,"abstract":"<p>Retrospective, propensity-score-adjusted (PSA) studies have indicated to practitioners in the field that contrast-induced acute kidney injury (AKI) after contrast-enhanced CT (CECT) is of minor importance or even non-existent. This has led to controversies between clinicians demanding CECT not to miss any diagnoses and radiologists reluctant or even refusing CECT in risky patients. A critical review of AKI/dialysis risk post-CECT in PSA studies was performed based on a Cochrane Library/Embase/PubMed search up to December 2024 with stratification for various populations. Among unselected emergency-/inpatients with chronic kidney disease, CECT was associated with significantly higher AKI incidence than in controls in 8/10 cohorts (weighted absolute risk increase 4.0 percentage points (pp), cohort range −4 to 16.9 pp at glomerular filtration rate (GFR) &lt;30 mL/min/1.73 m²) and dialysis in 5/6 cohorts (weighted absolute risk increase 1.8 pp, cohort range 1.0–5.9 pp at GFR &lt;30 mL/min/1.73 m²). Corresponding figures regarding cohorts with presumed/potentially unstable renal function were 1/10 and 3/8 cohorts, respectively. No increased risk was found in the five miscellaneous cohorts, but with a few patients with low GFR. Associations between individual contrast medium (CM) doses and AKI/dialysis were generally lacking. Marked selection bias was evident in one cohort. Thus, the analyses support an association between CECT and AKI in emergency-/inpatients, including a non-negligible dialysis risk, especially at GFR &lt;30 mL/min/1.73 m². PSA studies reporting no increased risk of CECT must be interpreted with caution due to risk for selection bias and the potential masking effects of acute kidney functional recovery. Studies on CM dose or gram-iodine/GFR ratio correlation with AKI/dialysis are warranted.</p>","PeriodicalId":196,"journal":{"name":"Journal of Internal Medicine","volume":"300 1","pages":"5-25"},"PeriodicalIF":9.2,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/joim.70095","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721195","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}