Amiodarone increases the risk of thyroid dysfunction, but the prognostic significance of this complication in patients with heart failure (HF) is uncertain. This study investigates the association between amiodarone-related thyroid dysfunction and risk of HF hospitalization or death in a nationwide cohort.
Cases and controls were identified from a source population of all HF patients who initiated treatment with amiodarone from 1996 to 2021. Patients diagnosed with and/or treated for thyroid dysfunction within 3 years of starting amiodarone were classified as cases and comprised the study population together with controls matched 1:2 based on age, sex, calendar year, and HF duration. The primary outcome was a composite of HF hospitalization and death within 1 year from onset of thyroid dysfunction, analyzed using Kaplan–Meier curves and Cox regression models adjusted for comorbidities.
Of 21,947 HF patients who initiated amiodarone, 2972 (14%) developed thyroid dysfunction. After matching, the study population consisted of 2953 cases and 5857 controls, mean age 70 years, and 65% men. At 1-year follow-up the primary outcome occurred in 1154 (39%) cases and 1826 (31%) matched controls, yielding an adjusted hazard ratio (HR) of 1.30 (95% CI 1.21–1.40). This increased risk was observed for both HF hospitalization (30% vs. 23%, HR 1.35 [1.24–1.47]) and all-cause death (19% vs. 15%, HR 1.21 [1.08–1.34]).
In this nested case–control study derived from a nationwide cohort of amiodarone-treated HF patients, new-onset thyroid dysfunction was associated with a 30% higher risk of a composite of HF hospitalization and death within 1 year.
Drug-induced liver injury (DILI) is an important medical condition. Recently, development of novel causality assessment tools has improved the diagnostic accuracy of idiosyncratic DILI, particularly RECAM (Revised Electronic Version of Roussel Uclaf Causality Assessment [RUCAM]). RECAM was found to be better than RUCAM in difficult cases and increased the precision of the DILI diagnosis but needs further refinement. In recent years, there has been an increased incidence of DILI with drugs, such as oncological drugs and herbal and dietary supplements (HDSs). DILI is commonly associated with checkpoint-induced liver injury. Treatment with corticosteroids has been the standard of care in this type of liver injury, but its use is controversial and potentially harmful. With the help of liver biopsy, 60% of subjects can avoid corticosteroids. In recent years, a number of dietary supplements have been found to lead to DILI, such as turmeric, Garcinia cambogia, kratom and ashwagandha. HLA-B*35:01 has been identified as a risk factor for green tea extract-induced liver injury. International collaborative efforts have tried to find candidate biomarkers, but no biomarker has yet demonstrated superior performance to standard liver tests. FDA has recently approved the use of serum glutamate dehydrogenase (GLDH) as a biomarker to distinguish liver injury from muscle injury. Serum GLDH should be used alongside standard liver injury monitoring in patients without pre-existing liver disease. In the current review, recent findings in DILI are presented on diagnostic strategies, new agents such as checkpoint inhibitors and HDSs leading to DILI, biomarkers and new therapies.
Hyperkalaemia is a serious complication in patients with chronic kidney disease (CKD) and heart failure (HF), often leading to the discontinuation of renin–angiotensin–aldosterone system inhibitors (RAASi; renin-angiotensin system inhibitors [RASi] and mineralocorticoid receptor antagonists [MRAs]) despite their cardiorenal benefits. Although potassium binders, especially second-generation potassium binders, reduce the risk of hyperkalaemia in clinical trials, real-world evidence on whether they enable RAASi continuation and influence clinical outcomes remains scarce.
This observational, population-based cohort study used Swedish healthcare data from the DEMONSTRATE database to identify adults with non-dialysis (ND) CKD and/or HF who initiated potassium binders (2018–2022). Patients were stratified by potassium binder generation. RASi and MRA treatment changes were assessed at 6 months, and clinical outcomes (all-cause mortality, hospitalization and three-point major adverse cardiovascular events [3P-MACE]) were evaluated over a 3-year follow-up using propensity-score-weighted Kaplan–Meier analyses.
Of 7913 potassium binder episodes (6232 patients), 7.1% used second-generation binders. These episodes were associated with increased RAASi persistence at 6 months: 76.9% and 57.5% of second-generation users maintained RASi and MRA therapy, respectively, compared with 66.4% and 47.8% in the first-generation group. Patients who maintained RASi had lower observed all-cause mortality and hospitalization rates, but no difference in incidence of 3P-MACE was found.
Second-generation potassium binders were associated with higher RAASi persistence than first-generation binders. RASi persistence was associated with lower observed rates of all-cause mortality and hospitalization, with no clear differences in 3P-MACE. These findings suggest that potassium binders may enable sustained RAASi use in patients with ND-CKD and/or HF.
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.
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.
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.
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.
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.
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.
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