Background: Current guidelines recommend factor IIa- or Xa-specific inhibitors over warfarin analogs for preventing thromboembolic stroke in patients with atrial fibrillation (AF).However, their plasma concentrations in Korean patients are not well understood. Methods: We conducted a single-center laboratory study to determine the distribution ranges of peak and trough concentrations of three factor Xa inhibitors (apixaban, edoxaban, and rivaroxaban) prescribed for preventing strokes in patients with AF. Patients receiving one of these drugs and undergoing blood specimen collection for laboratory tests were screened. Blood specimens were obtained from patients who had adhered to the prescribed drug regimen consistently for at least 1 week. Drug plasma concentrations were measured using heparin liquid-reagent technology-based anti-Xa chromogenic assays. Results: We selected 459 patients who were taking standard or on-label-reduced doses of apixaban (N = 252), edoxaban (N = 182), or rivaroxaban (N = 25). The 5th–95th percentile ranges of the peak concentrations were 84–414 ng/mL (apixaban), 72–424 ng/mL (edoxaban), and 97–517 ng/mL (rivaroxaban). The respective 5th–95th percentile ranges of the trough concentrations were 44–237 ng/mL, 23–93 ng/mL, and 13–219 ng/mL. Approximately 19.6% (apixaban), 33.3% (edoxaban), and 64.0% (rivaroxaban) of patients in each group had peak concentrations out of the predicted distribution ranges based on pharmacokinetic data. Approximately 7.3%, 52.8%, and 8.3% of patients had trough concentrations out of the predicted distribution ranges. Conclusions A considerable proportion of Korean patients with AF taking factor Xa inhibitors may require population-specific reference ranges to guide therapeutic monitoring.

Purpose: Endoscopic submucosal dissection (ESD) has become a standard minimally invasive treatment for selected patients with early gastric cancer (EGC). This study presents the first nationwide survey of patients with EGC treated with ESD in 2023, conducted by the Korean College of Helicobacter and Upper Gastrointestinal Research. Materials and Methods: Data were retrospectively collected from participating referral centers across Korea using a standardized case report form covering patient characteristics, tumor features, procedural details, histopathological findings, and clinical outcomes.Descriptive and comparative analyses were conducted to summarize nationwide ESD practice patterns and outcomes. Results: Data from 5,460 ESD cases from 5,250 patients across 27 institutions were analyzed. The mean age was 67.4 years, with 74.1% males. Multiple synchronous lesions were identified in 3.7%. Most lesions were located in the lower third of the stomach (64.0%), and differentiated-type adenocarcinomas accounted for 87.8%. The en bloc and complete resection rates were 99.2% and 91.4%, respectively. Curative resection was achieved in 80.5%, whereas local non-curative resection (L-NCR) and surgical non-curative resection (S-NCR) were identified in 2.8% and 16.7%, respectively. Additional surgery was performed more frequently in patients with S-NCR than in those with L-NCR (59.3% vs. 24.7%). The bleeding and perforation rates were 3.6% and 0.9%, respectively, and were mostly managed conservatively or endoscopically. The median length of hospitalization was 4.0 days. Conclusions This first nationwide survey provides a comprehensive overview of the current practice of EGC treatment using ESD in Korea, demonstrating high technical success and safety, and establishing a baseline dataset for future longitudinal research.

Popliteal artery entrapment syndrome (PAES) can mimic ankle pathology in young athletes and may lead to irreversible ischemia if a diagnosis is delayed. A 13-year-old Taekwondo athlete had exertional ankle pain unresponsive to synovectomy. Computed tomography angiography revealed a 5-cm popliteal artery occlusion. The patient underwent decompression surgery, but the arterial occlusion persisted, and bypass surgery was planned. This case highlights the importance of considering PAES as part of a differential diagnosis in young athletes presenting with persistent ankle pain, particularly when symptoms persist despite appropriate orthopedic treatment.

This study aimed to describe the technical feasibility and clinical outcome of unilateral biportal endoscopy (UBE)-assisted posterior C1–2 fusion for irreducible traumatic atlantoaxial rotatory dislocation (AARD) with facet fracture and locking. A 67-year-old man presented with severe neck pain following a motor vehicle accident. Computed tomography revealed C1–2 rotatory dislocation with a right C2 facet fracture and locking, while magnetic resonance imaging demonstrated left vertebral artery hypoplasia without cord compression. Traction for 3 days failed to achieve reduction. Surgery was subsequently performed using UBE under continuous saline irrigation. Following muscle-splitting exposure, facet release and reduction were achieved with a curette. Because the bulky right C2 nerve root obstructed access, it was transected proximal to the dorsal root ganglion. Facet distraction was then performed, the articular cartilage removed, and the subchondral bone prepared. Bilateral screws were inserted, and a polyether ether ketone cage filled with demineralized bone matrix was placed for fusion. The procedure was completed successfully without complications. Blood loss was minimal. The patient’s visual analogue scale score improved from 8 preoperatively to 2 on postoperative day 1. He was discharged uneventfully on postoperative day 7. At the 3-month follow-up, he remained pain-free with stable fixation and no loss of reduction on imaging. UBE-assisted posterior C1–2 fusion enables precise facet release, safe instrumentation, and minimal tissue trauma in irreducible AARD with facet fracture and locking. This minimally invasive approach may yield favorable short-term outcomes and represents a viable alternative to conventional open posterior fusion techniques.

This study aimed to describe the technical feasibility and clinical outcome of endoscope-assisted anterior odontoid lag screw fixation in a patient with ankylosing spondylitis, in whom the conventional open anterior approach was limited due to cervical rigidity. A 56-year-old man with longstanding ankylosing spondylitis presented with severe neck pain and right-sided tingling sensations following trauma. Imaging revealed a type III odontoid fracture. Because of rigid cervical alignment, adequate neck extension required for the conventional open anterior approach was not achievable. Endoscope-assisted anterior odontoid screw fixation was performed using a biplane C-arm. The procedure involved endoscopic dissection of the prevertebral corridor and insertion of the cannulated lag screw under fluoroscopic guidance. The screw was successfully placed across the fracture site without intraoperative complications. Postoperative imaging confirmed appropriate screw trajectory and fracture reduction. The patient’s pain improved immediately, allowing early ambulation. He was discharged uneventfully, and follow-up examinations demonstrated stable fixation. Endoscope-assisted anterior odontoid lag screw fixation appears to be a safe and effective alternative for treating odontoid fractures in patients with ankylosing spondylitis. This technique minimizes soft-tissue injury and facilitates optimal screw trajectory in cases where rigid cervical alignment precludes the conventional open approach.

Endocrine-disrupting chemicals (EDCs) and persistent organic pollutants (POPs) cross the placenta and accumulate during gestation and early postnatal life, periods of heightened hormonal and neurodevelopmental plasticity. Exposure to contaminants such as bisphenol A (BPA), phthalates, polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) during these critical windows can reprogram endocrine and neural circuits, resulting in persistent behavioral alterations. This review synthesizes mechanistic evidence from animal models and epidemiological studies linking developmental EDC/POP exposure to attention deficits, impulsivity, anxiety and altered reward sensitivity—phenotypes defined here as addiction vulnerability (addiction-relevant endophenotypes) rather than clinically diagnosed substance-use disorder (SUD). We propose a two-hit, adverse outcome pathway (AOP)-informed model in which prenatal EDC/POP exposure induces endocrine-related perturbations that prime reward and stress circuitry. Subsequent exposure to psychoactive drugs and/or chronic stress then acts on these sensitized systems to increase the probability of maladaptive reinforcement learning and impaired behavioral control. Mechanistically, early-life exposures disrupt thyroid and sex-steroid signaling, dysregulate the hypothalamic–pituitary–adrenal axis, and alter dopaminergic, serotonergic, and glutamatergic neurotransmission with additional modulation by epigenetic reprogramming, oxidative stress, and neuroinflammation. Human cohort studies consistently associate prenatal BPA and phthalate exposures with adverse neurobehavioral and externalizing symptoms in children, supporting this framework while underscoring the limited availability of longitudinal data linking early exposure to SUD outcomes. Integrating these findings within an AOP perspective highlights the importance of developmental timing, sex, dose, genetic background, and co-exposures, and supports risk-assessment strategies that account for sequential environmental and drug exposures.

Limited data exist regarding the real-world practices and clinical outcomes in patients with ischemic heart failure with reduced left ventricular ejection fractions (LVEFs).Using nationwide registry data from South Korea, we aimed to investigate long-term outcomes and clinical practices, especially implantable cardioverter defibrillators (ICDs) implantation, in patients with reduced LVEFs at least 40 days after acute myocardial infarction (AMI). Of 13,056 patients with AMI between 2011 and 2015, we analyzed 350 (median age, 66 years [interquartile range, 56-75]) who had LVEFs <40% on follow-up transthoracic echocardiogram 40 days after the index event. The primary outcome was cardiac-cause mortality at 3 years. Secondary outcomes comprised major cardiovascular events as well as outcomes defined by the use of ICDs, cardiac resynchronization therapy defibrillators (CRT-Ds), and electrophysiology studies. Among 350 patients, 39 (11.1%) died from cardiac causes during 3 years of follow-up. Eleven (3.1%) were hospitalized for ventricular tachycardia. The rate of ICD or CRT-D implantation up to 3 years was 5.7% (20/350). Cox time-to-event analysis revealed older age, LVEF <30%, diabetes mellitus, and previous MI or revascularization as positively associated with cardiac death, whereas the use of statins and body weight <67 kg were negatively associated. This nationwide Korean registry demonstrated that only 5.7% of patients who had reduced LVEFs after 40 days of AMI underwent ICD implantations over 3 years. Considering the high mortality, concerted efforts are needed to improve clinical outcomes for patients who may have been candidates for ICD implantation.

Early neurologic deterioration (END) is common and occurs within a few hours to days after an ischemic stroke. Traditionally, END has been treated as a collective entity, including the occurrence of new deficits (recurrence) and the aggravation of pre-existing neurologic deficits (progression). END arises from distinct mechanisms that require different therapeutic approaches. We reviewed clinical and experimental studies addressing the epidemiology, mechanisms, and treatment of END, focusing on differentiating END due to recurrence from END due to progression and on interventions including antiplatelet therapy, direct thrombin inhibition, and induced hypertension. Early recurrence is closely associated with thrombus growth and new ischemic events, particularly in atherothrombotic disease. Early recurrence is also common in patients with cancer-associated stroke. Thrombin and platelet activation play central roles under both conditions. In contrast, progression is mainly driven by infarct growth, that is, the evolution from incomplete infarction to complete infarction due to impaired perfusion, especially in lesions involving the subcortical fiber tracts. Therapeutic implications differ accordingly. Recurrence may respond to potent antithrombotic strategies, including combined antiplatelet and direct thrombin inhibition, whereas progression may benefit from induced hypertension. However, recurrence and progression often occur simultaneously, making clinical differentiation challenging. END should be conceptualized as a spectrum of clinical presentations arising from distinct mechanisms. Recognizing recurrence and progression as separate processes is essential for mechanism-oriented treatments. Future trials should adopt this framework to develop individualized strategies and improve outcomes in patients with acute stroke.

Autoimmune hemolytic anemia (AIHA) is a rare immune-mediated disorder in children that can present as primary or secondary to other diseases. Here, we report an unusual case of steroid-refractory warm AIHA in an 11-year-old girl whose condition was ultimately cured after removal of a benign ovarian tumor. Despite receiving multiple lines of therapy—including corticosteroids, rituximab, cyclosporine, sirolimus, and mycophenolate mofetil—the patient experienced recurrent hemolysis and steroid dependence for nearly four years. Abdominopelvic imaging performed to evaluate fever revealed bilateral ovarian cystic lesions, including a left-sided dermoid cyst. Surgical resection of the tumor led to complete and sustained hematologic remission, with normalization of hemoglobin, bilirubin, and reticulocyte counts, allowing discontinuation of all immunosuppressive agents. No recurrence of hemolysis was observed during 18 months of follow-up. This case highlights the potential for benign ovarian tumors to act as a rare secondary cause of AIHA through paraneoplastic or immune cross-reactive mechanisms. Awareness of such associations is crucial when evaluating pediatric patients with refractory or relapsing AIHA, as identification and removal of an occult tumor may achieve definitive resolution of hemolysis and avoid long-term immunosuppression.

Abrupt vessel closure (AVC) is a complication of percutaneous coronary intervention (PCI) and is defined as the sudden cessation of forward coronary blood flow due to a variety of mechanisms. The incidence of AVC has markedly decreased from approximately 3.0% in the early era to about 0.3% today. Nevertheless, cardiovascular interventionists must remain prepared to manage AVC effectively, given its significant impact on clinical outcomes.AVC can arise from several mechanisms, including dissection, intramural hematoma, intracoronary thrombosis, air embolism, vasospasm, and no-reflow. The clinical impact of AVC varies depending on the extent of myocardium affected, ranging from asymptomatic events or transient ischemic chest pain to cardiogenic shock or cardiac arrest. Both a general approach for stabilizing hemodynamic consequences and an etiology-specific management strategy are essential. Hasty decision-making may worsen the situation, whereas a structured approach—focused on hemodynamic stabilization, logical diagnostic processes, and targeted interventions—can improve outcomes. In this narrative review, we describe the mechanisms underlying each etiology, outline mechanism-specific management strategies, and discuss general approaches to managing patients with AVC through logical diagnostic and treatment processes. We hope this review offers valuable insights into this uncommon but significant complication and enhances readers’ skills in managing AVC more effectively during PCI.