Objective: To evaluate the diagnostic performance of the “probable hepatocellular carcinoma (HCC)” category in the Korean Liver Cancer Association-National Cancer Center (KLCA-NCC) v2022 guidelines. Materials and Methods: This multicenter retrospective study included patients at risk of HCC who underwent gadoxetic acid-enhanced MRI between January 2015 and June 2018; a subgroup of these patients also underwent liver CT. Eligible patients had at least one non-cystic lesion (≥10 mm) with a reference standard. Four radiologists interpreted the images independently and the results were pooled. The performance of “definite HCC” and “probable HCC” together and “probable HCC” alone were compared between v2018 and v2022. Results: A total of 2,237 patients (1,666 men; mean age, 59 ± 11 years) with 2,445 lesions were included. In v2022, 1.5% (143/9,780) of the lesions were additionally categorized as “probable HCC” by four reviewers on MRI; among these, 104 lesions were not HCCs. Focal nodular hyperplasia (FNH) or FNH-like nodules constituted 90.4% (94/104) of the false positives. When “definite HCC” and “probable HCC” were combined, v2022 showed higher sensitivity (83.7% [5,670/6,776] vs. 83.1% [5,631/6,776]) but lower specificity (77.1% [2,316/3,004] vs. 80.6% [2,420/3,004]) than v2018 (P < 0.001). For “probable HCC” alone, v2022 showed a lower positive predictive value (PPV) than v2018 (64.1% [373/582] vs. 76.1% [334/439], P < 0.001). In v2022, lesions with non-rim arterial-phase hyperenhancement (APHE) showed a lower PPV than those without APHE (42.3% [91/215] vs. 76.8% [282/367], P < 0.001). In the CT subgroup (n = 1,590), 1.6% (99/6,360) of the lesions were reassessed as “probable HCC,” and its PPV was 83.8% (83/99) in v2022 whereas no lesions were classified as “probable HCC” under v2018. Conclusion The revised “probable HCC” category in the KLCA-NCC v2022 aligns with updates in the diagnostic flow, demonstrating acceptable performance on MRI and CT. Notably, FNH or FNH-like nodules can be misclassified as “probable HCC” when MRI is used.

Subarachnoid hemorrhage (SAH) is a stroke subtype with high mortality and poor functional outcomes. Prompt occlusion of a ruptured aneurysm at an early stage is crucial to prevent rebleeding, which can result in even higher mortality and more severe disabilities. The most critical initial decision in SAH management is the choice of treatment method with surgical clipping or endovascular coiling. We aimed to develop an evidence-based clinical guideline to select the optimal initial treatment in patients with SAH. We developed this guideline based on evidence from systematic reviews and meta-analyses via a de novo process. A systematic literature review was conducted across four databases (MEDLINE, Embase, Cochrane, and KoreaMed) to answer two population, intervention, comparison, outcome questions comparing clipping and coiling. The risk of bias was assessed using ROB 2.0 and the Newcastle-Ottawa Scale. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses flow diagrams and meta-analyses were generated for functional outcome and mortality. We included six randomized control trials (RCTs) and 58 observational studies. Meta-analysis of RCTs showed that coiling improved functional outcomes compared to clipping (odds ratio [OR], 0.91; 95% confidence interval [CI], 0.86–0.97). No significant mortality difference was observed in RCTs (OR, 1.38; 95% CI, 0.91–2.09), but non-RCTs favored clipping for reduced mortality (OR, 0.77; 95% CI, 0.69–0.86). However, it is difficult to generalize these findings to all clinical situations, as patients with SAH have a highly variable clinical course. Final treatment decision should be tailored to the individual patient’s status, including aneurysm location, morphology, and the expertise available at the treatment center. Such decisions are best made by specialists such as a board-certified physician and should be explained to the patient and their caregivers, along with the rationale for selecting the most appropriate treatment at the given hospital. Korea has many certified endovascular neurosurgeons, cerebrovascular surgeons, and certified cerebrovascular centers. Proper selection of the most suitable treatment method by certified physicians and centers would greatly benefit patient outcomes and healthcare professionals.

Accurate and early identification of stroke and large vessel occlusion (LVO) in emergency settings is essential for improving patient outcomes and ensuring the efficient allocation of medical resources. This clinical practice guideline systematically reviews domestic and international literature and conducts meta-analyses to evaluate the utility and diagnostic accuracy of stroke assessment tools used in prehospital emergency medical services (EMS). We developed a guideline based on evidence from systematic reviews and meta-analyses via a de novo process. A systematic literature review was conducted to evaluate the usefulness of diagnostic EMS assessment tools for diagnosing stroke and LVO. Overall, 70 non-randomized control studies were selected for this study. A meta-analysis was conducted with a subgroup analysis to distinguish between patients with stroke and those with LVO. EMS tools demonstrated high sensitivity but low specificity for diagnosing stroke. In the prehospital setting, using validated EMS stroke assessment tools is recommended for the early identification of stroke and LVO. Upon hospital arrival, stroke specialists should conduct further evaluation and triage to confirm the diagnosis and guide appropriate management. Delays in diagnosing LVO are frequently unacceptable. While experts advocate for the use of EMS assessment tools to facilitate early identification of LVO, these tools alone lack adequate sensitivity. Therefore, further diagnostic evaluations and consultation with stroke specialists upon hospital arrival are recommended.

The mothership (MS) model, where patients are directly transferred to a thrombectomy-capable center, and the drip-and-ship (DS) model, where thrombolysis is initiated at the nearest primary stroke center before transfer for thrombectomy, are the primary transport modes for patients with stroke. We aimed to establish guidelines for selecting the appropriate transfer strategy based on emergent large vessel occlusion (LVO). We developed this guideline based on evidence from systematic reviews and meta-analyses via a de novo process. A systematic literature review was conducted across four databases (MEDLINE, Embase, Cochrane, and KoreaMed) to answer three Population, Intervention, Comparison, and Outcome questions comparing MS and DS models. The risk of bias was assessed using the Newcastle-Ottawa Scale. Preferred Reporting Items for Systematic Reviews and Meta-Analyses flow diagrams and meta-analyses were generated for functional outcomes, mortality, and successful recanalization. Twenty-six non-randomized controlled studies showed that the MS model improved good functional outcomes by approximately 14% compared with the DS model (odds ratio [OR], 1.14; 95% confidence interval [CI], 1.00–1.30). Fifteen studies reported that mortality in the MS and DS models showed no significant differences (OR, 0.97; 95% CI, 0.84–1.11). Twenty-four studies revealed no significant difference in successful recanalization between the MS and DS models (OR, 0.87; 95% CI, 0.68–1.10). The MS model should be considered first to improve the functional outcome of patients with LVO. However, if thrombectomy cannot be performed immediately after thrombolysis, or if a thrombectomy-enabled hospital is not nearby, the DS model should be considered by stroke specialists depending on transportation time and regional factors. We suggest a mixed approach with the DS model based on specific circumstances or regions to ensure the optimum treatment of patients with acute ischemic stroke (AIS). Appropriate transport for patients with LVO improves the prognosis of AIS.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Background/Aims: The optimal duration and interval of follow-up for cystic lesions of the pancreas (CLPs) is not well established. This study was performed to investigate the optimal duration and interval of follow-up for CLPs in clinical practice. Methods: Patients with CLPs without worrisome features or high-risk stigmata underwent followup with computed tomography at 6, 12, 18, and 24 months and then every 12 months thereafter. A retrospective analysis of prospectively collected data was performed. Results: A total of 227 patients with CLPs detected from 2000 to 2008 (mean initial diameter, 1.3±0.6 cm) underwent follow-up for a median of 120 months. Twenty-two patients (9.7%) underwent surgery after a median of 47.5 months. Malignancies developed in four patients (1.8%), one within 5 years and three within 10 years. One hundred and fourteen patients (50.2%) were followed up for more than 10 years. No malignancy developed after 10 years of follow-up. During surveillance, 37 patients (16.3%) experienced progression to surgical indication. In patients with CLPs less than 2 cm in diameter, development of surgical indications did not occur within 24 months of follow-up. Conclusions CLPs should be continuously monitored after 5 years because of the persistent potential for malignant transformation of CLPs. An interval of 24 months for initial follow-up might be enough for CLPs with initial size of less than 2 cm in clinical practice.

Background/Aims: A previous history of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) is a risk factor for PEP, suggesting that there may be a genetic predisposition to PEP. However, nothing is known about this yet. The aim of this study was to identify genetic variations associated with PEP. Methods: A cohort of high-risk PEP patients was queried from December 2016 to January 2019. For each PEP case, two propensity score-matched controls were selected. Whole exome sequencing was performed using blood samples. Genetic variants reported to be related to pancreatitis were identified. To discover genetic variants that predispose to PEP, a logistic regression analysis with clinical adjustment was performed. Gene-wise analyses were also conducted. Results: Totals of 25 PEP patients and 50 matched controls were enrolled. Among the genetic variants reported to be associated with pancreatitis, only CASR rs1042636 was identified, and it showed no significant difference between the case and control groups. A total of 54,269 non-synonymous variants from 14,313 genes was identified. Logistic regression analysis of these variants showed that the IRF2BP1 rs60158447 GC genotype was significantly associated with the occurrence of PEP (odds ratio 2.248, FDR q value = 0.005). Gene-wise analyses did not show any significant results. Conclusions This study found that the IRF2BP1 gene variant was significantly associated with PEP. This genetic variant is a highly targeted PEP risk factor candidate and can be used for screening high-risk PEP groups before ERCP through future validation. (ClinicalTrials.gov no. NCT02928718)