Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

BACKGROUND: Mast cells are immune sentinels in the skin that respond to a wide range of pathological and environmental stimuli; they owe their function to the expression of Toll-like receptors (TLRs). We previously found that tonsilderived mesenchymal stem cells (T-MSCs) were able to effectively attenuate TLR7-mediated skin inflammation in mice, which was accompanied by an increase in mast cell number. The present study investigated whether T-MSC extracellular vesicles, such as exosomes, are able to regulate mast cell activation in response to TLR7 stimulation. METHODS: The HMC-1 human mast cell line was treated with a TLR7 agonist in the presence or absence of T-MSC exosomes, and the levels of expressed inflammatory cytokines were assessed. Additionally, mice were repeatedly injected with a TLR7 agonist with or without interval treatments with T-MSC exosomes and assessed dermal distribution of mast cells and related immune cells. RESULTS: We showed that T-MSC exosomes containing microRNAs that target inflammatory cytokines significantly reduced the expression of inflammatory cytokines in TLR7 agonist-treated HMC-1 cells. In addition, T-MSC exosomes inhibited the increase in the number of both dermal mast cells and CD14-positive cells in TLR7 agonist-treated mice. CONCLUSION Our data suggest that T-MSC exosomes have regulatory effects on mast cell activation under inflammatory conditions, including TLR7 stimulation.

Background: and Purpose The natural course of adult-onset moyamoya disease (MMD) is unknown, and there is no medical treatment that halts its progression. We hypothesized that progressive shrinkage of large intracranial arteries occurs in adult-onset MMD, and that cilostazol inhibits this process. Methods: Serial high-resolution magnetic resonance imaging (HR-MRI) was performed on 66 patients with MMD: 30 patients received cilostazol, 21 received other antiplatelets, and 15 received no antiplatelets or had poor compliance to them. Serial HR-MRI was performed (interval between MRI scans: 29.67±18.02 months, mean±SD), and changes in outer diameter, luminal stenosis, and vascular enhancement were measured. Factors affecting HR-MRI changes were evaluated, including vascular risk factors and the ring finger protein 213 gene variant. Results: The progression of stenosis to occlusion, recurrent ischemic stroke, and the development of new stenotic segments were observed in seven, seven, and three patients, respectively. Serial HR-MRI indicated that the degree of stenosis increased with negative remodeling (outer diameter shrinkage). Patients who received cilostazol presented significantly larger outer diameters and lower degrees of stenosis compared with other groups (p=0.005 and p=0.031, respectively). After adjusting for clinical and genetic factors, only cilostazol use was independently associated with negative remodeling (odds ratio=0.29, 95% confidence interval=0.10–0.84, p=0.023). While vascular enhancement was observed in most patients (61 patients), the progression of enhancement or the occurrence of new vascular enhancement was rarely observed on follow-up HR-MRI (6 and 1 patients, respectively). Conclusions Adult-onset MMD induces progressive shrinkage of large intracranial arteries, which cilostazol treatment may prevent. Further randomized clinical trials are warranted.

Objective: Unlike common acute urinary tract infections, obstructive urinary tract infections caused by urinary calculus can be fatal because they can progress to sepsis and cause shock or disseminated intravascular coagulation. The evidence of patients with obstructive urinary tract infections caused by urinary tract stones visiting the emergency center is still lacking. Methods: Seventy-seven patients who visited the emergency room with obstructive urinary tract infections caused by urinary calculus from January 2016 to December 2018 were enrolled in this study and divided into two groups: sepsis group and non-sepsis group. Results: The lymphocyte count, platelet count, neutrophil-lymphocyte ratio, serum creatinine, and C-reactive protein were significantly different in the sepsis-positive and negative groups. Percutaneous nephrostomy was also significantly higher in the sepsis-positive group. The area under the receiver operating characteristic curve was calculated to evaluate the ability of the neutrophil-lymphocyte ratio and platelet-lymphocyte ratio to predict a septic urinary tract infection. The neutrophil-lymphocyte ratio and platelet-lymphocyte ratio were 0.659 and 0.550, respectively. Multivariate logistic regression analysis showed that diabetic patients, percutaneous nephrostomy, and serum creatinine were associated with septic obstructive urinary tract infection. Conclusion In patients with an obstructive urinary tract infection who were referred to the emergency center, diabetic patients and those with high blood urea nitrogen and creatinine levels are at high risk of sepsis. In such cases, rapid diagnosis and treatment, such as percutaneous nephrostomy, are necessary.

OBJECTIVE: Syncope is mostly benign, but it can also be caused by a life-threatening situation. In Korea, no studies have investigated application of the Canadian Syncope Risk Score (CSRS) to patients with syncope; therefore, this study was started to evaluate the usefulness of CSRS. METHODS: A total of 222 patients who visited the emergency room with syncope for one year from January 2016 to December 2016 were enrolled in this study. Patients were divided into two groups, a serious adverse events (SAE) group and a non-serious adverse events group. The scores of the nine CSRS variables were added and the CSRS was then calculated after the addition. RESULTS: The CSRS score for patients with SAE ranged from 0 to 8. The CSRS score was 18.6%, 31.7%, 55.6%, and 58.8% for 0, 1, 2, and 3, respectively. In the case of CSRS 0 and 1, 17 patients (81.0%) and 11 patients (84.6%) were non-cardiac. In the case of CSRS 2, 7 were non-cardiac (70.0%). In the case of CSRS 3, 6 cases (60.0%) were cardiogenic and 4 cases (40.0%) were non-cardiogenic. The area under the receiver operating characteristic curve of CSRS to predict SAE was 0.71. Setting the CSRS cutoff value to 0, we found that sensitivity and specificity of predicting SAE was 67.19% and 67.09%, respectively. CONCLUSION: CSRS may be difficult to predict for acute intracranial disease or acute hemorrhagic disease requiring transfusion; therefore, it is necessary to supplement it further.
Emergencies* ; Emergency Service, Hospital ; Humans ; Korea* ; Risk Factors ; ROC Curve ; Sensitivity and Specificity ; Syncope*

OBJECTIVE: The aim of this study was to evaluate the clinicopathological features of minimal deviation adenocarcinoma (MDA) and to analyze its prognostic factors. METHODS: We retrospectively analyzed the medical records of 17 patients who were diagnosed with MDA at a single institution between January 2005 and December 2015. RESULTS: The median age of the patients was 47.7 years (33–75 years). MDA was diagnosed in 7 patients (41.2%) before performing definitive surgery. Stage IB disease was diagnosed in 12 patients (70.6%) and advanced stage disease (stage II: 3, stage III: 2) in 5. MDA was incidentally diagnosed following hysterectomy for benign conditions in 6 patients. Adjuvant therapy was administered to 13 patients (76.5%). During median follow-up over 33.6 months (7–99 months), 11 patients (64.7%) showed no evidence of disease, 6 (35.3%) showed persistent or recurrent disease and 5 died of the disease. Peutz-Jeghers syndrome was not suspected in any patient, and no mutation was detected in the 3 patients who underwent genetic testing. Univariate analysis showed that advanced stage disease (P=0.016) and lymphovascular space invasion (P=0.002) demonstrated a statistically significant association with poor overall survival (OS) rates. Advanced stage disease continued to show a significant association with poor OS rates (hazard ratio, 2.92; 95% confidence interval, 1.097–7.746; P=0.032) even after multivariate analysis. CONCLUSION: Early diagnosis is important to manage MDA. Clinicians should consider MDA among the differential diagnoses in patients with a suspicious clinical presentation even with negative cervical screening tests.
Adenocarcinoma* ; Cervix Uteri* ; Diagnosis, Differential ; Early Diagnosis ; Female ; Follow-Up Studies ; Genetic Testing ; Humans ; Hysterectomy ; Mass Screening ; Medical Records ; Multivariate Analysis ; Peutz-Jeghers Syndrome ; Retrospective Studies ; Uterine Cervical Neoplasms

PURPOSE: In patients with altered mentality caused by drugs or unknown causes, ammonia is checked to facilitate differential diagnosis or diagnose hepatic coma. This helps early prevention and treatment of brain damage due to hyperammonemia. This study was conducted to evaluate clinical characteristics of intoxicated adult patients with hyperammonemia. METHODS: We evaluated 95 patients with hyperammonemia among intoxicated patients above the age of 15 who visited our ED from January 2013 to December 2015. We analyzed the demographic characteristics and type of poisoning substance, reason for ingestion, toxicological characteristics such as elapsed time from ingestion to hospital visit, lab, clinical progression and complications. Data were evaluated using the student's t test or Mann-Whitney U test for continuous variables, and Chi-square test and Fisher's exact test for frequency analysis of categorical variables. RESULTS: When compared to healthy individuals, patients with hyperammonemia showed statistical significance on their SOFA score (p=0.016) and poison severity score (p<0.001). Additionally, patients with hyperammonemia showed significantly different initial serum AST level (p=0.012) and maximum serum AST level during the hospital stay (p=0.026) when compared to healthy individuals. Moreover, individuals with sustained hyperammonemia compared to transient hyperammonemia showed clinically significant SOFA scores (p<0.001), poison severity scores (p=0.007), mortality rates in the ICU (p=0.021), as well as different duration of hospital stay (p=0.037), serum creatinine level (p=0.002), erythrocyte sedimentation rate (p=0.025), and serum myoglobin (p=0.015). CONCLUSION: Most poisoning-induced hyperammonemia cases were transient and recovered without special treatment. Therefore, hyperammonemia is almost non-specific among poisoning patients.
Adult ; Ammonia ; Blood Sedimentation ; Brain ; Creatinine ; Diagnosis, Differential ; Eating ; Hepatic Encephalopathy ; Humans ; Hyperammonemia* ; Length of Stay ; Mortality ; Myoglobin ; Poisoning