Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Background/Aims: Noninvasive methods have become increasingly critical in the diagnosis of fibrosis in chronic liver diseases. Herein, we compared the diagnostic performance of serum Mac2 binding protein glycosylation isomer (M2BPGi) and other serological panels for fibrosis in patients with nonalcoholic fatty liver disease (NAFLD) and proposed an improved two-step diagnostic algorithm for advanced fibrosis. Methods: We enrolled 231 patients diagnosed with NAFLD who underwent a liver biopsy. We subsequently evaluated the diagnostic performance of serological panels, including serum M2BPGi, a fibrosis index based on four factors (FIB-4), aspartate aminotransferase-to-platelet ratio index (APRI), and NAFLD fibrosis score (NFS), in predicting the stage of liver fibrosis. We then constructed a two-step algorithm to better differentiate advanced fibrosis. Results: The areas under the receiver operating characteristic curves of serum M2BPGi, FIB-4, APRI, and NFS for advanced fibrosis (≥F3) were 0.823, 0.858, 0.779, and 0.827, respectively. To reduce the performance of unnecessary liver biopsy, we propose a two-step algorithm using FIB-4 as an initial diagnostic tool and serum M2BPGi (≥0.6) as an additional diagnostic method for patients classified as intermediate (23%). Using the proposed algorithm, the sensitivity, specificity, accuracy, positive predictive value, and negative predictive value were 0.812, 0.814, 0.814, 0.600, and 0.927, respectively. Conclusions Serum M2BPGi is a simple and effective test for advanced fibrosis in patients with NAFLD. Application of the two-step algorithm based on FIB-4 and M2BPGi proposed here can improve diagnostic performance and reduce unnecessary tests, making diagnosis easily accessible, especially in primary medical centers.

Viral load and the duration of viral shedding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are important determinants of the transmission of coronavirus disease 2019.In this study, we examined the effects of viral doses on the lung and spleen of K18-hACE2 transgenic mice by temporal histological and transcriptional analyses. Approximately, 1×105 plaque-forming units (PFU) of SARS-CoV-2 induced strong host responses in the lungs from 2 days post inoculation (dpi) which did not recover until the mice died, whereas responses to the virus were obvious at 5 days, recovering to the basal state by 14 dpi at 1×102 PFU. Further, flow cytometry showed that number of CD8+ T cells continuously increased in 1×102 PFU-virusinfected lungs from 2 dpi, but not in 1×105 PFU-virus-infected lungs. In spleens, responses to the virus were prominent from 2 dpi, and number of B cells was significantly decreased at 1×105PFU; however, 1×102 PFU of virus induced very weak responses from 2 dpi which recovered by 10 dpi. Although the defense responses returned to normal and the mice survived, lung histology showed evidence of fibrosis, suggesting sequelae of SARS-CoV-2 infection. Our findings indicate that specific effectors of the immune response in the lung and spleen were either increased or depleted in response to doses of SARS-CoV-2. This study demonstrated that the response of local and systemic immune effectors to a viral infection varies with viral dose, which either exacerbates the severity of the infection or accelerates its elimination.

Objective: To investigate the relationship between reduced glutathione (GSH), a key molecule of the antioxidant defense system in the blood, and glutathione reductase (GR), which reduces oxidized glutathione (glutathione disulfide [GSSG]) to GSH and maintains the redox balance, with the prevalence of Alzheimer’s dementia and cognitive decline. Methods: In all, 20 participants with Alzheimer’s dementia who completed the third follow-up clinical evaluation over 6 years were selected, and 20 participants with normal cognition were selected after age and sex matching. The GSH and GR concentrations were the independent variables. Clinical diagnosis and neurocognitive test scores were the dependent variables indicating cognitive status. Results: The higher the level of GR, the greater the possibility of having normal cognition than of developing Alzheimer’s dementia. Additionally, the higher the level of GR, the higher the neurocognitive test scores. However, this association was not significant for GSH. After 6 years, the conversion rate from normal cognition to cognitive impairment was significantly higher in the lower 50th percentile of the GR group than in the upper 50th percentile. Conclusion The higher the GR, the lower the prevalence of Alzheimer’s dementia and incidence of cognitive impairment and the higher the cognitive test scores. Therefore, GR is a potential protective biomarker against Alzheimer’s dementia and cognitive decline.

Despite the availability of direct-acting antivirals (DAAs) for chronic hepatitis C virus (HCV) infection in Korea, need remains for pangenotypic regimens that can be used in the presence of hepatic impairment, comorbidities, or prior treatment failure. We investigated the efficacy and safety of sofosbuvir–velpatasvir and sofosbuvir–velpatasvir–voxilaprevir for 12 weeks in HCV-infected Korean adults. Methods: This Phase 3b, multicenter, open-label study included 2 cohorts. In Cohort 1, participants with HCV genotype 1 or 2 and who were treatment-naive or treatment-experienced with interferon-based treatments, received sofosbuvir–velpatasvir 400/100 mg/day. In Cohort 2, HCV genotype 1 infected individuals who previously received an NS5A inhibitor-containing regimen ≥ 4 weeks received sofosbuvir–velpatasvir–voxilaprevir 400/100/100 mg/day. Decompensated cirrhosis was an exclusion criterion. The primary endpoint was SVR12, defined as HCV RNA < 15 IU/mL 12 weeks following treatment. Results: Of 53 participants receiving sofosbuvir–velpatasvir, 52 (98.1%) achieved SVR12. The single participant who did not achieve SVR12 experienced an asymptomatic Grade 3 ASL/ALT elevation on day 15 and discontinued treatment. The event resolved without intervention. All 33 participants (100%) treated with sofosbuvir–velpatasvir–voxilaprevir achieved SVR 12. Overall, sofosbuvir–velpatasvir and sofosbuvir–velpatasvir–voxilaprevir were safe and well tolerated. Three participants (5.6%) in Cohort 1 and 1 participant (3.0%) in Cohort 2 had serious adverse events, but none were considered treatment-related. No deaths or grade 4 laboratory abnormalities were reported. Conclusions: Treatment with sofosbuvir–velpatasvir or sofosbuvir–velpatasvir–voxilaprevir was safe and resulted in high SVR12 rates in Korean HCV patients.

Background/Aims: We used next-generation sequencing (NGS) to analyze resistance-associated substitutions (RASs) and retreatment outcomes in patients with chronic hepatitis C virus (HCV) infection who failed direct-acting antiviral agent (DAA) treatment in South Korea. Methods: Using prospectively collected data from the Korean HCV cohort study, we recruited 36 patients who failed DAA treatment in 10 centers between 2007 and 2020; 29 blood samples were available from 24 patients. RASs were analyzed using NGS. Results: RASs were analyzed for 13 patients with genotype 1b, 10 with genotype 2, and one with genotype 3a. The unsuccessful DAA regimens were daclatasvir+asunaprevir (n=11), sofosbuvir+ribavirin (n=9), ledipasvir/sofosbuvir (n=3), and glecaprevir/pibrentasvir (n=1). In the patients with genotype 1b, NS3, NS5A, and NS5B RASs were detected in eight, seven, and seven of 10 patients at baseline and in four, six, and two of six patients after DAA failure, respectively. Among the 10 patients with genotype 2, the only baseline RAS was NS3 Y56F, which was detected in one patient. NS5A F28C was detected after DAA failure in a patient with genotype 2 infection who was erroneously treated with daclatasvir+asunaprevir. After retreatment, 16 patients had a 100% sustained virological response rate. Conclusions NS3 and NS5A RASs were commonly present at baseline, and there was an increasing trend of NS5A RASs after failed DAA treatment in genotype 1b. However, RASs were rarely present in patients with genotype 2 who were treated with sofosbuvir+ribavirin. Despite baseline or treatment-emergent RASs, retreatment with pan-genotypic DAA was highly successful in Korea, so we encourage active retreatment after unsuccessful DAA treatment.