Echinococcosis, caused by the tapeworm Echinococcus, is rare in Korea and is primarily imported from endemic areas. We report a case of a 37-year-old Korean man with multiple large hepatic cysts, initially diagnosed as simple cysts at a local clinic in 2018. The patient had lived in Oman, an endemic area, for several months in 2016. Upon referral to a tertiary hospital in 2023, due to progressive cyst enlargement, liver magnetic resonance imaging revealed three large cysts with a water lily sign. Serum IgG against Echinococcus was positive by enzyme-linked immunosorbent assay. After diagnosis of echinococcosis, treatment with albendazole and puncture-aspiration-injection-reaspiration (PAIR) was performed.Microscopic and molecular analysis of cyst aspirates confirmed Echinococcus granulosus infection. Follow-up computed tomography demonstrated a reduction in cyst size, yet the emergence of a new right pleural effusion and consolidation in the left lower lobe of the lung necessitated the continuation of albendazole therapy. This case highlights the importance of thorough travel history, imaging findings, and the effectiveness of PAIR combined with albendazole in treating imported echinococcosis.

Background: Gout is a type of inflammatory arthritis caused by monosodium urate crystal deposits, and the prevalence of this condition has been increasing. This study aimed to determine the combined effects of genetic risk factors and lifestyle habits on gout, using data from a Korean cohort study. Identifying high-risk individuals in advance can help prevent gout and its associated disorders. Methods: We analyzed data from the Korean Genome and Epidemiology Study-Urban Health Examinees cohort (KoGES-HEXA). Genetic information of the participants was collected at baseline, and gout cases were identified based on patient statements. The polygenic risk score (PRS) was calculated using nine independent genome-wide association study datasets, and lifestyle factors and metabolic syndrome status were measured for each participant using the KoGES. Logistic regression models were used to estimate the odds ratios (ORs) for gout in relation to genetic risk, lifestyle habits, and metabolic health status, after adjusting for age and sex. Results: Among 44,605 participants, 617 were diagnosed with gout. Gout was associated with older age, higher body mass index, and higher prevalence of hypertension, diabetes, and hypertriglyceridemia. High PRS, unfavorable lifestyle habits, and poor metabolic profiles were significantly associated with an increased risk of gout. Compared with that in the low-genetic-risk and healthy lifestyle group or ideal metabolic profile group, the risk of gout was increased in the high-genetic-risk plus unfavorable lifestyle (OR, 3.64; 95% confidence interval [CI], 2.32–6.03) or poor metabolic profile (OR, 7.78; 95% CI, 4.61–13.40) group.Conversely, adherence to favorable lifestyle habits significantly reduced gout risk, especially in high-genetic-risk groups. Conclusion Genetic predisposition and unhealthy lifestyle habits significantly increase the risk of gout. Promoting healthy lifestyle habits is crucial to prevent the development of gout, particularly in individuals with high genetic susceptibility.

Background/Aims: We aim to compare the remission of erosive esophagitis (EE) among individuals with different phenotypes based on their metabolic health and obesity status and investigate the impact of changes in metabolic health on the EE remission. Methods: Asymptomatic adults (n = 16 845) with EE at baseline, who underwent follow-up esophagogastroduodenoscopy (EGD) were categorized into 4 groups as follows: metabolically healthy (MH) nonobese, metabolically unhealthy (MU) nonobese, MH obese, and MU obese. EE was defined as grade A or higher mucosal breaks observed using esophagogastroduodenoscopy. Results: During a median follow-up of 2.2 years, the remission rates of EE were 286.4/10 3 , 260.1/10 3 , 201.5/10 3 , and 219.9/10 3 person-years in MH nonobese, MU nonobese, MH obese, and MU obese groups, respectively. Multivariate-adjusted hazard ratios (95% CI) for EE remission among the MH nonobese, MU nonobese, and MH obese groups versus that of the MU obese group were 1.30 (1.23-1.37), 1.17 (1.12-1.23), and 0.98 (0.90-1.06), respectively, whereas those of the persistent MH, progression of MH to MU, and remission of MU to MH compared with the persistent MU group were 1.37 (1.23-1.52), 1.15 (1.01-1.30), and 1.28 (1.12-1.46), respectively.Increased EE remission in the persistent MH group was consistently observed in individuals with and without obesity (or abdominal obesity). Conclusions Metabolic health and nonobesity independently and favorably impact EE remission. Maintaining normal weight and healthy metabolic status may contribute to EE remission.

Background/Aims: This study aimed to evaluate the performance of the Model for End-Stage Liver Disease (MELD) 3.0 for predicting mortality and liver-related complications compared with the Child-Pugh classification, albumin-bilirubin (ALBI) grade, the MELD, and the MELD sodium (MELDNa) score. Methods: We evaluated a multicenter retrospective cohort of incorporated patients with cirrhosis between 2013 and 2019. We conducted comparisons of the area under the receiver operating characteristic curve (AUROC) of the MELD3.0 and other models for predicting 3-month mortality. Additionally, we assessed the risk of cirrhosis-related complications according to the MELD3.0 score. Results: A total of 3,314 patients were included. The mean age was 55.9±11.3 years, and 70.2% of the patients were male. Within the initial 3 months, 220 patients (6.6%) died, and the MELD3.0had the best predictive performance among the tested models, with an AUROC of 0.851, outperforming the Child-Pugh classification, ALBI grade, MELD, and MELDNa. A high MELD3.0score was associated with an increased risk of mortality. Compared with that of the group with a MELD3.0 score <10 points, the adjusted hazard ratio of the group with a score of 10–20 pointswas 2.176, and that for the group with a score of ≥20 points was 4.892. Each 1-point increase inthe MELD3.0 score increased the risk of cirrhosis-related complications by 1.033-fold. The risk of hepatorenal syndrome showed the highest increase, with an adjusted hazard ratio of 1.149, followed by hepatic encephalopathy and ascites. Conclusions The MELD3.0 demonstrated robust prognostic performance in predicting mortality in patients with cirrhosis. Moreover, the MELD3.0 score was linked to cirrhosis-related complications, particularly those involving kidney function, such as hepatorenal syndrome and ascites.

Cynaropicrin, a sesquiterpene lactone found in artichoke leaves exerts diverse pharmacological effects. This study investigated whether cynaropicrin has a paraptosis-like cell death effect in human hepatocellular carcinoma Hep3B cells in addition to the apoptotic effects reported in several cancer cell lines. Cynaropicrin-induced cytotoxicity and cytoplasmic vacuolation, a key characteristic of paraptosis, were not ameliorated by inhibitors of necroptosis, autophagy, or pan caspase inhibitors in Hep3B cells. Our study showed that cynaropicrin-induced cytotoxicity was accompanied by mitochondrial dysfunction and endoplasmic reticulum stress along with increased cellular calcium ion levels. These effects were significantly mitigated by endoplasmic reticulum stress inhibitor or protein synthesis inhibitor. Moreover, cynaropicrin treatment in Hep3B cells increased reactive oxygen species generation and downregulated apoptosis-linked gene 2-interacting protein X (Alix), a protein that inhibits paraptosis. The addition of the reactive oxygen species scavenger N-acetyl-L-cysteine (NAC) neutralized cynaropicrin-induced changes in Alix expression and endoplasmic reticulum stress marker proteins counteracting endoplasmic reticulum stress and mitochondrial impairment. This demonstrates a close relationship between endoplasmic reticulum stress and reactive oxygen species generation. Additionally, cynaropicrin activated p38 mitogen activated protein kinase and a selective p38 mitogen activated protein kinase blocker alleviated the biological phenomena induced by cynaropicrin. NAC pretreatment showed the best reversal of cynaropicrin induced vacuolation and cellular inactivity. Our findings suggest that cynaropicrin induced oxidative stress in Hep3B cells contributes to paraptotic events including endoplasmic reticulum stress and mitochondrial damage.

Purpose: The association between the fecal microbiota and colorectal cancer (CRC) risk has been suggested in epidemiologic studies. However, data from large-scale population-based studies are lacking. Materials and Methods: In this case-control study, we recruited 283 CRC patients from the Center for Colorectal Cancer, National Cancer Center Hospital, Korea to perform 16S rRNA gene sequencing of fecal samples. A total of 283 age- and sex-matched healthy participants were selected from 890 cohort of healthy Koreans that are publicly available (PRJEB33905). The microbial dysbiosis index (MDI) was calculated based on the differentially abundant species. The association between MDI and CRC risk was observed using conditional logistic regression. Sparse Canonical Correlation Analysis was performed to integrate species data with microbial pathways obtained by PICRUSt2. Results: There is a significant divergence of the microbial composition between CRC patients and controls (permutational multivariate analysis of variance p=0.001). Those who were in third tertile of the MDI showed a significantly increased risk of CRC in the total population (odds ratio [OR], 6.93; 95% confidence interval [CI], 3.98 to 12.06; p-trend < 0.001) compared to those in the lowest tertile. Similar results were found for men (OR, 6.28; 95% CI, 3.04 to 12.98; p-trend < 0.001) and women (OR, 7.39; 95% CI, 3.10 to 17.63; p-trend < 0.001). Bacteroides coprocola and Bacteroides plebeius species and 12 metabolic pathways were interrelated in healthy controls that explain 91% covariation across samples. Conclusion Dysbiosis in the fecal microbiota may be associated with an increased risk of CRC. Due to the potentially modifiable nature of the gut microbiota, our findings may have implications for CRC prevention among Koreans.

Echinococcosis, caused by the tapeworm Echinococcus, is rare in Korea and is primarily imported from endemic areas. We report a case of a 37-year-old Korean man with multiple large hepatic cysts, initially diagnosed as simple cysts at a local clinic in 2018. The patient had lived in Oman, an endemic area, for several months in 2016. Upon referral to a tertiary hospital in 2023, due to progressive cyst enlargement, liver magnetic resonance imaging revealed three large cysts with a water lily sign. Serum IgG against Echinococcus was positive by enzyme-linked immunosorbent assay. After diagnosis of echinococcosis, treatment with albendazole and puncture-aspiration-injection-reaspiration (PAIR) was performed.Microscopic and molecular analysis of cyst aspirates confirmed Echinococcus granulosus infection. Follow-up computed tomography demonstrated a reduction in cyst size, yet the emergence of a new right pleural effusion and consolidation in the left lower lobe of the lung necessitated the continuation of albendazole therapy. This case highlights the importance of thorough travel history, imaging findings, and the effectiveness of PAIR combined with albendazole in treating imported echinococcosis.

Background: Gout is a type of inflammatory arthritis caused by monosodium urate crystal deposits, and the prevalence of this condition has been increasing. This study aimed to determine the combined effects of genetic risk factors and lifestyle habits on gout, using data from a Korean cohort study. Identifying high-risk individuals in advance can help prevent gout and its associated disorders. Methods: We analyzed data from the Korean Genome and Epidemiology Study-Urban Health Examinees cohort (KoGES-HEXA). Genetic information of the participants was collected at baseline, and gout cases were identified based on patient statements. The polygenic risk score (PRS) was calculated using nine independent genome-wide association study datasets, and lifestyle factors and metabolic syndrome status were measured for each participant using the KoGES. Logistic regression models were used to estimate the odds ratios (ORs) for gout in relation to genetic risk, lifestyle habits, and metabolic health status, after adjusting for age and sex. Results: Among 44,605 participants, 617 were diagnosed with gout. Gout was associated with older age, higher body mass index, and higher prevalence of hypertension, diabetes, and hypertriglyceridemia. High PRS, unfavorable lifestyle habits, and poor metabolic profiles were significantly associated with an increased risk of gout. Compared with that in the low-genetic-risk and healthy lifestyle group or ideal metabolic profile group, the risk of gout was increased in the high-genetic-risk plus unfavorable lifestyle (OR, 3.64; 95% confidence interval [CI], 2.32–6.03) or poor metabolic profile (OR, 7.78; 95% CI, 4.61–13.40) group.Conversely, adherence to favorable lifestyle habits significantly reduced gout risk, especially in high-genetic-risk groups. Conclusion Genetic predisposition and unhealthy lifestyle habits significantly increase the risk of gout. Promoting healthy lifestyle habits is crucial to prevent the development of gout, particularly in individuals with high genetic susceptibility.

Background/Aims: We aim to compare the remission of erosive esophagitis (EE) among individuals with different phenotypes based on their metabolic health and obesity status and investigate the impact of changes in metabolic health on the EE remission. Methods: Asymptomatic adults (n = 16 845) with EE at baseline, who underwent follow-up esophagogastroduodenoscopy (EGD) were categorized into 4 groups as follows: metabolically healthy (MH) nonobese, metabolically unhealthy (MU) nonobese, MH obese, and MU obese. EE was defined as grade A or higher mucosal breaks observed using esophagogastroduodenoscopy. Results: During a median follow-up of 2.2 years, the remission rates of EE were 286.4/10 3 , 260.1/10 3 , 201.5/10 3 , and 219.9/10 3 person-years in MH nonobese, MU nonobese, MH obese, and MU obese groups, respectively. Multivariate-adjusted hazard ratios (95% CI) for EE remission among the MH nonobese, MU nonobese, and MH obese groups versus that of the MU obese group were 1.30 (1.23-1.37), 1.17 (1.12-1.23), and 0.98 (0.90-1.06), respectively, whereas those of the persistent MH, progression of MH to MU, and remission of MU to MH compared with the persistent MU group were 1.37 (1.23-1.52), 1.15 (1.01-1.30), and 1.28 (1.12-1.46), respectively.Increased EE remission in the persistent MH group was consistently observed in individuals with and without obesity (or abdominal obesity). Conclusions Metabolic health and nonobesity independently and favorably impact EE remission. Maintaining normal weight and healthy metabolic status may contribute to EE remission.

Tooth wear is a physiologic process, but when accelerated by specific factors, it is considered pathologic wear, leading various issues that require prosthodontic intervention. Full-mouth prosthetic rehabilitation is often considered to restore adequate vertical dimension and esthetics for patients with severely worn dentition.However, a minimally invasive prosthodontic approach through multidisciplinary collaboration may be feasible for patients with localized anterior or posterior wear. This clinical case addressed the treatment for excessive anterior deep bites and pathologic wear of the anterior teeth, leading to deteriorated esthetics and function. Orthodontic extrusion was employed in the posterior teeth to increase the vertical dimension of occlusion and secure adequate space for the anterior restorations. A minimally invasive treatment was possible by limiting the scope of treatment to the anterior region. As a result, function and esthetics were improved by restoring only the teeth with pathologic wear without removing healthy tooth structure.