Anticancer treatment for acute lymphocytic leukemia is based on drugs such as methotrexate, 6-mercaptopurine, vincristine, and asparaginase. Asparaginase-related pancreatitis is known to have an incidence of up to 18%, and is a major cause of discontinuation of anticancer treatment for leukemia due to acute onset and chronic complications. There were various cases of treatment of peripancreatic fluid retention caused by anticancer drugs in leukemia patients. Use of lumen-apposing metal stents (LAMS) for walled-off necrosis (WON) drainage has recently increased. The electrocautery-enhanced delivery system allowed simpler and faster stent placement, streamlining the overall procedure and potentially reducing procedure time. Therefore, favorable outcomes have been reported with the use of LAMS for endoscopic drainage of various conditions. In this paper, we discuss a case in which hot-system LAMS was performed to treat L-asparaginase-induced acute pancreatitis and pancreatic pseudocyst in an adult patient with acute lymphoblastic leukemia.

Anticancer treatment for acute lymphocytic leukemia is based on drugs such as methotrexate, 6-mercaptopurine, vincristine, and asparaginase. Asparaginase-related pancreatitis is known to have an incidence of up to 18%, and is a major cause of discontinuation of anticancer treatment for leukemia due to acute onset and chronic complications. There were various cases of treatment of peripancreatic fluid retention caused by anticancer drugs in leukemia patients. Use of lumen-apposing metal stents (LAMS) for walled-off necrosis (WON) drainage has recently increased. The electrocautery-enhanced delivery system allowed simpler and faster stent placement, streamlining the overall procedure and potentially reducing procedure time. Therefore, favorable outcomes have been reported with the use of LAMS for endoscopic drainage of various conditions. In this paper, we discuss a case in which hot-system LAMS was performed to treat L-asparaginase-induced acute pancreatitis and pancreatic pseudocyst in an adult patient with acute lymphoblastic leukemia.

Anticancer treatment for acute lymphocytic leukemia is based on drugs such as methotrexate, 6-mercaptopurine, vincristine, and asparaginase. Asparaginase-related pancreatitis is known to have an incidence of up to 18%, and is a major cause of discontinuation of anticancer treatment for leukemia due to acute onset and chronic complications. There were various cases of treatment of peripancreatic fluid retention caused by anticancer drugs in leukemia patients. Use of lumen-apposing metal stents (LAMS) for walled-off necrosis (WON) drainage has recently increased. The electrocautery-enhanced delivery system allowed simpler and faster stent placement, streamlining the overall procedure and potentially reducing procedure time. Therefore, favorable outcomes have been reported with the use of LAMS for endoscopic drainage of various conditions. In this paper, we discuss a case in which hot-system LAMS was performed to treat L-asparaginase-induced acute pancreatitis and pancreatic pseudocyst in an adult patient with acute lymphoblastic leukemia.

Anticancer treatment for acute lymphocytic leukemia is based on drugs such as methotrexate, 6-mercaptopurine, vincristine, and asparaginase. Asparaginase-related pancreatitis is known to have an incidence of up to 18%, and is a major cause of discontinuation of anticancer treatment for leukemia due to acute onset and chronic complications. There were various cases of treatment of peripancreatic fluid retention caused by anticancer drugs in leukemia patients. Use of lumen-apposing metal stents (LAMS) for walled-off necrosis (WON) drainage has recently increased. The electrocautery-enhanced delivery system allowed simpler and faster stent placement, streamlining the overall procedure and potentially reducing procedure time. Therefore, favorable outcomes have been reported with the use of LAMS for endoscopic drainage of various conditions. In this paper, we discuss a case in which hot-system LAMS was performed to treat L-asparaginase-induced acute pancreatitis and pancreatic pseudocyst in an adult patient with acute lymphoblastic leukemia.

Anticancer treatment for acute lymphocytic leukemia is based on drugs such as methotrexate, 6-mercaptopurine, vincristine, and asparaginase. Asparaginase-related pancreatitis is known to have an incidence of up to 18%, and is a major cause of discontinuation of anticancer treatment for leukemia due to acute onset and chronic complications. There were various cases of treatment of peripancreatic fluid retention caused by anticancer drugs in leukemia patients. Use of lumen-apposing metal stents (LAMS) for walled-off necrosis (WON) drainage has recently increased. The electrocautery-enhanced delivery system allowed simpler and faster stent placement, streamlining the overall procedure and potentially reducing procedure time. Therefore, favorable outcomes have been reported with the use of LAMS for endoscopic drainage of various conditions. In this paper, we discuss a case in which hot-system LAMS was performed to treat L-asparaginase-induced acute pancreatitis and pancreatic pseudocyst in an adult patient with acute lymphoblastic leukemia.

Background and Objectives: Lipid lowering therapy is essential to reduce the risk of major cardiovascular events; however, limited evidence exists regarding the use of statin with ezetimibe as primary prevention strategy for middle-aged adults. We aimed to investigate the impact of single pill combination therapy on clinical outcomes in relatively healthy middleaged patients when compared with statin monotherapy. Methods: Using the Korean National Health Insurance Service database, a propensity score match analysis was performed for baseline characteristics of 92,156 patients categorized into combination therapy (n=46,078) and statin monotherapy (n=46,078) groups. Primary outcome was composite outcomes, including death, coronary artery disease, and ischemic stroke. And secondary outcome was all-cause death. The mean follow-up duration was 2.9±0.3 years. Results: The 3-year composite outcomes of all-cause death, coronary artery disease, and ischemic stroke demonstrated no significant difference between the 2 groups (10.3% vs.10.1%; hazard ratio [HR], 1.022; 95% confidence interval [CI], 0.980–1.064; p=0.309).Meanwhile, the 3-year all-cause death rate was lower in the combination therapy group than in the statin monotherapy group (0.2% vs. 0.4%; p<0.001), with a significant HR of 0.595 (95% CI, 0.460–0.769; p<0.001). Single pill combination therapy exhibited consistently lower mortality rates across various subgroups. Conclusions Compared to the statin monotherapy, the combination therapy for primary prevention showed no difference in composite outcomes but may reduce mortality risk in relatively healthy middle-aged patients. However, since the study was observational, further randomized clinical trials are needed to confirm these findings.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Background and Objectives: Lipid lowering therapy is essential to reduce the risk of major cardiovascular events; however, limited evidence exists regarding the use of statin with ezetimibe as primary prevention strategy for middle-aged adults. We aimed to investigate the impact of single pill combination therapy on clinical outcomes in relatively healthy middleaged patients when compared with statin monotherapy. Methods: Using the Korean National Health Insurance Service database, a propensity score match analysis was performed for baseline characteristics of 92,156 patients categorized into combination therapy (n=46,078) and statin monotherapy (n=46,078) groups. Primary outcome was composite outcomes, including death, coronary artery disease, and ischemic stroke. And secondary outcome was all-cause death. The mean follow-up duration was 2.9±0.3 years. Results: The 3-year composite outcomes of all-cause death, coronary artery disease, and ischemic stroke demonstrated no significant difference between the 2 groups (10.3% vs.10.1%; hazard ratio [HR], 1.022; 95% confidence interval [CI], 0.980–1.064; p=0.309).Meanwhile, the 3-year all-cause death rate was lower in the combination therapy group than in the statin monotherapy group (0.2% vs. 0.4%; p<0.001), with a significant HR of 0.595 (95% CI, 0.460–0.769; p<0.001). Single pill combination therapy exhibited consistently lower mortality rates across various subgroups. Conclusions Compared to the statin monotherapy, the combination therapy for primary prevention showed no difference in composite outcomes but may reduce mortality risk in relatively healthy middle-aged patients. However, since the study was observational, further randomized clinical trials are needed to confirm these findings.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.