Search

BackgroundAmiodarone is a class III antiarrhythmic drug that is commonly used in the clinic to treat ventricular arrhythmias and atrial fibrillation. We present a case report of the adverse effects of amiodarone and review its characteristics.Case reportA 73-year-old Asian female with a history of paroxysmal atrial fibrillation managed with amiodarone, well-controlled hypertension, and no substance abuse presented with gastrointestinal distress and dizziness, without chest pain or palpitations. Despite normal annual check-ups, she developed abnormal liver and thyroid function tests, and imaging revealed lung and liver changes suggestive of amiodarone toxicity. Discontinuation of amiodarone for sotalol led to symptom improvement and normalization of thyroid and liver functions, with imaging indicating recovery from interstitial fibrosis and reduced liver density.DiscussionAmiodarone, a widely used for treating ventricular and atrial arrhythmias, and with significant benefits in improving patient survival in cases of ventricular fibrillation. However, its long-term use is associated with serious adverse effects, including thyroid dysfunction, liver injury, and pulmonary toxicity, necessitating careful monitoring and management. Despite its efficacy, the need for research on early detection and management of amiodarone's side effects is crucial, highlighting the importance of regular monitoring and possibly adjusting therapy to mitigate these risks.

Pancreatic cancer (PC) is one of the deadliest gastrointestinal cancers, accounting for the fourth highest number of cancer-related fatalities. Increasing data suggests that mesenchymal stem cells (MSCs) might influence the drug resistance of GC cells in the tumor microenvironment and play essential roles in drug resistance development. However, the precise underlying process remains a mystery. The purpose of this study was to look at the control of MSC-induced SNHG7 in pancreatic cancer. In vitro and in vivo sphere formation, colony formation, and flow cytometry investigations revealed the stemness and Folfirinox resistance in pancreatic cancer cells. To confirm the direct connections between SNHG7 and other related targets, RNA pulldown and immunoprecipitation tests were performed. MSC co-culture enhanced the stemness and Folfirinox resistance in pancreatic cancer cells according to the findings. MSC co-culture increased SNHG7 expression in pancreatic cancer cells, contributing to the stemness and Folfirinox resistance. We demonstrated that Notch1 interacted with SNHG7 and could reverse the facilitative effect of SNHG7 on the stemness and Folfirinox resistance in pancreatic cancer cells. Finally, our findings showed that MSCs increased SNHG7 expression in pancreatic cancer cells, promoting the stemness and Folfirinox resistance via the Notch1/Jagged1/Hes-1 signaling pathway. These findings could provide a novel approach and therapeutic target for pancreatic cancer patients.