ObjectiveTo summarize the research progress of diagnosis and treatment in hypertriglyceridemia pancreatitis in recent years.MethodsThrough the retrieval of relevant literatures, the progress of diagnosis and treatment in hypertriglyceridemia pancreatitis were reviewed.ResultsHypertriglyceridemia pancreatitis is a rare acute pancreatitis, but with the improvement of living standard and the change of diet structure, the incidence of this disease in recent years was increasing, and more likely to lead to complications, causing serious consequences. The treatment of hypertriglyceridemia pancreatitis in addition to the routine treatment of pancreatitis, attention should also be paid to the rapid reduction of blood triglyceride levels, including plasma exchange, the use of low molecular weight heparin and insulin, and the use of lipid-lowering drugs.ConclusionsHypertriglyceridemia pancreatitis is more severe than acute pancreatitis caused by other causes, and the incidence of complications is higher. Maintaining a lower level of blood triglycerides is of great significance for the improvement of this pancreatitis and the prevention of the recurrence of pancreatitis.
ObjectiveTo systematically review the pathophysiological mechanisms and clinical characteristics of hypertriglyceridemia-associated acute pancreatitis, with a particular focus on the role of the gut microbiota and the gut–pancreas axis, and to summarize emerging microbiota-targeted therapeutic strategies and future research directions. MethodsRelevant literature published in recent years was reviewed and analyzed. Evidence regarding epidemiological features, pathogenic mechanisms, alterations in gut microbial composition, and microbiota-based therapeutic approaches was synthesized to establish an integrated framework linking dyslipidemia, gut microbial dysbiosis, and acute pancreatitis. ResultsCurrent evidence suggests that hypertriglyceridemia contributes to the initiation and progression of acute pancreatitis through multiple mechanisms, including lipotoxic injury, inflammatory cascade activation, and microcirculatory dysfunction. Gut microbiota dysbiosis and impairment of intestinal barrier integrity are closely associated with disease severity. Microbial metabolites and immune-regulatory pathways may play important roles in disease progression. Microbiota-targeted interventions have demonstrated potential in modulating inflammation, maintaining intestinal barrier function, and restoring metabolic homeostasis; however, their clinical efficacy and safety require further validation. ConclusionsThe gut microbiota and the gut–pancreas axis may represent key regulatory links between hypertriglyceridemia and acute pancreatitis. Further elucidation of the underlying mechanisms and advancement of precision microbiome-based interventions may provide novel approaches for risk stratification, early intervention, and comprehensive management of hypertriglyceridemia-associated acute pancreatitis.
