Current knowledge of hypertriglyceridemic pancreatitis

Abstract Severe hypertriglyceridemia (HTG) is a well established and the most common cause of acute pancreatitis (AP) after alcohol and gall stone disease. It is alleged to account for up to 10% of all pancreatitis episodes. Studies suggest that in patients with triglyceride (TG) levels > 1000 mg/dL (> 11.3 mmol/L), hypertriglyceridemia-induced acute pancreatitis (HTGP-AP) occurs in approximately 15–20% of all subjects referred to Lipid Clinics. Until now, there is no clear evidence which patients with severe HTG will develop pancreatitis and which will not. Underlying pathophysiological concepts include hydrolysis of TG by pancreatic lipase and excessive formation of free fatty acids with inflammatory changes and capillary injury. Additionally hyperviscosity and ischemia may play a decisive role. The clinical features of HTG-AP patients are supposed to be no different from patients with AP of other etiologies. Yet, there are well-conducted studies suggesting that HTG-AP is associated with a higher severity and complication rate. Therapeutic measurements in HTG-AP include dietary modifications, different antihyperlipidemic agents, insulin and/or heparin treatment. The beneficial use of plasmapheresis is repeatedly reported and suggested in many studies. Yet, due to the lack of randomized and controlled trials, it is currently unknown if plasmapheresis may improve morbidity and mortality in the clinical setting of HTG-AP. Since there are no commonly accepted clinical guidelines in the management of HTG-AP, there is a definite need for an international, multicenter approach to this important subject.