Key result
Survivors of acute hypertriglyceridaemic pancreatitis showed no significant differences in postheparin lipoprotein lipase activity (69 vs 92 mU/mL, p=0.057) or mass compared to patients with severe hypertriglyceridaemia without pancreatitis.
Why the study?
Are there differences in lipoprotein lipase activity, apolipoprotein mass, and polymorphisms between patients with severe hypertriglyceridaemia who develop acute pancreatitis and those who do not?
Population
24 survivors of acute hypertriglyceridaemic pancreatitis and 31 patients with severe hypertriglyceridaemia
Design
Case-control
Authors
Loading...
May identify protein differences linked to pancreatitis susceptibility in severe hypertriglyceridaemia; leaves open causal validation in prospective studies.
Case-Control (n=55)
No
Are there differences in lipoprotein lipase activity, apolipoprotein mass, and polymorphisms between patients with severe hypertriglyceridaemia who develop acute pancreatitis and those who do not?
Absolute Event Rate: 69% vs 92%
p-value: p=0.057
Primary defects in lipoprotein lipase and apolipoprotein C-II are rare in survivors of acute hypertriglyceridaemic pancreatitis, suggesting lipase activity measurements should be restricted to those with childhood onset.
Coca‐Prieto et al. (2009) conducted a case-control in Severe hypertriglyceridaemia with or without acute pancreatitis (n=55). Acute hypertriglyceridaemic pancreatitis vs. Severe hypertriglyceridaemia without pancreatitis was evaluated on Postheparin lipoprotein lipase (LPL) activity (mU/mL) (p=0.057). Survivors of acute hypertriglyceridaemic pancreatitis showed no significant differences in postheparin lipoprotein lipase activity (69 vs 92 mU/mL, p=0.057) or mass compared to patients with severe hypertriglyceridaemia without pancreatitis.