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[Hypertriglyceridemic acute pancreatitis. Is its clinical course different from lithiasic acute pancreatitis?]
Salvador Navarro1, Joaquín Cubiella, Fausto Feu
1Servicio de Gastroenterología, Institut de Malalties Digestives, Hospital Clínic de Barcelona, Barcelona, Spain. snavarro@clinic.ub.es
Background And Objective:
Although hypertriglyceridemia is an accepted cause of acute pancreatitis, its clinical course is not well defined. What is more, lipemic serum may interfere with an accurate pancreatic enzyme measurement and may hinder the diagnosis of acute pancreatitis. The objective was to analyze the clinical performance of hypertriglyceridemic acute pancreatitis and the diagnosis value of the serum measurement of pancreatic enzymes.
Patients And Method:
31 demographic, clinical, analytical and radiological data of 19 hypertriglyceridemic acute pancreatitis were retrospectively analyzed and their results were compared with data of 19 lithiasic acute pancreatitis without hypertriglyceridemia. Diagnosis of acute pancreatitis was based on clinical, radiological and/or laparotomical findings. Serum levels of triglycerides higher than 1,000 mg/dl were considered the cause of acute pancreatitis when other causes were excluded. Acute pancreatitis was considered lithiasic when gallstones were identified by ultrasonography, serum levels of triglycerides were lower than 200 mg/dl and there was no history of alcohol consumption.
Results:
Compared with lithiasic acute pancreatitis, hypertriglyceridemic acute pancreatitis showed more personal and family hypertriglyceridemia (9 vs 0), more previous episodes of pancreatitis (13 vs 2), pancreatitis was more severe (13 vs 5) and had more complications (29 vs 5). There was no mortality in either group. The serum levels of amylase and lipase supported the diagnosis in 26% and 58% of patients with hypertriglyceridemic acute pancreatitis compared with 58% and 79% of patients with lithiasic acute pancreatitis, respectively. Hospital stay was longer in hypertriglyceridemic than in lithiasic acute pancreatitis (24 [45] vs 7.6 [3.1] days; p = NS). Demographic and analytical factors which could permit to predict the severity of acute pancreatitis could not be identified.
Conclusions:
Hypertriglyceridemic acute pancreatitis is relapsing and its clinical course is more severe than lithiasic acute pancreatitis. The measurement of amylase and lipase levels is less useful in the diagnosis of hypertriglyceridemic than in lithiasic acute pancreatitis.
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