[Acute pancreatitis caused by hypertriglyceridemia]. / Hypertriglyceridaemia okozta akut pancreatitis sajátosságai beteganyagunkban.

UNLABELLED: Hypertriglyceridemia is reported to cause 1-7% of the cases of acute pancreatitis. AIM: The aim of the present study was to assess the clinical features and management of pancreatitis with hypertriglyceridemia in our tertiary center. METHODS: Between 1 January 2007 and 31 December 2009, patients with a diagnosis of hypertriglyceridemia-induced acute pancreatitis were reviewed. Patients with pancreatitis and serum triglyceride levels greater than 11.3 mmol/l (≈1000 mg/dl) were included. Acute pancreatitis with other etiologies was excluded. RESULTS: 26 patients (2 women, 24 men; median age at presentation 42 years; range: 22-70) were diagnosed with hypertriglyceridemia­induced acute pancreatitis; 3 patients had altogether 7 relapses. The total number of cases was 33, which accounted for 4.71% of the total number of acute pancreatitis cases in the examined period. There was a failure in diet in 30.3% and a history of regular alcohol abuse in 57.6% of the cases. A history of diabetes mellitus was present in 38.1%, and gallstones in 9.1% of the cases. Lactescent serum was described on admission in 27.3%. Mean triglyceride level was 47.24 mmol/l (≈4181 mg/dl; 12.4-103.8 mmol/l). Amylase level was elevated to three times the normal in 54.5%, and that of lipase to three times the normal in 58.8%. Necrotizing acute pancreatitis was diagnosed in 7 patients (26.9%), and pseudocyst in 8 patients (30.7%). Administration of insulin, heparin, plasmapheresis and fibrates lowered the triglyceride to 3.71 mmol/l (≈328 mg/dl). CONCLUSION: The clinical course of acute pancreatitis with hypertriglyceridemia does not differ from acute pancreatitis of other causes. Interestingly, levels of serum pancreatic enzymes may be normal or only minimally elevated. Insulin, heparin, plasmapheresis and fibrates effectively reduce lipid levels and relieve symptoms. A low triglyceride level is necessary to prevent relapses.

Hyperlipidemia induced by a cholesterol-rich diet aggravates necrotizing pancreatitis in rats.

The aim of the present study was to investigate whether hyperlipidemia can cause acute pancreatitis or alter its severity. Male Wistar rats were fed a 3% cholesterol-enriched diet or a normal diet for 16 weeks. Edematous and necrotizing pancreatitis was induced with 3x75 mug/kg body weight of cholecystokinin s.c. and 2x2 g/kg body weight of L-arginine i.p., respectively, in separate groups of normal and hyperlipidemic rats. The severity of the pancreatitis was assessed. We studied the influence of hyperlipidemia on the formation of oxygen-derived free radicals, endogenous scavengers, nitric oxide synthases (NOS), peroxynitrite (ONOO(-)), heat shock protein 72 (HSP72) and nuclear factor-kappa B (NF-kappaB) activation in the pancreas during acute edematous and necrotizing pancreatitis. Hyperlipidemia did not worsen edematous, but aggravated necrotizing pancreatitis. The cholesterol-enriched diet significantly reduced the catalase and Mn-superoxide dismutase (SOD) and constitutive NOS (cNOS) activities and increased the inducible NOS (iNOS) in the pancreas relative to those in the rats on the normal diet. The pancreatic nitrotyrosine level, as a marker of ONOO(-), and the NF-kappaB DNA-binding activity in the pancreas, were significantly elevated in the cholesterol-fed rats. The pancreatic HSP72 expression during necrotizing pancreatitis was not influenced by the hyperlipidemia. The pancreatic Mn-SOD, Cu, Zn-SOD, glutathione peroxidase, total glutathione and cNOS activities were significantly reduced, while the catalase, iNOS and NF-kappaB DNA-binding activities were significantly increased in the animals with necrotizing pancreatitis on the cholesterol diet as compared with those with pancreatitis and receiving the normal diet. Hyperlipidemia induced with this cholesterol-enriched diet leads to decreases in endogenous scavenger and cNOS activities, results in iNOS and NF-kappaB activation and stimulates ONOO(-) generation in the pancreas, which may be responsible for the aggravation of acute necrotizing pancreatitis.