There is a well-recognised association between hyperlipidaemia and acute pancreatitis. However, the role of hyperlipidaemia in modulating disease course is not clear. The aim of the study was to conduct a prospective study in acute pancreatitis to assess the relation between hyperlipidaemia and disease severity using current disease descriptors. The study population constituted 43 patients with acute pancreatitis, admitted during the calendar year 2001. There were 19 (44%) males. The median (range) age was 50 (21-86) years. Serum triglycerides, cholesterol and high-density lipids were measured on admission. Patients were followed-up for at least 6 months after discharge. Principal outcomes were relation between hyperlipidaemia and peri-pancreatic complications and end-of-episode disease severity. The results showed that hypertriglyceridaemia was present in 14 patients (33%). There was a significant difference in mean (SEM) serum triglyceride levels between patients with alcohol-induced pancreatitis compared with pancreatitis of other aetiologies [3.07 (1.0) mmol/l vs. 1.26 (0.11) mmol/l; p = 0.03, Fisher's exact test]. There was no correlation between admission hypertriglyceridaemia and admission APACHE II score (r(2) = 0.0015). Similarly, there was no correlation between triglyceride level and either pancreatic inflammatory complications or final outcome. In conclusion, this study has demonstrated that there was no significant correlation between hypertriglyceridaemia and either complications of disease or overall end-of-episode severity in this population of patients with acute pancreatitis.
The nuclear factor-kappaB (NF-kappaB) is a transcription factor that plays a pivotal role in the induction of genes involved in the response to injury and inflammation. Dithiocarbamates are antioxidants that are potent inhibitors of NF-kappaB. This study tested the hypothesis that pyrrolidine dithiocarbamate (PDTC) attenuates experimental acute pancreatitis. Intraperitoneal injection of cerulein in mice resulted in severe, acute pancreatitis characterized by edema, neutrophil infiltration, tissue hemorrhage and necrosis, and elevated serum levels of amylase and lipase. Infiltration of pancreatic and lung tissue with neutrophils (measured as increase in myeloperoxidase activity) was associated with enhanced lipid peroxidation (increased tissue levels of malondialdehyde). Immunohistochemical examination demonstrated a marked increase in immunoreactivity for nitrotyrosine and intracellular adhesion molecule-1 in the pancreas and lung of cerulein-treated mice. In contrast, the degree of 1) pancreas and lung injury, 2) upregulation/expression of intracellular adhesion molecule-1, 3) staining for nitrotyrosine, and 4) lipid peroxidation was markedly reduced by pretreatment with PDTC. This study demonstrates that prevention of the activation of NF-kappaB by PDTC ameliorates the tissue injury associated with experimental murine acute pancreatitis and provides an important insight into the molecular biology of acute pancreatitis.
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