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Hypertriglyceridemia: HELP
Articles by Bjørn Christophersen
Based on 2 articles published since 2009
(Why 2 articles?)
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Between 2009 and 2019, B. Christophersen wrote the following 2 articles about Hypertriglyceridemia.
 
+ Citations + Abstracts
1 Article [Why hypertriglyceridemia leads to pancreatitis]. 2013

Christophersen, Bjørn / Sørby, Randi / Osmundsen, Harald / Olivecrona, Gunilla / Nordstoga, Knut. ·Institutt for klinisk biokjemi, Rikshospitalet, Universitetet i Oslo, Norway. bjorn.christophersen@medisin.uio.no ·Tidsskr Nor Laegeforen · Pubmed #23306986.

ABSTRACT: -- No abstract --

2 Article Pancreatitis in hyperlipemic mink (Mustela vison). 2012

Nordstoga, K / Sørby, R / Olivecrona, G / Smith, A J / Christophersen, B. ·Norwegian School of Veterinary Science, Department of Basic Sciences and Aquatic Medicine, PO Box 8146 Dep., 0033 Oslo, Norway. ·Vet Pathol · Pubmed #21900541.

ABSTRACT: In both man and animals, inflammatory changes in the pancreas often occur with disturbances in lipid metabolism, including hypertriglyceridemia and an excess of free fatty acids. Hyperlipoproteinemia type I is a human condition caused by a deficiency of lipoprotein lipase. A similar metabolic disturbance that occurs in mink is of considerable comparative interest, as it is also followed by pancreatitis. Pancreatic lesions in hyperlipoproteinemic mink included overt variably sized nodules with hemorrhage and necrosis. These lesions began as intralobular necrosis of exocrine cells and progressed to total lobular destruction, with eventual involvement of interlobular tissue. Remnants of epithelial cells and lipid-filled macrophages were seen in necrotic areas, along with other types of inflammatory cells scattered in a lipid-rich exudate. Granulation tissue developed rapidly in necrotic areas. Additional observations included ductal proliferation, replacement of epithelial cells with fat, and mural arterial thickening, most conspicuously with vacuolated cells and endothelial proliferation. Extravasation of lipid-rich plasma is thought to be a major intensifier of the inflammatory response.