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Lipoprotein lipase activity and mass, apolipoprotein C-II mass and polymorphisms of apolipoproteins E and A5 in subjects with prior acute hypertriglyceridaemic pancreatitis

Coca-Prieto, Inmaculada (author)
Unidad de Lípidos, Servicio de Medicina Interna, Hospital Virgen de la Victoria, Málaga and Departamento de Medicina, Universidad de Málaga, Malaga, Spain
Valdivielso, Pedro (author)
Unidad de Lípidos, Servicio de Medicina Interna, Hospital Virgen de la Victoria, Málaga and Departamento de Medicina, Universidad de Málaga, Malaga, Spain
Olivecrona, Gunilla (author)
Umeå universitet,Fysiologisk kemi
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Ariza, María José (author)
Laboratorio de Lípidos y Arteriosclerosis, Centro de Investigaciones Médico-Sanitarias, Universidad de Málaga, Malaga, Spain
Rioja, José (author)
Laboratorio de Lípidos y Arteriosclerosis, Centro de Investigaciones Médico-Sanitarias, Universidad de Málaga, Malaga, Spain
Font-Ugalde, Pilar (author)
Departamento de Medicina, Facultad de Medicina, Universidad de Córdoba, Cordoba, Spain
García-Arias, Carlota (author)
Unidad de Lípidos, Servicio de Medicina Interna, Hospital Virgen de la Victoria, Málaga and Departamento de Medicina, Universidad de Málaga, Malaga, Spain
González-Santos, Pedro (author)
Unidad de Lípidos, Servicio de Medicina Interna, Hospital Virgen de la Victoria, Málaga and Departamento de Medicina, Universidad de Málaga, Malaga, Spain
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 (creator_code:org_t)
2009
2009
English.
In: BMC Gastroenterology. - 1471-230X. ; 9, s. 46-
Related links:
https://urn.kb.se/re...
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https://doi.org/10.1...
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  • Journal article (peer-reviewed)
Abstract Subject headings
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  • BACKGROUND: Severe hypertriglyceridaemia due to chylomicronemia may trigger an acute pancreatitis. However, the basic underlying mechanism is usually not well understood. We decided to analyze some proteins involved in the catabolism of triglyceride-rich lipoproteins in patients with severe hypertriglyceridaemia. METHODS: Twenty-four survivors of acute hypertriglyceridaemic pancreatitis (cases) and 31 patients with severe hypertriglyceridaemia (controls) were included. Clinical and anthropometrical data, chylomicronaemia, lipoprotein profile, postheparin lipoprotein lipase mass and activity, hepatic lipase activity, apolipoprotein C II and CIII mass, apo E and A5 polymorphisms were assessed. RESULTS: Only five cases were found to have LPL mass and activity deficiency, all of them thin and having the first episode in childhood. No cases had apolipoprotein CII deficiency. No significant differences were found between the non-deficient LPL cases and the controls in terms of obesity, diabetes, alcohol consumption, drug therapy, gender distribution, evidence of fasting chylomicronaemia, lipid levels, LPL activity and mass, hepatic lipase activity, CII and CIII mass or apo E polymorphisms. However, the SNP S19W of apo A5 tended to be more prevalent in cases than controls (40% vs. 23%, NS). CONCLUSION: Primary defects in LPL and C-II are rare in survivors of acute hypertriglyceridaemic pancreatitis; lipase activity measurements should be restricted to those having their first episode during childhood.

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