title: Lipoprotein lipase activity and mass, apolipoprotein C-II mass and polymorphisms of apolipoproteins E and A5 in subjects with prior acute hypertriglyceridaemic pancreatitis.
abstract: 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Unidad de Lípidos, Servicio de Medicina Interna, Hospital Virgen de la Victoria, Malaga, Spain. inmacopri@hotmail.com
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Coca-Prieto
authors.forename: Pedro
authors.initials: P
authors.lastname: Valdivielso
authors.forename: Gunilla
authors.initials: G
authors.lastname: Olivecrona
authors.forename: María José
authors.initials: MJ
authors.lastname: Ariza
authors.forename: José
authors.initials: J
authors.lastname: Rioja
authors.forename: Pilar
authors.initials: P
authors.lastname: Font-Ugalde
authors.forename: Carlota
authors.initials: C
authors.lastname: García-Arias
authors.forename: Pedro
authors.initials: P
authors.lastname: González-Santos
mesh_terms: D000208:Acute Disease; D000328:Adult; D000072040:Apolipoprotein A-V; D053304:Apolipoprotein C-II / Q000097:blood*; D001054:Apolipoproteins A / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood* / Q000150:complications / Q000235:genetics*; D008071:Lipoprotein Lipase / Q000097:blood*; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000097:blood* / Q000453:epidemiology / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: C437704:APOA5 protein, human; D000072040:Apolipoprotein A-V; D053304:Apolipoprotein C-II; D001054:Apolipoproteins A; D001057:Apolipoproteins E; D014280:Triglycerides; D008071:Lipoprotein Lipase