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Editorials: Valentine Charlton-Menys and Paul N. Durrington Apolipoprotein A5 and Hypertriglyceridemia Clin Chem 2005; 51: 295-297 [Full text] [PDF]

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Apo A5 S19W in ApoE 2/2 causes hypertriglyceridemia

Juergen R. Schaefer   (14 March 2005)

eLetter reply to Juergen R. Schaefer's eLetter

Paul N. Durrington   (28 March 2005)

Apo A5 S19W in ApoE 2/2 causes hypertriglyceridemia 14 March 2005
Juergen R. Schaefer, head of the laboratory of preventive cardiology Send letter to journal: Re: Apo A5 S19W in ApoE 2/2 causes hypertriglyceridemia juergen.schaefer{at}mailer.uni-marburg.de Juergen R. Schaefer	Dear editor, thank you for the very important publication of Peter J O Brien et al (Clin Chem 51:2, 351-359, 2005) as well as for the helpful and highly interesting editorial by Charlton Menys and Durrington on apolipoprotein A5 and hypertriglyceridemia. We are missing one piece of information that we feel is crucial in the discussion of the role of apo A5 in patients with hypertriglyceridemia. Most recently we could show that apo A5 plays an important (maybe the most important) role in patients with hypertriglyceridemia having the apo E 2/2 phenotype. So far we were unable to identify any normolipidemic patient with the combination of apo E 2/2 and the apo A5 S19W mutation; in contrast, all subjects with this combination suffered severe hypertriglyceridemia (J.R. Schaefer et al; Hyperlipidemia in patients with apolipoprotein E2/2 phenotype: apolipoprotein A5 S19W mutation as a cofactor. Clin Chem 50: 11, 2214, 2004). Accordint to this, not only apo C2 or apo C3 is interacting with apo A5, as discussed in the most recent publications, but also apo E. It would have been interesting to learn the apo A5 distribution in different apo E phenotypes and the interaction of these two fascinating triglyceride regulating apolipoproteins. Sincerely yours, Juergen R. Schaefer
eLetter reply to Juergen R. Schaefer's eLetter 28 March 2005
Paul N. Durrington Manchester Royal Infirmary Send letter to journal: Re: eLetter reply to Juergen R. Schaefer's eLetter pdurrington{at}manchester.ac.uk Paul N. Durrington	Dear Editor This is a fascinating observation. Apolipoprotein E2 homozygosity is present in about 1% of the population and acting on its own is associated with lower than average LDL levels. Some 90% of people with type III hyperlipoproteinaemia, however, have apolipoprotein E2 homozygosity, but type III hyperlipoproteinaemia is rare affecting fewer than 1 in 5000 people. It has therefore generally been considered that some other condition predisposing to hypertriglyceridaemia must also occur in association with apolipoprotein E2 homozygosity for type III hyperlipoproteinaemia to occur. This could be an acquired cause such as diabetes, but undoubtedly too familial hypertriglyceridaemia can interact with the apolipoprotein E genotype [1]. Apolipoprotein A5 variants predisposing to hypertriglyceridaemia would thus be ideal candidate genes to explain the phenomenon. Yours sincerely, Paul Durrington [1] Hazzard, W.R., Warnick, G.R., Utermann, G., Albers, J.J. Genetic transmission of isoapolipoprotein E phenotypes in a large kindred: relationship to dysbetalipoproteinemia and hyperlipidemia.Metabolism. 1981;30:79-88.