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Hypertriglyceridaemia: a commentary
  1. Aidan Ryan1,2,
  2. William G Simpson3,
  3. Patrick Twomey4,5
  1. 1Chemical Pathology, Cork University Hospital, Cork, Ireland
  2. 2Pathology, School of Medicine, University College Cork, Cork, Ireland
  3. 3Clinical Biochemistry, Aberdeen Royal Infirmary and the University of Aberdeen, Aberdeen, UK
  4. 4St Vincent's University Hospital Department of Pathology and Laboratory Medicine Clinical Biochemistry, Dublin, Ireland
  5. 5School of Medicine, University College Dublin, Dublin, Ireland
  1. Correspondence to Professor Patrick Twomey, Clinical Biochemistry, St Vincent's University Hospital Department of Pathology and Laboratory Medicine, Dublin D04 T6F4, Ireland; ptwomey{at}svhg.ie

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The diagnosis and specific management of hypertriglyceridaemia (HTG) is overshadowed and often ignored in favour of low-density lipoprotein cholesterol (LDL-C).1 General practitioners will often not request it; partly because most cardiovascular disease (CVD) risk calculators do not require it, and partly because of the potential need for patients to be fasting. So why bother? The answer is twofold—accurate diagnosis and assessment of risk (of CVD and of acute pancreatitis (AP)).

Wierzbicki et al2 discuss the diagnosis and management of HTG in a best practice update. Classically, the full traditional profile consisted of total cholesterol, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG) and a calculated LDL-C based on the Friedewald equation, which involved a fasting sample. Recent guidelines have moved away from recommending fasting lipid profiles based on large observational cohort studies (Danish) showing that, for most patients, fasting has little impact on lipid measurement.3 TG levels>4.5 mmol/L, the upper limit of validity of the Friedewald equation, were found in 3%–5% of non-fasting individuals in populations.1 There are two exceptions—one where an accurate LDL is acquired (usually calculated) and the other where TG is >10 mmol/L. A recently published meta-analysis has highlighted the use of non-HDL-C or apoB as superior metrics at least for assessing CVD risk.4 Part of this relates to evidence suggesting that some cholesterol in LDL particles is replaced by TGs, which makes the amount of cholesterol in LDL-C, an unreliable marker of LDL particle number.

It must be remembered that even with mild HTG>4.5 mmol/L, many HDL-C and indeed direct LDL assays become less reliable, potential affecting CVD risk and treatment decisions.5 In the presence of HTG over 10 mmol/L, the proportion of cholesterol, which is in triglyceride-rich lipoproteins (TRLs), will be raised, and the correlation between atherogenic potential and total cholesterol/HDL-C (commonly used in CVD …

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Footnotes

  • Handling editor Tahir S Pillay.

  • Correction notice This article has been corrected since it was published online. The article title has been changed from “Thoughts on hypertriglyceridaemia in clinical practice” to "Hypertriglyceridaemia: a commentary" and two new authors ('Aidan Ryan' and 'William G Simpson') have been added to the paper

  • Funding The author has not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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