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Friedewald equation underestimates low‐density lipoprotein cholesterol at low concentrations in young people with and without Type 1 diabetes
Author(s) -
Sibal L.,
Neely R. D. G.,
Jones A.,
Home P. D.
Publication year - 2010
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2009.02888.x
Subject(s) - medicine , apolipoprotein b , endocrinology , triglyceride , lipoprotein , very low density lipoprotein , cholesterol , ldl cholesterol , diabetes mellitus , type 2 diabetes , low density lipoprotein
Diabet. Med. 27, 37–45 (2010) Abstract Aims  Although the limitations of the Friedewald‐calculated serum low‐density lipoprotein cholesterol (LDL‐C) are well recognized, many diabetes and lipid guidelines propose LDL‐C as a therapeutic target. The validity of calculated LDL‐C in people with Type 1 diabetes (T1DM) is uncertain and the use of alternatives such as non‐high‐density lipoprotein cholesterol (non‐HDL‐C) or apolipoprotein measurement unexplored. We have therefore measured LDL‐C with the designated reference method and examined some of the potential sources of such bias, including plasma concentrations of other lipids and apolipoproteins. Methods  Seventy‐four people with T1DM and 80 healthy control subjects were recruited. Fasting samples were collected for analysis of lipid profiles by a beta‐quantification (BQ) reference method and by routine laboratory methods including direct HDL‐C and calculation of LDL‐C using the Friedewald formula. Results  Overall, Friedewald LDL‐C was 0.29 ± 0.02 (mean ±  se ) mmol/l ( P  < 0.001) lower in the two groups than by the BQ method. This resulted in misclassification of approximately 50% of people with a calculated LDL‐C < 2.0 mmol/l. Overestimation of HDL‐C by the routine assay [0.08 ± 0.01 mmol/l ( P  < 0.001)] accounted for ∼28% of the error in calculation of LDL‐C and the remainder appeared to be as a result of triglyceride in lipoprotein particles other than very‐low‐density lipoprotein (VLDL). Correlation of non‐HDL‐C with apolipoprotein B was better than LDL‐C with apolipoprotein B for both assays in both diabetic and non‐diabetic populations. Conclusions  Calculated LDL‐C is unsuitable as a therapeutic target in T1DM. Consideration should be give to the greater use of apolipoprotein B or non‐HDL‐C in clinical practice.

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