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Pathophysiology/Complications

Triglyceride–to–HDL Cholesterol Ratio in the Dyslipidemic Classification of Type 2 Diabetes

  1. Ana María Wägner, MD, PHD1,
  2. Antonio Pérez, MD, PHD1,
  3. Jose Luis Sánchez-Quesada, PHD2 and
  4. Jordi Ordóñez-Llanos, MD, PHD23
  1. 1Endocrinology Department, Hospital Sant Pau, Barcelona, Spain
  2. 2Biochemistry Department, Hospital Sant Pau, Barcelona, Spain
  3. 3Biochemistry Department, Universitat Autònoma de Barcelona, Barcelona, Spain
  1. Address correspondencereprint requests to Ana Ma Wägner, Steno Diabetes Center, Niels Steensens vej 2. 2820 Gentofte, Denmark. E-mail: awgn{at}steno.dk
Diabetes Care 2005 Jul; 28(7): 1798-1800. https://doi.org/10.2337/diacare.28.7.1798
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  • apoB, apolipoprotein B

Although LDL cholesterol is the main target in the treatment of diabetic dyslipidemia, it does not fully account for the cardiovascular risk associated with diabetes, neither alone nor in combination with triglycerides and HDL cholesterol. On the other hand, diabetic dyslipidemia also includes an overall increase in atherogenic particles identifiable, by measuring apolipoprotein B (apoB), and a predominance of small, dense LDL particles (phenotype B). The latter, although associated with increased cardiovascular risk, is not routinely assessed because its measurement is not available to most clinical laboratories. Therefore, easily measurable predictors of LDL size, such as triglycerides or LDL cholesterol/apoB and triglyceride–to–HDL cholesterol ratios, have been proposed, with the latter being suggested as the best surrogate (1,2,3). However, no study has been conducted that compares all of these predictors.

The aim of the present study is to evaluate the triglyceride–to–HDL cholesterol ratio, non-HDL cholesterol, and apoB to predict LDL phenotype and to assess them in the risk classification of patients with type 2 diabetes.

RESEARCH DESIGN AND METHODS

A total of 107 type 2 diabetic patients (68% male, age 59 ± 10 years [means ± SD], time since diagnosis 8.5 years [range 0–37], HbA1c 7.35% [3.7–16]) were consecutively included in the study. None of the patients were taking drugs or were in situations (not related to diabetes) known to affect lipoprotein metabolism.

Total cholesterol and triglycerides were measured by enzymatic methods and HDL cholesterol by a direct method (Roche Diagnostics, Basel, Switzerland). Hypertriglyceridemia was defined by triglycerides >2.25 mmol/l (4,5). LDL cholesterol was obtained by Friedewald’s formula (if triglycerides <3.39 mmol/l) or by ultracentrifugation. Non-HDL cholesterol was calculated by subtracting HDL cholesterol from total cholesterol. High non-HDL cholesterol was defined by the equivalent to an LDL cholesterol > 3.36 mmol/l, when pharmacological intervention is recommended, i.e., non-HDL cholesterol >4.13 mmol/l (4). The triglyceride–to–HDL cholesterol ratio was expressed in mmol/l over mmol/l. Previously described cutoff points were used (1,2,6), as well as that calculated from the regression equation obtained from the samples included in the present study: triglyceride–to–HDL cholesterol ratio = 42.122 − 1.576 × LDL size (R = 0.625) for an LDL size of 25.5 nm. ApoB was measured by an immunoturbidimetric method (Tina-quant, Roche Diagnostics) calibrated against the World Health Organization/International Federation of Clinical Chemistry reference standard SP3–07. Its cutoff point (0.97 g/l) was defined as the equivalent to an LDL cholesterol of 3.36 mmol/l (7) in a previously described nondiabetic normolipidemic control group (8). LDL size was determined by polyacrylamide gradient (2–16%) gel electrophoresis (3), and LDL phenotype B was defined by a predominant LDL diameter <25.5 nm.

Patients were classified according to their triglyceride and apoB concentrations as well as according to their triglycerides, triglyceride–to–HDL cholesterol ratio, and their non-HDL cholesterol.

Statistical analysis was performed using the SPSS 10.0 statistical package for Windows (SPSS, Chicago, IL). Results are expressed as means ± SD (Gaussian distribution), median and ranges (non-Gaussian distribution), or as percentages. Nonparametric, bivariate correlations (Spearman) were performed between LDL size and other parameters. Concordance between the dyslipidemic phenotypic classifications was assessed using the kappa index (κ). Values between 0.21 and 0.40, 0.41 and 0.60, 0.61 and 0.80, and 0.81 and 1.0 showed fair, moderate, good, and very good concordance, respectively (9).

RESULTS

The patients showed the following lipoprotein concentrations (in mmol/l unless otherwise indicated): triglycerides 1.38 (0.56–9.25), LDL cholesterol 3.58 (0.94), HDL cholesterol 1.20 (0.29), non-HDL cholesterol 4.42 (1.18), apoB 1.16 (0.25) g/l, and LDL size 25.8 (24.4–27.0) nm. When comparing patients with phenotypes A and B, the former showed lower triglyceride–to–HDL cholesterol ratios (0.88 [0.30–3.17] vs. 2.33 [0.53], P < 0.0005). LDL size showed a direct correlation with HDL cholesterol (R = 0.439) and LDL cholesterol/apoB (R = 0.583) and an inverse correlation with triglycerides (R = −0.626) and the triglyceride–to–HDL cholesterol ratio (R = −0.643, P < 0.0005 for all). No correlation was found with non-HDL cholesterol or apoB. When patients were classified according to previously proposed cutoff points for triglycerides–to–HDL cholesterol, the concordance with their classification into LDL phenotypes A and B was fair (κ = 0.390 for a cutoff point of 0.9) to moderate (κ = 0.478 for a cutoff point of 1.33 and κ = 0.545 for a cutoff point of 1.64). When using the regression equation triglycerides/HDL cholesterol = 42.122 − 1.576 × LDL size (R = 0.625), for an LDL size of 25.5 nm, a triglyceride/HDL cholesterol cutoff point of 1.93 was obtained. When this cutoff point was used, the concordance of the patients’ classification with LDL phenotype was also moderate, though slightly better than with the other cutoff points (κ = 0.554). It showed a sensitivity of 60% and a specificity of 92% to predict LDL phenotype B. We used 1.93 as the cutoff point to classify the patients (normal-high triglyceride–to–HDL cholesterol ratio) and compare their distribution with when the classification was performed using apoB and triglycerides (Fig. 1). Using these cutoff points, the concordance between hyperapoB and the hypertriglyceride–to–HDL cholesterol ratio was poor (κ = 0.175), whereas the concordance between hyperapoB and hyper–non-HDL cholesterol was moderate (κ = 0.522). Results were similar when cutoff points equivalent to LDL cholesterol of 2.59 mmol/l were used for non-HDL cholesterol and apoB, as well as when men and women were analyzed separately (data not shown).

CONCLUSIONS

The present study shows that the triglyceride–to–HDL cholesterol ratio is not superior to non-HDL cholesterol in classifying patients with type 2 diabetes into dyslipidemic phenotypes. The triglyceride–to–HDL cholesterol ratio is cheap and easy to calculate and is a good predictor of LDL size. However, it does not identify most of the patients with hyperapoB, has a high biological variability that is inherent to triglycerides (10), as reflected by the wide range of recommended cutoff points, and its determination should be made in the fasting state. On the other hand, non-HDL cholesterol is as cheap and easy to measure as the triglyceride–to–HDL cholesterol ratio, with the additional advantage that its biologic variability is much lower and fasting samples are not needed. ApoB reflects the total number of atherogenic particles and is superior to non-HDL cholesterol both as a cardiovascular risk predictor and as a predictor of the risk reduction following treatment of dyslipidemia (11). Its determination can also be made in the nonfasting state (12), its biological variability is lower than for other lipidic components, and the introduction of an international standard has made results from different labs comparable (13).

We have previously shown that in hypertriglyceridemic patients, apoB and non-HDL cholesterol are equivalent in classifying them into dyslipidemic phenotypes (14). This is also true for the triglyceride–to–HDL cholesterol ratio. In normotriglyceridemic subjects, however, non-HDL cholesterol identifies around half of the individuals with hyperapoB (14), whereas the triglyceride–to–HDL cholesterol ratio identifies <10% (Fig. 1).

Therefore, based on current and previous results and the cost-effectiveness of the different components, a strategy consisting of the estimation of non-HDL cholesterol (as a surrogate of apoB) in all of the subjects and the measurement of apoB itself in the normotriglyceridemic subjects with normal non-HDL cholesterol is proposed for dyslipidemic risk classification of patients with type 2 diabetes. The triglyceride–to–HDL cholesterol ratio does not add useful information to the previously mentioned strategy.

Figure 1—
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Figure 1—

Distribution of the patients into apoB-dependent dyslipidemic phenotypes according to their triglyceride–to–HDL cholesterol ratio (A) and their non-HDL cholesterol (B). Tg, triglyceride; HDLc, HDL cholesterol.

Acknowledgments

The study was partially funded by grants from Fondo de Investigaciones Sanitarias (no. C03/01 and C03/08).

Footnotes

  • A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

    • Accepted March 28, 2005.
    • Received February 24, 2005.
  • DIABETES CARE

References

  1. ↵
    Boizel R, Benhamou PY, Lardy B, Laporte F, Foulon T, Halimi S: Ratio of triglyceride to HDL cholesterol is an indicator of LDL particle size in patients with type 2 diabetes and normal HDL cholesterol levels. Diabetes Care 23: 1679–1685, 2000
    OpenUrlAbstract/FREE Full Text
  2. ↵
    Hanak V, Muñoz J, Teague J, Stanley A, Bittner V: Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B. Am J Cardiol 94: 219–222, 2004
    OpenUrlCrossRefPubMedWeb of Science
  3. ↵
    Wägner AM, Jorba O, Rigla M, Alonso E, Ordoñez-Llanos J, Pérez A: LDL-cholesterol/apolipoprotein B ratio is a good predictor of LDL phenotype B in type 2 diabetes. Acta Diabetol 39: 215–220, 2002
    OpenUrlCrossRefPubMedWeb of Science
  4. ↵
    Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults: Executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation and treatment of high blood cholesterol in adults (Adult Treatment Panel III). JAMA 285: 2486–2496, 2001
    OpenUrlCrossRefPubMedWeb of Science
  5. ↵
    American Diabetes Association: Management of dyslipidemia in adults with diabetes. Diabetes Care 27(Suppl. 1): S68–S71, 2004
  6. ↵
    Maruyama C, Imamura K, Teramoto T: Assessment of LDL particle size by triglyceride/HDL-cholesterol ratio in non-diabetic, healthy subjects without prominent hyperlipidemia. J Atheroscler Thromb 10: 186–191, 2003
    OpenUrlCrossRefPubMed
  7. ↵
    Contois JH, McNamara JR, Lammi-Keefe CJ, Wilson PW, Massov T, Schaeffer E: Reference intervals for plasma apolipoprotein B determined with a standardized commercial immunoturbidimetric assay: results from the Framingham Offspring Study. Clin Chem 42: 515–523, 1996
    OpenUrlAbstract/FREE Full Text
  8. ↵
    Wägner AM, Pérez A, Calvo F, Bonet R, Castellví A, Ordóñez J: Apolipoprotein B identifies dyslipidemic phenotypes associated with cardiovascular risk in normocholesterolemic type 2 diabetic patients. Diabetes Care 22: 812–817, 1999
    OpenUrlAbstract/FREE Full Text
  9. ↵
    Altman DG. Some common problems in medical research. In Practical Statistics for Medical Research. Altman DG, Ed. New York, Chapman and Hall, 1991, p. 396–439
  10. ↵
    Ortolá J, Castineiras MJ, Fuentes-Arderiu X: Biological variation data applied to the selection of serum lipid ratios used as risk markers of coronary heart disease. Clin Chem 38: 56–59, 1992
    OpenUrlAbstract/FREE Full Text
  11. ↵
    Sniderman AD, Furberg CD, Keech A, Roeters van Lennep JE, Frohlich J, Jungner I, Walldius G: Apolipoproteins versus lipids as indices of coronary risk and as targets for statin treatment. Lancet 361: 777–780, 2003
    OpenUrlCrossRefPubMedWeb of Science
  12. ↵
    Walldius G, Jungner I, Holme I, Aastveit AH, Kolar W, Steiner E: High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet 358: 2026–2033, 2001
    OpenUrlCrossRefPubMedWeb of Science
  13. ↵
    Marcovina SM, Albers JJ, Kennedy H, Mei JV, Henderson LO, Hannon WH: International Federation of Clinical Chemistry standardization project for measurement of apolipoproteins A-I and B: comparability of apolipoprotein B values by use of International Reference Material. Clin Chem 40: 586–592, 1994
    OpenUrlAbstract/FREE Full Text
  14. ↵
    Wägner AM, Pérez A, Zapico E, Ordóñez-Llanos J: Non-HDL cholesterol and apolipoprotein B in the dyslipidemic classification of type 2 diabetic patients. Diabetes Care 26: 2048–2051, 2003
    OpenUrlAbstract/FREE Full Text
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Triglyceride–to–HDL Cholesterol Ratio in the Dyslipidemic Classification of Type 2 Diabetes
Ana María Wägner, Antonio Pérez, Jose Luis Sánchez-Quesada, Jordi Ordóñez-Llanos
Diabetes Care Jul 2005, 28 (7) 1798-1800; DOI: 10.2337/diacare.28.7.1798

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Triglyceride–to–HDL Cholesterol Ratio in the Dyslipidemic Classification of Type 2 Diabetes
Ana María Wägner, Antonio Pérez, Jose Luis Sánchez-Quesada, Jordi Ordóñez-Llanos
Diabetes Care Jul 2005, 28 (7) 1798-1800; DOI: 10.2337/diacare.28.7.1798
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