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Departments of Laboratory Medicine and Pathology, Children's Hospital and Harvard Medical School, Boston, MA 02115.
a Address correspondence to this author, at: Department of Laboratory Medicine, Farley 705, Children's Hospital, 300 Longwood Ave., Boston, MA 02115. Fax 617 355-6081; e-mail harris n{at}a1.tch.harvard.edu
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResults and DiscussionReferences |
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4.9%, and all results correlated highly with
those of a modified reference procedure (r 
0.96). At
triglycerides concentrations <4000 mg/L, these field methods showed an
acceptable systematic error (y =
1.12x - 47, 1.05x - 23, and
0.96x + 8 for the phosphotungstate, Spinpro, and N-geneous
assays, respectively), and the total error of the field methods met the
current National Cholesterol Education Program (NCEP) performance goal
of 22%. Regression analyses of results for samples with
triglycerides >4000 mg/L produced the following results for the above
respective assays: y = 1.08x - 4.2,
1.02x + 3.6, and 0.85x + 108. In this
hypertriglyceridemic group, only the N-geneous assay (at an
HDL-cholesterol content of 240 mg/L) had a total error (35%) that
exceeded the NCEP limit. Bilirubin and ascorbate produced a negative
interference with the phosphotungstate and Spinpro assays but had
little effect on the N-geneous assay.
Key Words: indexing terms: triglycerides • method comparison • performance goals
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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600 mg/L is considered
protective (5). Further evidence suggests that HDL-C
determinations in the pediatric population have a positive predictive
value of 100% in identifying children with increased LDL-C, when used
in combination with total cholesterol (TC) measurements
(6). In most clinical chemistry laboratories, determination of HDL-C is a two-step procedure: First, apolipoprotein (apo) B-containing (non-HDL) particles are precipitated with solutions containing divalent cations (magnesium, calcium, or manganese) and polyanions (7)(8)(9)(10)(11)(12)(13), e.g., sulfated polysaccharides (heparin or dextran sulfate), sodium phosphotungstate (2Na2O · P2O5 · 12WO3 · 18H2O); then, the precipitated lipoproteins are removed by centrifugation, and HDL-C is determined by measuring the cholesterol remaining in the supernatant liquid. Among the problems of existing HDL-C methods are their labor-intensive nature and susceptibility to interference from particles rich in triglycerides (TG). These drawbacks have prompted investigators to improve the analytical performance of the HDL-C assay and facilitate specimen manipulation, hence developing second- and third-generation HDL-C assays.
Second-generation procedures still require sample precipitation. However, recovery of the HDL-C supernate is easier and the assays are designed to be performed on-line. Also, these assays are less affected by lipemia than are the first-generation assays. The third-generation procedures are the direct or homogeneous HDL-C assays, which use only a small sample volume and obviate all centrifugation and precipitation steps (14)(15)(16)(17).
We report the analytical performance of three assays of HDL-C concentrations in the clinical laboratory. Each procedure is representative of one of the three HDL-C assay generations: a phosphotungstic acid (PT)/Mg2+ (first-generation) protocol, the modular Spinpro® (Sigma Diagnostics, St. Louis, MO) second-generation HDL-C precipitation device, and a new homogeneous (third-generation) method, N-geneousTM HDL-C (Genzyme Diagnostics, Cambridge, MA). We also compare these assays with the ultracentrifugation/dextran sulfate–Mg2+ method, the modified Reference Method of the Centers for Disease Control and Prevention (CDC) for HDL-C.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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VLDL isolation.
VLDL particles were isolated by
ultracentrifugation of hypertriglyceridemic specimens under the
conditions described in the next section. Briefly, plasma was
ultracentrifuged for 3 h at 300 000g, and the <1.006
kg/L supernatant fraction was isolated by slicing the polyallomer tube.
The VLDL fractions from several pools were combined, after which their
TG content was determined enzymatically.
HDL-C assays.
In the modified Reference Method for
HDL-C, 230-µL plasma samples were centrifuged at 300 000g
for 3 h at 4 °C in 7 x 20 mm polyallomer tubes in a TL100
rotor (Beckman Instruments, Palo Alto, CA). The tubes were then sliced
to isolate the >1.006 kg/L infranatant, i.e., the fraction containing
the VLDL and chylomicron particles. The volume of the remaining
infranatant was restored to that of the original sample by adding 9 g/L
NaCl solution (isotonic saline). The HDL-C in this infranatant was
determined after precipitation by MgCl2 and dextran sulfate
(Mr 50 000) of the particles containing apo B,
i.e., LDL, intermediate-density lipoproteins, and lipoprotein(a).
For the PT assay of HDL-C, 200 µL of sample was mixed with 500 µL of precipitating reagent (Boehringer Mannheim), i.e., PT, 0.55 mmol/L, and MgCl2, 25 mmol/L. Precipitation proceeded at room temperature for 10 min. Samples were centrifuged (12 000g for 2 min) and the supernatant was collected for enzymatic determination of HDL-C.
The Spinpro HDL-C assay was performed according to the manufacturer's instructions. This assay uses a self-contained polystyrene device that can fit into a regular benchtop centrifuge. Briefly, 550–600 µL of specimen is transferred to the sample cone of the Spinpro device, which is then centrifuged at 1500g for 5 min in a swing-out rotor. After the centrifuge has come to a complete stop, it is restarted at 1500g for an additional 10 min, which allows the sample to mix with a calcium/dextran sulfate precipitating reagent. After centrifugation, the HDL-C-containing supernatant is recovered and analyzed with a routine enzymatic cholesterol reagent. The final dilution factor is 2x.
All reagents for the N-geneous HDL-C assay were obtained from Genzyme Diagnostics and were reconstituted according to the manufacturer's instructions. Reagent 1 contains a polyanion and a synthetic polymer; reagent 2 is a mixture of enzymes (cholesterol esterase, cholesterol oxidase, peroxidase), 4-aminoantipyrine (2 mmol/L), detergent, and buffer. Additional constituents are listed in the manufacturer's instructions. A small volume (3 µL) of specimen is mixed with 300 µL of reagent 1 and incubated at 37 °C for 5 min. The polymer and polyanion together form complexes with chylomicrons, VLDL, and LDL particles and prevent them from reacting with reagent 2. Reagent 2 (100 µL) is then added. The HDL particles are disrupted by the detergent, thereby releasing the cholesterol and cholesteryl esters. The HDL-C concentration is then determined enzymatically with the Hitachi 911 analyzer, and the two-point reaction at 37 °C is monitored at 546 nm (secondary wavelength, 660 nm).
samples
For the method comparison study we obtained 76 blood samples
from the daily pool of new specimens received at regional clinical
chemistry laboratories, including the Children's Hospital, the Beth
Israel Hospital, the Brigham and Women's Hospital, and
MetPathTM Laboratories of Boston, MA.
performance evaluation
Precision.
Run-to-run precision was determined with
~20 separate assays of two HDL-C controls. The level 2 control (500
mg/L) was pooled normal human plasma. The level 1 control (240 mg/L)
was prepared by diluting the above plasma pool twofold with isotonic
saline. All controls were stored in aliquots at -80 °C.
Ascorbate and bilirubin interference.
We chose 20–30
patients' specimens at random and combined them to give five 10-mL
pools of plasma. The mean TC and TG concentrations (mg/L) for each of
the five pools were as follows: pool 1, TC 1960, TG 2200; pool 2, TC
1840, TG 2130; pool 3, TC 2250, TG 1550; pool 4, TC 1690, TG 1660; pool
5, TC 2390, TG 2750. Ascorbic acid (Sigma) was dissolved in isotonic
saline to give a stock solution of 1000 mg/L. Each plasma pool was
divided into four 850-µL aliquots, to which we added 150 µL of
appropriately diluted ascorbate stock or saline to give final ascorbate
concentrations of 0, 50, 100, and 150 mg/L (the ascorbate
concentrations were determined by HPLC (18)).
Bilirubin for interference studies was prepared as follows: Hyperbilirubinemic plasma was processed in a 100-kDa-cutoff Centricon® device (Amicon, Beverly, MA). The ultrafiltrate (containing bilirubin) was extracted with 80% methanol and dried under nitrogen to ~50% of the original volume. We then diluted 5 parts of specimen with 1 part of albumin reagent, 70 g/L in isotonic saline. The total bilirubin content was measured as 305 mg/L, direct bilirubin as 15 mg/L.
As in the ascorbate analysis, we used five plasma pools for testing bilirubin interference. Each pool was divided into four 700-µL aliquots, and 300 µL of diluted bilirubin (in isotonic saline containing albumin, 20 g/L) was added to each to give final total bilirubin concentrations of 3–70 mg/L. Total bilirubin concentrations were measured with the Hitachi 911 at 570 nm with use of 2,5-dichlorophenyldiazonium tetrafluoroborate as the diazonium salt.
Total error
. Total error is the sum of
systematic error plus random error (19)(20).
Systematic error is calculated from the linear regression equation
y = bx + a, where b is the slope of the
regression equation, and a is the y-axis intercept.
Systematic error at an HDL-C concentration of xc
is defined as the absolute value of yc -
xc, where yc =
bxc + a. Random error is 1.96 x the SD of
the run-to-run precision study.
Stability study.
Specimens were combined to give five
10-mL plasma pools (as for the interference study). The TC and TG
concentrations (mg/L) of each pool were as follows: pool 1, TC 1750, TG
1060; pool 2, TC 1780, TG 1250; pool 3, TC 1540, TG 890; pool 4, TC
1780, TG 1270; pool 5, TC 1810, TG 1450. The pools were divided into
aliquots and stored at either 4, -20, or -80 °C for as long as 4
weeks. HDL-C concentrations in each pool were measured weekly with the
three field methods.
cost analysis
Total labor cost was estimated by averaging the total amount of
time taken to run 20, 30, and 50 samples and assuming a technologist's
salary of $20/h. Instrument cost was determined by calculating the
combined cost of the analyzer and the maintenance package over a 5-year
period and dividing this by 2.5 x 106, the number of
tests expected to be run with the analyzer during that time. The cost
of reagents was determined by multiplying the list price of the test by
1.2, because an estimated 20% of the reagents would be used for
calibration, controls, and repeats. Interactive labor was determined by
calculating the actual amount of "hands-on" bench work such as
pipetting, pouring specimens, loading the centrifuge, and loading and
programing the automated analyzer; it does not include centrifugation
or analysis time.
statistical analysis
Means, medians, and SDs were calculated with Microsoft Excel
Version 5.0® (Microsoft, Redmond, WA). Student's
t-test and least-squares linear regression analysis were
calculated by the SigmaPlot® statistics program (Jandel
Scientific, San Rafael, CA); t-tests were judged significant
at P <0.05. Bias was calculated as: test method result
minus Reference Method result.
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Results and Discussion |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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The N-geneous HDL-C assay had the smallest CV, both within-run and
day-to-day (Table 1
). The current NCEP guidelines
(21)(21) for the precision of HDL-C
assays recommend the use of SDs for low HDL-C concentrations (<420
mg/L) and of CVs for HDL-C 420 mg/L. The day-to-day precision of the
three field assays all met these current guidelines for HDL-C
concentrations of 240 mg/L (SD <25 mg/L) and 500 mg/L (CV <6%).
Although the precision of all three assays fell within the 1998
precision goals (SD <17 mg/L) at a low HDL-C concentration of 240
mg/L, only the PT and N-geneous assays met the future precision goal
(CV <4%) for the higher HDL-C concentrations (500 mg/L).
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In the 76 randomly chosen specimens used to define the accuracy of the
HDL-C methods, TG concentrations ranged from 260 to 12 890 mg/L. For
determinations by the three field methods and by the modified reference
procedure, the data were analyzed as two separate groups according to
TG concentration: <4000 mg/L in group 1 (mean ± SD TC and TG
1700 ± 470 and 1400 ± 820 mg/L, respectively) and 4000
mg/L in group 2 (TC and TG 2520 ± 1450 and 5960 ± 1990
mg/L, respectively). The results are displayed in Table 2
. The comparison-of-methods scatter plot and the linear
regression analysis are shown in Fig. 1
, with the modified HDL-C Reference Method values on the
x-axis.
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All assays correlated highly with the modified reference procedure
(r 0.96). In group 1, the mean bias of the field assays
ranged from +1.4 to -8.0 mg/L (Table 2
). In group 2, VLDL particles
were incompletely precipitated in two samples in the PT and the Spinpro
analyses and were eliminated from the data analysis for these methods
(hence n = 24); N-geneous HDL data analysis was based on n =
26. As Table 2
shows, the N-geneous HDL assay of group 2 samples had a
constant systematic error of 108 mg/L and a 15% proportional
systematic error (i.e., a slope of 0.85). The net effect of this was
the introduction of a TG-dependent positive bias, especially at low
HDL-C concentrations. Hence the mean bias of the N-geneous HDL-C was
+67 mg/L (Table 2
). The PT and the Spinpro assays gave both a smaller
proportional and constant systematic error in this hypertriglyceridemic
group, the mean bias of these assays being +16 and +9.2 mg/L,
respectively (Table 2
). However, the lower mean bias for the latter two
assays should be interpreted with caution because data for the
incompletely precipitated samples were excluded from the analysis.
Figure 2
shows the assay bias data (field method result minus Reference
Method result) plotted as a function of TG content over the full range
of TG concentrations (260–12 890 mg/L). Only the N-geneous HDL assay
(Fig. 2C
) showed a significant correlation (P <0.01)
between the TG concentration and the assay bias. The TG-dependent bias
was apparent at both high (group 2, n = 26, r =
0.56, P <0.01) and low (group 1, n = 50,
r = 0.36, P <0.05) TG concentrations. This
tendency was confirmed by adding an isolated VLDL fraction to three
pools of plasma: The mean N-geneous HDL-C concentration increased as
more VLDL was added (Table 3
), although the increase was not statistically significant.
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Systematic error (the absolute value of y -
x), or analytical bias, of each assay
(19)(20) was calculated by linear regression
analysis comparison with the Reference Method. The total error, a
measure of the overall analytical performance of an assay
(19)(20), was calculated by combining the
systematic error with the random error (1.96 x SD of the
run-to-run precision). Total error analyses were performed at low (240
mg/L) and high (500 mg/L) HDL-C concentrations. For 50 group 1
specimens (TG <4000 mg/L), all three field assays met the current NCEP
performance goal (21)(22) for total error,
22% (Table 4
). All three methods also met the 1998 NCEP
(21)(22) performance goal (<13%) for the
samples with HDL-C of 500 mg/L; at 240 mg/L HDL-C, only the N-geneous
HDL assay was within the 1998 total error goal (Table 4
). In the
hypertriglyceridemic (group 2) study, the total error of all three
field assays lay within the current 22% NCEP limits except for the
N-geneous assay of specimens with low HDL-C (240 mg/L). This is because
specimens with a low HDL-C and a high TG show a large systematic error
(or bias) when assayed by the N-geneous assay. Because the not fully
precipitated specimens were eliminated from hypertriglyceridemic PT and
the Spinpro HDL-C assay data, the total error data for group 2 samples
is biased towards these first- and second-generation assays.
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The NCEP Adult Treatment Panel II recommends an initial screening with measurement of HDL-C in nonfasting samples. Therefore, we assayed HDL-C by the three field methods in 16 subjects both after an overnight fast and 3–5 h after a high-fat meal. The mean ± SD fasting TC and TG concentrations in this group were 1980 ± 380 and 1250 ± 820 mg/L, respectively; in the postprandial samples, the respective values were 1980 ± 420 and 2090 ± 1660 mg/L. Neither the PT nor the Spinpro methods showed any significant change in results before and after the meal. The N-geneous HDL-C procedure, however, noted a slight but significant decrease (P <0.01) in HDL-C in the postprandial state—both in heparinized plasma and in serum samples. In plasma samples, the fasting HDL-C was 482 ± 100 mg/L, whereas the postprandial HDL-C was 456 ± 94 mg/L (P = 0.002). For serum samples, fasting and postprandial HDL-C measurements were 498 ± 104 and 484 ± 99 mg/L, respectively (P = 0.008). These N-geneous data agree with the finding of Cohn et al., using ultracentrifugation followed by precipitation (23), that plasma HDL-C decreases by 5–10% in the postprandial state. The N-geneous HDL-C assay therefore apparently reflects the expected postprandial physiological changes.
Both ascorbic acid and bilirubin are reducing agents that interfere
with routine peroxidase-dependent cholesterol determinations. Although
bilirubin did decrease the apparent N-geneous HDL-C concentration (Fig. 3
A), the effects were much less apparent than with the other
enzymatic cholesterol procedures. The presence of ascorbic acid
markedly affected both the PT and the Spinpro assays (Fig. 3B
); the
N-geneous HDL-C assay, however, was unaffected, even at high ascorbate
concentrations. The N-geneous HDL-C assay is therefore apparently
resistant to these reducing reagents.
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We cannot readily explain the mechanism of this resistance because all three generations of HDL-C assays depend, in principle, on the same enzymatic reaction (catalyzed by cholesterol oxidase) that generates H2O2 via a 2-electron reduction of O2. The peroxide, in turn, undergoes a further reduction to H2O by oxidizing a substrate such that the latter changes color. Reducing agents, however, scavenge the peroxide and decrease the extent of color change. In practice, the PT and Spinpro assays use the same enzymatic reagent, whereas the agent in the N-geneous assay is adapted to a homogeneous reaction. The N-geneous HDL-C assay has a major advantage over the first- and second-generation assays in this regard.
To assess the stability of the HDL-C assays, we made serial HDL-C
determinations in plasma samples stored at 4, -20, and -70 °C for
4 weeks (Fig. 4
). All HDL-C concentrations showed an apparent decrease over
this time period. As a general rule, the Spinpro assay showed the
greatest overall decrease over the 4 weeks (>15%), whereas the
N-geneous HDL-C assay showed the least (<8%). The significance of
this decrease was judged by a paired t-test comparing the
means of the five specimen pools (see Materials and Methods)
with the initial (week 0) or baseline value. "Instability" was
therefore defined as a statistically significant (P <0.05)
variation from the zero time-point. Specimens stored at 4 °C were
stable for at least 2 weeks when analyzed by all three HDL-C assays
(Fig. 4
). Furthermore, specimens frozen at -20 °C were stable for 2
weeks when assayed with the N-geneous HDL-C procedure. In contrast,
significant variations from baseline were evident after 1 week at
-20 °C when measured with the PT or Spinpro HDL-C methods. No
additional advantage was gained if samples were stored at -70 °C
(Fig. 4
). Of course, between-run analytical imprecision must also be
considered in interpreting the stability data.
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Because the N-geneous HDL-C assay requires no centrifugation or sample
preparation, the total labor cost of this assay was less than that of
the PT and the Spinpro assays. Estimated instrumentation disposable
costs were also lower with the N-geneous assay (Table 5
).
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The N-geneous HDL-C assay has the best analytical precision of
all the HDL-C methods we assessed. No centrifugation or preparation of
the sample is required. Although this assay showed a statistically
significant TG-dependent bias at TG concentrations <4000 mg/L, the
mean analytical bias of this assay (relative to the reference
procedure) was low—as was its total error, which met both current and
proposed (1998) guidelines for HDL-C determinations. However, at TG
4000 mg/L, the N-geneous HDL-C assay demonstrated a consistent
positive bias directly proportional to the TG concentration; in the
same high-TG group, the PT and Spinpro assays did not always completely
precipitate the VLDLs. Reducing agents such as bilirubin or ascorbate
showed little or no interference with the N-geneous HDL-C assay, in
comparison with their effect in other procedures. In conclusion, we
envisage an important role for the N-geneous HDL-C assay in
determinations of HDL-C in the routine clinical biochemistry
laboratory.
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Acknowledgments |
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Footnotes |
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1 To convert cholesterol values from mg/L to mmol/L, multiply by 0.2586; for triglycerides, multiply by 0.001129.
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References |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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-cyclodextrin. Clin Chem 1995;41:717-723.
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, Group 1 (TG <4000 mg/L); 
, group 2 samples (TG 
, P <0.05; *,
P <0.01.
), and -70 °C (
): (A)
PT HDL-C; (B) Spinpro HDL-C; (C) N-geneous HDL.