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N Rifai

Publications and source records attributed to N Rifai.

At least 109 records · Page 6Linked to original sources
PubMed1998

Analytical evaluation of particle-enhanced immunonephelometric assays for C-reactive protein, serum amyloid A and mannose-binding protein in human serum.

Against a background of growing interest in more sensitive assays for quantifying various acute phase proteins, we evaluated the performance of recently developed tests for C-reactive protein (CRP), serum amyloid A (SAA) and mannose-binding protein (MBP) on the Behring nephelometer II (BNII). Sample results outside the calibration ranges of 3.5 to 220 mg/L for CRP, 3.3 to 215 mg/L for SAA and 0.09 to 5.6 mg/L for MBP were automatically re-measured at another dilution. The lower limits of detection were 0.01, 0.7 and 0.01 mg/L for CRP, SAA and MBP, respectively. The coefficients of variation (CV) for intra- (n > or = 20) and inter- (n > or = 15) assay precision were < 5.2% and < 8.5%, respectively, for the three proteins at concentrations representing low, normal and high. Linearity for each method was within 5% of the expected values throughout the calibration range. We observed no significant interference from bilirubin (up to 300 mg/L) or haemoglobin (up to 10 g/ L) for the three tests. Method comparison studies performed for CRP and SAA yielded the following results: y (CRP on BNII) = 0.75x (ELISA, Hemagen) -0.25 mg/L (r = 0.981, Sy/x = 2.1 mg/L; y (SAA on BNII) = 1.44x (ELISA, Hemagen) -9.9 mg/L (r = 0.972, Sy/x = 6.9 mg/L), where ELISA is enzyme-linked immunosorbent assay. Reference intervals established in 261 adult blood donors (aged 36.2 +/- 9.0 years) were found to be log-normal with 2.5th, 50th, and 97.5th centiles of < 0.17, 1.00 and 10.1 mg/L for CRP, < 0.84, 2.10 and 9.70 mg/L for SAA; and 0.30, 1.28 and 4.10 mg/L for MBP. We observed no relationship with CRP concentration and age; however, SAA levels increased with age while MBP levels decreased. The BNII provides a simple, rapid and sensitive system for measuring CRP, SAA and MBP in human serum.

Adult↗
PubMed1998

Early high dose antioxidant vitamins do not prevent bronchopulmonary dysplasia in premature baboons exposed to prolonged hyperoxia: a pilot study.

The antioxidant vitamins ascorbic acid (AA) and alpha-tocopherol (alpha-TP) effectively inhibit oxygen free radical-induced lipid peroxidation. Using a premature baboon model of hyperoxia-induced bronchopulmonary dysplasia (BPD), we measured concentrations of AA, alpha-TP, and conjugated dienes (CD, marker of lipid peroxidation) in four animals (hyperoxic antioxidant group) receiving high dose antioxidant vitamin supplementation (AA, 100 mg x kg x(-1) x d(-1); alpha-TP; 20 mg x kg x(-1) x d(-1)) and one animal receiving standard dose antioxidant vitamin supplementation (AA, 10 mg x kg x(-1) x d(-1); alpha-TP, 1 mg x kg x(-1) x d(-1)). Respiratory and histopathologic data were compared with data from 10 historical animals exposed to hyperoxia (hyperoxic control group) and 11 historical animals treated as required with oxygen (normoxic control group) who had received standard dose antioxidant vitamin supplementation. Compared with standard dose antioxidant vitamin supplementation, high dose antioxidant vitamin supplementation effectively raised AA concentrations in plasma (37 +/- 22 micromol/L and 395 +/- 216 micromol/L, respectively) and tracheal aspirates (62 +/- 35 micromol/L and 286 +/- 205 micromol/L, respectively), and alpha-TP concentrations in plasma (10.1 +/- 2.5 micromol/L and 24.6 +/- 17.5 micromol/L, respectively). However, there was no apparent effect on tracheal aspirate CD concentrations (482 +/- 333 micromol/L and 1050 +/- 1111 micromol/L, respectively), and respiratory parameters in the hyperoxic antioxidant group were comparable to those of the hyperoxic control group but significantly worse than in the normoxic control group. Finally, no protective effect of high dose antioxidant vitamin supplementation was noted at the histopathologic level.

Animals↗
PubMed1998

Analytical and clinical performance of a homogeneous enzymatic LDL-cholesterol assay compared with the ultracentrifugation-dextran sulfate-Mg2+ method.

LDL-cholesterol (LDL-C) concentration is currently determined in most clinical laboratories by the Friedewald calculation. This approach has several limitations and may not meet the current total error requirement in LDL-C measurement of < or = 12%. We evaluated the analytical and clinical performance of the direct N-geneous LDL-C assay (Equal Diagnostics). The N-geneous method correlated highly with the modified beta-quantification assay (r = 0.95; y = 0.91x + 70.6 mg/L; n = 199), showed no significant effect of increased triglyceride or other common interferants, and performed adequately in serum samples from nonfasting individuals. This assay demonstrated a mean total error of 6.75% over a wide range of LDL-C concentrations. In addition, at the medical decision cutoff points, this LDL-C assay showed positive predictive values of 78-95% and negative predictive values of 84-99%. We conclude that the N-geneous LDL-C meets the currently established analytical performance goals and appears to have a role in the diagnosis and management of hypercholesterolemic patients.

Cholesterol, LDL↗
PubMed1998

Assessment of interlaboratory performance in external proficiency testing programs with a direct HDL-cholesterol assay.

Direct assays for the determination of HDL-cholesterol (HDL-C) have recently become available. The methods are precise, require small sample volume, and appear to be less affected by increased triglycerides than traditional precipitation methods. In this study, we describe the inter- and intralaboratory variability of the Boehringer Mannheim Corporation direct HDL-C assay and its performance in external proficiency testing surveys. A comparison study among three laboratories, using different analyzers and 85 serum specimens, showed a correlation coefficient (r) of 0.99. The direct HDL-C assay also showed good agreement with the ultracentrifugation-dextran sulfate-Mg2+ method (r = 0.98) and the Cholesterol Reference Method Laboratory Network-Designated Comparison Method (a = 0.98x + 4.75 mg/L, r = 0.98). Total error at medical decision levels ranged from -0.8% to +11.1%. Furthermore, this assay performed adequately in the College of American Pathologists and the ALERT surveys as well as the CDC Lipid Standardization Program and met all performance criteria of regulatory agencies.

Centers for Disease Control and Prevention, U.S.↗
PubMed1998

International Federation of Clinical Chemistry standardization project for the measurement of lipoprotein(a). Phase I. Evaluation of the analytical performance of lipoprotein(a) assay systems and commercial calibrators.

A secondary reference material for lipoprotein(a) is required to standardize the measurement of lipoprotein(a) in clinical laboratories worldwide. Towards this aim, the International Federation of Clinical Chemistry Working Group for the Standardization of Lipoprotein(a) Assays has initiated a standardization project involving a total of 33 diagnostic company and clinical chemistry laboratories from 12 countries. In Phase 1, the analytical performance of 40 lipoprotein(a) assay systems was evaluated by testing sera and manufactured lipoprotein(a) calibrator materials for precision, linearity, and parallelism. Twenty test systems were nonoptimized according to the results for a pooled serum, which tested nonlinear in 16 systems and imprecise in 4. Acceptable analytical properties and harmonization of lipoprotein(a) values were shown by some commercial calibrators, suggesting their possible use as reference materials. This study highlights the problems that currently occur for lipoprotein(a) measurement in existing assay systems.

Calibration↗
PubMed1997

Evaluation and clinical application of a direct low-density lipoprotein cholesterol assay in normolipidemic and hyperlipidemic adults.

This study examines the performance and clinical use of a commercial immunoseparation assay for low-density lipoprotein (LDL) cholesterol in a sample population of normolipidemic and hyperlipidemic adult volunteers. Using paired fasting and nonfasting samples, we compared the direct LDL assay with the beta quantification method and the Friedewald calculation. Overall, the direct LDL assay correctly classified 82% and 60% of fasting and nonfasting subjects, respectively, into National Cholesterol Education Program risk groups. The Friedewald method correctly classified 84% of subjects. The fasting direct LDL assay has comparable positive and negative predictive values to the Friedewald method, except at an LDL cholesterol of 100 mg/dl. The nonfasting direct LDL assay demonstrates unacceptable positive predictive values when LDL cholesterol decreases to the 130 to 159 and > or = 160 mg/dl categories. Overall, direct LDL assay demonstrates limitations in the nonfasting state and at the LDL cholesterol level of 100 mg/dl used for patients with established coronary heart disease.

Adult↗
PubMed1997

Predictive value of cardiac troponin T in pediatric patients at risk for myocardial injury.

BACKGROUND: Biochemical markers have not been routinely used in children at risk for myocardial damage. Yet, because of somatic growth and the duration of survival, a low level of myocardial damage may ultimately be of more consequence in children than in adults. METHODS AND RESULTS: We investigated the utility of cardiac troponin T (cTnT) blood levels (CARDIAC T ELISA Troponin T, Boehringer Mannheim Corp) in 51 consecutively sampled patients from 1 day to 34 years of age (median=5.7 years) undergoing cardiovascular (n=19) or noncardiovascular (n=17) surgery or who received doxorubicin for acute lymphoblastic leukemia (ALL) (n=15). Minimum detectable cTnT elevations were 0.03 ng/mL. cTnT was measurable in children of all ages with myocyte damage. In patients who underwent cardiovascular surgery, a correlation was noted between a score of increasing surgical severity and the mean level of postoperative cTnT (r=.79, P<.0001). Postoperative cTnT levels were elevated in children who completed cardiovascular surgery with an open chest compared with those with a closed chest (P=.0083). In addition, cTnT levels before cardiovascular surgery predicted postoperative survival (P=.007). cTnT elevations were observed after initial doxorubicin therapy for ALL. The magnitude of elevation predicted left ventricular dilatation (r=.80 when variables were treated as continuous, P=.003) and wall thinning (r=.61, P=.044) 9 months later. CONCLUSIONS: Elevations of blood cTnT in children relate to the severity of myocardial damage and predict subsequent subclinical and clinical cardiac morbidity and mortality.

Adolescent↗
PubMed1997

Asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia.

To further elucidate the incidence and potential mechanism of asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia (ALL), we serially obtained fasting lipid and lipoprotein studies on 38 of the 43 consecutively diagnosed children with ALL before, during, and after asparaginase therapy. We also evaluated a second population of 30 long-term survivors of childhood ALL; a fasting lipid and lipoprotein profile was obtained once at study entry. The mean peak triglyceride level during asparaginase of 465 mg/dL (standard deviation [SD] 492) was significantly higher (P = .003) than the level of 108 mg/dL (SD 46) before the initiation of asparaginase therapy. Sixty-seven percent of the newly diagnosed patients had fasting triglyceride levels greater than 200 mg/dL during asparaginase therapy; 15 patients (42%) had levels greater than 400 mg/ dL, 7 with levels greater than 1,000 mg/dL. The incidence of hypertriglyceridemia did not vary by type of asparaginase or risk status of ALL (defined by white blood cell count and age). None of the 7 patients with triglyceride levels greater than 1,000 mg/dL developed pancreatitis. In contrast, 4 of the 13 patients without triglyceride elevation developed pancreatitis; 3 of the 4 patients had fasting studies at the height of their abdominal pain. Nuclear magnetic resonance analysis of lipid subclasses showed a significant increase in the smaller, denser forms of very low density lipoprotein (VLDL) and negligible chylomicron fraction in a subset of patients with marked triglyceride elevation. Lipoprotein lipase activity was consistently above normative values for all levels of triglyceride and could not be explained by obesity or hyperglycemia. Apolipoprotein B(100) levels increased during asparaginase therapy, although the mechanism of this remains unclear. LDL reciprocally decreased with increased VLDL during asparaginase therapy. After asparaginase therapy, triglyceride levels (mean, 73 mg/dL [SD 33]) were significantly lower than levels obtained during asparaginase therapy. Triglyceride levels for survivors did not differ from the normal range or postasparaginase levels in the newly diagnosed patients. These data show a striking temporal association between asparaginase therapy and hypertriglyceridemia. Changes in cholesterol, in contrast, were not temporally related to asparaginase treatment. Cholesterol levels were elevated (>200 mg/dL) in 20% of the patients after asparaginase, which may be due to continued treatment with corticosteroids. The mean cholesterol level of long-term survivors of 177 mg/dL was significantly higher than the norm (P = .045). High-density lipoprotein (HDL) levels were significantly lower than normal at all time periods and for both populations; 25% of survivors had HDL levels less than 35 mg/dL. We conclude that modifications in asparaginase therapy are not necessary. In cases of triglyceride elevation greater than 2,000 mg/dL when the risk of pancreatitis is increased, close clinical monitoring is imperative. Larger studies are needed to determine the incidence of dyslipidemia in long-term survivors of ALL as well as the relationship between lipid abnormalities and other late effects of treatment, notably obesity and cardiomyopathies.

Adolescent↗
PubMed1997

Measurement of plasma busulfan concentration by high-performance liquid chromatography with ultraviolet detection.

Busulfan is widely used in bone marrow transplantation. Increased area under the plasma concentration curve has been shown to correlate with venoocclusive disease, which occurs in approximately 20% of these patients. The authors developed a high performance liquid chromatography assay for the determination of plasma busulfan concentration using ultraviolet detection and a single-step derivatization and extraction. The absolute retention times of busulfan and the internal standard were 2.8 and 5.6 min, respectively. The assay possessed linearity up to 200 mumol/l, sensitivity to at least 0.2 mumol/l, average recovery of 101%, and run-to-run precision (n = 34) of < 7%. Furthermore, the assay proved to be free of interference from 59 medications and correlated highly with a validated method employing gas chromatography with electron capture detection (slope = 0.90, intercept = 0.17, r = 0.98, n = 31). The authors conclude that the method described here is ideally suited for the therapeutic monitoring of busulfan.

Busulfan↗
PubMed1997

Measurement of plasma ketoprofen by a rapid high-performance liquid chromatography assay.

The authors developed a high performance liquid chromatography assay for the determination of plasma ketoprofen concentration using a single-step extraction, a short chromatographic separation of 3 min, and a sample volume of 50 microliters. The assay possessed linearity up to 500 mg/l, sensitivity down to at least 1 mg/l, average recovery of 100.1%, and run-to-run precision (n = 20) of 4.6% at a level of 10 mg/l and 2.2% at a level of 40 mg/l. Furthermore, the assay was free of interference from 51 prescription and over-the-counter medications. The authors conclude that the method described here is ideally suited for the determination of ketoprofen concentration in a clinical laboratory setting for the purpose of therapeutic monitoring and assessment of toxicity.

Chromatography, High Pressure Liquid↗
PubMed1997

Three generations of high-density lipoprotein cholesterol assays compared with ultracentrifugation/dextran sulfate-Mg2+ method.

We report on the analytical performance of three generations of HDL-cholesterol assays: phosphotungstic acid/Mg2+, Spinpro, and a homogeneous method, N-geneous. The run-to-run imprecision (CV) of all assays was < or = 4.9%, and all results correlated highly with those of a modified reference procedure (r > or = 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 < or = 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.

Ascorbic Acid↗
PubMed1996

Effects of a single bout of ultraendurance exercise on lipid levels and susceptibility of lipids to peroxidation in triathletes.

OBJECTIVE: To determine the effects of a single bout of ultraendurance exercise, as a model for physiologic stress, on lipid and lipoprotein levels, and oxidative susceptibility of lipids in highly trained athletes. DESIGN: Observational trial. POPULATION AND SETTING: Thirty-nine volunteer subjects (26 mean, 13 women; mean age, 38 +/- 10 years) who competed in and completed the 1994 Hawaii Ironman World Championship Triathlon consisting of a consecutive 3.9-km (2.4-mi) swim, 180.2-km (112-mi) bike ride, and a 42.2-km (26.2-mi) run. Subjects answered questionnaires and had blood samples obtained 2 days prior to and within 15 minutes of completion of the triathlon. MAIN OUTCOME MEASURES: Prerace vs postrace changes in lipid and lipoprotein levels, and susceptibility of lipids to peroxidation. RESULTS: The mean duration of exercise was 753 +/- 128 minutes. With exercise, plasma volume-corrected levels of triglycerides decreased 39% from 1.58 +/- 0.83 to 0.97 +/- 0.68 mmol/L (139.6 +/- 73.6 to 85.8 +/- 60.5 mg/dL) (P < .001). Levels of total cholesterol decreased 9% from 4.94 +/- 0.88 to 4.50 +/- 0.79 mmol/L (190.8 +/- 33.8 to 173.8 +/- 30.6 mg/dL) (P < .001), low-density lipoprotein cholesterol decreased 11% from 2.59 +/- 0.77 to 2.30 +/- 0.86 mmol/L (100.1 +/- 29.9 to 88.7 +/- 33.3 mg/dL) (P = .02), and apolipoprotein B decreased 10% from 0.91 +/- 0.20 to 0.82 +/- 0.18 g/L (90.7 +/- 20.0 to 82.0 +/- 17.9 mg/dL) (P < .001). High-density lipoprotein cholesterol and apolipoprotein A-I increased with exercise but not significantly. The susceptibility of lipids to peroxidation decreased significantly (4.51 +/- 1.91 micromol/L, preexercise, vs 2.42 +/- 2.27 micromol/L, postexercise, P < .001), an effect that was not related to antioxidant use or levels of vitamins A, C, or E. Serum iron, a potential pro-oxidant, also decreased by 45% with exercise from 15.75 +/- 5.55 to 8.59 +/- 4.30 micromol/L (88 +/- 31 to 48 +/- 24 micrograms/dL) (P < .001), an effect that was weakly correlated with changes in lipid peroxidation (P = .05). CONCLUSIONS: These data suggest that a single bout of prolonged exercise can reduce lipid and lipoprotein risk factors for developing cardiovascular disease. Moreover, susceptibility of lipids to peroxidation is reduced by exercise, thereby adding to the benefits of physical activity. This effect appears to be independent of antioxidant supplement use and may be mediated by induction of endogenous antioxidants. These observations may explain in part the reduced risk of developing vascular and other diseases in individuals who are physically active.

Adult↗
PubMed1996

Therapy with oral clotrimazole induces inhibition of the Gardos channel and reduction of erythrocyte dehydration in patients with sickle cell disease.

Pathologic water loss from sickle erythrocytes concentrates the abnormal hemoglobin and promotes sickling. The Ca2+-activated K+ channel (Gardos channel) contributes to this deleterious dehydration in vitro, and blockade of K+ and water loss via this channel could be a potential therapy in vivo. We treated five subjects who have sickle cell anemia with oral clotrimazole, a specific Gardos channel inhibitor. Patients were started on a dose of 10 mg clotrimazole/kg/d for one week. Protocol design allowed the daily dose to be escalated by 10 mg/kg each week until significant changes in erythrocyte density and K+ transport were achieved. Blood was sampled three times a week for hematological and chemical assays, erythrocyte density, cation content, and K+ transport. At dosages of 20 mg clotrimazole/kg/d, all subjects showed Gardos channel inhibition, reduced erythrocyte dehydration, increased cell K+ content, and somewhat increased hemoglobin levels. Adverse effects were limited to mild/moderate dysuria in all subjects, and a reversible increase in plasma alanine transaminase and aspartic transaminase levels in two subjects treated with 30 mg clotrimazole/kg/d. This is the first in vivo evidence that the Gardos channel causes dehydration of sickle erythrocytes, and that its pharmacologic inhibition provides a realistic antisickling strategy.

Administration, Oral↗
PubMed1996

The role of lipoproteins in the transport and uptake of cyclosporine and dihydro-tacrolimus into HepG2 and JURKAT cell lines.

OBJECTIVES: We wish to examine the role of lipoproteins in the transport and cellular uptake of cyclosporine (CsA) and tacrolimus. DESIGN AND METHODS: The distribution of tritiated CsA and tacrolimus among lipoproteins was determined in normo- and hypertriglyceridemic sera. The uptake of these two drugs into HepG2 and JURKAT cell lines was assessed in the presence of various concentrations of low density lipoproteins. (LDL). RESULTS: Our data showed that about 60% of these drugs were transported by high density lipoprotein in normolipidemic sera, while about 50-60% were carried by very low density lipoprotein in hypertriglyceridemic sera. Almost 80% of CsA and 70% of tacrolimus entered HepG2 and JURKAT cells within the first hour of incubation in lipoprotein free media. However, the uptake was decreased (CsA by 60% and tacrolimus by 40%) in the presence of LDL. CONCLUSIONS: Lipoproteins play a major role in the transport of CsA and tacrolimus, but not in their cellular uptake.

Biological Transport, Active↗
PubMed1996

Vitamin A status in acute exacerbations of cystic fibrosis.

Vitamin A is an essential nutrient for epithelial cell maintenance and repair, and it is known that infectious stresses may depress plasma vitamin A concentrations. Patients with cystic fibrosis are at risk for vitamin A deficiency because of fat malabsorption as well as for the inflammatory stresses of pulmonary exacerbations of their underlying disease. We therefore hypothesized that acute pulmonary exacerbations of CF would depress plasma retinol concentrations, and that these concentrations would return to baseline values when clinical symptoms improved. We prospectively studied 35 CF patients (mean age: 24.2 y) consecutively admitted with pulmonary exacerbations. Plasma retinol, vitamin E, retinol binding protein (RBP), and C-reactive protein (CRP) concentrations were measured on hospital admission and discharge. Dietary intake was measured by using a semiquantitative food-frequency questionnaire. Regression analysis was used to identify significant clinical and laboratory correlates of retinol concentrations. On admission, mean (+/- SD) concentrations of plasma retinol were 1.14 +/- 0.5 mumol/L compared with 1.70 +/- 0.6 mumol/L on discharge (P = 0.0001). Of 35 subjects, 8 (22.9%) had plasma retinol concentrations considered to be in the deficient range (< 0.70 mumol/L). Concurrently, mean concentrations of plasma RBP increased during hospital admission (from 1.46 to 2.24 mumol/L, P = 0.003), and the mean CRP concentration declined (from 25.7 to 9.8 mg/L, P = 0.002). Significant positive correlations were found between plasma retinol concentrations at admission and age, weight, body mass index, triceps-skinfold-thickness percentile, midupper arm circumference percentile, plasma vitamin E, and RBP concentration, thus suggesting that better-nourished patients had more optimal vitamin A status. At admission, plasma retinol concentrations were negatively correlated with maximum body temperature and CRP concentrations, which indicated that the body's acute-phase response was associated with the depression in retinol concentrations. We conclude that plasma retinol concentrations are depressed in acute pulmonary exacerbations of cystic fibrosis, and that concentrations considered to be in the deficient range are common. Vitamin A metabolism during acute inflammatory stress deserves further study.

Acute Disease↗
PubMed1996

Three routine methods for measuring high-density lipoprotein cholesterol compared with the Reference Method.

We compared the performance of three methods for quantifying high-density lipoprotein cholesterol (HDL-C) with the Reference Method for HDL-C, using samples with a wide range of triglyceride (TG) concentrations (290-18000 mg/L). All three comparison assays-- utilizing a magnetic dextran sulfate precipitating reagent, a direct method, and a standard MgCl2-dextran sulfate reagent--were precise, with a run-to-run CV of less than or equal to 4.1%. However, the systematic error of these assays exceeded the National Cholesterol Education Program (NCEP) performance goal of less than or equal to 10% in half of the concentration ranges tested. Nevertheless, the total error of the assays generally meets the current 22% limit set by the NCEP. Although both the magnetic dextran sulfate precipitation reagent and the direct assay can be performed more rapidly than the MgCl2-dextran sulfate assay, the direct assay involves no sample preparation and requires only 4 microL of sample excluding the dead space. Although precipitation is frequently inadequate with the MgCl2-dextran sulfate reagent at TG concentrations >6000 mg/L, both the magnetic and the direct reagent show no interference from high TG concentrations as great as 18 000 mg/L.

Chemical Precipitation↗
PubMed1996

Analytical performance and clinical utility of a direct LDL-cholesterol assay in a hyperlipidemic pediatric population.

This study compares a new latex immunoseparation method for the direct determination of plasma low-density lipoprotein cholesterol (LDL-C) with the reference procedure for LDL-C (beta-quantification) in a pediatric hyperlipidemic population. The direct LDL-C assay has a mean bias of -98 mg/L in a fasting group (n = 96) of patients (mean triglycerides 1057 +/- 720 mg/L) and a bias of +177 mg/L in a nonfasting group (n = 42, mean triglycerides 4854 +/- 5457 mg/L). The mean total analytical error calculated from our data is 13.8%. The direct LDL-C assay and the commonly used Friedewald calculation respectively classified 81% and 84% of fasting patients correctly, according to the cutoffs of 1100 and 1300 mg/L for LDL-C set by the National Cholesterol Education Program for pediatric patients. Of combined fasting and nonfasting patients, 80% were correctly classified by the direct LDL-C assay. Therefore, despite several analytical shortcomings, the direct LDL-C assay may be useful in managing hyperlipidemic children without the need for a fasting specimen.

Adolescent↗