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Biomedical subjects

G R Warnick

Publications and source records attributed to G R Warnick.

At least 55 records · Page 3Linked to original sources
PubMed1983

Interlaboratory proficiency survey of high-density lipoprotein cholesterol measurement.

Proficiency surveys of Seattle-area laboratories suggest only slight improvement in overall performance in high-density lipoprotein (HDL) measurement between 1978 and 1982, although the reported workload for HDL has increased by 15%. The mean interlaboratory SD was 64 mg/L (ranging from 34 for a pool averaging 299 mg/L to 136 for a pool averaging 886 mg of HDL cholesterol per liter) in 1982, compared with 79 mg/L (range 48-155) in 1978-79. Of the individual laboratory results in the current survey, 39% deviated by more than 50 mg/L from target values as compared with 37% in 1978-79. The discrepant values were primarily ascribable to method inaccuracy: only 30% of laboratories in 1982 reported results that averaged within 30 mg/L of target values (vs 50% in 1978). For within-run precision, 80% of laboratories in 1982 had SDs of less than 30 mg/L, vs 70% in 1978. The 1982 survey included a lyophilized serum prepared by spray freezing and bulk lyophilization (Hyland Omega), identical to the pools used in the College of American Pathologists Comprehensive Chemistry Survey, and five pools of frozen plasma. Interlaboratory variation and biases for the Omega pool were similar to those for the frozen pools.

Chemistry, Clinical↗
PubMed1982

Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis.

The effects of stanozolol, 17-methyl-2H-5 alpha-androst-2-eno [3,2-c] pyrazol-17 beta-ol, on lipoprotein levels were assessed in a short-term (6 wk) prospective study of 10 normolipidemic, postmenopausal, osteoporotic women. While total cholesterol and triglyceride levels remained constant, equal and offsetting responses were seen in low density lipoprotein (LDL) cholesterol (+30.9 +/- 28.1 mg/dl [mean +/- S.D.], p less than 0.01, a 21% increase) and high density lipoprotein (HDL) cholesterol (-32.5 +/- 11.9 mg/dl [mean +/- S.D.], p less than 0.001, a 53% decline). Hence the LDL/HDL ratio increased dramatically, from 2.5 +/- 0.7 to 6.8 +/- 2.5. Within HDL, stanozolol was associated with a greater decline in HDL2 (from 26.0 +/- 7.4 mg/dl to 3.8 +/- 1.9 mg/dl, p less than 0.001, an 85% decrease) than HDL3 (which diminished from 35.7 +/- 3.2 to 24.1 +/- 5.8 mg/dl. p less than 0.001, a 35% decrease). The major HLD apolipoproteins also declined (A-I by a mean of 41% and A-II by 24%, both p less than 0.001). Postheparin hepatic triglyceride lipase increased (off treatment 74 +/- 42 nmole free fatty acid min-1 mole-1, on treatment 242 +/- 110, n = 6, p = 0.06). All changes were reversed by 5 wk following termination of the drug. These lipoprotein changes suggest caution in the long term prescription of stanozolol, particularly in those without overriding clinical indications for its use.

Aged↗
PubMed1982

HDL cholesterol quantitation by phosphotungstate-Mg2+ and by dextran sulfate-Mn2+-polyethylene glycol precipitation, both with enzymic cholesterol assay compared with the lipid research method.

Two methods using commercial kits for high density lipoprotein (HDL) cholesterol quantitation were compared with the Lipid Research Clinics (LRC) procedures. HDL cholesterol quantitations on 50 patient specimens by the Lancer HDL cholesterol Rapid Stat Kit (Lancer) with phosphotungstate-Mg2+ precipitation and enzymic cholesterol assay averaged 424 mg/L, and by a method with dextran sulfate-Mn2+-polyethylene glycol (dextran sulfate) precipitation and enzymic cholesterol assay averaged 474 mg/L. By comparison, the LRC method (heparin-Mn2+ precipitation combined with a Liebermann-Burchard reagent cholesterol assay) averaged 478 mg/L. Supernates obtained by the three precipitation methods had similar cholesterol values when analyzed by the LRC assay, suggesting that the observed differences were primarily due to differences between the cholesterol assays. Results were consistent with underestimation by the enzymic assay of cholesterol in the supernates, offset by a positive interference of Mn2+ in the dextran sulfate-produced supernates. Among-day CVs of 4-5% were observed for the Lancer method, and 6-7% for the dextran sulfate method. Sedimentation of precipitates in hypertriglyceridemic specimens was excellent by both methods.

Chemical Precipitation↗
PubMed1982

Lipoprotein quantification: an electrophoretic method compared with the Lipid Research Clinics method.

We compared a turbidimetric electrophoretic method (Lipidophor) for lipoprotein quantification with the standardized Lipid Research Clinics (LRC) method. In the Lipidophor procedure, major lipoproteins are separated by electrophoresis on agarose gels, precipitated on the gels with phosphotungstate-Mg2+ reagent, and the resulting turbidity is measured densitometrically. Measurements of relative turbidity were converted into lipoprotein cholesterol values by the use of numeric constants provided by the manufacturer. Among-day CVs (n = 46) for the Lipidophor method were 6.0%, 3.6%, and 9.9% for cholesterol in the alpha-, beta-, and pre-beta lipoproteins, respectively. The Lipidophor alpha-cholesterol was significantly lower (n = 171 specimens) than the LRC high-density lipoprotein (HDL) cholesterol (514 vs 586 mg/L), and beta-cholesterol was significantly higher than the corresponding LRC low-density lipoprotein (LDL) cholesterol values (1505 vs 1409 mg/L). The linear relation between the two methods for lipoprotein cholesterol quantification is as follows: Lipidophor alpha = 0.77 LRC HDL + 63 mg/L with correlation coefficient (r) of 0.87; Lipidophor beta = 0.95 LRC LDL + 166 mg/L (r = 0.96); Lipidophor pre-beta = 0.57 LRC very-low-density lipoprotein + 39 mg/L (r = 0.82). We derived a revised algorithm for estimating lipoprotein cholesterol from turbidity measurements. Lipoprotein cholesterol values by the Lipidophor method agree well with those obtained by the LRC method when these constants are used.

Adult↗
PubMed1981

Association of isoapolipoprotein-E3 deficiency with heterozygous familial hypercholesterolaemia: implications for lipoprotein physiology.

A prepubertal girl with both homozygous isoapolipoprotein-E3 deficiency (the genetic defect underlying type-III hyperlipoproteinaemia) and heterozygous familial hypercholesterolaemia (familial type-IIa hyperlipoproteinaemia) presented with severe hypercholesterolaemia and antecubital and popliteal planar xanthomas. She responded dramatically to clofibrate. Her mother was normolipidaemic and heterozygous for apo-E3-deficiency. Her father, an obligate apo-E3-deficient heterozygote, and his similarly affected brother died prematurely with severe hypercholesterolaemia which had been refractory to clofibrate. Her paternal grandfather, who had the same combination of disorders as the proband, also responded to clofibrate, whereas her grandmother was normolipidaemic. Hence homozygous apo-E3 deficiency may present during childhood as severe hypercholesterolaemia when combined with familial hypercholesterolaemia, suggesting that the low-density-lipoprotein receptor may represent one mechanism whereby apo-E3-deficient remnants of very-low-density lipoproteins and chylomicrons are cleared from the plasma compartment. The removal of such apo-E3-deficient remnants is especially facilitated by clofibrate.

Apolipoprotein E3↗
PubMed1981

Relationships of gender, sex hormone use, and age with lipoprotein cholesterol/triglyceride ratios in an adult population. The Pacific Northwest Bell Telephone Company health survey.

UNLABELLED: Effects of gender, sex hormone use, and age on lipoproteins composition have been evaluated in 603 Caucasian subjects, ages 20-59, randomly selected from employees participating in the Pacific Northwest Bell Telephone Company Health Survey. Lipoprotein composition in this analysis is defined as the cholesterol to triglyceride (C/TG) ratio in each lipoprotein fraction. The lipoprotein C/TG ratio is inversely related to the lipoprotein triglyceride concentrations in VLDL, LDL and HDL; the ratio falling in each instance as lipoprotein triglyceride concentration increases. Plots of this relationship are virtually superimposable among women hormone users and nonusers and men in VLDL and HDL and between men and nonhormone taking women in LDL. A consistently lower C/TG ratio is observed in LDL for hormone-treated women compared to the other 2 groups. Age in these analysis is without effect. CONCLUSIONS: We hypothesize that a lower LDL (C/TG) ratio is hormone-treated women may render the lipoprotein less crystalline or smectic and potentially less atherogenic. No such difference exists in the lipoprotein C/TG ratio between men and nonhormone-treated women and therefore cannot explain the observed difference in atherosclerosis sick. Nonetheless, the C/TG ratios may predict atherosclerosis if the ratio is high in VLDL or in LDL. However, the significance of the HLD (C/TG) ratio remains to be established.

Adult↗
PubMed1981

Distribution of lipoproteins triglyceride and lipoprotein cholesterol in an adult population by age, sex, and hormone use- The Pacific Northwest Bell Telephone Company health survey.

This report describes the distribution of lipoprotein triglyceride and lipoprotein cholesterol in employees of the Pacific Northwest Bell Telephone Company. Means, medians, and selected percentiles are presented for very low, low, and high density lipoproteins (VLDL, LDL, and HDL, respectively) in 606 randomly selected white subjects aged 20-59. Results are specific for age decade, sex, and female sex hormone usage. Women who use sex hormones have significantly higher concentrations of triglycerides in all of the fractions across all age decades from 20 to 59 than do women not taking hormones. The average VLDL, LDL, and HDL triglyceride levels in women taking hormones are 69, 25 and 18 mg/dl which are considerably higher than the corresponding averages of 44, 17 and 12 mg/dl noted in women not taking hormones. Men have the highest average VLDL triglyceride value (85 mg/dl) but their average triglyceride concentrations in the LDL and HDL fractions (18 and 12 mg/dl) approximate those of women not taking hormones. This study in a well-defined population provides references standards for lipoprotein triglyceride concentrations. These results can be used to evaluate the effect of sex hormone treatment on the lipoprotein triglyceride content in VLDL, LDL and HDL, and to assess triglyceride content as a potential risk factor in men and older women.

Adult↗
PubMed1981

Genetic transmission of isoapolipoprotein E phenotypes in a large kindred: relationship to dysbetalipoproteinemia and hyperlipidemia.

The largest reported kindred of a proband with type III hyperlipoproteinemia was investigated by assessment of lipid and lipoprotein levels and very low density lipoprotein (VLDL) isoapolipoprotein E distributions in all accessible family members (56% of the 124 living blood relatives and 59% of the 37 spouses). The results confirm in this kindred a trimodal distribution of apoE3/E2 ratios, and segregation analysis of 16 informative matings classified according to E3/E2 ratio demonstrated classical Mendelian inheritance of the autosomal codominant type: the E3/E2 ratio is determined by two alleles, apoE3d and apoE3n, which produce three phenotypes apoE3-D, apoE3-ND, and apoE3-N, corresponding to the low, intermediate, and high modes, respectively. Vertical transmission of the apoE3-D phenotype occurred in two branches of the second generation. In both instances this represented pseudodominance; i.e., products of heterozygous (apoE3-ND) x homozygous (apoE3-D) matings. Hyperlipidemia (defined as a low density lipoprotein cholesterol and/or plasma triglyceride level exceeding the respective age-, sex-, and sex-steroid-specific 95th percentiles derived from Lipid Research Clinics population studies) was present in 15 blood relatives in multiple lipoprotein patterns, consistent with the presence of familial combined hyperlipidemia in this kindred. Eight of nine members with the apoE3-D phenotype had either type III hyperlipoproteinemia or, in the absence of hyperlipidemia, beta-VLDL and at least marginally cholesterol-rich VLDL (VLDL-cholesterol/plasma triglyceride greater than 0.25) (defined as dysbetalipoproteinemia). The ninth such member, the only child with this phenotype, was normal. beta-VLDL and marginally cholesterol-rich VLDL was seen in but one of six hyperlipidemic family members of phenotype apoE3-ND, in none of seven hyperlipidemic blood relatives of phenotype apoE3-N, in no normolipidemic family members of phenotype apoE3-ND or apoE3-N, and in no spouses (three of whom were hyperlipidemic and nine of phenotype apoE3-ND). Thus, among adult members of the O'D kindred the apo3-D phenotype was nearly specifically associated with dysbetalipoproteinemia or, when hyperlipidemia was present, type III hyperlipoproteinemia.

Adolescent↗
PubMed1981

Multilaboratory evaluation of an ultrafiltration procedure for high density lipoprotein cholesterol quantification in turbid heparin-manganese supernates.

High density lipoprotein (HDL) can be quantitated by measurement of cholesterol in supernates after precipitation of low and very low density lipoprotein (LDL and VLDL) with heparin and Mn(2+). Supernatant turbidity, often observed with hypertriglyceridemic specimens, indicates incomplete sedimentation of LDL/VLDL and precludes accurate quantitation of HDL. Ten Lipid Research Clinic Laboratories compared an ultrafiltration technique for clearing turbid heparin-Mn(2+) supernates to current methods involving repeat precipitation of either the original specimen after dilution or the d > 1.006 g/ml fraction after removal of VLDL from the initial specimen by ultracentrifugation. Results for ultrafiltration of 429 turbid supernates averaged only slightly higher (1.0-1.1 mg/dl) than results by the dilution or ultracentrifugation methods on the same specimens, but this difference was found to be significant (P < 0.005). The agreement of the ultrafiltration method with the other two methods is indicated by the following linear regression equations: a), ultrafiltration = (0.964 x ultracentrifugation) + 2.4 mg/dl, and correlation coefficient = 0.926; and b), ultrafiltration = (0.936 x dilution) + 3.3 mg/dl, and correlation coefficient = 0.933. We conclude that ultrafiltration of turbid heparin-Mn(2+) supernates is a convenient alternative to precipitation after either dilution or removal of VLDL.-Warnick, G. R., J. J. Albers, P. Bachorik, J. Turner, C. Garcia, C. Breckinridge, K. Kuba, S. McNeely, G. Hillerman, P. King, R. Muesing, B. Most, and K. Lippel. Multi-laboratory evaluation of an ultrafiltration procedure for high density lipoprotein cholesterol quantification in turbid heparin-manganese supernates.

Chemical Phenomena↗
PubMed1981

Evaluation of quality-control materials for high-density-lipoprotein cholesterol quantitation.

Commercial quality-control materials and frozen plasma and serum pools were evaluated for high-density lipoprotein (HDL) cholesterol quantitation by the heparin-Mn2+ and phosphotungstate-Mg2+ precipitation methods and by ultracentrifugal and electrophoretic methods. We evaluated among-day precision; inter-method differences in HDL cholesterol quantitation; lipid composition and electrophoretic mobility of th lipoprotein density fractions; and the effects of modifications in reagent concentration and temperature. Frozen plasma pools (in-house) and frozen serum pools (prepared by the Center for Disease Control) were determined to be suitable HDL controls. Also, a commercial lyophilized serum free of very-low-density lipoprotein (VLDL) to which VLDL is added in a diluent solution (Analytical Control) also appeared suitable as an HDL control material. Conventional lyophilized pools (Lyphochek Elevated, Monitrol I, Ortho Normal, Precilip) were less suitable as control materials because of poor between-day precision for one or both of the precipitation methods and, in some cases, because of large absolute differences observed between the HDL methods. A serum pool stabilized with ethylene glycol (Beckman Level I) was the least as appropriate as an HDL control material. Other lyophilized pools--Lipid Fraction Control (Hyland) prepared by a modified lyophilization process and Lipidophor (Immuno Diagnostika) prepared by lyophilization with a stabilizing agent--appear promising.

Apolipoproteins↗
PubMed1979

Gel isoelectric focusing method for specific diagnosis of familial hyperlipoproteinemia type 3.

We describe a gel isoelectric focusing procedure for resolving into at least five bands the arginine-rich protein of very-low-density lipoproteins, and use the method in diagnosis of hyperlipoproteinemia type 3. We find that deficiency of one band, designated E3, relative to E2, expressed as an E3/E2 ratio less than or equal to 0.3, is specifically associated with hyperlipoproteinemia type 3 as diagnosed by traditional criteria in a large family study. In addition, we used the procedure to test 47 referral samples with demonstrable beta-migrating very-low-density liproprotein grouped by very-low-density lipoprotein cholesterol/total triglyceride ratios of greater than or equal to 0.3, from 0.25 to 0.3, and less than 0.25. All 24 of the first group, three of six in the second, and only one of 17 in the third had E3/E2 ratios of less than or equal to 0.3. Also, two normolipidemic children, without detectable lipoprotein abnormalities but related to subjects with hyperlipoproteinemia type 3, had E3/E2 ratios of less than or equal to 0.3. Use of our procedure improves the specificity of diagnosis and allows sensitive detection of asymptomatic subjects who may be at risk of developing the disorder.

Apolipoproteins↗
PubMed1979

Evaluation of commercial heparin preparations for use in the heparin-Mn2+ method for measuring cholesterol in high-sensity lipoprotein.

Commercial heparin preparations (18 lots) from seven manufacturers were compared in the heparin-Mn2+ procedure for high-density-lipoprotein cholesterol quantitation. With normotriglyceridemic samples, 16 heparin lots, isolated from porcine intestinal mucosa, gave mean values for supernatant cholesterol that did not differ statistically; all were within 7 mg/L. Two heparin preparations from bovine lung gave results that were slightly (16 mg/L, average) but significantly (p less than 0.005) lower. With hypertriglyceridemic samples, we observed greater variation in supernatant cholesterol among the heparin preparations, which was ascribable to variable sedimentation by centrifugation of very-low-density and low-density lipoproteins precipitated by heparin-Mn2+ treatment. If the precipitated lipoproteins were completely removed by an ultrafiltration procedure, we saw no significant difference among the heparin preparations for results with hypertriglyceridemic samples.

Animals↗
PubMed1979

Comparison of current methods for high-density lipoprotein cholesterol quantitation.

We compared six precipitation methods for high-density-lipoprotein cholesterol quantitation with an ultracentrifugation method, the accuracy of which was improved by correcting for 4% manipulative loss in the d greater than 1.063 fractions. For purposes of comparison, the apoprotein B-associated cholesterol (average 56 mg/L) measured by immunoassay in the d greater than 1.063 fractions was subtracted. In 65 plasma samples from men, women, and children, a heparin-Mn2+ procedure with Mn2+ at 46 mmol/L produced results slightly higher (+16 mg/L), while results with Mn2+ at 92 mmol/L averaged slightly lower (-8 mg/L) than the comparison ultracentrifuge method. Results that were about 5% low were obtained by the dextran sulfate 500-Mg2+ (-25 mg/L) and phosphotungstate-Mg2+ (-31 mg/L) methods. A heparin-Ca2+ method produced results 10% high (+58 mg/L). Results by a polyethylene glycol-6000 precipitation method were 12% low (-64 mg/L). Precision was better with the two heparin-Mn2+ and the dextran sulfate 500-Mg2+ procedures, with CVs of 4%, intermediate with phosphotungstate-Mg2+ and polyethylene glycol-6000 (CV 6-7%), and poorest with heparin-Ca2+ (CV 10%). Precipitation by phosphotungate-Mg2+ appeared more sensitive to reagent concentration and temperature variations than either the heparin-Mn2+ or dextran sulfate 500-Mg2+ methods. We conclude that these precipitation methods are not equivalent, but give rise to significant systematic differences in high-density-lipoprotein cholesterol quantitation.

Adult↗