Cancer risk in relation to serum copper levels.

A nested, matched case-control study was conducted to assess the relationship between serum levels of copper and the subsequent risk of cancer. One hundred thirty-three cases of cancer were identified during 1974-1984 among 5000 members of a northwest Washington State employee cohort from whom serum specimens had been previously obtained and stored. Two hundred forty-one controls were selected at random from the cohort and were matched to the cases on the basis of age, sex, race, and date of blood draw. Serum copper levels were measured by atomic absorption spectrometry. Risk of a subsequent diagnosis of cancer was positively associated with serum copper levels, but only among those cases diagnosed within 4 years of the time the serum specimens were collected. Among cases diagnosed more than 4 years after specimen collection, there was no consistent association between serum copper levels and risk. Adjustment for age, sex, race, occupational status, cigarette smoking, family history of cancer, alcohol consumption, and, among females, use of exogenous hormones had no appreciable effect on these relationships. The findings suggest that the presence of cancer may increase serum copper levels several years prior to its diagnosis. They are less supportive of the hypothesis that serum copper levels affect cancer risk.

Comparison of plasma lipoproteins and apoproteins in Chinese and American non-insulin-dependent diabetic subjects and controls.

Plasma lipoproteins and apoproteins were compared among Chinese and American controls and non-insulin-dependent diabetic (NIDDM) subjects in the same laboratory. Apoprotein AI concentrations in Chinese subjects, both NIDDM subjects and controls (men, 147 and 158 mg/dl, respectively), were significantly higher than those in American subjects (men, 104 and 124 mg/dl, respectively). Apoprotein AII concentrations, however, were comparable between Chinese and American subjects. Chinese NIDDM subjects had lower high-density lipoprotein cholesterol (HDLC), higher low-density lipoprotein cholesterol (LDLC), and higher apoprotein B levels than Chinese controls. Chinese subjects with NIDDM had HDLC and LDLC levels similar to those of American controls but trends of higher HDLC and lower LDLC compared with American subjects with NIDDM. These differences may in part explain the relatively higher incidence of atherosclerotic vascular disease in Americans.

Oral contraceptive and postmenopausal estrogen effects on lipoprotein triglyceride and cholesterol in an adult female population: relationships to estrogen and progestin potency.

PIP: A study of the prevalence of hyperlipidemia has been conducted among female telephone company employees using oral contraceptives (OCs) or estrogenic hormones. This paper relates hormone formulation and estrogen/progestin potency to striglyceride and cholesterol concentrations in total plasma and lipoprotein fractions and relative lipid composition. Changes in these lipid parameters are of interest because they may predict atherosclerosis risk. Results in 148 hormone users are compared with those in 306 nonhormone users. All data are adjusted for the effects of age, relative body weight, cigarette smoking, and alcohol intake. Triglyceride concentrations in whole plasma, very low density lipoprotein (VLDL), and high density lipoprotein (HDL) are elevated 1.5-2.5 fold with increasing estrogen potency. Low density lipoprotein (LDL) triglyceride concentration is elevated to a similar degree among OC users regardless of estrogen potency, but there is no significant effect of postmenopausal estrogen use on LDL triglyceride concentrations. The LDL cholesterol concentration shows an increasing trend with increasing estrogen potency in a random sample of OC-treated women, but is slightly lower than control in postmenopausal women treated with estrogen alone. The HDL cholesterol concentration in plasma is highest with hormones having the greatest estrogen potency and lowest with those having the greatest progestin potency. The VLDL cholesterol to triglyceride ratio adjusted for triglyceride concentration is significantly increased with the use of Ovral, a progestin-predominant contraceptive preparation. The LDL cholesterol to triglyceride ratio is reduced with the use of all OCs examined, except for Ovral, where the ratio is above average. The HDL cholesterol to triglyceride ratio is reduced for all combination OCs examined. The use of a sequential OC or postmenopausal estrogens is not associated with a significant alteration in the cholesterol to triglyceride ratio in any lipoprotein fraction. Knowledge of estrogen and progestin potency and kind of progestin are important in predicting the effect of OCs on plasma and lipoprotein lipids. On the basis of observed differences in lipoprotein lipid concentrations and relationships, the potential arteriosclerotic risk from sex hormones may vary among OC formulations.^ieng

Capabilities of compact analyzers for decentralized testing of lipids and lipoproteins.

Advances in compact analyzer technology have provided the capability to move laboratory testing to the patient, the bedside, the physician office, wellness sites and even into the home. The future has arrived in the sense that lipid testing can be performed in a simple manner similar to blood pressure testing with results immediately available to facilitate treatment decisions. The realities of access and utilization as well as the rate of future technology developments will be determined to a large degree by government regulatory and reimbursement decisions.

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.

PIP: A study of lipoprotein triglyceride and lipoprotein cholesterol distribution was done between 1973-76 on a randomly selected group of 606 white male and female employees, aged 20-59, of the Pacific Northwest Bell Telephone Company. Data obtained were used to ascertain whether triglyceride content of lipoprotein differs in men and women by observing mean, standard and percentile distribution of VLDL, LDL, and HDL (very low, low, and high density lipoprotein). A high proportion of women, i.e. 50% in the age group 20-29, and 50-59, reported current use of some form of exogenous sex hormone preparation. The average VLDL, LDL, and HDL triglyceride level in women taking hormones were 69, 25, and 18 mg/dl, considerably higher than the corresponding averages of 44, 17, and 12 mg/dl observed in women not taking hormones. For VLDL triglyceride, the youngest and oldest male groups had lower average levels than females in the same age taking hormones; in the middle-age group the levels were the same among men and women. For VLDL cholesterol, the 20-29 year old male and female hormone users had similar concentration levels, but male values were higher in each of the remaining age strata. These data confirm the fact that lipoprotein triglyceride rise is associated with the type of oral contraceptives used in the U.S., and with postmenopausal treatment as well.

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.

Effect of fenofibrate treatment on plasma lipoprotein lipids, high-density lipoprotein cholesterol subfractions, and apolipoproteins B, AI, AII, and E.

In this segment of a multicenter study, 36 hypercholesterolemic patients were randomly assigned to fenofibrate or placebo treatment to assess effects on plasma concentrations of lipoprotein cholesterol and triglyceride, high-density lipoprotein-cholesterol subfractions, and apolipoproteins E, B, Al, and All. All of these factors are of known or potential value in determining the patient's risk of arteriosclerosis. Observations were made during initial screening and placebo phases, a 24-week, double-blind treatment phase, and a subsequent 24-week, open-label fenofibrate phase. There were three possible expressions of fenofibrate efficacy. Changes in lipoprotein cholesterol and total triglyceride concentrations observed in these patients were very similar to those seen with the larger multicenter cohort: total triglyceride levels decreased 38 to 46 percent, low-density lipoprotein cholesterol levels decreased 13 to 20 percent, and high-density lipoprotein cholesterol levels increased 4 to 13 percent. Triglyceride concentrations were significantly reduced (p less than 0.01) in very low-density lipoprotein (50 to 56 percent, similar to those of total triglyceride and very low-density lipoprotein cholesterol), and in low-density lipoprotein cholesterol levels (17 to 21 percent). A slight but statistically insignificant decrease in high-density lipoprotein triglyceride was observed (9 to 15 percent). High-density lipoprotein2 cholesterol levels did not change significantly, whereas high-density lipoprotein3 cholesterol levels increased 8 to 16 percent, accounting for all of the increase in high-density lipoprotein cholesterol. Apoprotein All levels increased significantly (13 to 20 percent) whereas those of apolipoprotein Al did not, consistent with an increase in high-density lipoprotein3 levels, where apolipoprotein All is more abundant relative to apolipoprotein Al than in high-density lipoprotein2. Apolipoprotein B levels decreased 20 to 26 percent and those of apolipoprotein E went from 29 to 34 percent, relative to the 16 to 20 percent decreases in very low-density lipoprotein and low-density lipoprotein triglyceride and cholesterol levels. Five patients with combined elevations of triglyceride and low-density lipoprotein cholesterol treated with fenofibrate, had reductions primarily in triglyceride, total apolipoprotein E (50 percent reduction), and apolipoprotein B (18 percent) levels. High-density lipoprotein3 cholesterol levels increased 19 percent and high-density lipoprotein2 cholesterol levels were unchanged. Low-density lipoprotein cholesterol levels declined slightly in four patients and a slight rise was observed in a fifth patient.(ABSTRACT TRUNCATED AT 400 WORDS)

Standardization of lipoprotein reporting.

We wanted to ascertain whether the current format of lipid laboratory reports seemed adequate to promote identification and treatment of patients with dyslipidemia. In a random survey of lipid laboratory reports from 25 laboratories, we found great inconsistencies among reporting formats and contents. Fewer than half the laboratories correctly reported the ranges for cholesterol, only 4 correctly reported ranges for high-density lipoprotein cholesterol, only 2 correctly reported ranges for triglycerides, and none presented low-density lipoprotein cholesterol ranges in terms of risk factors for coronary heart disease. Reports typically were disjointed and difficult to read. The current practice of reporting results for lipid panels is confusing and does not follow the National Cholesterol Education Program (NCEP) guidelines. We recommend that reporting of results be standardized, and a "model" standardized report is presented herein, based on consensus from a team of experts. The standardized report uses current recommendations for ranges, follows the flowcharts of the NCEP guidelines, and takes the patient's clinical condition (the number of risk factors and the presence of coronary heart disease) into consideration. Standardizing lipid reports should decrease confusion and perhaps increase application of the guidelines and patient compliance with treatment.

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.

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.

Lp(a) lipoprotein: relationship to sinking pre-beta lipoprotein hyperlipoproteinemia, and apolipoprotein B.

To assess the relationship between the Lp(a) and the "sinking pre-beta" (d smaller than 1.006) lipoprotein, the concentration of Lp(a) was quantified by radial immunodiffusion and the presence or absence of sinking pre-beta was assessed by agarose electrophoresis in overnight fasting plasma samples from 485 adults, comprised of 320 with normal lipid levels, 48 with type IIa, 40 with type IIb, and 77 with type IV lipoprotein phenotypes. The median Lp(a) level was 7.6 mg/100 ml, 89% (433 of 485) having detectable Lp(a) levels. Twenty-two per cent (107 of 485) had detectable pre-beta lipoprotein in the d greater than 1.006 plasma fraction (sinking pre-beta). Of the sinking pre-beta positive plasma samples, 96% (102 and 107) exceeded the median Lp(a) level, and sinking pre-beta was detected in all 44 samples with an Lp(a) concentration exceeding 40 mg/100 ml. The relationship of Lp(a) and sinking pre-beta to lipoprotein phenotype was assessed. Compared to the normolipidemic group, the type IIa group had higher Lp(a) percentile values (p smaller than 0.02), whereas the IIb and type IV groups had significantly lower Lp(a) values than the normolipidemic group. Ninety-two per cent (296 of 320) of the normolipidemic subjects had detectable levels of Lp(a) and 22% (70 of 320) had detectable sinking pre-beta lipoprotein. Ninety-four per cent (45 of 48) of the type IIa plasmas had detectable Lp(a) levels and 27% (13 of 48) had sinking pre-beta lipoproteins. Contrasted with the IIa group, only 80% (32 of 40) of the IIb plasmas had detectable Lp(a) levels and 18% (7 of 40) had sinking pre-beta lipoprotein. In the type IV plasmas 78% (60 of 77) had detectable Lp(a) and 22% (17 of 77) had sinking pre-beta lipoprotein. Lp(a) or log Lp(a) levels were not correlated with apolipoprotein B levels (n = 485, r = 0.002 or 0.037, respectively). Furthermore, Lp(a) levels remained essentially constant in three subjects whose aprptein B levels were altered in response to pharmacological and/or dietary manipulation. A fourth subject had a 50% increase in Lp(a) but this change did not correlate with apoprotein B changes. Thus, these findings suggest that Lp(a) is metabolically independnet of low density lipoprotein even though it shares the same structural protein, apoprotein B.

Contrasting effects of unmodified and time-release forms of niacin on lipoproteins in hyperlipidemic subjects: clues to mechanism of action of niacin.

To minimize the cutaneous flushing symptoms associated with niacin use, a time-release capsule form of niacin has been formulated. Thus study compares the effects of time-release niacin with those of unmodified niacin on lipoprotein lipids, including HDL2 and HDL3, apoproteins A-I and A-II, clinical chemistries, symptomatic side effects, and adherence to the medication regimen. Seventy-one primarily hypercholesterolemic subjects were randomized to either unmodified niacin or time-release niacin ad took medication for a six-month period. The two groups were closely matched on anthropomorphic and lipid variables. Adherence to the therapeutic regimen at a dose of 1.5 g/d in the first month of treatment was similar in the two groups. Thereafter, at a dose of 3.0 g/d, adherence was in excess of 90% among subjects taking unmodified niacin but only 64% among those taking time-release niacin, chiefly because of aggravated gastrointestinal symptoms; cutaneous flushing side effects, however, were slightly less common with time-release niacin. At these levels of adherence, LDL cholesterol (C) was reduced 21% by unmodified niacin and 13% by the time release form. Plasma total triglyceride was reduced more with unmodified niacin (27%) than with time-release niacin (8% maximum), and HDL-C and HDL2-C were increased significantly with unmodified niacin (26% and 36%) and were not significantly changed by time-release niacin. Increased to a similar degree on both regimens were HDL3-C (approximately 35%) and apoA-I (approximately 12%). ApoA-II was not affected by either drug regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Lipid and lipoprotein triglyceride and cholesterol interrelationships: effects of sex, hormone use, and hyperlipidemia.

The interrelationships of lipid and lipoprotein cholesterol and triglyceride concentrations in normolipidemic and hyperlipidemic employees of the Pacific Northwest Bell Telephone Company were examined bivariately using correlation analysis and multivariately by factor analysis. Application of the latter resulted in the identification of three distinct lipoprotein lipid clusters, which succinctly describes their metabolic relationships. Among normolipidemic subjects, the interrelationships were found to be similar in male and female subjects, but hormone use by women considerably altered interrelationships that involved high-density lipoprotein cholesterol (HDL-C) and triglyceride. Among hyperlipidemic subjects, we found that elevation in cholesterol level alone rarely altered relationships, but elevation in triglyceride level either alone or in conjunction with an elevation in cholesterol concentration was associated with substantial changes in relationships involving the low-density lipoprotein (LDL) fraction. In many instances, positive relationships between LDL cholesterol (LDL-C) and other lipoprotein lipids became inverse in the presence of triglyceride elevation. We conclude that hormone use by women and hypertriglyceridemia with or without an elevation in cholesterol level clearly alter lipoprotein relationships, whereas pure hypercholesterolemia does not. These alterations provide a basis for investigating pathophysiologic mechanisms in hypertriglyceridemia.

PIP: The interrelationships between lipid and lipoprotein cholesterol and triglyceride concentrations in normolipidemic and hyperlipidemic employees of the Pacific Northwest Bell Telephone Company were examined bivariately using correlation analysis and multivariately by factor analysis. Factor analysis resulted in the identification of 3 distinct lipoprotein lipid clusters, which succinctly describes their metabolic relationships. Among normolipidemic subjects, the interrelationships were found to be similar in males and females, but hormone use by women considerably altered interrelationships that involved high-density lipoprotein cholesterol (HDL-C) and triglyceride. Among hyperlipidemic subjects, elevation in cholesterol level alone rarely altered relationships, but elevation in triglyceride level either alone or in conjunction with an elevation in cholesterol concentration was associated with substantial changes in relationships involving the low-density lipoprotein (LDL) fraction. In many instances, positive relationships between LDL-C and other lipoprotein lipids became inverse in the presence of triglyceride elevation. It is concluded that hormone use by women and hypertriglyceridemia with or without an elevation in cholesterol level clearly alter lipoprotein relationships, whereas pure hypercholesterolemia does not. These alterations provide a basis for investigating pathophysiologic mechanisms in hypertriglyceridemia.

Type III hyperlipoproteinemia: a comparative study of current diagnostic techniques.

Research into the prevalence, genetic transmission and pathophysiology of Type III hyperlipoproteinemia has suffered from the lack of a practical specific diagnostic procedure. In this study, very low density lipoprotein (VLDL) compositional criteria were established in a population lacking the beta-migrating VLDL characteristic of this disorder. Diagnosis by these criteria was compared to diagnosis using current criteria for the Type III lipoprotein pattern. In addition two techniques for detecting Type III without preliminary VLDL isolation by ultracentrifugation were evaluated. Plasma triglyceride (TG) concentration dependent cutlines for the compositional criteria reduced false positives at low TG levels and false negatives at high TG levels. Furthermore, an agarose electrophoresis heparin-manganese precipitation technique was effective for screening for a possible Type III pattern in plasma whereas the combination agarose-polyacrylamide gel electrophoresis system was not effective.

Measurement of cholesterol, triglycerides, and HDL using compact analysis systems.

The compact analyzers facilitate rapid measurement of cholesterol and other lipid parameters outside the conventional laboratory setting. The current generation of instruments has very different features, operating parameters, and performance characteristics, and they must be selected in accordance with the intended application. All three of the common screening instruments, the DT-60, the Reflotron, and the VISION, have demonstrated the capability to meet current performance guidelines, provided they are operated correctly. Attention to quality assurance will, nevertheless, be essential in achieving reliable results. Further refinements in the instruments, reagents, and applications will improve their utility in screening programs.

Physiological and analytical variation in cholesterol and triglycerides.

Plasma cholesterol and triglyceride levels were determined, on each of two AutoAnalyzer systems in 11 healthy subjects, weekly over a 10-week and monthly over a 12-month period. Analytical variation was 1-2% for cholesterol and 2-5% for triglyceride. Cholesterol and triglyceride values on frozen quality control serum pools were not indicative of absolute values on fresh plasma. Even though the two AutoAnalyzer systems averaged within 1-2 mg/dl for triglyceride and cholesterol on the serum quality control pools during the 12-month period, the two systems differed by 7-8 mg/dl on fresh or frozen plasma samples. The coefficient of physiological variation on the 10 weekly samples averaged 5% (range 3-10%) for plasma cholesterol and 18% (range 9-27%) for plasma triglyceride. Analysis of the monthly samples suggested significant (P less than 0.05) seasonal trends: cholesterol was highest in the winter months and lowest in October, whereas triglyceride was highest in January and February and lowest in May and December. We conclude that intra-individual variation can be an important source of error in attempting to make a genetic diagnosis of hyperlipidemia and/or in evaluating hypolipidemic regimens in a given subject.

Studies of lipoproteins and fatty acids in maternal and cord blood of two racial groups in Trinidad.

The high mortality rate from coronary heart disease (CHD) among Indians compared to Negroes in Trinidad led us to test plasma lipid profiles to see whether dietary or genetic factors might be involved. There were no interracial differences in the composition of plasma cholesterol ester fatty acids of the tested women and neonates. This finding suggests that dietary fat does not account for the interracial difference in CHD, nor does the cause appear to be due to genetic differences in lipid profiles, as there was no significant difference between values for plasma triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, apo-I, apo-II, apo B or cholesterol ester fatty acids in the cord blood of each racial group. Blood samples were collected from 69 nonpregnant and 71 postpartum, fasted Negro and Indian women. Also taken were 71 umbilical cord blood samples. The mean triglyceride level was significantly lower in the Negro nonpregnant and postpartum women than in the Indians. HDL cholesterol and apo-I values were lower in the Indian women. There were no significant differences in the total cholesterol and apo B measurements. The triglyceride values for postpartum women were higher than those of the nonpregnant Negroes and Indians (75% and 47%, respectively), whereas the total cholesterol and HDL cholesterol, apo A-I and apo A-II ranged from 9% to 29% higher in the postpartum women. Apo B was about 40% higher postpartum in both ethnic groups. The high CHD rate of Indians in Trinidad cannot be explained by dietary factors, plasma total cholesterol or fatty acid composition.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma and lipoprotein lipid responses to four hypolipid drugs.

The responses of 14 hyperlipidemic subjects to 4 hypolipidemic agents were compared by measuring cholesterol and triglyceride in whole plasma, very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL) monthly for 2 months before and 3 months during treatment with each of 4 drugs: clofibrate, 2 g/d; colestipol, 20 g/d; para-aminosalicylic acid-ascorbate (PAS-C), 6-8 g/d; and oxandrolone, 7.5 mg/d. Lipid responses proved to be stable by the first monthly evaluation both off and on each drug. Mean adherence was high and similar for all agents (81-92% of the prescribed dose). Clofibrate was associated with significant decreases in mean plasma cholesterol (-16%, p less than .01), plasma triglyceride (-51%, p less than .005), VLDL-cholesterol (-61%, p less than .005) and VLDL-triglyceride (-61%, P less than .005), while HDL cholesterol increased (+20%, p less than .01), and the LDL-cholesterol/HDL ratio declined (-24%, p less than .05). Colestipol was associated with decreases in mean plasma cholesterol (-15%, p less than .01) and LDL-cholesterol (-22%, p less than .05), while VLDL-triglyceride increased (+41%, p less than .05), and the LDL-cholesterol/HDL-cholesterol radio declined (-25%, p less than .05). PAS-C was associated with decreases in VLDL-cholesterol (-30%, p less than .05), and VLDL-triglyceride (-29%, p less than .05), while the LDL-cholesterol/HDL-cholesterol ratio remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholesterol in fingerstick capillary specimens can be equivalent to conventional venous measurements.

Current interest in coronary heart disease and cholesterol has led to the development of a new generation of compact analysis systems designed for fingerstick whole blood measurement. Since reliable classification of patients based on national cut-points for serum cholesterol concentration requires accurate results, the question whether results from fingerstick capillary specimens are equivalent to those from conventional venous-derived serum specimens, the basis for the national cut-points, is germane. Earlier studies in the literature are contradictory, with fingerstick differences ranging from 9% low to 6% high. We developed guidelines for reliable fingerstick collection and, following these guidelines, achieved results that were comparable to results derived from concurrently collected venous serum specimens. Results measured either by an accurate, standardized enzymatic assay or by the AccuMeter, a new noninstrumented device, were in close agreement with serum results, ie, within 1% and 1.7%, respectively, suggesting that fingerstick measurements are appropriate for identifying individuals with elevated cholesterol levels and monitoring their treatment.