Normolipidemic planar xanthomatosis associated with benign monoclonal gammopathy

This report describes a patient with advanced planar xanthomatosis and benign monoclonal gammopathy who had normal plasma concentrations of cholesterol and triglycerides (TG). Decreased electrophoretic mobilities of very low density lipoprotein (VLDL), intermediate density lipoproteins (IDL) and chylomicrons were found. No changes in electrophoretic mobility were found for low density lipoprotein (LDL) and high density lipoproteins (HDL). The patient's disease was associated with a progressive decline in plasma-TG and VLDL-TG over a 2 yr period. He also appeared to develop an increased rate of clearance of VLDL-TG and chylomicrons. These changes in the metabolism of TG-containing lipoproteins were unaccompanied by alterations in the synthesis of either cholesterol or bile acids. The observations in this patient led us to the conclusion that his normal to low levels of VLDL-TG could be explained by both enhanced tissue uptake and increased lipolysis of VLDL-TG. The most likely explanation for these findings is that the patient had immune complexes between his TG-rich lipoproteins and an abnormal monoclonal gamma globulin. This patient is another example of an expanding group of subjects in whom xanthomatosis can develop without hyperlipidemia.     

Characteristics of cholesterol transport by various classes of lipoproteins and their apolipoproteins in hypo- and hyperalphalipoproteinemia]

The content in the blood plasma of the main apolipoproteins of lipoproteins of very low and low density apo-B and tetramethylurea-soluble apo-LP as well as lipoproteins of high density apo-A and the relation to apo-LP cholesterol of these classes of lipoproteins were studied in 34 males with different levels of alpha-LP cholesterol. It is shown that in hypoalphacholesterolemia the plasma apo-A content is reduced with the cholesterol/apo-A ratio being less than in normoalphacholesterolemia; at the same time, the content in the plasma of total triglycerides, cholesterol, and protein of very low density lipoproteins is increased and cholesterol saturation calculated for protein of very low and low density lipoproteins does not change. In hyperalphacholesterolemia the plasma apo-A content is increased both in the absolute amount and in relation to apo-B and TMU-soluble proteins; the content of cholesterol on apo-A in high density lipoproteins is the same as under normal conditions and higher than in hypoalphacholesterolemia. The results obtained are discussed in association with the data in the literature concerning the functions of lipoproteins and apo-LP in relation to the transport of cholesterol into the vascular wall and its drainage.     

Increased free cholesterol in plasma low and very low density lipoproteins in non-insulin-dependent diabetes mellitus: its role in the inhibition of cholesteryl ester transfer.

Recombination of low and very low density lipoproteins (VLDL and LDL) from normal subjects with plasma from patients with non-insulin-dependent diabetes mellitus significantly increased the reduced rate of transfer of cholesteryl ester to these lipoproteins, which is characteristic of diabetic plasma, whereas diabetic VLDL and LDL reduced cholesteryl ester transfer rates in normal plasma. VLDL and LDL from diabetic plasma had an increased ratio of free cholesterol to phospholipid compared to normal, and unlike normal VLDL and LDL spontaneously lost free cholesterol to high density lipoprotein. These data suggest that the block to cholesteryl ester transfer to these lipoproteins in non-insulin-dependent diabetes is mediated by their increased free cholesterol content and may be related to the increased risk of these patients for developing atherosclerosis.     

Effects of clofibrate, nicotinic acid and diet on the properties of the plasma lipoproteins in a subject with type III hyperlipoproteinemia.

A patient with familial type III hyperlipoproteinemia (HLP) was subjected to a clinical trial in which the effects of different diet regimens and drugs on all plasma lipoprotein density classes were studied. In this patient, whose plasma cholesterol and triglyceride were within normal limits under clofibrate treatment, medication was discontinued in favor of a diet enriched in carbohydrate. This management resulted, within eight days, in the development of a type III phenotype featuring all of the most widely used criteria typical for this form of lipid disorder. Very low density lipoproteins contained an increased amount of cholesterol and the “arginine-rich” apolipoprotein at both the beginning of the trial and at the eighth day. When the carbohydrate-enriched diet was replaced by a diet commonly used in type III hyperlipoproteinemia, the plasma cholesterol and triglyceride values were lowered to upper normal limits. However, after zonal ultracentrifugation, a lipoprotein profile typical for a type III subject without treatment was observed. Administration of either clofibrate or nicotinic acid to the type III diet resulted in a further decrease of the plasma levels of cholesterol and triglyceride. Zonal ultracentrifugation indicated that these decreases were caused by lowering the plasma concentrations of very low density, intermediate density, and low density lipoproteins. Furthermore, both drugs raised the two high density lipoprotein classes from their initially decreased levels to normal plasma values. These results suggest that drug and diet treatment of a type III hyperlipoproteinemic not only lowers the amount of very low, intermediate, and low density lipoproteins but also increases the high density lipoproteins which are considered protective against atherosclerosis.     

Effects of long-term negative energy balance with exercise on plasma lipid and lipoprotein levels in identical twins

Plasma lipid and lipoprotein concentrations were measured before and after a 58,000kcal (244MJ) negative energy balance protocol induced entirely by supervised endurance exercise over a 93-day period in seven pairs of young sedentary and healthy male monozygotic twins. The negative energy balance induced significant changes in all measures of body weight and composition except fat free mass. The mean weight loss was 5.0+/-0.6kg, and it was entirely accounted for by the loss of body fat. In response to the program, improvement in the plasma lipid profile was seen including decreases in plasma total (P=0.028) and low density lipoprotein (LDL) (P=0.004) cholesterol; total cholesterol/high density lipoprotein (HDL) cholesterol ratio (P=0.002); and HDL apolipoprotein A-I concentration (P=0.062). Statistically significant within-pair resemblance was found for the changes in total and very low density lipoprotein (VLDL) cholesterol; total, VLDL and LDL triglycerides, and total, VLDL and LDL apolipoprotein B. The findings suggest that favorable changes in the lipid profile can be obtained through chronic negative energy balance achieved by clamping daily energy intake and adding daily moderate intensity exercise even in persons with relatively normal lipid levels at baseline. Furthermore, within-pair resemblance among twin brothers strongly suggests that genetic differences partially account for the variation in the response of lipids and lipoproteins to the negative energy balance protocol.     

Clinical Thermofiltration: Initial Application

Guest Editor's Introduction: This paper was submitted for publication in June 1985 and published in the “Thought and Progress” section of Artificial Organs, Vol. 9, No. 4, 1985, pages 425–427. The first clinical thermofiltration procedures (plasma filtration near and above normal physiologic temperature) were performed on a secondary hypercholesterolemia patient. The intent of this filtration scheme is the selective removal of low density lipoprotins (LDL) and maintenance of high density limpoproteins (HDL) and other essential plasma proteins including albumin. The EVAL 4A filter, at a filtration temperature of 37°C, was selected for on‐line thermofiltration. The sieving coefficients of LDL + very low density lipoproteins (VLDL) cholesterol, HDL cholesterol, and albumin were 0.02, 0.75, and 0.78, respectively. These results were comparable to in vitro filtration tests using the plasma of the same patient. This system is simple to apply and does not require replacement solution. Compared with plasma exchange, a high return of HDL and other essential plasma solutes can be returned to the patient by this method. Abstract: The first clinical thermofiltration procedures (plasma filtration near or above normal physiologic temperature) were performed on a secondary hypercholesterolemia patient. The intent of this filtration scheme is the selective removal of low density lipoproteins (LDL) and maintenance of high density lipoproteins (HDL) and other essential plasma proteins including albumin. The EVAL 4A filter, at a filtration temperature of 37°C, was selected for on‐line thermofiltration. The sieving coefficients of LDL + very low density lipoproteins (VLDL) cholesterol, HDL cholesterol, and albumin were 0.02, 0.75, and 0.78, respectively. These results are comparable to in vitro filtration tests using the plasma of the same patient. This system is simple to apply and does not require replacement solution. Compared with plasma exchange, a high return of HDL and other essential plasma solutes can be returned to the patient by this method.     

Abnormalities in plasmas concentrations of lipoproteins and fibrinogen in Type 1 (insulin-dependent) diabetic patients with increased urinary albumin excretion

Summary Type 1 (insulin-dependent) diabetic patients with clinical nephropathy have a more than ten-fold increase in mortality of cardiovascular diseases compared with diabetic patients without nephropathy. The risk factors for cardiovascular disease, plasma concentrations of lipoproteins and fibrinogen, were investigated in 74 long-term diabetic patients: 37 with normal urinary albumin excretion, 20 with incipient nephropathy and 17 with overt clinical nephropathy based on urinary albumin excretion. The groups were matched according to sex, age and diabetes duration. The concentration of plasma cholesterol, very low density lipoprotein cholesterol, low density lipoprotein cholesterol, triglyceride and fibrinogen rose with increasing urinary albumin excretion. The plasma concentrations of these lipoproteins and fibrinogen were 11–14% higher in the patients with incipient nephropathy and 26–87% higher in the patients with overt clinical ne phropathy compared with the patients without nephropathy. The plasma concentration of high density lipoprotein cholesterol was unaffected by albuminuria. Patients with normal urinary albumin excretion and HbA_1c>8.0% had significantly higher very low density lipoprotein- and lower high density lipoprotein cholesterol concentrations compared with patients with HbA_1c<8.0%. Simple addition of the described risk factors can only account for a minor part of the greatly increased cardiovascular mortality in patients with diabetic nephropathy. An additional and possibly more decisive factor might be a change in the arterial wall, a change which promotes lipid accumulation and/or facilitates thrombus formation.     

Changes in the levels and composition of lipoproteins and apolipoproteins of blood plasma in patients with ischemic heart disease after hemosorption

Prior to and following activated charcoal hemosorption, concentrations of lipids, apolipoproteins AI and B and lipid and protein composition in lipoprotein fractions isolated by ultracentrifugation were determined in the plasma from patients with coronary heart disease. The majority of the patients showed a parallel proportional decrease in plasma atherogenic parameters and all components of very low density lipoproteins and low density lipoproteins, triglycerides in particular. Antiatherogenic parameters, such as high density lipoprotein and apo-AI cholesterol, and all the components in high density lipoprotein subfractions were less reduced. In 19% of the patients, hemosorption failed to affect plasma lipids and apolipoproteins. The findings suggest that, in case of successful hemosorption, apoB-containing lipoproteins are chiefly eliminated as whole complexes from the plasma and that this procedure is most beneficial in hypertriglyceridemia.     

Abnormal plasma lipoproteins and lecithin-cholesterol acyltransferase deficiency in alcoholic liver disease.

Serial studies of plasma lipids and lipoproteins were performed in 4 patients with acute alcoholic liver disease characterized by a massive fatty liver and laboratory evidence of intrahepatic cholestasis. There were striking alterations in the plasma lipoprotein electrophoretic patterns characterized by the absence of alpha- and pre-beta-lipoprotein bands and the presence of a single band of abnormal mobility. These changes were associated with an extreme decrease in plasma lecithin-cholesterol acyltransferase activity, resulting in greatly reduced levels of plasma cholesteryl esters and increased levels of unesterified cholesterol. In 2 patients hypertriglyceridemia and hypercholesterolemia were present, the latter because of an increase in unesterified cholesterol. Lipoproteins were isolated from the plasma by sequential ultracentrifugation at the densities used for separation of normal very low density, low density, and high density lipoproteins; however, the patients' lipoproteins were different from normal in lipid composition and ultrastructure. All of the lipoprotein fractions were decreased in cholesteryl esters and the major lipoprotein was a triglyceride-rich low density lipoprotein. Electron microscopic studies of the low and high density lipoprotein fractions revealed the presence of bilamellar vesicles and stacked discs. All of the changes in lipoprotein composition and ultrastructure gradually returned to normal with clinical improvement. These observations indicate that alcoholic liver injury is associated with profound alterations in lipoprotein composition and metabolism which may be related in part to lecithin-cholesterol acyltransferase deficiency.     

Exogenous estrogens attenuate dietary hypercholesterolemia and atherosclerosis in the rabbit

The effect of exogenous estrogens upon the response to dietary cholesterol was tested in New Zealand White rabbits. Cholesterol-fed, untreated rabbits had a 10-fold increase in plasma cholesterol in 12 wk. The major increase of cholesterol occurred in very low density lipoproteins (VLDL, 43.5-fold) followed by intermediate density lipoproteins (IDL, 26-fold) and low density lipoproteins (LDL, 6-fold) with no change in high density lipoproteins (HDL). These diet induced changes were markedly attenuated in the estrogen treated animals, in whom plasma cholesterol increased only 5-fold. This increase was distributed among LDL (6-fold), IDL (7.5-fold), and VLDL (9-fold), similarly with no change in HDL. All the lipoproteins in both groups of animals were considerably enriched in cholesterol during cholesterol feeding as indicated by a high cholesterol/protein and cholesterol/triglyceride ratio. However, these ratios were lower in estrogen treated animals. There were no differences in the feed consumption, body weight or cholesterol absorption between the two groups of animals. Rabbits fed a cholesterol-rich diet but not treated with estrogen had well developed lesions in all parts of the aorta with higher content of cholesterol and phospholipids as compared to those injected with estrogen, whose aortas were completely clear of visible atherosclerosis. Equivalent total hypercholesterolemia was induced in other estrogen-treated rabbits by feeding twice the cholesterol dietary content (0.2%) as in nonestrogen-treated animals. Aortic atherosclerosis was far more evident in the latter, which had higher proportions of cholesterol-rich lipoproteins of d < 1.006 g/ml.     

Comparative characteristics of serum lipids in healthy persons and in patients with coronary arteriosclerosis living in low and medium altitude areas of Tadzhikistan

Clinical symptoms, atherogenic (cholesterol, triglycerides, beta-lipoproteins + pre-beta-lipoproteins, low-density lipoprotein cholesterol, very low density lipoprotein cholesterol, atherogenic coefficient) as well as antiatherogenic (alpha-lipoproteins, high density lipoprotein cholesterol and its proportion in total cholesterol) lipoproteins, and phenotypes were examined in 727 individuals (330 normal subjects and 397 atherosclerotic patients), living in two different areas of Tadzhikistan (830 and 2200 m above sea-level). In midaltitude dwellers coronary atherosclerosis was associated with low incidence of clinical and electrocardiographic coronary signs and a comparatively favorable clinical course, apparently due to low atherogenic and high antiatherogenic lipid parameters, the absence of type-4-hyperlipoproteinemia and low incidence of type-2B hyperlipoproteinemia.     

Arterial blood derived low density lipoprotein increases platelet aggregation and macrophage cholesterol content in comparison to lipoprotein derived from veinous blood

We studied the biochemical and biological properties of plasma lipoproteins taken from blood derived from either the aorta or femoral vein of patients with normal coronary arteriography. There were no significant differences in concentrations of cholesterol, triglycerides, apoprotein A-1 and apoprotein B derived from either source. The cholesterol content of very low density lipoprotein (VLDL) and high density lipoprotein (HDL) was similar in both aortic and venous blood. The low density lipoprotein (LDL) concentration, however, was significantly higher in the aortic blood sample. Arterial LDL significantly enhanced in vitro platelet aggregation when compared to venous LDL. (p less than 0.02). When incubated with mouse peritoneal macrophages (MPM) arterial LDL and VLDL caused an increased cholesterol accumulation and enhanced cholesterol esterification within these macrophages. The venous lipoproteins had little effect. The differences noted in the arterial lipoproteins in composition and biological function when compared to venous lipoproteins might be related to the much higher incidence of atherosclerosis found in the arterial tree.     

Relationship between plasma insulin levels and high density lipoprotein cholesterol levels in healthy men

Summary Insulin and high density lipoproteins are considered to play a role in the development of atherosclerosis. In order to study whether there was a relationship between endogenous plasma insulin response and high density lipoproteins, an acute intravenous glucose tolerance test (0.5 g glucose/kg body weight) was performed in 94 healthy men, aged 20–49 years. Cholesterol and triglyceride levels were measured in very low density lipoproteins, low density lipoproteins and high density lipoproteins isolated from fasting serum by preparative ultracentrifugation. The subjects were divided into quartiles according to their fasting and post-glucose load plasma insulin and high density lipoprotein cholesterol levels. The results obtained in the subjects of the upper quartiles were compared with the results obtained in the subjects of the lower quartiles. The mean glucose disappearance rates were within the normal range and did not differ between the upper and lower quartiles. Subjects with high fasting plasma insulin had lower high density lipoprotein cholesterol levels (1.11±0.34 mmol/l, p=0.01) than men with low fasting plasma insulin (1.40±0.37 mmol/l). Higher mean post-glucose plasma insulin was associated with lower high density lipoprotein cholesterol levels (1.18±0.32 mmol/l, p<0.05) and increased high density lipoprotein triglyceride levels (0.14±0.07 mmol/l, p<0.01) when compared with the men with low post-glucose plasma insulin (1.40±0.36 mmol/l and 0.09±0.03 mmol/l respectively). These observations reflect the close relationship between endogenous insulin and lipoprotein metabolism.     

Plasma lipids and lipoproteins of a patient with cholesteryl ester storage disease

The plasma lipids, lipoproteins and lipolytic enzymes of a patient suffering from cholesterol ester storage disease were investigated and followed over a time period of 3 years. The patient was hypertriglyceridacmic and cholesterolaemic and exhibited very low levels of high density lipoproteins. These lipoproteins consisted almost exclusively of the HDL-subfraction-3. Apolipoprotein-B was elevated and apoAI and AII were grossly reduced. The activity of lipoprotein lipase was normal, but hepatic lipase values were increased. Lecithin : cholesterol acyltransferase was in the upper normal range. The corresponding lipoprotein and enzyme values of one brother were within normal limits but some components measured in the plasma of the father were abnormal. It is speculated that the low plasma HDL levels in this disease may be a consequence of increased hepatic lipase activity in addition to a derangement in the reverse cholesterol flow.     

Changes in plasma lipid and apoprotein levels in patients with ischemic heart disease after hemosorption]

All the patients who had undergone a course of non-specific hemosorption (HS) for clinical indications showed lower plasma lipid levels and largely lower triglyceride concentrations. The patients with hypercholesterolemia alone simultaneously displayed decreased levels of cholesterol, high density lipoproteins, and apoprotein A-I. Apoprotein B levels reduced in patients having normal lipid values and in those with isolated hypercholesterolemia. The changes in the levels of lipids and apoproteins were different for 2 weeks after hemosorption in relation to the baseline lipid spectrum. The patients with coronary heart disease with hyperlipidemias had positive trends in lipid spectral changes: the parameters of atherogenic classes of lipids tended to decrease, whereas those of antiatherogenic lipid classes tended to show a slight increase. There was a negative direction in the dynamics of the studied parameters in renal patients, in those who had normal baseline lipid values, and in those with isolated hypo-alpha-cholesterolemia, i. e. higher plasma cholesterol and triglyceride, low density lipoprotein cholesterol and apoprotein B levels.     

High density lipoprotein and low density lipoprotein utilization by human granulosa cells for progesterone synthesis in serum-free culture: respective contributions of free and esterified cholesterol

Human preovulatory granulosa cells cultured in serum- and gonadotropin-free medium secreted progressively less progesterone as time elapsed. Addition of purified high density lipoproteins (HDL) as well as low density lipoproteins [very low density (VLDL) plus low density lipoproteins (LDL)] restored optimal synthesis of progesterone, and HDL was as effective as VLDL + LDL. The use of cholesterol doubly labeled lipoproteins allowed calculation of the proportions of free and esterified cholesterol converted into progesterone. Granulosa cells used either free or esterified cholesterol from VLDL + LDL. In contrast, HDL-esterified cholesterol was a poor substrate for progesterone synthesis, while HDL-free cholesterol was used preferentially. LH increased the use of both kinds of lipoproteins without changing the way in which they were used. Pretreatment of HDL by purified phospholipase A2 increased the conversion of free cholesterol into progesterone. Similar treatment of VLDL + LDL had little effect on progesterone secretion. We conclude that HDL as well as VLDL + LDL can provide cholesterol to human preovulatory granulosa cells and that utilization of HDL-cholesterol may depend on gonadotropin (LH) and enzymatic (phospholipase) regulation.     

Changes in plasma lipoprotein constituents during constant infusions of heparin.

Constant infusions of heparin of 4 to 6 hours' duration were used to estimate the transfer of very low density lipoprotein constituents to other plasma lipoproteins. Eleven subjects were studied, 3 with Type III and the remainder with either Type IV or V hyperlipoproteinemia. Whereas only about 5% of the triglyceride lost from VLDL was recovered in the other lipoproteins, 44% of the cholesterol was retained in the circulation, in equal amounts within low density (d 1.019-1.063) and intermediate density (d 1.006-1.019) lipoproteins. By contrast, there was no apparent loss of protein, more than half of that originally in VLDL being recovered in high density lipoprotein. In subjects with Type III hyperlipoproteinemia, lipid and protein was lost from the intermediate density lipoprotein as well as from VLDL. In subjects with marked hypertriglyceridemia, cholesterol became redistributed from larger to smaller VLDL. The esterification of plasma cholesterol as measured in vitro, was apparently suppressed during the early phase of the heparin infusions, but tended to recover later.     

Prevalence of ischaemic heart disease and associations with serum lipoproteins in subjects aged 45 to 64 years. The Speedwell study.

A longitudinal study has been set up to examine the incidence of ischaemic heart disease and its associations with serum lipoproteins including high density lipoprotein cholesterol and its subfractions, certain haemostatic factors, and other "risk' factors. We report here on our pilot study findings. Cross-sectional data were available on 283 men and 68 women aged 45 to 64 representing 85% of the available population randomly selected from the lists of 16 general practitioners. Reproducibility of the measurements of total serum cholesterol, triglyceride, and low density lipoprotein cholesterol was acceptable. The reproducibility of some of the other serum lipid fractions, for example high density lipoprotein cholesterol, was less good, in part because of the small range of the values found for these components. Univariate associations of physical and behavioural characteristics and serum lipoproteins of men and women, with and without ischaemic heart disease, disclosed small and statistically nonsignificant differences except for levels of blood pressure. In particular, there was no significant difference in mean levels of serum high density lipoprotein cholesterol between men with ischaemic heart disease (0.91 mmol/l) and men without it (0.94 mmol/l). In examining our data for the determinants of serum high density lipoprotein cholesterol using a linear multiple regression model, sex, serum high density lipoprotein cholesterol, and very low density lipoprotein triglyceride were the major factors, each individually explaining about 7% of the variance of serum high density lipoprotein cholesterol levels. In addition, alcohol intake and obesity each explained a further 2% of the variance. The experience of the pilot study has led to modifications in the collection of blood samples and the subsequent estimation of lipid fractions.     

Effect of characterologic risk factors of ischemic heart disease on lipid metabolism indices in young persons during adaptation to long-term psychoemotional and physical loads

A study of changes in lipid metabolism in young men throughout their adaptation to lasting physical and mental/emotional stress demonstrated an increase in blood cholesterol, triglycerides, cholesterol of low and of very low density lipoproteins, and a significant decrease in cholesterol of high density lipoproteins. This period of time particularly favors the activation of atherogenic developments in the body. Changes were the greatest in people of behavior type A. They are assumed to be living under constant emotional stress because of their specific character traits, hence the marked shifts in their blood lipid composition.     

Deficiency of Hepatic Lipase Activity in Post-heparin Plasma in Familial Hyper-α-Triglyceridemia

ABSTRACT. Hyper-α-triglyceridemia is a rare dyslipoproteinemia characterized by a pronounced increase in the concentration of triglycerides in the plasma high density lipoprotein (HDL) fraction. One case with this condition, an apparently healthy 61-year-old man, has been studied. Additional lipoprotein abnormalities were present, such as abnormally cholesterol-rich very low density lipoproteins (VLDL) with retarded electrophoretic mobility (β-VLDL) and triglyceride enrichment of low density lipoproteins-(LDL). The patient's plasma concentration of apolipoproteins A-I, A-II and B were normal and those of C-I, C-II, C-III and E were elevated. No abnormal forms of the soluble apolipoproteins of VLDL and high density lipoproteins (HDL) were found after analysis by isoelectric focusing. Lecithin: cholesterol acyltransferase activities, plasma cholesterol esterification rates and lipid transfer protein activities were normal. Post-heparin plasma activity of hepatic lipase was virtually absent and that of lipoprotein lipase was reduced by 50%. In plasma of this patient, HDL was almost exclusively present as large triglyceride-rich particles corresponding in size to particles of the HDL₂ density fraction. The only brother of the patient also had hyper-α-triglyceridemia together with the other lipoprotein abnormalities described for the index case and deficiency of postheparin plasma activity of hepatic lipase. The findings presented below support the hypothesis that one primary function of hepatic lipase is associated with degradation of plasma HDL₂. Deficiency of this enzyme activity thus causes accumulation of HDL₂ in plasma leading to hyper-α-triglyceridemia. The results further suggest that the abnormal chemical and electrophoretic properties of VLDL and LDL in plasma from the patient, reminiscent of type III hyperlipoproteinemia, are secondary to the lack of the action of hepatic lipase on the HDL particles.