Observations on the passage of apoproteins from plasma lipoproteins into peripheral lymph in two men.

1. The passage of radioactive apolipoproteins into lymph draining the foot was investigated in two men, each given a single intravenous injection of low-density lipoprotein containing 131I-labelled apoprotein B and of very-low-density lipoprotein containing 125I-labelled apoprotein A and apoprotein C. 2. Protein-bound 125I and 131I appeared in the lymph of both subjects. Immunoelectrophoresis of lymph lipoproteins against anti-(high-density lipoprotein) and anti-(low-density lipoprotein) showed the presence of apo-high-density lipoprotein and apo-low-density lipoprotein with faster mobilities than plasma high-density and low-density lipoprotein respectively. Most of the protein-bound 131I in lymph was recovered in the precipitin line formed by the apoprotein B-containing lipoprotein after immunoelectrophoresis. Polyacrylamide gel electrophoresis of the lymph lipoprotein fraction showed the presence of 125I-containing bands with mobilities similar to those of the apoprotein A of high-density lipoprotein and of three of the fast-moving C apoproteins. 3. These results suggest that most, if not all, of the apoproteins of plasma lipoproteins reach the interstitial fluids and that some lipoproteins undergo modification during their passage into peripheral lymph.     

Abnormal plasma lipoprotein composition in hypercholesterolaemic patients induces platelet activation

Increased platelet activation has been shown to be a feature of patients with familial hypercholesterolaemia. Plasma lipoprotein concentration and composition were studied in eleven male patients with familial hypercholesterolaemia and in ten age-matched healthy controls. Increased levels of cholesterol were found in very-low- and low-density lipoproteins (53 and 275%, respectively), whereas in high-density lipoprotein, both cholesterol and apolipoprotein A-I were decreased by 21 and 26%, respectively. On incubation of gel-filtered platelets derived from normolipidaemic controls with identical concentrations of lipoproteins derived from either nomolipidaemic controls or hypercholesterolaemic patients very-low- and low-density lipoproteins from the patients caused significantly greater thrombin-induced platelet aggregation (P less than 0.01). High-density lipoprotein from normal subjects reduced platelet release by 22%, whereas the patients' high-density lipoprotein had no significant effect on platelet release. Lipoprotein-deficient plasma from both groups augmented platelet function to a similar extent. Lipoprotein composition has an important effect on platelet function in vitro. The abnormal lipid and protein composition of the lipoproteins derived from hypercholesterolaemic patients appears to be the cause of platelet hyperactivity observed in these patients.     

The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high-density lipoproteins

The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low-density and high-density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very-low- plus low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P less than 0.02), and an effect of treatment duration was observed. The changes in high-density lipoprotein total cholesterol (P less than 0.02), free cholesterol (P less than 0.001), triacylglycerol (P less than 0.05) and the free cholesterol/cholesteryl ester molar ratio in high-density lipoproteins (P less than 0.01) were inversely-related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high-density lipoprotein lipids observed in hypothyroidism.     

Assessment of cyclosporine A interactions with human plasma lipoproteins in vitro and in vivo in the rat

The interaction of cyclosporine A (cyclosporine) with human plasma lipoproteins has been investigated by combining in vitro and in vivo methods. Binding parameters were derived in vitro from an erythrocyte partitioning method, and provided reliable Ka (product of the number of binding sites by the association constant) estimates: high-density lipoprotein, 2.21 +/- 0.48; low-density lipoprotein, 1.23 +/- 0.12; and very low-density lipoprotein, 0.53 +/- 015 liters/g, showing that high-density lipoprotein was the major carrier of plasma cyclosporine. The effects of cyclosporine binding to lipoproteins were investigated in vivo by the intracarotid injection technique of Oldendorf in the rat. The brain extraction of cyclosporine was related inversely to the lipoprotein concentration in the injected solution, allowing estimation of nKa in vivo: high-density lipoprotein, 2.25 +/- 0.59; low-density lipoprotein, 0.62 +/- 0.13; and very low-density lipoprotein, 0.57 +/- 0.14 liters/g. This showed that brain uptake occurred from the free drug pool and possibly from a small part of the originally lipoprotein-bound pool of cyclosporine, at least for low-density lipoprotein-bound cyclosporine. These results allow the calculation of an index of the unbound plasma cyclosporine fraction.     

癌症与血脂水平的相关性初探

目的探讨癌症与血脂水平的相关性。方法采用1∶1病例对照研究的方法 ,病例组选自住院的癌症患者,对照组是社区中与病例性别和年龄匹配的健康人群。分析病例组与对照组的血脂水平比较。结果病例组血浆三酰甘油（TG）、极低密度脂蛋白胆固醇（VLDL）和低密度脂蛋白胆固醇/高密度脂蛋白胆固醇（LDL/HDL）水平均高于对照组,而血浆HDL水平低于对照组（P〈0.001）;TC和LDL则无差异（P〉0.05）。高TG患癌症的相对危险度为1.757（95%C I：1.020~3.025）;低HDL患癌症相对危险度为2.677（95%C I：1.266~5.662）;其余血脂异常指标的相对危险度无统计学意义。结论血脂水平与癌症发生有一定的相关性。其中高TG是癌症发生的可疑危险因素,而HDL是保护因素。     

Use of the TLX ultracentrifuge for the isolation of different density lipoproteins and effects of freeze/thawing of human plasma before ultracentrifugation

Abstract Background: Isolation of different density lipoproteins by ultracentrifugation can require lengthy centrifugation times and freeze/thawing of plasma may influence recovery. Methods: We isolated a range of lipoproteins using a preparative ultracentrifuge and the TLX micro-ultracentrifuge and determined the effect of freeze/thawing of plasma beforehand. Results: In fresh plasma, there was no significant difference in results for small-dense low-density lipoprotein apolipoprotein B (LDL apoB) (density >1.044 g/mL) or cholesterol at density >1.006 g/mL. Freeze/thawing had no effect on closely correlated results for small-dense LDL apoB (r=0.85; p<0.0001) or high-density lipoprotein (r=0.93; p<0.0001). Conclusions: The TLX micro-ultracentrifuge is a reliable alternative to the preparative ultracentrifuge and freeze/thawing has only a small effect on small-dense LDL apoB or high-density lipoprotein cholesterol. Clin Chem Lab Med 2008;46:1285-8.     

Distribution of apolipoprotein(a) in the plasma from patients with lipoprotein lipase deficiency and with type III hyperlipoproteinemia. No evidence for a triglyceride-rich precursor of lipoprotein(a).

Lipoprotein(a) consists of a low-density lipoprotein containing apolipoprotein (apo) B-100 and of the genetically polymorphic apo(a). It is not known where and how lipoprotein(a) is assembled and whether there exists a precursor for lipoprotein(a). We have determined the phenotype, concentration, and distribution of apo(a) in plasma from patients with lipoprotein lipase (LPL) deficiency (type I hyperlipoproteinemia, n = 14), in apo E 2/2 homozygotes with type III hyperlipoproteinemia (n = 12) and in controls (n = 16). In the two genetic conditions, there is grossly impaired catabolic conversion of apo B-100-containing precursor lipoproteins to low-density lipoproteins. Considering apo(a) type, the plasma concentration of apo(a) was normal in type III patients but significantly reduced in LPL deficiency. Despite the defects in the catabolism of other apo B-containing lipoproteins, the distribution of apo(a) was only moderately affected in both metabolic disorders, with 66.7% (type I) and 74.7% (type III) being present as the characteristic lipoprotein(a) in the density range of 1.05-1.125 g/ml (controls 81.6%). The remainder was distributed between the triglyceride-rich lipoproteins (type I 12.4%, type III 8.5%, controls 4.7%) and the lipid-poor bottom fraction (type I 19.3%, type III 15.3%, controls 12.6%). In all conditions most apo(a) (57-88%) dissociated from the triglyceride-rich lipoproteins upon recentrifugation and was recovered as lipoprotein(a). These data suggest that lipoprotein(a) is not generated from a triglyceride-rich precursor. Lipoprotein(a) may be secreted directly into plasma or may be formed by preferential binding of secreted apo(a) to existing low-density lipoprotein.     

Lipopolysaccharide (LPS)-binding protein is carried on lipoproteins and acts as a cofactor in the neutralization of LPS

Lipoproteins isolated from normal human plasma can bind and neutralize bacterial lipopolysaccharide (LPS) and may represent an important mechanism in host defense against gram-negative septic shock. Recent studies have shown that experimentally elevating the levels of circulating high-density lipoproteins (HDL) provides protection against death in animal models of endotoxic shock. We sought to define the components of HDL that are required for neutralization of LPS. To accomplish this we have studied the functional neutralization of LPS by native and reconstituted HDL using a rapid assay that measures the CD14- dependent activation of leukocyte integrins on human neutrophils. We report here that reconstituted HDL particles (R-HDL), prepared from purified apolipoprotein A-I (apoA-I) combined with phospholipid and free cholesterol, are not sufficient to neutralize the biologic activity of LPS. However, addition of recombinant LPS binding protein (LBP), a protein known to transfer LPS to CD14 and enhance responses of cells to LPS, enabled prompt binding and neutralization of LPS by R- HDL. Thus, LBP appears capable of transferring LPS not only to CD14 but also to lipoprotein particles. In contrast with R-HDL, apoA-I containing lipoproteins (LpA-I) isolated from plasma by selected affinity immunosorption (SAIS) on an anti-apoA-I column, neutralized LPS without addition of exogenous LBP. Several lines of evidence demonstrated that LBP is a constituent of LpA-I in plasma. Passage of plasma over an anti-apoA-I column removed more than 99% of the LBP detectable by ELISA, whereas 31% of the LBP was recovered by elution of the column. Similarly, the ability of plasma to enable activation of neutrophils by LPS (LBP/Septin activity) was depleted and recovered by the same process. Furthermore, an immobilized anti-LBP monoclonal antibody coprecipitated apoA-I. The results described here suggest that in addition to its ability to transfer LPS to CD14, LBP may also transfer LPS to lipoproteins. Since LBP appears to be physically associated with lipoproteins in plasma, it is positioned to play an important role in the neutralization of LPS.     

The plasma lipoproteins in familial chylomicronemia. Analysis by zonal ultracentrifugation

Familial chylomicronemia is a rare genetic disorder attributable to the absence of lipoprotein lipase activity or the absence of apo-CII, i.e., the cofactor for the same enzyme. Plasma lipoproteins were analyzed by zonal ultracentrifugation under rate flotation conditions in four patients with lipoprotein lipase deficiency and two patients with apo-CII deficiency. Lipoproteins of density less than 1.006 gm/ml, and particularly lipoproteins with Sf greater than 100, were present in very high concentrations. Low levels of density greater than 1.006 gm/ml lipoproteins were observed. This fraction was composed of some different and discrete lipoprotein populations: intermediate-density lipoproteins (in three of six patients, density = 1.006 to 1.019 gm/ml); low-density lipoprotein LDL2 (in all patients, density = 1.019 to 1.045 gm/ml); low-density lipoprotein LDL3 (in all patients, density = 1.045 to 1.063 gm/ml); high-density lipoprotein HDL2 (in four of six patients); and high-density lipoproteins HDL3 (in all patients). LDL3 was never observed in normal participants by means of zonal ultracentrifugation; this subclass of low-density lipoproteins seems to correspond to LDL particles of very low Sf (2 to 5) previously identified by analytical ultracentrifugation in patients with severe hypertriglyceridemia. LDL3 was isolated by means of zonal ultracentrifugation as a single and discrete peak in all patients. Lipoproteins of density greater than 1.006 gm/ml were rich in triglycerides and poor in cholesterol in comparison with normal lipoproteins. The heterogeneity of low-density lipoproteins (particularly the appearance of LDL3), low levels of total high-density lipoproteins, and lower HDL3 flotation rate than normal are typical aspects of serum lipoproteins in these patients. No significant differences in the lipoprotein profiles of the patients with lipoprotein lipase deficiency in comparison with patients with apo-CII deficiency were found. In both groups of patients, the plasma lipoproteins profile and the altered lipoprotein composition could be related to the impaired catabolism of triglyceride-rich lipoproteins caused by the absence of lipoprotein lipase activity.     

Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes

ABSTRACT: INTRODUCTION: Apolipoprotein M (apoM) is present in 5% of high-density lipoprotein (HDL) particles in plasma. It is a carrier of sphingosine-1-phosphate (S1P), which is important for vascular barrier protection. The aim was to determine the plasma concentrations of apoM during sepsis and systemic inflammatory response syndrome (SIRS) and correlate them to levels of apolipoprotein A-I (apoA1), apolipoprotein B (apoB), HDL-, and low-density lipoprotein (LDL)-cholesterol. METHODS: Plasma samples from patients with (1), severe sepsis with shock (n = 26); (2), severe sepsis without shock (n = 44); (3), sepsis (n = 100); (4), infections without SIRS (n = 43); and (5) SIRS without infection (n = 20) were analyzed. The concentrations of apoM, apoA1, and apoB were measured with enzyme-linked immunosorbent assays (ELISAs). Total, HDL-, and LDL-cholesterol concentrations were measured with a commercial HDL/LDL cholesterol test. RESULTS: ApoM concentrations correlated negatively to acute-phase markers. Thus, apoM behaved as a negative acute-phase protein. Decreased values were observed in all patient groups (P < 0.0001), with the most drastic decreases observed in the severely sick patients. ApoM levels correlated strongly to those of apoA1, apoB, HDL, and LDL cholesterol. The HDL and LDL cholesterol levels were low in all patient groups, as compared with controls (P < 0.0001), in particular, HDL cholesterol. ApoA1 and apoB concentrations were low only in the more severely affected patients. CONCLUSIONS: During sepsis and SIRS, the plasma concentrations of apoM decrease dramatically, the degree of decrease reflecting the severity of the disease. As a carrier for barrier-protective S1P in HDL, the decrease in apoM could contribute to the increased vascular leakage observed in sepsis and SIRS.     

Safety, pharmacokinetics, pharmacodynamics, and plasma lipoprotein distribution of eritoran (E5564) during continuous intravenous infusion into healthy volunteers

Eritoran, a structural analogue of the lipid A portion of lipopolysaccharide (LPS), is an antagonist of LPS in animal and human endotoxemia models. Previous studies have shown that low doses (350 to 3,500 microg) of eritoran have demonstrated a long pharmacokinetic half-life but a short pharmacodynamic half-life. The present study describes the safety, pharmacokinetics and pharmacodynamics, and lipid distribution profile of eritoran during and after a 72-h intravenous infusion of 500, 2,000, or 3,500 microg/h into healthy volunteers. Except for the occurrence of phlebitis, eritoran administration over 72 h was safe and well tolerated. Eritoran demonstrated a slow plasma clearance (0.679 to 0.930 ml/h/kg of body weight), a small volume of distribution (45.6 to 49.8 ml/kg), and a relatively long half-life (50.4 to 62.7 h). In plasma, the majority (approximately 55%) of eritoran was bound to high-density lipoproteins. During infusion and for up to 72 h thereafter, ex vivo response of blood to 1- or 10-ng/ml LPS was inhibited by > or =85%, even when the lowest dose of eritoran (500 microg/h) was infused. Inhibition of response was dependent on eritoran dose and the concentration of LPS used as an agonist. Finally, in vitro analysis with purified lipoprotein and protein fractions from plasma obtained from healthy volunteers indicated that eritoran is inactivated by high-density but not low-density lipoproteins, very-low-density lipoproteins, or albumin. From these results, we conclude that up to 252 mg of eritoran can be safely infused into normal volunteers over 72 h and even though it associates extensively with high-density lipoproteins, antagonistic activity is maintained, even after infusion ceases.     

Quantification of high-density-lipoprotein cholesterol by precipitation with phosphotungstic acid/MgCl2

We evaluated the use of a modified phosphotungstic acid/MgCl2 precipitation procedure for the precipitation of apolipoprotein B-containing lipoproteins. Precipitation of these lipoproteins [very-low- and low-density lipoproteins, and lipoprotein (a)] is complete, with negligible coprecipitation of high-density lipoprotein subfractions (HDL1, HDL2, HDL3), even in hypertriglyceridemic sera. In comparison with ultracentrifugation, the precipitation method yields, on the average, values that are 0.17 mmol/L lower for cholesterol values but almost identical for apolipoprotein A-I and phosphatidylcholine. Looking for delta 3,5-cholestadiene formed from cholesterol in the precipitation residue, we used "high-performance" liquid chromatography and "high-performance" thin-layer chromatography and found none.     

Comparison of two micromethods for determination of lipoprotein cholesterol in plasma.

We compared the results obtained by a micromethod for the determination of plasma lipoprotein cholesterol, in which electrophoresis is used to separate the lipoprotein fractions (beta-, pre-beta-, and alpha-lipoproteins), with those determinations with ultracentrifugation (low-density, very-low-density, and high-density lipoproteins). Precision of determination (coefficient of variation, CV, %) was the same for beta- and low-density lipoproteins (1.6%), and for pre-beta- and very-low-density lipoproteins (3.7%); however, determination of alpha-lipoprotein cholesterol was more precise (1.4%) than that of high-density lipoprotein cholesterol (3.1%). Analytical recovery of lipoprotein cholesterol was the same for both methods (98--100%) and the results were closely correlated (r = 0.943). The procedure has been used to determine the cholesterol content of plasma lipoprotein fractions of apparently healthy adults (both sexes). Lipoprotein cholesterol concentrations in our population sample compare well with those reported for other groups of similar age, in particular Stanford long-distance runners.     

Decrease of lipoprotein(a) with improved glycemic control in IDDM subjects.

OBJECTIVE: Recently, lipoprotein(a) [Lp(a)] has been identified as a major risk factor for coronary heart disease. There are few data available on the influence of metabolic control on plasma Lp(a) concentrations in subjects with insulin-dependent diabetes mellitus (IDDM), a group at high risk for coronary heart disease. RESEARCH DESIGN AND METHODS: We examined the effects of improved metabolic control on plasma lipid and lipoproteins and Lp(a) concentrations in 12 subjects before and after 21 days of tight metabolic control. RESULTS: Glycosylated hemoglobin declined from 8.4 to 6.9% (P less than 0.001), and Lp(a) declined from 29.7 to 27.1 mg/dl (P = 0.022). There were no significant differences in total, low-density lipoprotein, or high-density lipoprotein cholesterol, although the decline in triglyceride concentrations were borderline statistically significant. The distribution of apolipoprotein(a) isoforms in IDDM patients was not unusual, and the apolipoprotein(a) isoform phenotypes did not change with improved metabolic control. Lp(a) concentrations were also significantly higher than in a population-based control group of nondiabetic subjects from the San Antonio Heart Study. CONCLUSIONS: Although the number of subjects was small and the degree of improvement in metabolic control was modest, the results suggest that improved metabolic control may decrease the risk of coronary heart disease mediated by Lp(a) in IDDM.     

Effects of fish oil fatty acids on plasma lipids and lipoproteins and oxidant-antioxidant imbalance in healthy subjects.

The purpose of this study was to investigate the effect of eicosapentaenoic and docosahexaenoic acids on plasma lipids and lipoproteins, lipid peroxidation and antioxidant status in healthy humans. A total of 19 healthy volunteers consumed 6 g/day Maxepa fish oil for 3 weeks (1.8 g n-3 fatty acids/day). At baseline and at day 21, we evaluated plasma lipoproteins, plasma and low-density lipoprotein fatty acids, lipid peroxidation markers (malondialdehyde concentration, low-density lipoprotein peroxidation in vitro), and the content of a number of antioxidants (reduced and oxidized glutathione in whole blood, plasma and erythrocyte glutathione peroxidases, plasma vitamin E and beta carotene). Plasma concentrations of total cholesterol, triglycerides, phospholipids, low-density lipoprotein cholesterol and low-density lipoprotein size did not differ significantly after 3 weeks of supplementation. Adding the fish oil to the diet increased the concentration of n-3 very-long-chain polyunsaturated fatty acids and decreased the concentration of n-6 fatty acid and oleic acid in plasma and low-density lipoprotein. Eicosapentaenoic and docosahexaenoic acid supplementation caused elevated values of the high-density lipoprotein cholesterol due to an increment of the high-density lipoprotein 2 fraction and reduced low-density lipoprotein peroxidation rate in vitro. However, we observed an imbalance between oxidizable substrates and antioxidants with an increased lipid peroxidation, whereas the content of reduced glutathione and beta carotene decreased without any variation in vitamin E. Association of antioxidants with n-3 PUFA could prevent lipid peroxidation and enhance the antiatherogenic effects of n-3 polyunsaturated fatty acids.     

Low apolipoprotein A-I level at intensive care unit admission and systemic inflammatory response syndrome exacerbation

OBJECTIVE: Examine whether a low serum level of apolipoprotein A-I at intensive care unit (ICU) admission is associated with a further increase of the number of systemic inflammatory response syndrome (SIRS) criteria. DESIGN: Prospective observational study. SETTING: A 20-bed, university-affiliated, surgical ICU. PATIENTS: Patients admitted after major surgery, multiple trauma, or acute pancreatitis without septic shock. INTERVENTIONS: We defined as the SIRS Exacerb group patients who presented a further increase of the number of SIRS criteria during their ICU stay or, in the presence of four SIRS criteria at ICU admission, those who presented a further aggravation of organ failure. Other patients were attributed to the SIRS No Exacerb group. From day 1 to 6, we measured apolipoprotein A-I, high-density lipoprotein and total cholesterol, triglycerides, C-reactive protein, procalcitonin, serum amyloid A, interleukin 6, interleukin-1 receptor antagonist, albumin, and other nutrition-linked variables. We looked at laboratory values or factors present at ICU admission according to the two groups. MEASUREMENTS AND MAIN RESULTS: From 63 patients analyzed, 29 (46%) were assigned to the SIRS Exacerb group. Age, sex, and SAPS II and SIRS scores at ICU admission did not differ between the groups. Patients in the SIRS Exacerb group presented more often a septic event (5/29 vs. 0/34, p =.02), had a higher hospital mortality (6/29 vs. 0/34, p =.007), and had a longer ICU stay (p =.0023). At admission, inflammatory variables such as the C-reactive protein, serum amyloid A, interleukin 6, interleukin-1 receptor antagonist plasma levels, and other lipid or nutrition-linked variables were similar between the two groups. Apolipoprotein A-I levels were lower in the SIRS Exacerb group (median [interquartile range]: 68 [56-81] vs. 84 [69-94] mg/dL, p =.028). CONCLUSION: A low serum level of apolipoprotein A-I at ICU admission is associated with an increase of the number of SIRS criteria during the ICU stay.     

412例多发伤后全身炎症反应综合征临床分析

目的 :分析多发伤后全身炎症反应综合征 (SIRS)的发生率和病死率以及SIRS与休克的关系。方法 :多发伤 4 12例 ,分为SIRS组和非SIRS组 ,比较两组的病死率 ,并进行SIRS评分以及按休克严重程度分组 ,分析多发伤后SIRS与休克的关系及多发伤病死率与SIRS评分的关系。结果 :多发伤后SIRS发生率为 87 6 % ,SIRS组病死率明显高于非SIRS组 (P <0 0 5 )。随休克严重程度的增加 ,SIRS发生率明显升高 (r=1,P <0 0 0 1) ,同时多发伤病死率也随着SIRS分值的增加而增高 (P <0 0 0 5 )。结论 :大多数多发伤患者发生了SIRS,发生SIRS后病死率较高 ,SIRS的发生率与休克严重程度成正相关。积极抗休克治疗及早期进行脏器功能支持应是防治SIRS的有力的措施。     

Serum lipids and apolipoproteins in patients with psoriasis.

Psoriasis is characterized by defects in the normal cycle of epidermal development that lead to epidermal hyperproliferation, altered maturation of skin cells, vascular changes and inflammation. Also, psoriasis has been associated with an abnormal plasma lipid metabolism. Changes in plasma lipid and lipoprotein composition in patients with psoriasis may be the reason for the increased risk of atherosclerosis in these patients. We determined serum concentrations of lipids, lipoproteins and apolipoprotein Al and B (apo A1 and apo B) in 72 patients with psoriasis and 30 age matched controls. Serum lipoprotein (a) (Lp(a)), apo A1 and apo B were measured by immunoprecipitation assays, and the lipids and other biochemical parameters by enzymatic methods. Serum Lp(a) and triglyceride (TG) were significantly higher in patients with psoriasis than in healthy control subjects (p<0.01 for both). Apo B was also found to be higher in the patient group, but the difference was not significant. The levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and apo A1 did not differ significantly from those of the controls. These observations imply that serum Lp(a) and TG concentrations may play a role as risk factors for atherosclerotic disease in patients with psoriasis.     

Apolipoprotein E in hepatocellular liver disease

Apolipoprotein E concentrations in plasma were investigated in 17 patients with hepatocellular (non-cholestatic) liver disease. Ninety-five per cent of plasma apolipoprotein E was recovered in density fractions less than 1.063 kg/l and it was therefore associated with very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL). Very low-density lipoproteins and LDL apolipoprotein E correlated positively (r = 0.63, p less than 0.01) with plasma bile salt concentrations when a decrease in liver protein synthesis was taken into account. This may be due to a down-regulation of the hepatic apolipoprotein B, E receptors concomitant with increasing plasma bile salt concentrations.     

Serum lipids and lipoproteins are less powerful predictors of extracranial carotid artery atherosclerosis than are cigarette smoking and hypertension

The effect of serum lipids and lipoproteins on extracranial carotid artery atherosclerosis (CAS) was studied in patients who underwent carotid arteriography. Serum lipid and lipoprotein values along with data on other potential predictors of extracranial CAS were determined in 240 patients who had at least one extracranial carotid artery visualized. In a multiple logistic regression analysis, the independently significant predictors of the presence of extracranial CAS were, in decreasing order of significance, duration of smoking of cigarettes, hypertension, age, and low-density lipoprotein cholesterol. Serum cholesterol, triglycerides, high-density lipoprotein cholesterol, and apolipoprotein A-I did not show an independent effect. Although low-density lipoprotein cholesterol was an independent predictor of the presence of extracranial CAS, its effect as a predictor was far outweighed by the effects of the duration of smoking of cigarettes and a history of hypertension.