Changes in Lp(a) lipoprotein and other plasma proteins during acute myocardial infarction.

The sequential changes of Lp(a) lipoprotein concentrations in patients (n = 59) suffering acute myocardial infarction (AMI) were examined and compared with other plasma proteins. The temporal and quantitative characteristics of the responses in concentration of acute phase reactants (CRP, haptoglobin, alpha 1-antitrypsin, alpha-acid glycoprotein), lipids (total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol) and apolipoproteins AI and B were similar to previous reports. Lp(a) lipoprotein showed transient changes with an initial decrease of 10-25% compared to the 3-month control value, followed by rebound on day 7-11 above admission level, before again declining. We were able to demonstrate a quantitative relationship between infarct size and alterations in plasma levels of acute phase reactants. However, in addition to rather unusual significant fluctuations during AMI, Lp(a) lipoprotein changes seemed unrelated to infarct size. These findings do not support the view that Lp(a) lipoprotein acts as an acute phase reactant.

[Treatment of hypercholesterolemia in adults. A treatment program 1991]. / Behandling av hyperkolesterolemi hos voksne. Handlingsprogram 1991.

A Norwegian programme for treatment of hypercholesterolemia in adults was published in 1988. In 1990 the Norwegian Medical Association appointed a group to modify this programme in the light of current knowledge, and taking into consideration the recommendations of the Consensus Conference on Cholesterol of October 1989. The present article presents this modified programme. When evaluating the risk of developing coronary heart disease a combined risk score should be calculated which also takes into account important risk factors other than cholesterol, such as family history, sex, age, smoking, hypertension, presence of diabetes etc. For those considered to be at high risk of developing coronary heart disease, the programme gives guidelines on how to intervene. With regard to treatment, special emphasis is placed on changing the diet.

[Cholesterol-lowering effect of oat]. / Kolesterolsenkende effekt av havre.

Use of oat-supplement has been advocated to reduce serum cholesterol concentration. In order to study the effect of a daily dietary supplement of oats on lipid levels we performed three controlled clinical trials in healthy Norwegians and patients with hypercholesterolemia. The studies lasted 3-5 weeks, and oats were added to the diet in bread, breakfast cereals, porridge or crispbread. The serum cholesterol concentrations were reduced by 2.5-5% in four of the five groups with an oat-supplemented diet. No effect was found in the group who ate crispbread. Lipid levels remained unchanged in the three control groups. We conclude that oat products have a small but significant cholesterol-lowering effect when given as a supplement to the ordinary Norwegian diet.

[Drug therapy of hypercholesterolemia. Treatment of hypercholesterolemia in adults--a Norwegian therapeutic program 1988]. / Medikamentell behandling av hyperkolesterolemi. Behandling av hyperkolesterolemi hos voksne--norsk handlingsprogram 1988.

There are indications that treatment of hypercholesterolemia by means of drugs reduce risk of atherosclerosis in patients with increased concentrations of atherogenic lipoproteins. Such therapy should be initiated only after satisfactory exclusion of secondary causes of hyperlipoproteinemia, and should be regarded as an adjunct to appropriate dietary therapy. Drug therapy should be strongly considered in patients with total cholesterol above 8-9 mmol/l on diet therapy only. Drug therapy should be considered at even lower concentrations of cholesterol when coronary heart disease is present and in familial forms of hyperlipidemia when increased risk of atherosclerosis has been documented. In patients with increased plasma concentrations of total cholesterol the drugs of choice are agents which enhance the rate of LDL catabolism (resins) or reduce the rate of LDL synthesis (nicotinic acid). Fibrates should be used when triglycerides and cholesterol are both increased. HMG CoA reductase inhibitors offer considerable promise in the therapy of patients with primary hypercholesterolemia. Probucol may be used in combination with other drugs, particularly when xanthomas are present in patients with familial hypercholesterolemia.

[Hypercholesterolemia. Use of laboratory analysis]. / Hyperkolesterolemi. Bruk av laboratorieanalyser.

The article summarizes the use of laboratory analysis as described in the recently published Norwegian program for diagnosis and treatment of hypercholesterolemia in adults. Serum cholesterol is used both to diagnose hypercholesterolemia and to monitor the effect of treatment. Serum triglycerides should be measured when hypercholesterolemia has been found and dietetic treatment is considered. High density lipoprotein (HDL) cholesterol should be measured when dietetic treatment has not reduced hypercholesterolemia sufficiently and drug treatment is considered. We do not at present recommend measurement of apolipoproteins and factors within coagulation/fibrinolysis, but such measurements might be of importance in the near future. Blood cholesterol exhibits large biological variations, which makes retesting necessary before hypercholesterolemia is diagnosed. Analytical variation is usually less than biological variation, but requires use of quality control materials. This control is equally important for small dry chemistry analyzers as for wet chemistry analyzers.

The effect of serum lipoproteins on cholesterol content and sterol exchange in cultured human endothelial cells.

Cultured human endothelial cells preincubated with the infranatant of human serum increased their content of cholesterol when subsequently exposed to low density lipoproteins (LDL) as compared to control cultures further incubated in the presence of infranatant only. Replacing LDL with high density lipoproteins (HDL) resulted in no change in the cellular cholesterol content compared to the control. The addition of HDL did not influence the increase in cellular cholesterol content mediated by LDL. HDL stimulated the efflux of endogenously synthesized 14C-labelled sterols compared to the infranatant fraction, whereas LDL had only a slight effect. Cells preincubated with whole serum did not change their cholesterol content when subsequently exposed to LDL, compared to cultures further incubated in presence of whole serum. Replacing whole serum (during the final incubation) with infranatant, resulted in a decrease of the cellular cholesterol content, which was not influenced by further addition of HDL.

Low density lipoprotein metabolism in type IV and type V hyperlipoproteinemia.

Low density lipoproteins (LDL) are thought to arise largely from degradation of triglyceride-rich very-low-density lipoproteins (VLDL). LDL kinetics in patients with Type IV and Type V hyperlipoproteinmia were studied and compared with normal subjects. LDL labeled in the protein moiety with 125I was used as a tracer. There was no significant difference in LDL turnover between the three groups, suggesting that a catabolic defect in VLDL degradation to LDL may exist in both Type IV and Type V hyperlipoproteinemia.

Studies on the pre-alpha-lipoprotein of human serum. II. Evidence for the presence of an albumin-apo-A-I complex.

By combined column affinity chromatography and preparative electrophoresis, a lipoprotein was isolated from the electrophoretically defined pre-alpha-region. The isolated fraction, designated Fraction II1, demonstrated one band after electrophoresis in agarose, in polyacrylamide, and in sodium dodecylsulphate containing polyacrylamid. Double diffusion experiments disclosed the presence of albumin and apolipoprotein-A-I within the fraction. After reduction with mercaptoethanol and subsequent electrophoresis in sodium dodecylsulphate containing polyacrylamide gel, two bands appeared. One of the bands had an electrophoretic mobility similar to albumin monomer (mol.wt 67,000), the other had the same electrophoretic mobility as apolipoprotein-A-I with a mol.wt of 28,400. It is suggested that Fraction II1 contains an albumin-apolipoprotein-A-I complex.

Complement activation and phagocytosis of cryoglobulin particles in a patient with plasma cell proliferative disease.

The serum of a patient with a non-aggressive plasma cell proliferative disorder contained two monoclonal immunoglobulins: IgG3 lambda in moderate concentration and having cryoglobulin features, and IgA kappa in low concentration and without cryoprecipitability. The patient's serum had low complement concentration and C3 was partly converted into split products in vivo. Complement (C3) together with cryoglobulin and fibrinogen was found by immunofluorescence in sections from skin showing vasculitis. The cryoglobulin particles which formed at room temp. were vividly phagocytized in vitro by neutrophile granulocytes from the patient and from normal individuals as demonstrated in light microscopy and ultramicroscopy.

Studies on the pre-alpha-lipoprotein in patients with familial lecithin: cholesterol acyltransferase deficiency.

The present study shows that regular alpha1- and pre-alpha-lipoproteins cannot be detected in serum of patients with familial lecithin: cholesterol acyltransferase (LCAT) deficiency. After electrophoresis on agarose gel only one single band of albumin mobility was observed in the alpha1-pre-alpha-region. In contrast to sera of normal subjects neither the anodic front nor the cathodic part of this region revealed any lipoprotein bands in the patients studied. The lack of the cathodic part might be related to a low amount of alpha1-lipoprotein. The apparent lack of the anodic front could be related to a low amount of "albumin-Apo-A-I-containing lipoprotein" (AAL). AAL was not detected with conventional methods in LCAT deficient sera. The alpha1-lipoprotein was made up of two immunologically identical peaks, both of which had a Sudanophilic character. After incubation of lysolecithin with albumin and AAL and subsequent thin layer chromatography, a significant lysolecithin-binding capacity of AAL was demonstrated, superior to that possessed by albumin.

Effects of intravenous hyperalimentation of plasma-lipoproteins in severe familial hypercholesterolaemia.

The plasma-lipoprotein response to intravenous hyperalimentation was studied in three patients with severe familial hypercholesterolaemia. Hyperalimentation substantially lowered plasma concentrations of cholesterol, low-density lipoproteins (L.D.L.P.), and high-density lipoproteins. The chemical composition of L.D.L.P. did not change. Triglyceride levels increased slightly in two patients and decreased in the third. Turnover of radiolabelled L.D.L.P. was disturbed as L.D.L.P. concentration fell but then returned to normal. The mechanism by which intravenous hyperalimentation rapidly lowers plasma-cholesterol in severe hypercholesterolaemia is unknown.