Acta Medica ScandinavicaVolume 179, Issue 1 p. 1-4 Plasma Phospholipid Levels and Distribution in Human Maternal Blood and in Blood from the Umbilical Cord KIM CRAMÉR, KIM CRAMÉR Medical Services I and II and Obstetrical-Gynecological Service I, Sahlgren's Hospital, University of Göteborg, Göteborg, SwedenSearch for more papers by this authorOLLE VIKROT, OLLE VIKROT Medical Services I and II and Obstetrical-Gynecological Service I, Sahlgren's Hospital, University of Göteborg, Göteborg, SwedenSearch for more papers by this author KIM CRAMÉR, KIM CRAMÉR Medical Services I and II and Obstetrical-Gynecological Service I, Sahlgren's Hospital, University of Göteborg, Göteborg, SwedenSearch for more papers by this authorOLLE VIKROT, OLLE VIKROT Medical Services I and II and Obstetrical-Gynecological Service I, Sahlgren's Hospital, University of Göteborg, Göteborg, SwedenSearch for more papers by this author First published: January/December 1966 https://doi.org/10.1111/j.0954-6820.1966.tb05425.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume179, Issue1January/December 1966Pages 1-4 RelatedInformation

Plasma fibronectin was determined using a laser nephelometric method in 10 patients with acute myeloid leukaemia undergoing chemotherapy. There was a continuous fall during the first 3 weeks to about 50% of the normal level. The decrease of fibronectin may contribute to the lowered resistance against infection characteristic of these patients.

At our hospital 15 cases of leukaemic reticuloendotheliosis and 4 cases of legionnaires' disease have been diagnosed. 3 patients had both diseases. The clinical findings are reported. It is probable that patients with leukaemic reticuloendotheliosis have an increased susceptibility to Legionnaires' disease. Possible reasons for the decreased resistance are discussed.

Patients with pernicious anemia (PA) have been compared with a reference group concerning the concentration of lipids in plasma before (34 cases) and after (15 cases) treatment with vitamin B12. The lipid parameters in plasma and in postheparin plasma have been measured before and after 6 hours' incubation at 37degree C before and after specific treatment. In a limited number of cases the lecithin: cholesterol acyl transfer (LCAT) rate has been determined. In relapse, the PA cases showed increased free fatty acid (FFA) and triglyceride (TG) concentrations but decreased concentrations of total cholesterol (TC), unesterified cholesterol (UC) and all examined phospholipid fractions. After treatment, FFA remained unchanged and TG decreased, while TC and possibly also UC and the phospholipid frations were in line with reference levels. After incubations, UC and phosphatidylcholine (PC) decreased and lysolecithin (LL) increased. FFA increased and TG decreased. Incubation of postheparin plasma resulted in an augmented decrease in TG and PC and increase in FFA and LL, In relapse, the changes on incubation were less pronounced than after treatment. The LCAT was low but within the normal range before treatment in the six cases examined. After treatment, LCAT rates increased but were still normal in relation to the plasma lipid concentrations. The study showed a decreased net esterification of cholesterol and LL formation on incubation of plasma in PA cases in relapse. This finding might be explained by the low concentration of plasma substrates for the LCAT reaction and phospholipases. After treatment the concentration of lipid substrates was restored to normal, with subsequent normal LL formation and cholesterol esterification. The observations could also explain the frequent lack of stabilization of erythrocytes suspended in plasma of PA after incubation, resulting in virtually the same ESR after as before this procedure. Due to low LL formation following the insufficient substrate availability for LCAT and phospholipase, the previously reported critical level of the LL concentration is not reached and cannot achieve its normal reduction of the ESR.

Lecithin:cholesterol acyl transfer (LCAT) rate in plasma and lipid concentrations in total plasma and high density lipoproteins (HDL) were determined before and after oral fat loads in healthy human subjects. The changes of LCAT rate after fat loading were compared to the effect of chylomicrons or lipid emulsions added in vitro to fasting plasma. After the fat loads there was an increase of mean molar LCAT rate simultaneous with an increase of mean phospholipid (PL) and HDL-PL concentration but not simultaneous with the increase of mean triglyceride (TG) concentration. Individual changes of molar LCAT rate correlated positively with changes of PL, HDL-PL, and unesterified cholesterol (UC) concentration but not with changes of TG concentration in the separate plasma samples after the fat loads. If only the maximal changes in each subject in any sample at any time after the loads were taken into account, the maximal increase of molar LCAT rate correlated positively with the maximal increase of TG concentration. Molar LCAT rate was not influenced by addition of chylomicrons in vitro but increased after addition of a PL emulsion. It is suggested that LCAT rate is stimulated by an excess of PL in plasma and substrate lipoproteins. This excess of PL may be created in vivo temporarily during chylomicron catabolism. The stimulation of LCAT rate by fat ingestion emphasizes the importance of LCAT as a connecting link between triglyceride and cholesterol metabolism.

Information concerning variation in the lecithin:cholesterol acyl transfer (LCAT) rate in normal persons is scanty. We have therefore analyzed the LCAT rate and the lipid and lipoprotein concentrations in the plasma of healthy normolipidemic persons 20-60 years of age, 40 men and 40 women. 10 per decade and sex. Interindividual variation in molar LCAT rate was 57-130 mumol-u(-1)-h-1 (mean +/- 2 S.D.) with no sex difference. Intraindividual variation of molar LCAT rate studied in 8 women and 9 men was shown to be greater than expected from methodological error and was not explainable by the small changes in plasma lipid concentration during the observation period. In the women the molar LCAT rat was lower during the preovulatory phase of the menstrual cycle than during the postovulatory phase. There was positive correlations between the molar LCAT rate and most of the lipid parameters in plasma. By partial correlation analysis a positive correlation was shown between LCAT rate and triglyceride concentration irrespective of other lipid parameters. Keeping triglyceride concentration constant, there was a positive correlation between molar LCAT rate and total phospholipid, unesterified cholesterol, esterified cholesterol, or low-density lipoprotein (LDL) cholesterol concentration. No correlation was found between high-density lipoprotein (HDL) lipid concentration and LCAT rate. Thus in normal subjects there seems to be a direct relation between very low density lipoprotein and LDL lipid concentration and molar LCAT rate but no relation between HDL lipid concentration and LCAT rate.

Crucial and previously criticized points in a slightly modified version of the Stokke-Norum assay of fractional lecithin:cholesterol acyl transfer (LACT) rate in plasma were studied. LCAT activity in the albumin added to the assay medium and negative influence of remaining organic solvent were important sources of error that it was necessary to eliminate. The assumption of equilibration of labeled cholesterol among lipoproteins in vitro was supported experimentally. Addition of isolated chylomicrons had no influence on initial LACT rate. Incubation time was decreased to 20 minutes to obtain a better estimate of initial LCAT rate in normals. Using gas-liquid chromatography to determine unesterified cholesterol concentration, the precision of measurement of molar LCAT rate was 5.2 per cent (coefficient of variation). Molar LCAT rate in healthy males 20-60 years of age was 56-130 mumol-1(-1)-h-1 (mean +/- 2 S.D.) and compared well with reports from other laboratories and in vivo measurements. At present this methodology is considered to be suitable for studies of LCAT and cholesterol turnover in different metabolic situations and clinical materials.

Abstract. In an experimental study increasing amounts of lysolecithin have been added to aliquots of plasma from 18 patients with a high erythrocyte sedimentation rate (ESR) and the final concentration of lysolecithin in the samples has been determined by means of thin layer chromatography and subsequent phosphorus determination as well as determination of the ESR. It was found that the ESR remained high in the different plasma samples until a critical level of lysolecithin was reached, whereafter the ESR abruptly dropped to lower values. This change took place within a very narrow concentration range, usually between 4.5 and 5.5 μg lysolecithin P/ml, and at a concentration of 7–8 μg/ml the ESR was consistently very low. In additional experiments, using decreasing amounts of red cells to the various plasma samples, the ESR had a normal tendency to increase inversely to the hematocrit, but in this case no threshold level could be observed. These findings clearly demonstrate that the lysolecithin concentration is of considerable importance for the ESR value. A low lysolecithin content of the plasma means a higher ESR value than expected from the amount of protein components, and a high lysolecithin concentration means a low ESR in spite of an unchanged protein pattern. Normally a decrease of the ESR takes place on incubation of a plasma sample due to the enzymatic formation of lysolecithin from lecithin. This phenomenon is explained by an increase of the lysolecithin amount above the demonstrated critical level. In a number of pathological conditions this “heat-stabilization” process does not occur, and in these cases the lysolecithin concentration is characteristically low and does not rise above the critical level even after incubation. A number of possible explanations of this drastical decrease of the ESR at a certain lysolecithin level are discussed in this presentation, but the most likely is that lysolecithin is bound to plasma proteins, e.g. albumin. In this form it is unable to exert its physiological effect on the red cell surface membranes until the saturation limit of the carrier protein is reached and “free” lysolecithin appears.

Abstract. In ten patients with hypercholesterolemia plasma lipids, including individual phospholipids, were analyzed before and 2 to 18 months after high‐dose nicotinic acid therapy. Free fatty acids were increased, while cholesterol, triglycerides and total phospholipids decreased. Among the individual phospholipids there was a significant decrease of lysolecithin in absolute as well as relative amounts. The other phospholipid fractions did not change significantly. The possible mechanisms of nicotinic acid effects on plasma lipids are discussed.

Abstract. Individual phospholipids were determined in the plasma of 24 hypercholesterolemic subjects and in 13 healthy controls. In the hypercholesterolemic group total phospholipids were increased, as were the absolute amounts of lecithin and especially sphingomyelin. Expressed as percentage of total phospholipids, sphingomyelin was increased and lecithin decreased. The absolute amount of lysolecithin was unchanged and the percentage lower than normal. Phosphatidylethanolamine was not changed. The findings are compatible with an increase of beta‐lipoproteins of normal composition in hypercholesterolemia. It is speculated whether the alteration in the phospholipid pattern may be of importance for the tendency to atherosclerosis in hypercholesterolemia.

ABSTRACT Free fatty acids (FFA), triglycerides (TG), total and free cholesterol, total phospholipids and the individual phospholipids lysolecithin, sphingomyelin, lecithin and cephalin were determined in four groups of women, each consisting of nine or ten subjects. The determinations were performed before treatment and about every third month during one year of medication. Two combined drugs, Anconcene® (Chlormadinone acetate = CMA, 3 mg + mestranol 0.1 mg) and Conluten® (Norethindrone = NET, 2 mg + mestranol 0.1 mg) and two low-dose gestagen drugs, CMA 0.5 mg and NET 0.4 mg were used. FFA decreased in the Anconcene group. TG increased among those taking Anconcene, Conluten and NET. Slight increases of cholesterol were noted in the two groups taking combined drugs. Total phospholipids were increased in the Anconcene group and the Conluten group. Among the individual phospholipids, changes appeared similar to those found during pregnancy. They were most pronounced in the Anconcene group. It seems that it is the oestrogenic component of the combined drugs that is responsible for many of the alterations. It is suggested that the testosterone derivative NET but not the progesterone derivative CMA may have anti-oestrogenic effect in this connection.

Abstract. The individual phospholipids as well as the triglycerides, free fatty acids, total cholesterol and its non‐esterified fraction have been determined on a normal material comprising 37 men and women of different age groups. Young men exhibited significantly higher values of lysolecithin in comparison with elderly men and women irrespective of age.Incubation studies revealed a lecithin splitting activity with subsequent formation of lysolecithin and release of fatty acids. Simultaneously the well‐known lipase activity was found, splitting also the triglycerides and releasing further amounts of free fatty acids. Free cholesterol decreased to a significant extent, probably by transesterification of fatty acids released during the incubation from lecithin and probably also to a lesser degree from triglycerides. No change of sphingomyelin was noted and phosphatidylethanolamine also remained unchanged during the incubation. The reported lysolecithin increase in incubated plasma probably explains the previously reported reduced sedimentation rate of red cells added to such a plasma. The increment of free fatty acids may also contribute to the same result to a lesser extent.

Abstract.The increased lecithinase as well as lipase activity of post‐heparin plasma in comparison with native plasma subjected to incubation is reported. The enzymatic action gives rise to a further increased formation of lysolecithin, a concomitant diminution of lecithin and triglycerides with an appreciable liberation of fatty acids. In spite of the presence in abundance of free fatty acids no further esterification of free cholesterol takes place, in contrast to the considerable decrease of free cholesterol by transesterification from the enzymatically split lecithin when pre‐heparin plasma is subjected to incubation. Possibly an esterification “threshold level” exists in this respect. The effect of a single heparin injection on the lipid metabolism will last for about 3–4 h.Based on the available data from this report and earlier findings the possibility is discussed whether or not the clearing of lipemic plasma can be explained by the consecutive action of a lecithinase and a lipase, the first enzyme transferring the stabilizing surface layer of the chylomicra consisting of phospholipids and cholesterol into a more or less water‐soluble form, and thereafter the second enzyme can act directly on the chylomicron content of triglycerides. An experimental approach to in vitro clearing of lipemic plasma by the two enzyme systems from extraneous sources is discussed.

Abstract. A material of 22 cases of myocardial infarction has been analysed with regard to the lipid and phospholipid levels at the acute stage of the disease, and at the lime of discharge from hospital in 12 cases. Definitely decreased values of lysolecithin have been found which highly significantly differ from a reported normal material. A slight but probably significant decrease of phosphatidylethanolamine has been observed. The FFA level is also considerably elevated in comparison with the normal material. On incubation a lysolecithin increase takes place in the plasma of patients suffering from myocardial infarction as in normal subjects, and a concomitant decrease of lecithin occurs. Simultaneously triglycerides and FFA change, the former exhibiting a highly significant decrease and the latter an increase of the same significance level. As in normal subjects an esterification of free cholesterol occurs on incubation. Total cholesterol, total lipid phosphorus and sphingomyelin retain their preincubation levels as in the normal material.The increase of lysolecithin in absolute figures is distinctly below the normal one, indicating that a diminished lecithinase activity has been observed. Cholesterol esterification on incubation is also definitely decreased, suggesting a reduced fatty acid transferase activity.After the lapse of the initial disease period the same analyses were performed. At that time most patients had returned to or approached the normal lysolecithin level of their age group. The alterations after incubation at the re‐examination are the same as at the initial stage.The possible biological and clinical significance of the reported findings is discussed.

Acta Medica ScandinavicaVolume 181, Issue 2 p. 143-146 Individual Plasma Phospholipids in Women: A Comparison of Menstruating and Menopausal 48 Year-old Women L. HALLBERG, L. HALLBERG Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorA.-M. HÖGDAHL, A.-M. HÖGDAHL Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorA. SVANBORG, A. SVANBORG Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorO. VIKROT, O. VIKROT Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this author L. HALLBERG, L. HALLBERG Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorA.-M. HÖGDAHL, A.-M. HÖGDAHL Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorA. SVANBORG, A. SVANBORG Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorO. VIKROT, O. VIKROT Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this author First published: January/December 1967 https://doi.org/10.1111/j.0954-6820.1967.tb07239.xCitations: 6AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume181, Issue2January/December 1967Pages 143-146 RelatedInformation

Acta Medica ScandinavicaVolume 181, Issue 1 p. 83-87 Plasma Lipids in Recurrent Jaundice of Pregnancy Alvar Svanborg, Alvar Svanborg Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorOlle Vikrot, Olle Vikrot Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this author Alvar Svanborg, Alvar Svanborg Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this authorOlle Vikrot, Olle Vikrot Department of Medicine II (Head: E. Wassén, M. D.), University of Göteborg, Göteborg, SwedenSearch for more papers by this author First published: January/December 1967 https://doi.org/10.1111/j.0954-6820.1967.tb07230.xCitations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume181, Issue1January/December 1967Pages 83-87 RelatedInformation