Normal Lipoprotein Pattern Research Articles

Transiently Elevated TC and sdLDL-C Levels and Falsely Low LDL-C Levels in Patients with Extrahepatic Cholangiocarcinoma.

PurposeMost patients diagnosed with extrahepatic cholangiocarcinoma (ECCA) exhibit cholestasis caused by obstruction of the bile duct. Cholestasis is associated with lipid disorders, but studies focused on the changing lipid parameters in patients with ECCA are lacking. Here, we observed lipid profiles in patients with ECCA and investigated whether the removal of biliary obstruction could correct dyslipidemia.Patients and MethodsWe consecutively included patients admitted to the hepatobiliary surgery department at the Affiliated Hospital of Xuzhou Medical University. The patients were divided into an ECCA group or a non-ECCA group based on the disease assessment. Patients with histological confirmation of ECCA were included in the ECCA group. Blood samples were collected on admission as well as five days after treatment. An automatic biochemistry analyzer was used to test liver function and serum lipid levels. Serum lipoprotein electrophoresis was performed using barbitone sodium buffer and Sudan black B.ResultsA total of 180 patients met inclusion criteria and were enrolled for this study. Of these, 76 patients were diagnosed with ECCA; all other patients were enrolled in the non-ECCA group. Total cholesterol (TC) and small and dense low-density lipoprotein cholesterol (sdLDL-C) levels were significantly elevated in the ECCA group. LDL-C levels were found to be slightly lower in the ECCA group. In the ECCA group, serum samples were detained in sample wells and lipoproteins failed to be separated. TC and sdLDL-C levels significantly decreased after cholestasis relief in the ECCA group. Lipoprotein electrophoresis revealed that patients with ECCA showed normal lipoprotein patterns after treatment.ConclusionPatients with ECCA exhibited transiently elevated TC and sdLDL-C levels and falsely low LDL-C results. TC, sdLDL-C, and LDL-C levels could be restored to normal levels after biliary obstruction removal and cholestasis relief.

A common truncated variant of lipoprotein lipase in the Japanese population is characterized by pattern B phenotype.

To investigate the relationship between the lipoprotein lipase Ser447Ter (S447X) mutation, lipid profiles and risk of atherosclerotic disease, we studied two groups of Japanese subjects. These groups consisted of a dyslipidemic group (triglyceride (TG) > 1.69 mmol/l and high-density lipoprotein-cholesterol (HDL-C) < or = 0.91 mmol/l; n = 106) and a control group (TG < or = 1.69 mmol/l and HDL-C > or = 1.16 mmol/l; n = 106). All subjects in the control group were confirmed to the pattern A phenotype (normal low-density lipoprotein (LDL) pattern), and 21 individuals in this group were heterozygous for the S447X mutation, but not homozygous. In the patient group, pattern A was shown by 44 of 106 patients. The rest were of the pattern B phenotype, which is associated with an increased risk of coronary heart disease. Homozygosity was concentrated in the patient group (p < 0.05) and in those with the pattern B phenotype (p < 0.05). In contrast, heterozygosity between both groups was not statistically significant. In conclusion, heterozygous and homozygous status with respect to the LPL S447X mutation appears to have different meanings with respect to biochemical and clinical phenotypes of atherosclerosis.

Studies on lipoprotein metabolism in a family with jejunal chylomicron retention.

We describe two siblings with fat malabsorption and jejunal chylomicron retention. Plasma lipoproteins were studied in the patients and their first-degree relatives. The patients were a 14-year-old girl and her 8-year-old brother. Compared to healthy controls, they both had low fasting plasma concentrations of plasma total, HDL, and LDL cholesterol, as well as of apolipoproteins A-I and B. No increase in plasma lipoprotein levels or detectable apo B-48 was observed following an oral fat load. Histological studies of jejunal biopsy specimens obtained during fasting and 1 h postprandially showed severe steatosis, and an apparent block of chylomicron secretion from the endoplasmic reticulum into the Golgi apparatus was observed by electron microscopy. Liver biopsy specimens showed moderate steatosis and ultrastructural changes similar to those in the enterocytes. One healthy sister had a normal plasma lipoprotein pattern, and showed increased plasma triglyceride levels as well as the presence of apo B-48 following an oral fat load. Both parents had normal plasma total cholesterol levels, but clearly reduced fasting concentrations of HDL cholesterol and apo A-I. At least in this family, determination of plasma apo A-I levels might thus prove useful in the identification of heterozygotes.

Secondary hyperlipidaemia: beyond the primary debate.

There has been much recent controversy over the benefit and risks of the treatment of primary hyperlipidaemia. I Although clear guidelines exist from the British Hyperlipidaemia Association (BHA) and European Atherosclerosis Society (EAS)2,3 there are differing opinions over the merits of screening for and treating hyperlipidaemia. Secondary hyperlipidaemia is, however, a less contentious subject. If an underlying cause is identified, appropriate treatment may allow early intervention in the disease, avoid subsequent complications, restore normal lipoprotein patterns and may also obviate the need for lipid-lowering therapy. Series et al, have demonstrated that by using a total serum cholesterol cut-off of 8· 0 mrnollL an unequivocal increase in the frequency of undiagnosed hypothyroidism is observed in hyperlipidaemic patients. The most frequently encountered and previously unsuspected causes in the lipoprotein clinic at Glasgow Royal Infirmary are alcohol excess, hypothyroidism, chronic renal failure and diabetes mellitus, although rarer conditions including nephrosis have also been discovered. Questionnaires were sent to 46 practices in Glasgow, where public and practitioner awareness of hyperlipidaemia is high through local screening schemes, to assess general practitioner (GP) policies towards the systematic biochemical exclusion of causes of secondary hyperlipidaemia. As a secondary objective, GPs policies towards the referral of patients with hyperlipidaemia were also examined.

The association of lipoprotein and hepatic lipase activities with high density lipoprotein subclass levels in men with myocardial infarction at a young age

The relations between postheparin plasma lipase activities and concentrations of lipoproteins, in particular plasma high density lipoprotein (HDL) subclasses determined by gradient gel electrophoresis, were examined in 39 men who had survived a first myocardial infarction before the age of 45 years and in 20 age-matched control men. Reduced lipoprotein lipase (LPL) and hepatic lipase (HL) activities were found in the patients due to low LPL activity in patients with hypertriglyceridaemia, and low HL activity in those with a normal lipoprotein pattern or hypercholesterolaemia. Considerably lower plasma HDL 2b and HDL 2a protein concentrations and higher plasma HDL 3b and HDL 3c protein levels were found in the patients compared with the healthy control subjects. The subgroup of patients with hypertriglyceridaemia accounted for the major proportion of the case control differences for the HDL subspecies. However, significantly lower HDL 2b and HDL 2a concentrations were seen also among the normotriglyceridaemic patients. Analysis of the correlations between concentrations of HDL subclasses and lipase activities revealed positive associations between LPL and HDL 2b and negative associations between HL and HDL 2b. For LPL, this relationship was confined to hypertriglyceridaemic and for HL to normotriglyceridaemic subjects. HL was indicated to be positively connected with HDL 3b levels, irrespective of lipoprotein pattern, whereas LPL seemed to be unassociated with HDL 3b. It is concluded that low LPL and HL activities partly account for the change in HDL subclass distribution observed in patients with myocardial infarction at a young age.

Variations of serum lipoproteins during cell proliferation induced by lead nitrate

In the present study serum lipoproteins were investigated during cell proliferation induced by a potent mitogen, lead nitrate. A strong decrease in HDL 2 and a concomitant increase in HDL 3 were observed in lead-treated rats. The recovery of normal lipoprotein pattern took place together with the regression of hyperplastic process. Since a decrease in HDL also occurs under other conditions of cell growth, we hypothesize that a decrease in HDL, mainly in HDL 2 subfraction, may represent a generalized phenomenon related to massive cell proliferation.

Relation of hyperlipidemia in serum and loss of high density lipoproteins in urine in the nephrotic syndrome

The mechanism leading to hyperlipidemia in the nephrotic syndrome is not fully understood but may be related in part to loss of high density lipoproteins in the urine of patients with nephrosis. To prove this hypothesis, we compared serum lipoprotein profiles with the excretion of high density lipoproteins in urine in 19 nephrotic patients. Serum cholesterol ranged from 19–152 (median value 45) mg/dl in very low density lipoproteins (VLDL), from 130–443 (median 186) mg/dl in low density lipoproteins (LDL) and from 19–64 (median 33) mg/dl in high density lipoproteins (HDL). Hyperlipoproteinemia was found in 17 patients, which was classified as phenotype IIa (Fredrickson) in 2, as phenotype IIb in 9 and as phenotype IV in 6 subjects. Two patients showed normal lipoprotein patterns. VLDL- and LDL-cholesterol were not found in detectable amounts in urine, whereas HDL-cholesterol was measured in low concentrations from 0.1–8.3 mg/24 h in all samples. There was no correlation between serum HDL-cholesterol and urinary HDL-cholesterol, but a positive correlation between serum LDL-cholesterol and urinary HDL-cholesterol ( r= +0.54, p < 0.05). However, the total amount of the daily urinary loss of HDL (<1% of total plasma HDL) seems not to be sufficient to explain hyperlipoproteinemia in the nephrotic syndrome.

Amyotrophic choreoacanthocytosis: Is it really a very rare disease?

Amyotrophic choreoacanthocytosis (ACA) is a hereditary disease characterized by adult onset, hyperkinesias (with tongue and/or lip biting), neurogenic muscular atrophies, acanthocytosis and normal blood lipoprotein pattern. In this paper we cite 8 patients belonging to three families, describing 6 patients of two of the families. We query the supposed rarity of the disease.

Effect of saturated and unsaturated fat diets on molecular species of phosphatidylcholine and sphingomyelin of human plasma lipoproteins

Four healthy 21–23-year-old males with normal lipoprotein patterns and plasma lipid concentrations were subjected voluntarily to two diets of 5 weeks duration each: I, highly saturated fat diet; II, highly polyunsaturated fat diet. The VLDL, LDL and HDL 3 fractions were isolated by conventional ultracentrifugation from each subject on the high fat diets and the molecular species of the component phosphatidylcholines and sphingomyelins were identified and quantitated by GC-MS of the t-butyldimethylsilyl ethers of the corresponding diacylglycerols and ceramides. It was shown that the diet markedly and rather evenly affected the molecular species of the phosphatidylcholines of all lipoprotein classes. However, the changes in the corresponding major molecular species were reciprocal in nature and were consistent with a demonstrated relative resistance to alterations in surface fluidity. In contrast, the dietary fat had only a minor effect on the composition of the sphingomyelins, and did not alter the characteristic differential distribution of the molecular species among the low and high density lipoprotein classes. These results, which were free of the uncertainties introduced by analyses of derived fatty acid and which were obtained on samples isolated from the same subjects, clearly demonstrate that a complete equilibration of the molecular species of the phospholipids is not attained among the plasma lipoprotein classes even in the fasting state. The possible physico-chemical and metabolic basis of these observations is briefly discussed.

Lipoprotein electrophoresis in fat embolism: a preliminary report

Serum lipoprotein electrophoresis and other laboratory tests were made on 14 injured patients over 10 days. Reduction in the pre-beta fraction to an average of 6 per cent, with an elevation of the alpha lipoprotein fraction to an average of 41 per cent, were recorded. The patients without complications regained their normal lipoprotein pattern within 48 hours, while in the two cases who developed fat embolism, the deranged pattern lasted for up to 10 days. The clinical diagnosis of fat embolism is based on signs that appear generally within 3 days following injury. As prognosis depends on early diagnosis, in order to start treatment before full blown clinical signs are present, there is the need for a laboratory test which gives early results and is reliable and easy to perform. This study shows an apparently distinct pattern of the serum lipoproteins which may provide us with a warning about which patients are at risk of developing fat embolism.

Quantification of amounts of coronary arterial narrowing in patients with types II and IV hyperlipoproteinemia and in those with known normal lipoprotein patterns

The amount of cross-sectional area narrowing by atherosclerotic plaques in each 5 mm long segment of the left main, left anterior descending, left circumflex, and right coronary arteries was analyzed at necropsy in 15 patients with type II hyperlipoproteinemia (HLP), in 13 with type IV HLP, and in 10 with known normal lipoprotein patterns. All 38 study patients had clinical evidence of coronary heart disease. Of the 2593 five mm segments examined histologically, narrowing of 76% to 100% in cross-sectional area by atherosclerotic plaques was as follows: type II = 39%, type IV = 67%, and normal lipoprotein pattern = 35% (controls = 4%). Utilizing a scoring system of 1 to 4 for the four categories of narrowing (0% to 25%, 26% to 50%, 51% to 75%, 76% to 100%), the mean score per 5 mm segment for the patients with type IV HLP was significantly higher (3.5) than that for the patients with type II HLP (3.0), normal lipoprotein patterns (3.0), and the controls (2.3). Thus, our patients with type II HLP and those with normal lipoprotein patterns had similar amounts of severe coronary narrowing and significantly less severe coronary narrowing than the patients with type IV HLP.

Failure of thyroid hormones to maintain the normal lipoprotein pattern in rats after removal of the pituitary gland

Hypophysectomy was found to increase low density lipoprotein (LDL) cholesterol in rats from 0.18 to 1.18 mmol/l in 1 week, while very low density lipoprotein (VLDL) and high density lipoprotein (HDL) cholesterol decreased simultaneously from 0.08 to 0.03 mmol/l and from 2.12 to 1.01 mmol/l, respectively. Serum total cholesterol levels remained unchanged. Thyroid supplementation (T 3 or T 4) with doses causing a euthyroid state did not fully correct the lipoprotein pattern. The increase of LDL caused by hypophysectomy was significantly rectified, but the normal level could not be maintained, whilst the HDL level was not at all affected by thyroid hormones. Serum total cholesterol was markedly reduced in all groups with thyroid supplementation, indicating increased cholesterol catabolism. These results suggest that TSH and peripheral thyroid hormones modulate LDL but no effect on HDL could be detected. Other hormones, notably ACTH, growth hormone, lipotropins and gonadotropins are also involved in the control of lipoproteins at the pituitary level. Their exact impact cannot at present be assessed.

Familial LCAT Deficiency Report of Two Patients from a Canadian Family of Italian and Swedish Descent

A 16-year-old male (S.F.) and his 21-year-old sister (D.H.) from a large family of Italian and Swedish descent had virtually identical lipoprotein pattern and complete absence of LCAT activity. Both had typical corneal opacities and mild anemia with target cells. S.F., but not D.H., presented with proteinuria, which has increased over three years of follow-up. His kidney biopsy revealed lipid deposits in the glomerular basement membrane. Ten relatives in 4 generations had normal LCAT activity and/or lipoprotein pattern. The patients and their relatives had haptoglobin type 2. Factors that might influence the different clinical presentation in our patients (previous renal disease, diet, abnormal lipoproteins), prognosis, and treatment (diet, enzyme replacement, cholestyramine) are discussed.

Serum levels of thyroid-stimulating hormone in hyperlipoproteinemia

Similar serum lipoprotein abnormalities have been demonstrated in hyperlipoproteinemia type III and hypothyroidism. In this study the levels of thyroid-stimulating hormone in serum were determined in clinically euthyroid patients with different types of hyperlipoproteinemias and in subjects with a normal lipoprotein pattern. The mean value for thyroid-stimulating hormone was significantly higher in the group with hyperlipoproteinemia type III than in normal controls ( p < 0.01) and in the group with hyperlipoproteinemia type II A ( p < 0.02). The levels of thyroid-stimulating hormone were positively correlated to the triglyceride and cholesterol concentration in the very low density lipoprotein fraction and the “III-index”.

Dose-response effect of single and combined clofibrate (Atromidin ®) and niceritrol (perycit ®) treatment on serum lipids and lipoproteins in type II hyperlipoproteinaemia

The dose-response effects of clofibrate and niceritrol on serum cholesterol and triglycerides (TG) were studied in 29 patients with Type IIa and IIb hyperlipoproteinaemia. In 17 patients, clofibrate and niceritrol were then given as combined treatment, and the effects of this combination on serum lipoproteins were studied. Clofibrate was theen in three doses: 1.5, 2 and 2.5 g/day. The optimum effect on serum TG and cholesterol in patients with Type IIa was observed with the 1.5 g dose and higher doses did not lower the serum lipids further. In patients with Type IIb the optimal clofibrate dose was 1.5–2 g/day. Niceritrol was then given in three doses: 3, 4.5 and 6 g/day. In patients with Type IIa the serum TG concentration was not significantly affected by any dose used, whereas the reduction of the serum cholesterol concentration was dose dependent. In patients with Type IIb the reduction of both serum TG and cholesterol was dose dependent. Combined treatment with 2 g clofibrate and 3 g niceritrol resulted inaa normal lipoprotein pattern in 15 out of 17 patients. The reduction of the serum lipids was approximately the same as during treatment with 6 g niceritrol/day. No additional side-effects were observed during combined treatment.

Plasma lipid values and lipoprotein patterns during adolescence in boys

Lipid studies were performed on fasting plasma samples in 214 healthy adolescent boys, 11-19 years of age. Ranges of normal values for plasma cholesterol and triglyceride concentrations, and normal lipoprotein patterns were established for this age group. The boys were grouped according to puberty rating. A significant increase in triglyceride values was obtained with adolescent maturity. Plasma cholesterol values did not change with age or puberty rating. One boy had hypercholesterolemia and a lipoprotein pattern consistent with Type II hyperlipoproteinemia (Fredrickson). Seventeen boys, all of whom had reached adolescent maturity, had elevated triglyceride values and a marked increase in pre-beta-lipoprotein. It appears from this study that increased concentrations of triglyceride and Type IV hyperlipoproteinemia of Fredrickson may be detected as boys reach maturity at adolescence.

各種血清脂質異常例におけるリポ蛋白質PAG電気泳動像の観察

With the development of a practical method of polyacrylamide gel (PAG) electrophoresis of serum lipoproteins, sophisticated studies on serum lipid or lipoprotein disorders in atherosclerotic cardiovascular patients became possible. Qualitative and quantitative disorders of serum lipoproteins are estimated adequately even in modest to moderate hyperlipidemias which are quite prevalent among atherosclerotic cardiovascular patients. The objective of this presentation is to relate electrophoretic profiles of serum lipoproteins worked out with PAG disc method on an approximately 1815 clinical subjects.Serum lipoprotein PAG disc electrophoretic profiles could be classified as six basic lipoprotein patterns. Four of six basic patterns seemed being consistent with the patterns of four of the established cases with familia hyperlipoproteinemia of WHO and other classifications, though none of our subjects had any clinical evidence of familial disorders. Presence of the midband lipoproteins and chylomicrons were major sources of a considerable number of the variations of the six basic patterns.Occurrence of dense and wide midband was relatively rare in hyperpre-bata lipoproteinemia. In this abnormality, fluctuation of serum triglyceride concentration is evidently ascribable to chylomicrons which is clearly separated from pre-beta or beta lipoproteins with PAG method. The mixed hyperlipoproteinemia (referred to as the sixth phenotype by some) is detectable and identifiable with the method. Lipid chemistry of this abnormality was frequently indif f erentiable from those of other hyperlipoproteinemias. Dense and wide midband was detected frequently among hyperbeta lipoproteinemia with or without. moderately detectable pre-beta lipoprotein, though occurrence of the midband per se was not differred from the others. The midband showed considerable variations in electrophoretic characters. Hypercholesterolemia was common in these subjects, but triglyceride level was variable. Among the variations of normal lipoprotein pattern, the most interesting was those with dense and wide midband in addition to normal beta lipoprotein band. Some of them showed hypercholesterolemia and some others showed hypertriglyceridemia. Following drug therapy for hyperlipidemia, quantitative and qualitative changes of serum lipoprotein profiles were observable frequently.These observations suggest that serum lipid abnormalities may appear as variable forms of abnormal spectra of lipoprotein species, although there is a rough interrelationship between serum lipoprotein abnromalities and lipid abnormalities.

Cardiovascular pathology in hyperlipoproteinemia: Anatomic observations in 42 necropsy patients with normal or abnormal serum lipoprotein patterns

Certain clinical and cardiovascular necropsy findings are described in 28 patients with known hyperlipoproteinemia and 14 patients known to have a normal lipoprotein pattern. Of the 42 patients, 28 had symptomatic ischemic heart disease: 20 of these had hyperlipoproteinemia (9 type II, 2 type III, and 9 type IV), and 8 had a normal lipoprotein pattern. The average age at death in the 20 patients with hyperlipoproteinemia and symptomatic ischemic heart disease was 48 years, and in the 8 with a normal lipoprotein pattern and ischemic heart disease, 46 years. The degree of coronary arterial luminal narrowing was severe in all patients with ischemic heart disease whether their lipoprotein pattern was normal or abnormal. In all 28 patients with symptomatic ischemic heart disease, the lumen of at least 1 of the 3 major coronary arteries was narrowed more than 75 percent by old atherosclerotic plaques, and in 25 of these all 3 major coronary arteries were narrowed to this extent. With the exception of 1 of the 2 patients with a type III pattern, the composition of the coronary atherosclerotic plaques was similar among patients with type II, III and IV hyperlipoproteinemia and among those with a normal lipoprotein pattern. Attention is called to the unique type of valvular aortic stenosis that frequently develops in the homozygote with a type II pattern and also to the reversed distribution of the aortic atherosclerotic plaquing in the homozygote with a type II pattern. In these patients the amount of plaquing appears to be greater in the ascending than in the abdominal portion of the aorta. Lipid plaques were observed on left atrial endocardium in 2 patients: One had type I hyperlipoproteinemia without associated coronary or aortic atherosclerosis; the second had a type III pattern with extensive coronary and aortic atherosclerosis. These left atrial endocardial lipid deposits may be unique to these hyperlipoproteinemias. In conclusion, it appears clear that atherosclerosis is accelerated or occurs prematurely in patients with type II, III and IV hyperlipoproteinemia, but that hyperlipoproteinemia is not a prerequisite for premature development of severe atherosclerosis.

Cardiovascular Pathology in Hyperlipoproteinemia (HLP).

Meeting Abstracts1 May 1973Cardiovascular Pathology in Hyperlipoproteinemia (HLP).William C. Roberts, M.D., Victor J. Ferrans, M.D., Robert I. Levy, M.D., F.A.C.P., Donald S. Fredrickson, M.D., F.A.C.P.William C. Roberts, M.D.Search for more papers by this author, Victor J. Ferrans, M.D.Search for more papers by this author, Robert I. Levy, M.D., F.A.C.P.Search for more papers by this author, Donald S. Fredrickson, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-5-820_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptLittle information is available on the morphologic aspects of hyperlipoproteinemia. To begin to fill this void 28 patients known to have this disorder and 14 with normal lipoprotein patterns were studied at necropsy. Of the 42 patients, 28 had symptomatic ischemic heart disease—20 of these had hyperlipoproteinemia (type II, 9; type III, 2; type IV, 9), and 8 had normal lipoproteins. The average age at death in the 20 patients with hyperlipoproteinemia and symptomatic heart disease was 48 years; in the 8 with normal lipoproteins, 46 years. The degree of coronary arterial luminal narrowing was severe in all with heart... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Bethesda, Maryland PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1973Volume 78, Issue 5Page: 820-820KeywordsCardiovascular therapyHeartLipoproteins Issue Published: 1 May 1973 PDF downloadLoading ...

SUCROSE FEEDING IN MAN

Abstract. In four patients with hyperlipoproteinemia and in one with a normal serum lipoprotein pattern 800 kcal of the daily caloric intake were replaced by sucrose for two weeks. Studies of the adipose tissue metabolism in vitro showed that the lipid synthesis from glucose, the basal as well as the noradrenaline‐stimulated lipolysis, were considerably increased as compared to the controls. Furthermore, no antilipolytic effect of a physiological concentration of insulin was found. It was suggested that sucrose feeding induces changes in adipose tissue metabolism which may be of importance for the increased triglyceride levels noted in these patients.