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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human LDL were bound and internalized by cultured human fibroblasts. When an antilipoprotein IgA kappa from a case of myeloma with hyperlipidemia and xanthomatosis was introduced into the system, LDL uptake dropped by 50% but LDL binding to fibroblasts was unchanged. In the same system, IgG and IgA controls were inactive.
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PMID:In vitro interaction of LDL, anti-lipoprotein IgA and human fibroblasts. 21 34

LDL interact with fibroblasts through specific membrane sites. This reaction is the first step of a mechanism which leads to the regulation of intracellular cholesterol synthesis. When LDL form a complex with an IgA from a myeloma serum with mixed hyperlipidemia and xanthomatosis, they no longer function as a regulator, and the result is excess production of free intracellular cholesterol. No excess cholesterol production is observed when myeloma IgA is replaced by control IgG and IgA.
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PMID:Cholesterol synthesis by human fibroblasts in the presence of LDL and anti-LDL IgA. 22 98

Investigations performed in a patient with myeloma, hyperlipidemia, and xanthomatosis demonstrated the antilipoprotein activity of the monoclonal IgA directed against an antigenic site--called Ra.--different from those previously described. A complex IgA beta-lipoprotein has been firstly characterized. After isolation and purification of the IgA, it has been shown that the association between IgA and lipoprotein was immunologically mediated. The antibody is an IgA lambda bound via its Fab portion and in fixed combining ratio to an antigenic determinant shared only by LDL and VLDL of humans and some other mammalians to the exclusion of any other serum proteins. The results obtained with passive hemagglutination and inhibition of hemagglutination suggest that the antigenic site Ra. is not located on apoprotein B (major proteic moiety of LDL and VLDL), since the antigenic determinants of apolipoproteins are different in humans and in animals and since IgA Ra. fails to react with apolipoprotein B obtained by delipidation of LDL. On the other hand, the lack of reaction between IgA Ra. and HDL suggests that the antigenic determinant is not only present on the lipid hapten such as in the case of PG and AS determinants which are located on VLDL, LDL, and HDL from humans and animals. So the antigenic determinant revealed by IgA Ra. seems to be different from those previously described.
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PMID:[Monoclonal myelomatous IgA with antilipoprotein antibody activity of Ra specificity (author's transl)]. 51 6

This study was undertaken in 79 patients with retinal vein occlusion to assess the different systemic mechanisms contributing to the occlusion, namely, intrinsic vessel disease and abnormalities of the blood constituents and blood viscosity. In 55 patients older than 50 years of age, important associations were hypertension, abnormal results on glucose tolerance test, hyperlipidemia, chronic lung disease, and elevated serum IgA levels. In the 24 patients younger than 50 years of age, male incidence was high and important associations were head injuries, hyperlipidemia, and the use of estrogen-containing preparations. Hyperviscosity and cryofibrinogenemia were prominent in both groups. The pathogenesis of retinal venous occlusion is complex involving interaction between the vessel wall and blood constituents.
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PMID:Systemic factors contributory to retinal vein occlusion. 62 51

Autoimmune hyperlipidemia (AIH) may be induced a variety of antibodies which inhibit different stages of the lipolytic process by which the lipid load is removed from the circulating lipoproteins. In a patient having a monoclonal gammopathy and a nephrotic syndrome with a glomerulonephritis and a marked hypertriglyceridemia, it was found previously that the monoclonal IgG gamma Lac. reacted with human VLDL as well as with human serum albumin. Here it is demonstrated that the purified IgG gamma inhibits the lipolysis of triglyceride substrates by reacting with a substance (Lac. S) necessary for lipoprotein lipase activity. The interaction of IgG lambda Lac. with serum or HDL-activated triglyceride substrates inhibits the lipolytic activity of human and rat plasma post heparin and also adipose tissue lipases. It slightly inhibits the activity of swine pancreatic lipases. The Lac S. which reacts with IgG Lac. is associated to whole and delipidated VLDL and HDL and not to LDL or purified APo-A. It may be an Apo-C or a non-peptidic co-factor of the lipases which remains bound to the apoprotein core after delipidation. Its lack of species specificity and its presence as traces in HSA preparations favors the latter hypothesis. The Lac. substances is different from the Pg and As substances which were found to react with IgA anti-Pg and IgG anti-As antibodies in previously reported antilipoprotein AIH.
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PMID:Inhibition of lipoprotein lipase activity by a monoclonal immunoglobulin in autoimmune hyperlipidemia. 83 49

A 69-year-old white male with autoimmune hyperlipidemia for 19 years characterized by high serum levels (1,5000 to 3,400 mg. per deciliter) of IgA firmly bound to very-low- and low-density lipoproteins (serum total cholesterol 852 +/- 51 mg./dl., free cholesterol 340 +/- 52, triglyceride 1638 +/- 411, phospholipid 934 +/- 84) received intravenously a tracer dose of cholesterol-4-14C. Serum cholesterol specific activity was followed for 337 days and analyzed by two methods: (1) compartmental analysis which revealed the best fit of a two-compartment model with rapidly exchangeable pool 710 gm. (2,563 per cent of the mean of 15 normal subjects), slowly exchangeable pool 317 gm. (651 per cent), mean transit time 92.5 days (167 per cent), turnover rate 9.23 gm. per day (654 per cent), and excretory coefficient 0.013 (25 per cent); (2) a simulated five-compartment model involving serum free, esterified, red blood cell, and rapidly and slowly exchangeable tissue cholesterols for which pool sizes of 17, 25, 2.4, 674, and 350 gm., respectively, were calculated and a turnover rate of 9.44 gm./day agreed well with that of the two-compartment model. The extreme hyperlipoproteinemia and expanded body cholesterol pools were primarily due to the impairment of feedback control of cholesterol synthesis as a consequence of the complexing of lipoprotein and IgA.
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PMID:Cholesterol dynamics in autoimmune hyperlipidemia. 97 40

Eight patients with end-stage renal failure (plasma albumin less than 35 g/l) who were established on glucose CAPD exchanges, were studied for 4-week periods before, and after 12 weeks when 1% amino-acid solution had been used for the morning exchange. Anthropometric, biochemical, clinical and dietary assessments were made every 4 weeks. Dietary intakes of protein and calories were maintained. Studies with amino-acid solutions showed a mean of 13% and 8% amino acids remaining in the dialysate after 6 and 8 h respectively. Plasma amino acids increased to a maximum after 2 h of dialysis; however, fasting concentrations were constant over the 5 months. Osmolality of amino acids decreased comparably with 1.36% glucose during 8-h exchanges although the recovery of fluid was marginally less. Plasma transferrin increased significantly after 8 weeks of amino acids but subsequently decreased in one patient due to infection. No significant changes occurred in albumin, apolipoprotein A, IgG, IgA or prealbumin. Cholesterol and apolipoprotein B decreased in seven patients but increased in one due to rising calorie intake. Increases in urea and decreases in bicarbonate were not clinically significant. Amino-acid-based fluid was well tolerated with modest nutritional benefit and reduction in hyperlipidaemia. Optimal effects of amino acids are likely at higher concentrations using two or more exchanges in patients eating less than 0.9 g protein/kg per day.
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PMID:The use of an amino-acid-based CAPD fluid over 12 weeks. 250 36

Serum was examined for a cytotoxic effect on cultured human fibroblasts, using 8 normal controls and 4 patients. Three of the patients had secondary lipidoses associated with monoclonal gammapathies of IgA kappa, IgG kappa and IgG lambda types. The fourth had systemic lupus erythematosus (SLE) with hyperlipidemia. Only serum containing the monoclonal IgG lambda was found to be cytotoxic. This circulating IgG lambda was strongly bound to HDL and behaved like an antilipoprotein antibody. The circulating immune complexes may be the serum factor responsible for the cytotoxicity and the cutaneous plane xanthomas, thus giving another example of 'antibody-dependent' cellular cytotoxicity previously described for endothelial cells in other diseases.
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PMID:Cytotoxic effect of serum on fibroblasts in one case of normolipidemic plane xanthoma and myeloma IgG lambda. 309 2

In autoimmune hyper- or dislipidemia secondary to a monoclonal antilipoprotein gammapathy, immunoglobulin-lipoprotein (Ig-Lp) complexes are found in the circulating blood. In order to determine their possible significance in common types of hyperlipidemia we compared the Ig-Lp content of sera from 98 healthy blood donors and 155 outpatients from a Lipid Clinic, including 91 cases of hypercholesterolemia (55 familial and 36 non-familial), 15 cases of hypertriglyceridemia, 20 cases of mixed hyperlipidemia and 29 miscellaneous cases. Detection of the Ig-Lp was performed by an ELISA technique with polyclonal affinity purified anti-LDL + HDL as capture antibodies and peroxidase-labeled anti-Ig antibodies specific for IgA, IgG, IgM heavy chains as indicators. Two cases of monoclonal gammapathy (one IgA K and one IgG L) with dislipidemia served as positive controls for the test. IgG, IgA and IgM Lp were found in the sera of the blood donors, in very small quantities when compared with the monoclonal gammapathy cases. All three types of Ig-Lp were also found in the different hyperlipidemic populations studied. When blood donors were compared to hyperlipidemic patients, no difference was observed for IgG Lp. A significant increase in IgM Lp was found in patients with familial hypercholesterolemia (P less than 0.01). An increase in IgA Lp was also found in hypercholesterolemia, familial or not (P less than 0.01), and in patients with corneal arcus (P less than 0.0001), ischaemic disease (P less than 0.01), tendon xanthomas (P less than 0.05) or xanthelasma (P less than 0.05). Furthermore, in a group of 18 paired parents from 9 different families, positive interparent correlations were found for IgM Lp (r = 0.78; P = 0.013) and IgG Lp (r = 0.69; P = 0.038). Therefore IgM Lp may be markers for subpopulations of familial hypercholesterolemia, and IgA Lp markers for the risk of atherosclerotic ischemic disease and deposition of lipids in the cornea. It may be (1) that natural clones of autoanti-lipoprotein antibodies are responsible for the minute quantities of Ig-Lp found in normal people; (2) that the marked development of one of these clones is the cause of autoimmune hyper- or dyslipidemia and xanthomatosis associated with monoclonal gammapathy; (3) that the limited development of a clone produces the Ig-Lp particles found in hypercholesterolemic patients; (4) that there are types of Ig-Lp particles (IgA Lp) that may be harmful for tissues independently of hypercholesterolemia.
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PMID:Immunoglobulin-bound lipoproteins (Ig-Lp) as markers of familial hypercholesterolemia, xanthomatosis and atherosclerosis. 324 Mar 31

Human low density lipoproteins are metabolized by cultured human fibroblasts, through a specific metabolic pathway, which entails the regulation of intracellular cholesterol synthesis. When anti-lipoprotein IgA coming from patients with myeloma, mixed hyperlipidaemia and xanthomatosis were introduced into the system, we observed a decrease of the protein degradation of the LDL molecule, and a disappearance of the regulation of intracellular cholesterol synthesis. In the same system, an anti-lipoprotein IgA from a case of myeloma with mixed hyperlipidaemia, but without xanthomatosis, or control IgG and IgA were inactive and did not modify the LDL pathway.
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PMID:Interaction between fibroblasts, lipoproteins and three antilipoproteins IgA kappa. 677 Oct 77


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