Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed interference studies for IgG, IgA, IgM, haptoglobin, and alpha1-antitrypsin assayed in serum, using either fixed-time nephelometry on the BN 100 from Behring or rate nephelometry on two analyzers from Beckman Instruments. For clear serum samples, results for IgG, IgA, IgM, and haptoglobin obtained with the three nephelometers showed good agreement. Values for alpha1-antitrypsin in clear sera were lower with the BN 100 than with the Array 360 or Immage. In lipemic samples, the BN 100 gave higher values than the Array 360 or Immage for all analytes except IgG. Addition of Intralipid to serum produced atypical reactions with the BN 100 (fixed-time nephelometry) but not with the Array 360 or Immage (rate nephelometry). The interference of lipemia on the BN 100 was also seen when the Beckman antibody was used, indicating that the effect was reagent-independent. For hemolyzed samples, the BN 100 gave higher values than the Array 360 or Immage for haptoglobin but not for the other analytes. Addition of increasing amounts of a hemolysate to serum revealed a negative interference in all assay systems. This effect was more pronounced with the Beckman reagent than with the Behring reagent in all three nephelometers and was independent of the type of instrument (fixed-time vs rate nephelometry).
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PMID:Evaluation of interferences in rate and fixed-time nephelometric assays of specific serum proteins. 989 39

A calf having extremely high concentrations of triglycerides, cholesterol and phospholipids, in particular in chylomicrons (CM) and very low-density lipoprotein (VLDL) fraction was found. The purpose of the present study was to determine serum concentration and distribution of apolipoprotein (apo) C-III, a low molecular mass protein mainly distributed in high-density lipoprotein (HDL) fraction in normolipidemic cattle, in the calf with hyperlipidemia. The serum apoC-III concentration in the calf increased to more than 10-fold that of normolipidemic control calves, and apoC-III was distributed more in the CM than in the HDL. The concentration of apoA-I (a predominant apoprotein in the HDL) was also increased to nearly 4-fold that of controls in the serum from the calf, and its major distribution site was the CM. Haptoglobin was detected in the serum from the hyperlipidemic calf, and was distributed in the CM as well as in the HDL. Serum amyloid A was also induced. In contrast to apoC-III, apoA-I and haptoglobin, the majority of apoSAA was found in the HDL fraction, as observed in normolipidemic calves. Increased concentrations in the CM of apoC-III and apoA-I suggest that the two apolipoproteins may be involved in the pathogenesis of calf hyperlipidemia. The presence of haptoglobin in the CM and HDL also implies the relevance of this acute-phase protein in the regulation of lipid metabolism.
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PMID:Increased serum concentration of apolipoprotein C-III and its greater distribution to chylomicrons than to the high-density lipoprotein fraction in a calf with hyperlipidemia. 1107 72

This article describes the first autopsy case of heme oxygenase (HO)-1 deficiency. A 6-year-old boy who presented with growth retardation; anemia; leukocytosis; thrombocytosis; coagulation abnormality; elevated levels of haptoglobin, ferritin, and heme in serum; a low serum bilirubin concentration; and hyperlipidemia was diagnosed as HO-1 deficient by gene analysis several months before death. Autopsy showed amyloid deposits in the liver and adrenal glands and mesangioproliferative glomerular changes in kidneys, in addition to an irregular distribution of foamy macrophages with iron pigments. Fatty streaks and fibrous plaques were noted in the aorta. Compared with HO-1--targeted mice, the present case seems to more severely involve endothelial cells and the reticuloendothelial system, resulting in intravascular hemolysis, disseminated intravascular coagulation, and amyloidosis with a short survival. This contrasts to the predominant iron metabolic disorders of HO-1--targeted mice with a long survival.
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PMID:Heme oxygenase-1 deficiency: the first autopsy case. 1182 83

The Incstar(R) SPQ II human haptoglobin (Hpt) (Incstar Corporation, Stillwater, MN) immunoturbidimetric assay was validated for the determination of serum and plasma Hpt concentrations in dogs and horses. The anti-human Hpt antiserum supplied with the assay, displayed monospecificity to both dog and horse serum Hpt by immunoelectrophoresis and Western blotting techniques. The automated immunoturbidimetric assay results correlated well with the cyanmethemoglobin binding assay (r=0.953 for canine serum and r=0.941 for equine serum), and had excellent precision at both high and low serum Hpt concentrations (within run and between run coefficients of variation near or less than 5%). The assay was linear in both species by serial dilution of pooled-high serum with pooled-low serum, saline and with Hpt-free serum. Interference from hemolysis (> 25 mg/dl hemoglobin) and lipemia greater than 100 mg/dl caused a false decrease and false increase respectively in Hpt yield with the immunoturbidimetric assay. The anti-Hpt antibody supplied with the assay kit, once diluted with polymer diluent and stored at 4 degrees C, was stable for up to 6 days and gave consistent results.
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PMID:Validation of human haptoglobin immunoturbidimetric assay for detection of haptoglobin in equine and canine serum and plasma. 1266 Sep 62

The influence of interference by hemolysis, icterus and lipemia on the results of routine chemistries may lead to wrong interpretations. On Synchron LX-20 instruments (Beckman Coulter) serum or plasma indices can be used as reliable semi-quantitative measures of the magnitude of such interference. In an article recently published in this journal, we presented the results of a multicenter study carried out in Dutch hospitals in which we determined cutoff indices for analytes above which analytically significant interference exists. Clinically significant interference cutoff indices were also derived for these analytes. In this article, we describe the handling of patient samples with clinically significant interference by hemolysis, icterus or lipemia. We investigated several possible approaches for correction of the result: dilution of the interference; mathematical correction in the case of hemolysis; treatment with ferrocyanide to destroy bilirubin; and removal of lipids in lipemic patient samples. We concluded, that mathematical correction of potassium or lactate dehydrogenase results in hemolytic samples can only be carried out if intravascular hemolysis is ruled out. Hemoglobin quantification in serial patient samples, combined with measurement of haptoglobin, represents a useful tool to rule out in vivo hemolysis. We derived an algorithm for this situation. We do not simply recommend mathematical correction, unless it is clinically acceptable. We present formulas for potassium and lactate dehydrogenase: corrected potassium=measured potassium-(hemolytic index increment x 0.14); corrected lactate dehydrogenase=measured lactate dehydrogenase-(hemolytic index increment x 75). The dilution studies indicated that dilution is only applicable for bilirubin, C-reactive protein and iron. The results of treatment with ferrocyanide were poor, and we do not recommend this method. Removal of lipids using high-speed centrifugation or LipoClear (StatSpin Inc.), a non-toxic and non-ionic polymer, is a very effective approach, although C-reactive protein, creatine kinase-MB (CK-MB) and cholesterol cannot be removed using LipoClear. For all interferants (hemoglobin, bilirubin, lipids), relatively simple algorithms are derived that can easily be implemented in the clinical laboratory.
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PMID:Correction of patient results for Beckman Coulter LX-20 assays affected by interference due to hemoglobin, bilirubin or lipids: a practical approach. 1724 28

Hemoglobin (Hb) uniquely associates with proinflammatory HDL in atherogenic mice and coronary heart disease (CHD) patients. In this paper, we report that Hb and its scavenger proteins, haptoglobin (Hp) and hemopexin (Hx) are significantly increased in apoA-1-containing particles of HDL both in mouse models of hyperlipidemia and in CHD patients, when compared with wild type mice and healthy donors, respectively. We further demonstrate that the association of Hb, Hp, and Hx proteins with HDL positively correlates with inflammatory properties of HDL and systemic inflammation in CHD patients. Interestingly, HDL from Hp(-/-) mice under atherogenic conditions does not accumulate Hb and is anti-inflammatory, suggesting that (i) Hp is required for the association of Hb with HDL and (ii) Hb x Hp complexes regulate the inflammatory properties of HDL. Moreover, treatment of apoE(-/-) mice with an apoA-1 mimetic peptide resulted in significant dissociation of Hb x Hp complexes from HDL and improvement of HDL inflammatory properties. Our data strongly suggest that HDL can become proinflammatory via the Hb x Hp pathway in mice and humans, and dissociation of Hb x Hp x Hx complexes from apoA-1-containing particles of HDL may be a novel target for the treatment of CHD.
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PMID:Hemoglobin and its scavenger protein haptoglobin associate with apoA-1-containing particles and influence the inflammatory properties and function of high density lipoprotein. 1943 79

To investigate the influence of diet on serum protein pattern, mice were fed for 8 weeks either control chow or a high-fat diet (containing 21 % w/w milk fat and 0.2 % w/w cholesterol); sera were collected and analyzed by 2-DE. The main positive acute-phase reactant proteins, haptoglobin and hemopexin, were significantly up-regulated in animals receiving the high-fat diet. Data on all other proteins also pointed to an inflammatory condition in these animals. The largest change in concentration was observed for carboxylesterase N, a circulating enzyme seldom connected with lipid metabolism in earlier reports. These observations agree with the notion of a link between diet-induced hyperlipidemia and the inflammatory component of its cardiovascular sequels in humans, but the effects in the experimental animals are massive and obviously affect most of the major serum proteins.
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PMID:Inflammatory serum proteome pattern in mice fed a high-fat diet. 2322 24

Intravascular hemolysis produces injury in a variety of human diseases including hemoglobinopathies, malaria, and sepsis. The adverse effects of increased plasma hemoglobin are partly mediated by depletion of nitric oxide (NO) and result in vasoconstriction. Circulating plasma proteins haptoglobin and hemopexin scavenge extracellular hemoglobin and cell-free heme, respectively. The ability of human haptoglobin or hemopexin to inhibit the adverse effects of NO scavenging by circulating murine hemoglobin was tested in C57Bl/6 mice. In healthy awake mice, the systemic hemodynamic effects of intravenous coinfusion of cell-free hemoglobin and exogenous haptoglobin or of cell-free hemoglobin and hemopexin were compared with the hemodynamic effects of infusion of cell-free hemoglobin or control protein (albumin) alone. We also studied the hemodynamic effects of infusing hemoglobin and haptoglobin as well as injecting either hemoglobin or albumin alone in mice fed a high-fat diet (HFD) and in diabetic (db/db) mice. Coinfusion of a 1:1 weight ratio of haptoglobin but not hemopexin with cell-free hemoglobin prevented hemoglobin-induced systemic hypertension in healthy awake mice. In mice fed a HFD and in diabetic mice, coinfusion of haptoglobin mixed with an equal mass of cell-free hemoglobin did not reverse hemoglobin-induced hypertension. Haptoglobin retained cell-free hemoglobin in plasma, but neither haptoglobin nor hemopexin affected the ability of hemoglobin to scavenge NO ex vivo. In conclusion, in healthy C57Bl/6 mice with normal endothelium, coadministration of haptoglobin but not hemopexin with cell-free hemoglobin prevents acute hemoglobin-induced systemic hypertension by compartmentalizing cell-free hemoglobin in plasma. In murine diseases associated with endothelial dysfunction, haptoglobin therapy appears to be insufficient to prevent hemoglobin-induced vasoconstriction.NEW & NOTEWORTHY Coadministraton of haptoglobin but not hemopexin with cell-free hemoglobin prevents hemoglobin-induced systemic hypertension in mice with a normal endothelium. In contrast, treatment with the same amount of haptoglobin is unable to prevent hemoglobin-induced vasoconstriction in mice with hyperlipidemia or diabetes mellitus, disorders that are associated with endothelial dysfunction.
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PMID:Endothelial dysfunction inhibits the ability of haptoglobin to prevent hemoglobin-induced hypertension. 2831 63