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 evaluated the effect of hemolysis, icteric discoloration, lipemia, paraproteinemia, and uremia on enzymatic methods for determining sodium, potassium, and chloride, according to the National Committee for Clinical Laboratory Standards EP7-P proposals for testing interference from endogenous substances. The sodium, potassium, and chloride assays (reagent kits supplied by Boehringer Mannheim) were based on electrolyte-dependent beta-galactosidase, pyruvate kinase, and alpha-amylase, respectively. The results were compared with those obtained by indirect ion-selective electrodes (ISE), which in turn had been validated by flame photometry. We analyzed the samples with Hitachi 717, 737, and 911 chemistry analyzers and with an IL943 flame photometer. The enzymatic results were in good agreement with those by ISE, the interference-related differences generally being without clinical significance; however, none of the enzymatic methods could analyze grossly lipemic samples.
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PMID:Enzymatic determination of sodium, potassium, and chloride in abnormal (hemolyzed, icteric, lipemic, paraproteinemic, or uremic) serum samples compared with indirect determination with ion-selective electrodes. 804 91

The possible increase in total and low-density lipoprotein cholesterol following severe restriction of dietary NaCl was reported in 1990 and and 1991 from three experiments, one in the United States and two in Germany. Each of these experiments lasted only 1 week. To evaluate the clinical side effects we analyzed data collected from patients who completed a course of NaCl-restricted weight reduction at the Duke Diet and Fitness Center. Observations of lipid changes are not available for periods of less than 3 weeks; however, we were able to collect data on lipid and lipoprotein changes from 556 participants 25 days after they were referred for weight reduction. Total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels returned to normal in the majority of obese patients. In our slightly longer observation period in patients on a 1000 mg NaCl restricted diet we found no evidence of hyperlipidemic side effects. We believe that the hyperlipidemia resulting from severe sodium restriction in non-hypertensive, normal-weight individuals is not relevant to the problem of nonpharmacological and diuretic treatment of obese hypertensive patients. In clinically healthy, normal-weight, normotensive individuals severe salt restriction serves no practical or therapeutic purpose.
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PMID:Influence of dietary sodium restriction on lipid metabolism. 812 57

Gout is a disease caused by deposits of sodium urate crystals in tissues. This disease, already known of Hippocrates, is now due to new causes, notably iatrogenic, and has new clinical forms. The typical initial attack usually occurs in men in their fifties and affects the big toe; in the absence of treatment it evolves towards chronic tophaceous gout. When gout occurs in subjects younger than 30 years, these must be investigated for enzyme deficit which is usually partial. The incidence of gout in women is ever increasing, being encouraged by treatments with diuretic drugs. Gout is often atypical, affecting predominantly the hands and with rapid development of tophus. In transplanted patients other drugs, such as cyclosporin, may induce an early, polyarticular and tophaceous gout. Alcohol is a facilitating factor of hyperuricaemia. Disturbances of metabolism, such as hyperlipidaemia, obesity or arterial hypertension, are often associated with hyperuricaemia. With an early and well-conducted treatment the passage to chronicity and the occurrence of complications can be avoided.
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PMID:[What remains of gout in 1993?]. 817 71

The nephrotic syndrome is a consequence of urinary loss of intermediate-sized plasma proteins and the resulting homeostatic responses to those losses. Plasma protein composition is changed greatly. Pathophysiologic changes are a consequence of the nature of the proteins lost and of the proteins that are increased in plasma to replace them. Plasma oncotic pressure (pi) falls because of the replacement of relatively small plasma proteins by larger ones. Decreased pi increases transudation of fluid into the interstitium and favors edema. This is exacerbated by causing renal insensitivity to atrial natriuretic factor (ANF), primary renal sodium retention, and plasma volume expansion. Many proteins lost in the urine, such as erythropoietin and IgG, are not defended by increased synthesis. Their loss may result in reduced immunity, anemia, and endocrinopathies. Albumin synthesis can be increased by dietary protein augmentation; however, urinary protein losses also increase, offsetting any palliative effect of increased albumin synthesis on albumin stores. The synthesis of many other proteins secreted by the liver is also increased, causing an elevation in plasma levels of several large proteins, including lipoproteins and elements of the coagulation cascade. This results in hyperlipidemia and, in conjunction with the urinary loss of smaller proteins that impede coagulation, a hypercoagulable state. Lipoprotein catabolism is also reduced as a consequence of proteinuria contributing to increased lipid levels.
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PMID:Nonrenal complications of the nephrotic syndrome. 819 77

The plasma concentration, particle size, and chemical composition of high density lipoproteins (HDLs) are associated with the metabolism of triglyceride-rich lipoproteins (TGRLs). During alimentary lipemia there is active exchange of lipids and apolipoproteins between HDL and apolipoprotein B-containing lipoproteins. Whereas HDL has been assigned a protective role against the development of atherosclerosis, alimentary lipemia has been proposed to represent a potentially atherogenic state. We examined plasma HDL concentration, particle size, and composition and their relations to postprandial TGRLs in 32 postinfarction patients and 10 healthy control subjects after intake of a standardized oral fat load of a mixed-meal type. All patients had undergone coronary angiographies in connection with the myocardial infarction and around 5 years thereafter. The plasma HDL cholesterol concentration decreased significantly in response to the oral fat load, particularly in hypertriglyceridemic patients, with a concomitant increase of HDL triglycerides. A limited and reversible yet consistent increase of HDL particle size (1-2%) was seen 6 hours after intake of the oral fat load on nondenaturing gradient gel electrophoresis (GGE) in both patients and control subjects. Virtually no changes in the plasma concentration of HDL GGE subclasses, lipoproteins containing apolipoprotein A-I but no apolipoprotein A-II (LpA-I), or lipoproteins containing both apolipoproteins A-I and A-II (LpA-I:A-II) were induced in the postprandial state despite massive increases of large very low density lipoprotein (VLDL) and large chylomicron remnant levels (determined as apolipoproteins B-100 and B-48 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis). Strong inverse correlations with fasting plasma HDL cholesterol and the larger HDL GGE subspecies were found for large postprandial VLDL and large chylomicron remnants, whereas the corresponding relations for small VLDL and small chylomicron remnants were weaker. The relations of both large and small VLDL and chylomicron remnants to HDL cholesterol were confined to subjects in the lower fasting plasma HDL cholesterol range (< 1.2 mmol/l). None of the HDL parameters measured, either in the fasting or in the postprandial state (HDL cholesterol, HDL triglycerides, HDL GGE subclasses, LpA-I, and LpA-I:A-II), were related to the development of coronary atherosclerosis, whereas the postprandial plasma levels of small chylomicron remnants, which showed weak negative correlations with HDL, related positively to the progression of coronary atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:HDLs and alimentary lipemia. Studies in men with previous myocardial infarction at a young age. 842 32

Elevated fasting plasma cholesterol concentrations were identified in clinically healthy briards. Biochemical investigations revealed no other major abnormalities. Plasma lipoprotein electrophoresis demonstrated a marked increase in the intensity of the alpha 2 band (compared with control dogs) which was reduced by dextran sulphate-magnesium chloride or sodium phosphotungstate-magnesium chloride precipitation of apo B and apo E containing lipoproteins in the plasma. The study has identified a hyperlipidaemia in briards characterised by increased cholesterol but normal triglyceride concentrations. The absence of obvious metabolic changes associated with secondary hypercholesterolaemia, suggests the breed may have a primary abnormality in cholesterol metabolism. The increased density of the precipitable lipoprotein which migrates to the alpha 2 band suggests that the hypercholesterolaemia may be due to an abnormal accumulation of high density lipoprotein (HDL) possibly HDLc. The possibility that abnormality in lipid metabolism might play a role in the development of retinal pigment epithelial dystrophy in briards is currently being investigated.
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PMID:Hypercholesterolaemia in briards in the United Kingdom. 843 53

Insulin resistance in Type 1 (insulin-dependent) diabetes mellitus may be associated with raised erythrocyte sodium-lithium countertransport activity in patients with hypertension, or nephropathy, or both. However, in these circumstances it is difficult to separate the impact of hypertension, hyperlipidaemia and nephropathy on erythrocyte sodium-lithium countertransport from that of insulin resistance. We have therefore examined the relationship between insulin-mediated glucose disposal and erythrocyte sodium-lithium countertransport in 41 normotensive (mean blood pressure 120/74 mmHg), normoalbuminuric (mean albumin excretion 6.2 micrograms/min), normolipidaemic (mean serum cholesterol 4.3 mmol/l and mean serum triglycerides 1.0 mmol/l) Type 1 diabetic patients. Erythrocyte sodium-lithium countertransport was on average 0.31 mmol Li.h-1.l erythrocytes-1 (range 0.07-0.69). Nine patients had values above 0.40 mmol Li.h-1.l erythrocytes-1 (0.51 +/- 0.10 mmol Li.h-1.l erythrocytes-1). The patients with high erythrocyte sodium-lithium countertransport were matched for age, sex, BMI, HbA1 and duration of diabetes, with nine patients with normal erythrocyte sodium-lithium countertransport. Insulin-mediated glucose disposal was evaluated during the last hour of a euglycaemic clamp (insulin 0.015 U.kg-1.h-1; blood glucose clamped at 7.0 mmol/l). The free insulin levels were comparable between the patients with high and normal erythrocyte sodium-lithium countertransport (37.2 +/- 14.7 mU/l and 34.7 +/- 17.2 mU/l respectively). Insulin-mediated glucose disposal was on average 3.1 +/- 1.5 (range 0.8-6.8) mg.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Erythrocyte sodium-lithium countertransport activity and total body insulin-mediated glucose disposal in normoalbuminuric normotensive type 1 (insulin-dependent) diabetic patients. 843 53

Insulin resistance resolved in 3 dogs with hypothyroidism and diabetes mellitus after treatment with sodium levothyroxine. A thorough diagnostic evaluation failed to identify any other cause of insulin resistance in these dogs. Hypothyroidism was diagnosed in each dog on the basis of clinical signs, physical findings, hyperlipidemia, and results of thyrotropin or thyrotropin-releasing hormone stimulation test. Hypoglycemia was documented in each dog within 2 weeks of starting sodium levothyroxine administration. The insulin dosage was decreased by 60 to 62% during the ensuing months and good glycemic control was obtained at these lower insulin dosages in all dogs. These findings would suggest hypothyroidism-induced insulin resistance in these dogs.
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PMID:Insulin resistance in three dogs with hypothyroidism and diabetes mellitus. 849 4

As compared to 7 normolipidemic donors, the maximal velocity of sodium-lithium countertransport was accelerated by nearly 70% in 10 patients with elevated levels of triglyceride-rich lipoproteins and tended to be stimulated also in 5 patients with hypercholesterolemia. No significant differences were observed between normolipidemia and both hyperlipidemic groups for the apparent affinities of the transport system for intracellular sodium and extracellular lithium. Strong positive relations of the maximal activity of sodium-lithium countertransport to the percentages of red cell membrane phosphatidylcholine (r = 0.85, 2P < 0.001), the phosphatidylcholine/sphingomyelin (r = 0.82, 2P < 0.001) and the phosphatidylcholine/phosphatidylethanolamine ratio (r = 0.81, 2P < 0.001) were seen in all donors. A negative correlation was found to membrane sphingomyelin (r = -0.72, 2P < 0.001). Also plasma phosphatidylcholine and sphingomyelin exhibited positive and negative associations, respectively, to the maximal activity of sodium-lithium countertransport (r = 0.66, 2P < 0.01 and r = -0.78, 2P < 0.001). Among several plasma lipoprotein parameters investigated, total triglycerides or VLDL cholesterol levels showed independent relations to both the plasma and the membrane phosphatidylcholine/sphingomyelin ratio as well as to the maximal velocity of sodium-lithium countertransport. The results indicate that an increase in red cell membrane phosphatidylcholine and a concomitant fall in sphingomyelin are closely associated with the acceleration of sodium-lithium countertransport in hyperlipidemia.
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PMID:Relations of sodium-lithium countertransport kinetics to plasma and red cell membrane phospholipids in hyperlipidemia. 850 44

Patients who develop diabetic nephropathy, one of the leading causes of end-stage renal diseases in Western communities, have an increased red cell Li+/Na+ countertransport (CT). Li+/Na+ CT is a membrane function which exchanges intracellular Li for extracellular Na in vitro. High Li+/Na+ CT reflects abnormal kinetic properties of red cell membrane Na/H exchange. A widespread abnormality of Na/H exchange could play a major role in the pathogenesis of diabetic nephropathy as well as of cardiovascular diseases since Na/H exchange is involved in the regulation of cell pH and cell volume; in the cellular response to hormones, mitogens, and growth factors; and in the renal reabsorption of Na and bicarbonate. Li+/Na+ CT is under genetic control and raised in a subgroup of patients with essential hypertension. Among these patients, high Li+/Na+ CT is associated with increased glomerular filtration rate, filtration fraction, proximal fractional Na reabsorption, microalbuminuria, plasma renin activity, and kidney and cardiac volume. Increased Li+/Na+ CT is often associated with hyperlipidemia, hyperuricemia, reduced insulin sensitivity, and obesity. The whole of these observations may explain why patients with diabetes or essential hypertension and increased Li/Na CT are at risk of early renal and cardiac impairment.
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PMID:Red blood cell Li+/Na+ exchange in patients with diabetic nephropathy and essential hypertension: therapeutic implications. 851 86


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