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

The Corning 940 Titrator, which measures total calcium concentration by titration with [ethylenebis(oxyethylenenitrilo)]tetraacetic acid, was evaluated for use in hospital laboratory. Calcium values for patients' sera were about 0.3 mg/dl lower as measured with the Titrator than with the Technicon SMA 12/60 continuous-flow analyzer. A similar bias was evident when the results with the Titrator were compared with those from atomic absorption spectrophotometry. Agreement was better in the low range and worse in the high range. Within-day and between-day coefficients of variation on the Titrator were about 1.5% and 2.5%, respectively. We saw no interference from magnesium, phosphorus, bilirubin, or in the presence of lipemia. At extremely increased hemoglobin concentrations (500 mg/dl), there is a 5% inhibition. Titrator results for patients' urine samples correlated closely (n = 0.999) with those obtained with the SMA 12/60.
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PMID:Evaluation of the Corning 940 Calcium Titator for use with serum and urine. 111 34

Prolonged exposure (4 weeks) to 6.72 ppb of the organochlorine insecticide endosulfan induced disturbances in the blood and organ chemistry values of a common fish, Barbus conchonius. In blood the total lipids, cholesterol, and proteins were decreased in comparison to unexposed controls, while the free fatty acids (FFA), glucose, total phosphorus, and lactate were increased. Total lipids, FFA, and proteins were augmented in liver; cholesterol, in liver and ovary; and phosphorus and glycogen, in skeletal muscles. Compared to the controls, a decrease was seen in the total lipids (skeletal muscles and ovary), glycogen (liver, brain, and heart), and cholesterol (testes). Hyperlipemia, hyperproteinemia, and hyperlactemia persisted during a recovery period of 1 week in clean water following endosulfan poisoning.
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PMID:Effects of endosulfan on the blood and organ chemistry of freshwater fish, Barbus conchonius Hamilton. 206 Apr 89

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11

Patients who lose more than 50% of their functioning renal mass are at risk to develop progressive deterioration of their remaining kidney function, even though the process that caused the original loss of kidney function may no longer be present. The glomerular capillary hyperperfusion, hypertension, and hyperfiltration that occur in the surviving nephrons may play an important role in the natural tendency for renal function to deteriorate. Nevertheless, recent studies suggest that these glomerular hemodynamic events may not be the final common pathway for the natural deterioration of renal function, as was once thought. With regard to the general management of patients with impaired renal function, recent evidence suggests that controlling systemic blood pressure, reducing dietary protein and phosphorus intake, and controlling hyperlipidemia may be effective in slowing the loss of renal function.
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PMID:On the natural tendency to progressive loss of remaining kidney function in patients with impaired renal function. 219 55

Little notice has been paid in the surgical literature to problems with psychoeffective lithium, which by interfering with adenylate cyclase affects thyroid and parathyroid function, causing hypercalcemia, hyperparathyroidism, and hypothyroidism. Seven patients with lithiumogenic hyperparathyroidism occurring after years of lithium therapy underwent treatment and manifested osteoporosis (n = 2), hypertension (n = 2), nephrolithiasis (n = 1), coma (n = 1), rising hypercalcemia (n = 1), goitrous myxedema (n = 4), nephrogenic diabetes insipidus (n = 2), renal failure (n = 2), and hyperlipidemia (n = 1). Disease-directed parathyroidectomy (without morbidity) was curative. Unique laboratory findings included normal serum phosphorus and reduced urinary calcium and cyclic adenosine monophosphate values. Three separate cases of thyroid carcinoma after long-term lithium therapy were also treated, being preceded by myxedema (n = 2) and concurrent with hyperparathyroidism (n = 1). There has been only one previous report of lithium-associated thyroid carcinoma. All patients taking lithium should undergo surveillance for thyroid and parathyroid dysfunction and neoplasia, and appropriate surgical and medical treatment should be considered in each situation. Although hyperparathyroidism may be reversible with lithium discontinuance, such therapy may be obligatory for patient well-being, thus dictating parathyroidectomy.
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PMID:Lithiumogenic disorders of the thyroid and parathyroid glands as surgical disease. 224 24

A survey of dietitians at renal transplant centers in the United States was conducted to identify diet modifications currently used for nondiabetic adults after kidney transplantation. The survey focused on the diet recommended for the first 21 days after successful transplantation. Questionnaires were mailed to 100 centers randomly selected from a comprehensive list obtained through the Organ Transplant Coordinating Office of the Texas Medical Center, Houston. A 66% response rate was obtained. The results of the survey showed that dietitians were most frequently recommending 1.2 to 1.5 gm protein per kg body weight, 40% to 50% of total energy as carbohydrate, a fat intake of less than 30% of total energy, and an energy level consistent with achieving or maintaining desirable body weight. Sodium intake was most commonly restricted to 2 to 4 gm, whereas potassium and phosphorus intakes were individualized according to the patient's serum values. Comments on the returned questionnaires indicated that many institutions were reviewing and updating their transplant diet to include a polyunsaturated fat to saturated fat ratio and restrictions of cholesterol and simple sugars. The findings of the survey indicated that the renal transplant diet should focus on optimal protein and energy intake as well as restriction of simple sugars, total fat, cholesterol, and saturated fat to restore nitrogen balance and minimize clinical symptoms of post-transplant diabetes and hyperlipidemia.
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PMID:Renal transplant diet recommendations: results of a survey of renal dietitians in the United States. 234 58

The individual and combined effects of aflatoxin and deoxynivalenol (DON) were evaluated in young broiler chickens (Hubbard X Hubbard). The experimental design was a 2 X 2 factorial with treatments of 0 and 2.5 micrograms of aflatoxin/g of feed (ppm) and 0 and 16 micrograms of DON/g of feed. The broilers were maintained on these dietary treatments from hatching to 3 weeks of age in electrically heated batteries with feed and water available ad libitum. The aflatoxin treatment significantly (P less than .05) decreased body weight; weight gain; increased the relative weight of the spleen, liver, and kidney; induced hepatic hyperlipemia; decreased activity of lactic dehydrogenase; and decreased serum levels of protein, albumin, and phosphorus. The toxicity of DON was expressed through reduced growth rate, increased feed conversion; increased relative weight of the gizzard, anemia, decreased activity of lactic dehydrogenase, and decreased serum triglycerides. The interaction between aflatoxin and DON was characterized by reduced growth rates; increased feed conversion, increased relative weight of the proventriculus, gizzard, spleen, liver, and kidney, anemia, hepatic hyperlipemia, decreased activity of alkaline phosphatase, glutamic oxalacetic transaminase, and lactic dehydrogenase, and decreased serum levels of protein, albumin, uric acid, cholesterol, triglycerides, and calcium. These data demonstrate that both aflatoxin and DON can limit broiler performance and adversely effect broiler health. The effects of the combination of aflatoxin and DON on broiler performance and health was more severe than the individual effects of these mycotoxins; however, the interaction was not severe enough to represent toxic synergy and can best be characterized as additive toxicity.
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PMID:Individual and combined effects of aflatoxin and deoxynivalenol (DON, vomitoxin) in broiler chickens. 374 45

Evidence from animal and human studies indicate that calcium supplementation may ameliorate two risk factors for atherosclerotic cardiovascular disease, hypertension and hyperlipidemia. We sought to characterize dietary fat consumption and plasma lipid profiles in hypertensive and normotensive subjects and plasma lipid responses to supplemental calcium. A randomized, double-blind, placebo-controlled, crossover protocol was used to assess blood pressure and lipid response to 8 wk of 1000 mg of elemental calcium in 43 hypertensive and 27 normotensive subjects. Nutrient intakes and plasma lipids were measured repeatedly. Hypertensive female subjects consumed significantly less (p less than 0.05) phosphorus, potassium, and magnesium and had significantly higher triglycerides (p less than 0.04) and lower HDL-cholesterol (p less than 0.02) than did normotensive subjects. There were no significant changes in dietary plasma lipids with calcium supplementation. Mildly hyperlipidemic normotensive subjects had a significant decrease in total cholesterol (p less than 0.05). No significant changes in plasma lipids occurred with calcium supplementation in hypertensive subjects.
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PMID:Plasma lipids and hypertension: response to calcium supplementation. 379 5

A patient had hyperlipidemia associated with apparent hyperphosphatemia. Further tests on his serum and on the lipemic sera from 15 additional patients revealed a method-dependent overestimation of inorganic phosphorus values. The degree of overestimation was found to correlate positively with the serum triglyceride concentration. Unexplained elevation of the serum phosphorus level should alert the physician to the possibility of spurious hyperphosphatemia due to hyperlipidemia.
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PMID:Spurious hyperphosphatemia due to hyperlipidemia. 398 38

The chemical measurements on our Technicon SMAC of lipemic sera before and after clearing lipemia by ultracentrifugation showed that uric acid, creatinine, carbon dioxide, calcium, phosphorus, potassium, and alkaline phosphatase were not affected significantly by lipemia, whereas sodium, urea, glucose, chloride and total protein showed small but significant increases with averages of less than 1.9 percent. Albumin showed a significant decrease of 1.2 percent. In contrast, the results for the enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) showed striking differences between pre- and post-centrifuged sera in a number of specimens. With lactate dehydrogenase, thirty-two of fifty specimens registered an increase in activity while with the aminotransferases, thirty-five and forty-one out of fifty specimens showed a decrease in aspartate aminotransferase and alanine aminotransferase activities, respectively. Although much of the lipemic interference can be explained by the volume displacement of serum by lipids or by interference by lipemia with colorimetry, the anomalous effects observed with the enzymes indicate the possibility of other, as yet, undetermined factor(s).
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PMID:The effect of hyperlipidemia on Technicon SMAC measurements. 712 23


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