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

Anthropometric measurements, sixteen specific plasma proteins, triglycerides, cholesterol, urea and creatinine were measured at 4-monthly intervals for 1 year in 15 patients on CAPD. Delayed hypersensitivity skin tests were performed on 11 patients at the start and after 4 and 12 months. Body weight increased due mainly to a mean increase in 'calculated' body fat of 2.0 kg with increases in cholesterol, triglycerides and apolipoprotein B. Gain in fat correlated with the daily supply of dextrose in the dialysis fluid. Albumin, transferrin, prealbumin and retinol-binding protein decreased in 8 patients who intermittently ate less than 1.3 g protein/kg/day. A high concentration of dextrose in the dialysis fluid probably caused loss of appetite. Peritonitis resulted in increases in acute phase proteins although other plasma proteins decreased. Skin test responses indicated improvement in cell-mediated immunity during continuous ambulatory peritoneal dialysis (CAPD). The incidence of peritonitis and length of stay in hospital were greater in the patients who were hypoalbuminaemic probably due to impairment of the humoral mechanism. Dextrose in dialysis fluid may contribute to hyperlipidaemia and malnutrition with impairment of immunocompetence.
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PMID:Nutrition and delayed hypersensitivity during continuous ambulatory peritoneal dialysis in relation to peritonitis. 372 25

Glucose Tolerance Factor (GTF) is synthesized in vivo from absorbed dietary chromium, and acts as a physiological enhancer of insulin activity, binding to insulin and potentiating its action about three-fold. Since GTF is well absorbed orally, the development of sufficiently concentrated and stable supplementary sources of this agent may enable convenient and physiologically appropriate pharmacological modulation of insulin activity. A review of the numerous physiological actions of insulin suggests a number of therapeutic applications for GTF, in such diverse ailments as diabetes mellitus, hyperlipidemia, reactive hypoglycemia, obesity, cancer, protein malnutrition or malabsorption, endogenous depression, Parkinsonism, hypertension and cardiac arrhythmias. GTF supplementation may also have value in preventive medicine.
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PMID:The therapeutic potential of glucose tolerance factor. 700 27

A high rate of cardiovascular death in renal patients, particularly patients with endstage renal failure, has not been well appreciated in the past. It is obvious that cardiovascular lesions are more severe than can be explained by the classical risk factors of elevated blood pressure and dyslipidemia. In renal failure, a number of pathomechanisms are operative which may be paradigms of more general relevance, e.g. activation of the renin and sympathetic system, inhibition of the vasoconstrictor NO system, left ventricular hypertrophy in excess of what is expected for high blood pressure. A paradox inverse relation between lipid concentrations and cardiovascular death, i.e. a protective effect of hyperlipidemia, in dialysed patients, presumably results from the confounding effect of malnutrition, high lipid levels being a substitute marker of adequate nutrition.
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PMID:Excess cardiovascular mortality in the uremic patient--what does it teach for other risk factors in the non-renal patient? 773 91

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.
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PMID:Magnesium and ageing. II. Clinical data: aetiological mechanisms and pathophysiological consequences of magnesium deficit in the elderly. 815 90

Malnutrition as the cause of developing atherosclerosis is undoubtedly of major importance. For that reason, proper nutrition and eating habits among the population is of specific significance in preventive medicine. In order to establish a more pronounced food consciousness among the population of Styria, a questionnaire was issued to 1.354 persons attending the Graz Autumn Fair in 1991. The results showed above all that approximately 40% of the subjects investigated presented a disease due to malnutrition and metabolic disorder, mainly hyperlipidemia. The choice of various foods varied according to male and female tastes; roasted pork was more often a men's favourite dish (p < 0.001) while women had a prediction for vegetarian food (p < 0.001). There was, however, no difference in the choice of eating habits in persons with or without metabolic disorders. Thus, women in general do pursue a healthier consciousness was not so pronounced in man. Yet, it could not be established by means of the questionnaire that subjects with metabolic disorders showed different eating habits with respect to their disease.
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PMID:[Eating behavior of patients with metabolic diseases and metabolically healthy probands in Austria. Results of a questionnaire survey at the Graz Autumn Fair 1991]. 821 21

The objective of this paper is to examine the usefulness of plasmatic fructosamine finding as an indicator of glycemic control in patients with hypocaloric parenteral nutrition with glycerol. Thirty abdominal surgery patients were studied. None displayed malnutrition, diabetes mellitus, hepatopathy, nephropathy or hyperlipemia in the preoperative stage or during the five days of postoperative recovery they were administered hypocaloric parenteral nutrition with glycerol. Their plasma levels of glucose, fructosamine, triglycerides, albumin and total proteins were found in the preoperative stage and on the first and fourth day of postoperative recovery. Following surgery, findings showed an increase in triglycerides and a decrease in the protein compartment, while glycemia levels remained steady. Furthermore there was a positive correlation between the figures for glycemia and later fructosamine figures. The conclusion was that providing hypocaloric nutrition with glycerol does not increase fructosamine levels. This confirmed prior observations on the slightness of its effect on hydrocarbonic metabolisms.
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PMID:[The fructosamine monitoring of the effect on glycemic control of hypocaloric parenteral nutritional support with glycerol]. 847 51

We have previously demonstrated that low-casein diets supplemented with cystine and threonine reduced hyperlipidemia and proteinuria in nephritic rats without noticeable protein malnutrition. In the present study, we examined whether or not a low-casein diet supplemented with methionine, sulfur amino acid other than cystine, and threonine would ameliorate the symptoms without protein malnutrition in rats with nephrotoxic serum nephritis by feeding experimental diets for 10 days. A methionine-threonine-supplemented 8.5% casein diet (8.5 CMT), when compared with a basal 20% casein diet, improved hypoalbuminemia as well as hyperlipidemia and proteinuria without noticeable growth retardation and fatty liver induction in nephritic rats. Fecal bile acid excretion and microsomal cholesterol 7 alpha-hydroxylase activity were enhanced by 8.5CMT feeding. These results suggest that amino acid-balanced low protein diet would have a beneficial effect on the symptoms of nephritis. They also suggest that the hypocholesterolemic action of 8.5CMT may be, at least in part, due to increased fecal bile acid excretion accompanied by elevated microsomal cholesterol 7 alpha-hydroxylase activity.
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PMID:Improvement of hyperlipidemia and proteinuria without noticeable growth retardation by feeding a methionine and threonine supplemented low-casein diet to nephritic rats. 853 82

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.
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PMID:[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia]. 865 Sep 33

In summary, dyslipidemia is a common feature of various renal syndromes. Whether this perturbed lipid metabolism results in accelerated atherosclerosis and increased cerebrovascular and cardiovascular morbidity and mortality remains a subject of inquiry. Also undefined is the role of dyslipidemia in the progression of renal injury. The malnutrition that becomes a dominant morbid feature in patients on maintenance renal replacement therapy provides a caveat against aggressive intervention for modest hyperlipidemia once dialysis is instituted. Individualized assessment of end organ atherosclerotic disease and cardiovascular risk factors should form the basis for modification of the treatment plan (ie, pharmacological intervention) should nonpharmacological means prove ineffective.
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PMID:Dyslipidemia in renal disease. 873 63

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44


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