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)

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

A 38-year-old female was admitted to our hospital because of dyspnea. The diagnosis of total lipodystrophy was made by following findings: (1) gaunt appearance; (2) insulin-resistant diabetes mellitus; (3) hyperlipidemia; (4) fatty liver. Chest X-ray demonstrated cardiomegaly, pulmonary edema and pleural effusion. Echocardiogram was characterized by left ventricular hypertrophy with asymmetrical septal hypertrophy and left ventricular dysfunction. Renal biopsy revealed focal glomerulosclerosis. We reported a patient with total lipodystrophy combined with heart failure and renal failure, which have been rarely associated with the disease.
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PMID:Total lipodystrophy with heart failure and renal failure: report of a case. 253 Mar 77

Using a complex stimulating mixture containing ADP, epinephrine and collagen, a significantly (p less than 0.002) enhanced platelet aggregability, expressed as platelet sensitivity factor (PSF) was noted in platelet rich plasma of patients with proteinuria (PSF = 472 +/- 125), as against normal weight normolipidemic control subjects (PSF = 32.76 +/- 2.67). A significantly negative correlation (r. -0.579; p less than 0.001) was found between serum albumin concentration and the logarithmic values of platelet sensitivity factor. Plasma von Willebrand factor activity expressed as a percentage of normal was also significantly (p less than 0.001) higher in proteinuric patients (287% +/- 25.8) than in control subjects (99% +/- 5.02), but this hemostatic variable did not correlate with the logarithm of platelet sensitivity factor. Platelet aggregability was higher in hyperlipidemic nephrotic patients than in proteinuric patients with normal serum lipids, while renal failure led to a decrease of platelet function. The raised plasma levels of von Willebrand factor noted in proteinuric patients were not influenced by either hyperlipidemia or by chronic renal failure. It is concluded that changes affecting platelet function in the nephrotic syndrome are produced by other mechanisms than these leading to an increase of endothelia-derived von Willebrand factor. Both changes may, however, contribute to the thrombotic tendency of nephrotic patients.
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PMID:Plasma von Willebrand factor antigen and activity and platelet aggregability in patients with proteinuria. 261 81

Renal disease from a variety of causes often progresses to end-stage renal failure. The progression may be caused by factors accompanying, but not initiating, renal injury. These factors include glomerular hyperfiltration, glomerular hypertension, systemic hypertension, and hyperlipidemia. Studies, primarily in animals, indicate that causative factors may be altered by control of systemic hypertension, dietary protein restriction, administration of angiotensin-converting enzyme inhibitors or calcium channel blockers, and plasma lipid control. Whether such interventions will significantly alter progressive renal disease in humans is, as yet, uncertain.
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PMID:Can progression of renal disease be prevented? 266 51

Treatment of hypertension has succeeded in preventing the complications attributable to pressure, including heart failure and the arteriolar complications such as brain hemorrhage and renal failure. Recent understanding that antihypertensive drugs have effects on lipoproteins and flow disturbances that may be important in atherosclerosis progression, and the recent development of drugs that are more effective in treating hyperlipidemia, have given impetus to the design of studies to test whether interventions are anti-atherosclerotic. Since studies depending on clinical endpoints by necessity consume vast resources, it is desirable to develop methods for measurement of atherosclerosis, in order to make it possible to conduct intervention studies efficiently. Because angiographic methods are costly and associated with risk, and many patients are unable or unwilling to undergo followup angiography at the end of a study, we are developing an atherosclerosis severity index based on clinical and noninvasive ultrasound assessment. This scale can be used as a surrogate outcome in place of, or complementary to angiographic measurement of atherosclerosis, to avoid costly loss of subjects in intervention studies. It has the additional advantage that it is suitable for repeated assessment over time, permitting the power of analyses such as life table analysis which look at time to development of endpoints.
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PMID:Measurement of atherosclerosis: development of an atherosclerosis severity index. 267 64

Diabetes Mellitus represents an important public health problem in the most developed industrialized countries. Clinical presentations of diabetes are strongly related to the cardiovascular system, namely, coronary disease and angiopathic renal failure. Diabetes modifies the clinical course of arteriosclerosis by carrying the angiopathic process to a microvascular level, where typical microangiopathic lesions can be observed. The risk of developing atherosclerotic disease is 2-3 fold higher in diabetics than in nondiabetics and arterial hypertension reaches a prevalence of 40 to 80%. Authors analyse Arterial Hypertension in the context of Diabetes putting focus on the underlying pathophysiological mechanisms. Where considering the coronary disease (CD), its high prevalence among the diabetics is also emphasized, which is expressed by an increase of morbidity and mortality when compared to normal subjects. In diabetics not only the incidence of Acute Myocardial Infarction is higher, but also the long term prognosis is more complicated, a reality that the authors try to explain by anatomic and metabolic factors. The association of Diabetes plus hyperlipidemia represents undoubtedly one of the major factors that justify the worsening and progression of CD. Briefly, some interesting points that allow the understanding of this topic are described, pointing the pathogenic differences of types I and II and the clinical implications of their knowledge. Finally, the approach of Diabetes as a cardiovascular risk factor is discussed in a prophylactic perspective.
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PMID:[Diabetes mellitus and coronopathy]. 269 90

The treatment of high blood pressure with beta-blocking and other antihypertensive agents has been associated with a decrease in the incidence of stroke, progression of hypertension, heart failure, left ventricular hypertrophy, retinopathy and renal failure. Although hypertension increases the risk for developing coronary disease, the risk is heightened markedly if coexistent hyperlipidemia, smoking or glucose tolerance is present. Thiazide diuretics, primarily used as antihypertensive agents, compromise glucose tolerance and are associated with increases in plasma cholesterol, triglycerides and low density lipoprotein levels. Nonselective and beta 1-selective beta blockers have also been associated with increases in plasma triglycerides and very low density lipoproteins, as well as with decreases in high density lipoprotein levels. The effects of various antihypertensive agents on lipid levels, lipid metabolism, carbohydrate metabolism, left ventricular size and atherogenesis are discussed.
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PMID:Effects of beta blockers and other antihypertensive drugs on cardiovascular risk. 288 79

Serial changes in urine protein, blood chemistry, and histology of the kidney were investigated in rats for 28 weeks after injections of adriamycin (ADR). Massive proteinuria, hypoalbuminemia, and hyperlipidemia were observed at week 4 and throughout the experiment. Both BUN and serum creatinine began to increase at week 16 and reached the uremic level at week 28. Light microscopic study of the kidney demonstrated a normal appearance at week 4, vacuole formation in glomerular tuft at weeks 8 and 12, focal and segmental glomerular sclerosis at weeks 16 and 20, and extensive glomerular sclerosis with tubulointerstitial degenerations at weeks 24 and 28. Immunohistologically, IgM with a small amount of IgG and C3 appeared in the sclerosing glomeruli from week 16. Aggregated human IgG, injected intravenously at week 24, had accumulated mainly in the glomeruli. Electron microscopy revealed degenerative changes of glomerular epithelial cells with small vacuoles in the cytoplasm at week 4. Size of vacuoles increased at the later stage. In conclusion, ADR produced chronic, progressive glomerular changes in rats, which led to terminal renal failure. The segmental glomerular sclerosis and IgM-dominant glomerular deposition in these animals are similar to pathological characteristics of focal and segmental glomerular sclerosis seen clinically.
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PMID:Adriamycin-induced nephropathy as a model of chronic progressive glomerular disease. 348 12

This paper is a study of 117 patients with endstage renal failure, treated by continuous ambulatory peritoneal dialysis (CAPD) over periods of 1-56 months. The study has shown CAPD to be an effective form of dialysis with a number of advantages over intermittent peritoneal dialysis and hemodialysis (better control of salt and water status, hypertension and anemia, steady state biochemistry and greater ease of self-dialysis). Peritoneal clearance and ultrafiltration have remained adequate in all but a few patients. Hypoproteinemia, poor nutrition, obesity and abdominal herniae have been problems in a small percentage of patients. Hyperlipidemia has developed in half the patients but improved with diet. Peritonitis remains the major barrier to the more widespread use of CAPD, although its incidence can be considerably reduced by use of better connectors, bacterial filters and choice of patients.
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PMID:Continuous ambulatory peritoneal dialysis (CAPD): an established treatment for endstage renal failure. 636 Jan 16

Bilateral corneal opacities are the first clinical sign of a familial lecithin-cholesterol acyltransferase (LCAT) deficiency and can be found in early childhood. Familial LCAT deficiency includes the following typical clinical findings: corneal opacification, proteinuria, anemia, turbid or milky plasma, very low plasma HDL, very low plasma cholesterol esters and lysolecithin, hyperlipidemia, and very low or absent LCAT enzymatic activity. Several patients have had fundus findings including angioid streaks and papilledema. This disease is autosomal recessive and has been reported in a total of 19 patients previously. Progression of the disease has resulted in premature atherosclerosis, renal failure and transplantation, decreasing visual acuity and corneal transplantation.
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PMID:Corneal opacification and lecithin-cholesterol acyltransferase (LCAT) deficiency: a case report. 647 90


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