Long term hemodialysis aggravates lipolytic activity reduction and very low density, low density lipoproteins composition in chronic renal failure patients

<p>Abstract</p> <p>Background</p> <p>Dyslipidemia, particularly hypertriglyceridemia is common in uremia, and represents an independent risk factor for atherosclerosis.</p> <p>Methods</p> <p>To investigate the effects of hemodialysis (HD) duration on very low density lipoprotein (VLDL) and low density lipoprotein (LDL) compositions and lipopolytic activities, 20 patients on 5 to 7 years hemodialysis were followed-up during 9 years. Blood samples were drawn at T0 (beginning of the study), T1 (3 years after initiating study), T2 (6 years after initiating study) and T3 (9 years after initiating study). T0 was taken as reference.</p> <p>Results</p> <p>Triacylglycerols (TG) values were correlated with HD duration (r = 0.70, P < 0.05). An increase of total cholesterol was noted at T2 and T3. Lowered activity was observed for lipoprotein lipase (LPL) (-44%) at T3 and hepatic lipase (HL) (-29%) at T1, (-64%) at T2 and (-73%) at T3. Inverse relationships were found between HD duration and LPL activity (r = -0.63, P < 0.05), and HL activity (r = -0.71, P < 0.01). At T1, T2 and T3, high VLDL-amounts and VLDL-TG and decreased VLDL-phospholipids values were noted. Increased LDL-cholesteryl esters values were noted at T1 and T2 and in LDL-unesterified cholesterol at T2 and T3.</p> <p>Conclusion</p> <p>Despite hemodialysis duration, VLDL-LDL metabolism alterations are aggravated submitting patients to a greater risk of atherosclerosis.</p

High-density lipoprotein concentrations increase after stopping smoking.

Concentrations of plasma lipoproteins in 10 men who were habitual smokers were monitored for six weeks after they stopped smoking and related to changes in diet and body weight. The energy intake increased by 10% (p less than 0.05) owing to a higher consumption of carbohydrates and fat, and body weight increased by 2% (p less than 0.01). Plasma triglyceride, cholesterol, and low-density lipoprotein cholesterol concentrations did not change significantly. The most prominent finding was a rapid and pronounced increased in high-density lipoprotein concentrations. From comparatively low values (mean 0.82 mmol/1) they rose by 29% (p less than 0.01) within two weeks and remained at this value throughout the observation period. In three subjects who resumed smoking after the end of the study they again fell to initial values six weeks later. The initial increase in concentration could be accounted for mainly by an increase in the esterified fraction and only to a lesser extent in the free cholesterol fraction. The changes in concentrations were accompanied by similar but less pronounced rises in high-density lipoprotein phospholipid and in apolipoprotein AI concentrations (p less than 0.01), whereas high-density lipoprotein phospholipid and in apolipoprotein AI concentration (p less than 0.01), whereas high-density lipoprotein triglyceride concentrations did not change significantly. These findings confirm and extend those of earlier cross-sectional studies which showed low concentrations of high-density lipoproteins in cigarette smokers, A significant correlation between the rise in high-density lipoprotein cholesterol concentrations and the increase in fat consumption after stopping smoking indicate that the changes in high-density lipoprotein concentrations may be partly due to nutritional factors

Transient hypertriglyceridemia of infancy

A premature boy who had suffered from IRDS, bronchopulmonary dysplasia and retinopathy of prematurity developed massive hypertriglyceridemia (48.1 mmol/L) together with moderate hypercholesterolemia (12.6 mmol/L) at 5 months of age. Lipoprotein electrophoresis revealed a marked elevation of the level of the very low density lipoprotein fraction. There was a moderate decrease in the activity of a lipolytic enzyme, lipoprotein lipase (LPL). The child had neither liver or renal disorder nor any inflammatory disease. The hyperlipidemia disappeared spontaneously at the age of 3 years. The cause of the decreased LPL activity could not be established. A partial genetic deficiency in lipoprotein lipase appears the most likely explanation, since no signs of secondary lowering of LPL activity could be found