Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors quantified serum lipoprotein (a) (Lp) (a) by enzymo-immuno-analysis in 86 outpatient men suffering peripheral vascular disease (PVD) and in 53 age-matched healthy men. They further measured serum cholesterol, serum triglycerides, low density lipoproteins-cholesterol, high density lipoproteins (HDL)-cholesterol and serum apolipoprotein B. Serum triglycerides were significantly increased in patients with PVD versus controls (148 +/- 8 and 114 +/- 7 mg/dL, mean +/- SEM). HDL-cholesterol levels were significantly lower in patients versus controls (36 +/- 1 and 43 +/- 2 mg/dL, respectively). Serum Lp(a) levels in patients with PVD were 20 +/- 2 mg/dL, whereas in controls they were 16 +/- 3 (p: NS). Serum Lp(a) concentrations were identical in smoker and nonsmoker patients. There was no correlation between Lp(a) concentration and the other lipid parameters. Conversely, as occurs in coronary heart disease and in cerebrovascular disease, Lp(a) does not seem to be a marker for PVD, although a trend toward a higher mean levels was found.
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PMID:Serum lipoprotein (a) levels in men with peripheral vascular disease. 183 26

In order to evaluate whether Lp(a), a lipoprotein that is potentially thrombogenic and atherogenic, is a potential risk factor for CAD in non-insulin-dependent diabetes (NIDDM), we compared the Lp(a) and its distribution in 145 NIDDM patients with that in 94 healthy control subjects. Furthermore, we studied the effect of insulin treatment on serum Lp(a) in 108 patients with NIDDM. Male and female NIDDM patients had similar Lp(a) concentrations to healthy controls (median value 167 mg L-1, range 15-1550 mg L-1 vs. 157 mg L-1, range 15-919 mg L-1, NS and 92, range 15-1190 mg L-1 vs. 103 mg L-1, range 15-842 mg L-1, NS). Also, the cumulative distribution of Lp(a) did not differ between the NIDDM patients and healthy subjects. Insulin treatment increased Lp(a) in diabetics with a Lp(a) concentration of less than 300 mg L-1, but this effect was not related to the concomitant improvement in metabolic control (mean change (+/- SEM) of HbA1c from 9.80 +/- 0.15 to 8.00 +/- 0.12; P < 0.001). In subjects with elevated Lp(a) concentrations (> 300 mg L-1) the Lp(a) concentration was unaffected by insulin, despite a similar improvement in glycaemic control. These results suggest that insulin may modulate the concentration of Lp(a).
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PMID:Effect of insulin treatment on serum lipoprotein(a) in non-insulin-dependent diabetes. 778 67

Serum Lipoprotein(a) [Lp(a)] concentration was compared between middle-aged well-trained Caucasian male endurance runners (N = 57), (mean age +/- SEM 47.8 +/- 0.7 yr) and age-, body mass-, and body mass index (BMI)-matched male nonathletic control subjects (N = 62), (mean age +/- SEM 48.7 +/- 0.8). The mean weekly training distance of the runners was (60.7 +/- 2.8 km.wk-1) at the time of testing. Median Lp(a) levels were not significantly different (P > 0.05) between the runners (15.0 mg.dl-1) and the control subjects (12.5 mg.dl-1). As expected, compared with control subjects, in runners levels of other lipoproteins and apoproteins were significantly more favorable for cardiovascular health (all P < 0.01). There was no significant relationship between Lp(a) and any other measured variable (lipid, anthropometric, or dietary) in the runners group. In the control group, the significant positive correlation between Lp(a) and LDL-C was no longer significant after correction for the estimated contribution of Lp(a) cholesterol to LDL-C. These cross-sectional data suggest that a lifestyle of moderate to intense exercise training does not exert a significant impact on the Lp(a) level.
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PMID:Lipoprotein(a) [Lp(a)] levels in middle-aged male runners and sedentary controls. 779 78

Cardiovascular disease is the major cause of mortality in renal transplant recipients. Plasma levels of low-density lipoprotein cholesterol (LDL-C) are often elevated following renal transplantation, and the immunosuppressant cyclosporin A has been implicated as a predisposing factor for posttransplantation hyperlipidemia. Lipoprotein(a) [Lp(a)] is an LDL-like lipoprotein particle; elevated levels of Lp(a) provide an independent and significant risk factor for cardiovascular disease. Plasma concentrations of Lp(a) vary greatly among individuals, and the mechanisms that govern changes in their levels in transplant patients are unknown. The effect(s) of cyclosporin A on Lp(a) was studied in two groups of renal transplantation patients. In group I plasma lipoproteins including Lp(a) were measured before and after successful renal transplantation; this group received both prednisone and cyclosporin A for immunosuppression. Group II patients were studied after renal transplantation and received prednisone alone for immunosuppression. Following surgery, group I patients demonstrated increased plasma concentrations of LDL-C (mean +/- SEM range, 111 +/- 6 to 142 +/- 17 mg/dL; P < .005). In contrast, plasma Lp(a) levels for this group were markedly decreased after renal transplantation (median, 34.3 to 19.7 mg/dL). Patients not treated with cyclosporin A (group II) exhibited mean LDL-C and median Lp(a) levels (118 +/- 42 and 33.1 mg/dL, respectively) that were remarkably similar to those observed before renal transplantation (group I). These data confirm that hyperlipidemia following renal transplantation is associated with cyclosporin A therapy and show that this drug has opposing effects on plasma Lp(a) and LDL-C accumulations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporin A has divergent effects on plasma LDL cholesterol (LDL-C) and lipoprotein(a) [Lp(a)] levels in renal transplant recipients. Evidence for renal involvement in the maintenance of LDL-C and the elevation of Lp(a) concentrations in hemodialysis patients. 806 98

The influence of simvastatin, a competitive inhibitor of 3-hydroxy-3-methyl glutaryl coenzyme A reductase, on quantitative and qualitative changes in lipoprotein metabolism was investigated in 18 patients (group I, 10 with primary kidney disease and group II, 8 with diabetic nephropathy) with nephrotic syndrome. Nephrotic patients exhibited severe hyperlipidemia (serum cholesterol 390 +/- 17 mg/dl and triglyceride 335 +/- 42 mg/dl; mean +/- SEM) and had significantly higher lipoprotein (a) [Lp(a)] levels (54 +/- 12 mg/dl; median 31 mg/dl, p < 0.01) compared with 20 healthy subjects (mean 12 +/- 1.8 mg/dl; median 7 mg/dl). Fifty-six percent of the patients and 15% of the controls had values greater than 30 mg/dl. Treatment with simvastatin in increasing doses over a period of three months (13 patients received 40 mg/day and 5 patients 20 mg/day at the end of the third month) reduced LDL-cholesterol in both groups of patients (35% and 54%) as well as apolipoprotein B (apoB) (31% and 46%) significantly, but Lp(a) levels were not influenced (57 +/- 21 vs 59 +/- 20 and 50 +/- 14 vs 53 +/- 16 mg/dl, respectively). On the other hand a complex change in lipoprotein composition occurred. The ratio of LDL apoB/LDL cholesterol-ester increased significantly (0.75 +/- 0.03 to 0.84 +/- 0.03 and 0.80 +/- 0.03 to 1.02 +/- 0.1, respectively) and cholesterol concentration in VLDL (64 +/- 16 to 39 +/- 7 and 74 +/- 18 to 55 +/- 74 mg/dl, respectively) was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of simvastatin on lipoprotein (a) and lipoprotein composition in patients with nephrotic syndrome. 818 55

Recently, a high plasma level of lipoprotein(a) [LP(a)] has been considered an independent risk factor for atherosclerosis and its sequelae, particularly myocardial infarction. Patients with non-insulin-dependent diabetes mellitus (NIDDM) have an increased mortality rate from cardiovascular and cerebrovascular disease. Therefore, plasma concentrations of Lp(a) were determined and the relationship between fasting plasma Lp(a) level and diabetic control was investigated in NIDDM patients without any diabetic complications. Fasting plasma Lp(a) levels were measured using enzyme-linked immunosorbent assay kits [Terumo Medical Corp, Elkton, MD, Lp(a)] in 61 NIDDM subjects (30 men aged 56 +/- 2.0 years, 31 women aged 53 +/- 2.1 years [mean +/- SEM]) who were without any diabetic macroangiopathy and microangiopathy such as retinopathy, nephropathy, and neuropathy and in 56 healthy age- and sex-matched controls. Plasma Lp(a) levels were significantly higher in the diabetic group than in the control group (23.5 +/- 2.5 v 11.7 +/- 1.4 mg/dL [mean +/- SEM], P < .001). There was no significant correlation between log-transformed plasma Lp(a) levels and other factors such as age, sex, body mass index (BMI), blood pressure, duration of diabetes, fasting plasma glucose (FPG) level, glycosylated hemoglobin (HbA1C) level, and plasma lipid levels except for low-density lipoprotein cholesterol (LDL-C) levels in diabetic patients. A significant positive correlation was noted in diabetic patients between the changes of log Lp(a) and HbA1C levels after a 3-month follow-up period (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alteration of lipoprotein(a) concentration with glycemic control in non-insulin-dependent diabetic subjects without diabetic complications. 841 45

The relationship between lipoprotein(a) [Lp(a)] and metabolism of triglyceride-rich lipoproteins (TRL) was studied in 58 untreated patients with familial combined hyperlipidemia (FCH) from eight different kindreds, 17 spouse controls, and 17 unrelated controls. Lp(a) plasma concentrations were not significantly different between FCH subjects (343 +/- 61 mg/L, mean +/- SEM) and controls (249 +/- 52 mg/L). In FCH, log-transformed Lp(a) levels correlated positively with postheparin lipoprotein lipase ([LPL] r = .61, P = .0002) and hepatic lipase ([HL] r = .46, P = .008) activities and total plasma cholesterol level (r = .30, P = .03). In controls, Lp(a) correlated with LPL (r = .50, P = .04) and total plasma cholesterol level (r = .51, P = .003). In eight FCH patients, treatment with the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin resulted in significantly increased mean LPL activities and plasma Lp(a) concentrations. In three of these FCH patients, repeated measurements during 1 year demonstrated that changes in Lp(a) concentrations were paralleled by similar changes in LPL activity, but not HL activity. The observed correlation between postheparin plasma lipolytic activities and Lp(a) plasma concentrations suggests a connection between the metabolism of TRL and Lp(a).
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PMID:Lipoprotein(a) plasma concentrations associated with lipolytic activities in eight kindreds with familial combined hyperlipidemia and normolipidemic subjects. 851 May 21

To explore whether lipoprotein(a), Lp(a), may accumulate preferentially to LDL in the arterial wall at sites of injury, cholesterol-fed rabbits were injected intravenously with radiolabeled Lp(a) and/or LDL 3.1 +/- 0.1 days (mean +/- SEM, n = 30) after a balloon injury of the thoracic aorta. After 5 to 10 minutes' exposure to labeled lipoproteins, more labeled LDL than labeled Lp(a) was recovered in the intima-inner media of the balloon-injured segment (n = 9; paired t test, P < .0001); however, the amount of tightly bound labeled lipoprotein was similar for the two lipoprotein fractions. In the second set of experiments, 131I-Lp(a) (or 131I-LDL) was injected 26 hours before and 125I-Lp(a) (or 125I-LDL) 3 hours before the aorta was removed. Permeability and fractional loss of labeled Lp(a) (n = 8) versus LDL (n = 7) in the balloon-injured aortic intima-inner media were: permeability, 0.46 +/- 0.10 microL/cm2 per hour versus 1.41 +/- 0.32 microL/cm2 per hour (nonpaired t test, P < .0001); and fractional loss, 0.12 +/- 0.02 h-1 versus 0.44 +/- 0.05 h-1 (nonpaired t test, P = .0001), respectively. Finally, after 23 hours' exposure to labeled lipoproteins, the total accumulation and the amount of tightly bound labeled Lp(a) in the balloon-injured intima-inner media were, respectively, 174% (n = 6; ANOVA, P = .03) and 256% ANOVA, P = .005) of the values for labeled LDL. For labeled Lp(a) in the balloon-injured compared with the normal aortic intima-inner media, the recovery after 5 to 10 minutes, the permeability, and the accumulation after 23 hours were all increased, whereas the fractional loss was unchanged. These data suggest that the accumulation of Lp(a) is much larger in injured vessels than in normal vessels. Moreover, the data support the idea of a specific accumulation of Lp(a) compared with LDL in injured vessels.
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PMID:Specific accumulation of lipoprotein(a) in balloon-injured rabbit aorta in vivo. 863 19

Serum lipoprotein(a) [Lp(a)] levels were measured before and after a 12-wk program of moderate-intensity endurance training. The training program consisted of walking and/or jogging, at least three sessions.wk-1 of at least 30 min duration, at an intensity producing 60-85% HRmax reserve. Twenty-eight previously sedentary middle-aged Caucasian males matched for age, body mass, and body mass index (BMI) were randomly allocated to either an exercise (N = 17, mean age +/- SEM = 51.57 +/- 1.25 yr) or a control (N = 11, mean age +/- SEM = 50.0 +/- 1.15 yr) group. Pre- and post-training median Lp(a) levels, measured by immunoturbidimetric analysis, were not significantly different in either the exercise (pre 13.0, post 15.0 mg.dl-1) or the control subjects (pre 14.0, post 12.0 mg.dl-1) (P > 0.05). Kendall Rank correlation analysis revealed no significant relationship between the level of Lp(a) and any other variable in either group before or after training. In the exercisers, a significant increase (P < 0.05) was recorded in the estimated mean VO2max (pre 33.39 +/- 1.70, post 37.7 +/- 1.75 ml.kg-1 min-1). These data indicate that the level of Lp(a) was not influenced by a 12-wk program of moderate-intensity endurance training, and are consistent with previous reports suggesting that Lp(a) level is not altered by lifestyle factors.
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PMID:The effect of endurance training on lipoprotein(a) [Lp(a)] levels in middle-aged males. 878 64

The effect of L-thyroxine therapy on lipoprotein fractions was assessed in 15 patients with overt hypothyroidism (14 women and one man aged 45 +/- 3.9 years; thyrotropin [TSH]: mean +/- SEM, 42 +/- 6.5 mIU/L; range, 20.5 to 106.5) and 14 patients with subclinical hypothyroidism (13 women and one man aged 41 +/- 4 years; TSH: mean +/- SEM, 9.1 +/- 1 mIU/L ; range 5.1 to 17.3). Fasting serum lipid levels were measured initially and 4 months after achievement of a euthyroid state with incremental L-thyroxine therapy (TSH: mean +/- SEM, 1.8 +/- 0.4 mIU/L; range, 0.3 to 4.9 for both groups). In the overtly hypothyroid group, restoration of a euthyroid state was associated with a significant reduction in total cholesterol, and apo B. In the subclinically hypothyroid group, there was a significant reduction of only total cholesterol (199.6 +/- 13.2 v 183.4 +/- 11.6 mg/dL) and LDL-C (13.6 +/- 8.4 v 114 +/- 9.25 mg/dL). In contrast, lipoprotein(a) [Lp(a)] was unaffected by the incremental adjustment of L-thyroxine therapy in both groups (overt, 34.3 +/- 8.8 v 35.6 +/- 6.7 mg/dL; subclinical, 23.0 +/- 8.6 v 29.4 +/- 9.5 mg/dL). We conclude that restoration of a euthyroid state in patients with overt hypothyroidism has no significant effect on Lp(a) levels, and confirm that subclinical hypothyroidism is associated with a significant increase in LDL-C, known to have an atherogenic effect.
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PMID:Effect of L-thyroxine therapy on lipoprotein fractions in overt and subclinical hypothyroidism, with special reference to lipoprotein(a). 878 24


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