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H Drexel

Publications and source records attributed to H Drexel.

At least 37 records · Page 2Linked to original sources
PubMed1994

Relation of cyclosporine blood levels to adverse effects on lipoproteins.

Hyperlipidemia is common in renal allograft recipients. To elucidate the role of cyclosporine in posttransplant hyperlipidemia, we measured lipids, lipoprotein lipids, and apolipoproteins of thirty-five renal allograft recipients and evaluated their relation to trough cyclosporine blood levels. All patients were on a triple immunosuppressive regimen with equal doses of prednisone and azathioprine, and had stable graft function. Cyclosporine blood levels were significantly correlated to total plasma cholesterol (P = 0.028), low-density lipoprotein cholesterol (P = 0.022), apolipoprotein B (P = 0.017), and the cholesterol/high-density lipoprotein cholesterol ratio (P < 0.002), but not to plasma triglycerides. Significant inverse correlations were found between cyclosporine blood levels and high-density lipoprotein cholesterol (P = 0.034), high-density lipoprotein3 cholesterol (P = 0.025), and apolipoprotein A-1 (P = 0.047), but not high-density lipoprotein2 cholesterol. The independent relation of cyclosporine blood levels to each of the measured lipid parameters was investigated by a stepwise regression model including age, body mass index, interval from transplantation, diabetes mellitus, plasma creatinine, and intake of diuretics and beta-blockers. After correction for these 7 variables, cyclosporine blood levels remained significantly associated with high-density lipoprotein cholesterol, high-density lipoprotein3 cholesterol, apolipoprotein A-1, apolipoprotein B, low-density lipoprotein cholesterol, and the cholesterol/high-density lipoprotein cholesterol ratio. These data suggest that cyclosporine causes atherogenic dyslipidemia.

Adult↗
PubMed1994

Fenofibrate improves postprandial chylomicron clearance in II B hyperlipoproteinemia.

In 11 patients with IIB hyperlipoproteinemia we studied fasting lipids, lipoproteins, lipoprotein-modifying enzymes, and postprandial lipid metabolism after a standardized oral fat load supplemented with vitamin A before and 12 weeks after treatment with fenofibrate, a third-generation fibric acid derivative. Fasting plasma cholesterol, triglycerides, low-density lipoprotein cholesterol decreased significantly (P < 0.05, P < 0.01, P < 0.01), high-density lipoprotein subfraction 3 cholesterol increased significantly (P < 0.05), and high-density lipoprotein subfraction 2 cholesterol remained unchanged. Postprandial lipemia, i.e., the integrated postprandial triglyceride concentrations corrected for the fasting triglyceride level, and postprandial chylomicron concentrations, as assessed by biosynthetic labeling of chylomicrons with retinyl palmitate, decreased by 40.6% and 60.1% (P < 0.05; P < 0.05), respectively. The activity of lipoprotein lipase (LPL) increased by 33.6% (P < 0.05); the increase in LPL during fenofibrate treatment was positively correlated with the increase in high-density lipoprotein cholesterol (r = 0.84; P < 0.005). Hepatic lipase and cholesteryl ester transfer protein mass and activity remained unchanged. We conclude that lipid-lowering therapy with fenofibrate ameliorates fasting and, more profoundly, postprandial lipoprotein transport in hypertriglyceridemia by curbing postprandial triglyceride and chylomicron accumulation, at least in part, through an increase in LPL activity.

Adult↗
PubMed1994

Plasma triglycerides and three lipoprotein cholesterol fractions are independent predictors of the extent of coronary atherosclerosis.

BACKGROUND: The lipoprotein system has manifold links to atherosclerotic disease. LDL cholesterol is related to lesion formation and growth. The cholesterol of HDLs is indicative of protection against atherosclerosis. The status of triglycerides and of subfractions of high-density lipoproteins as risk factors is less certain. Also, the magnitude of the atherogenic/protective power of these factors is not known. METHODS AND RESULTS: Five hundred patients (418 men and 82 women) were enrolled in an angiographic study. A total of 1006 coronary lesions with > or = 50% narrowing were recorded as study end points. By extent of atherosclerosis, defined as the number of > or = 50% lesions, the study subjects were allocated to one of four ordered categories with 0, 1 to 3, 4 to 6, or 7 to 10 lesions, respectively. Subfractions of HDL cholesterol were determined by a dual precipitation method. By a polychotomous logistic regression model, it was found that, besides age and sex, LDL cholesterol, HDL2 cholesterol, HDL3 cholesterol, and triglycerides were independently predictive (P < .05) of the extent of coronary atherosclerosis. An increase in age by 10 years was associated with an increase of the odds ratio for falling into a higher-extent category by a factor of 1.64, and the same increase of the odds ratio was obtained by increasing LDL cholesterol by 0.92 mmol/L or triglycerides by 1.01 mmol/L and by decreasing HDL2 cholesterol by 0.20 mmol/L or HDL3 cholesterol by 0.46 mmol/L. The less sensitive coronary end point, presence of atherosclerosis (ie, observation of > or = 1 lesion of > or = 50%) depended significantly on age, sex, LDL cholesterol, and HDL2 cholesterol, but not on HDL3 cholesterol or triglycerides. CONCLUSIONS: In addition to LDL, HDL2, and HDL3 cholesterol, triglycerides also proved independently predictive of the extent of coronary atherosclerosis.

Cholesterol, HDL↗
PubMed1994

[Low dosage intravenous calcitriol bolus therapy in chronic hemodialysis patients].

Severe secondary hyperparathyroidism in patients on chronic renal replacement therapy is still an immense problem, even after the introduction of the oral calcitriol therapy. Because the current first choice treatment--intravenous calcitriol-bolus application--fails to decrease parathyroidhormone (PTH) in some patients, we decided to monitor 22 chronic hemodialysis patients receiving low dose therapy with 3 x 1 micrograms calcitriol per week for a period of 6 months. After 6 months the PTH increased from 430 +/- 318 to 573 +/- 508 pg/ml (p < 0.05), the serum calcium from 2.14 +/- 0.22 to 2.31 +/- 15 mmol/l (p < 0.01). There was no significant change in serum phosphate, alkaline phosphatase (APH) and osteocalcin. The patients were divided into 2 groups according to their basal PTH-levels. Group 1 (n = 7, PTH < 200 pg/ml) showed a significant decrease of the PTH-levels from 99 +/- 38 to 61 +/- 53 pg/ml (p < 0.05). There was no significant change in serum calcium, phosphate, APH and osteocalcin levels. In group 2 (n = 15, PTH > 300 pg/ml) the PTH increased significantly (p < 0.05) from 585 +/- 287 to 812 +/- 439 pg/ml. No significant change was found for APH or osteocalcin. Calcium and phosphate levels increased significantly from 2.11 +/- 0.20 to 2.31 +/- 0.12 mmol/l (p < 0.01) and from 2.29 +/- 0.47 to 2.74 +/- 0.60 mmol/l (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Lipids and blood vessels].

The key lesion in atherosclerosis is termed atheroma. It consists of intracellular and extracellular cholesterol esters. Because atheromas are located subendothelially, an interrelation with blood cholesterol has long been suspected. In the blood, cholesterol is wrapped in lipoproteins, with the largest amount being found in low-density lipoproteins (LDL), whereas a smaller amount is found in high-density lipoproteins (HDL). LDL (and their cholesterol) are removed from the plasma by receptor-mediated uptake. Impaired LDL-receptor interaction results in accumulation of LDL in plasma. LDL now penetrate the endothelial layer and become deposited in the arterial intima. This process initiates atheroma formation. Excess tissue cholesterol (e.g. in the arterial intima) is returned to the liver by HDL. The HDL2 subfraction is particularly effective in this reverse cholesterol transport. Patients with coronary atherosclerosis either have a defect in reverse cholesterol transport (i.e. low HDL2 levels) or an excess in cholesterol load (i.e. high LDL). The ratio between LDL and HDL2 cholesterol determines the risk for atherosclerotic disease. Triglycerides lower HDL2 levels and thereby exert indirect atherogenicity.

Arteriosclerosis↗
PubMed1993

[Therapy of hyperlipoproteinemia].

Triglycerides and cholesteryl esters are non-polar molecules and, therefore, insoluble in aqueous fluids such as blood. Lipid transport in blood is only possible the formation of lipoproteins. This article proposes a concept for the treatment of hyperlipidemias that is based on lipoprotein pathology. The liver secretes the triglycerides and cholesteryl esters in the form of very-low-density lipoproteins (VLDL). Lipolysis hydrolyzes VLDL triglycerides, providing tissues with fatty acids. and gives rise to relatively cholesterol-enriched intermediate-density lipo- proteins (IDL) and low-density lipoproteins (LDL). IDL and LDL are removed from plasma by receptor-mediated cellular uptake. An increased plasma concentration of VLDL ensues in predominant hypertriglyceridemia (e.g. triglycerides 9 mmol/l, cholesterol 7 mmol/l). VLDL are not considered to be directly atherogenic, but increased levels of VLDL often occur together with an atherogenic decrease of high-density lipoproteins (HDL). Elevated VLDL levels respond well to dietary measures; fibric acid derivatives, nicotinic acid and omega-3-fatty acids also effectively lower VLDL. An increase in IDL leads to both hypertriglyceridemia (e.g. 3 mmol/l) and hypercholesterolemia (e.g. 7 mmol/l). IDL are considered directly atherogenic. Hyperlipidemias due to IDL respond to the same interventions as those due to VLDL. An increased blood level of LDL leads to hypercholesterolemia (e.g. 7 mmol/l) with normal triglyceride levels (e.g. 1 mmol/l); LDL are considered directly atherogenic. Dietary measures can reduce LDL levels by about 10%, but pharmacological treatment by inhibitors of cholesterol synthesis ('statins') and by ion exchange resins is much more effective.(ABSTRACT TRUNCATED AT 250 WORDS)

Anticholesteremic Agents↗
PubMed1993

Plasma lipoprotein (a) concentration and phenotypes in diabetes mellitus.

Patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus are at increased risk of developing atherosclerotic vascular diseases. A variety of lipoprotein abnormalities have been described as being associated with this increased risk. In this study, apo(a) isoform frequencies and lipoprotein(a) [Lp(a)] concentrations were determined in Type 1 and Type 2 diabetic patients in order to investigate a possible contribution of Lp(a) to the increased risk for atherosclerosis in diabetes. No significant differences in plasma Lp(a) concentrations were found in two ethnically different populations (Austrians from the province of Tyrol and Hungarians from Budapest) in either type of diabetes when compared to respective control groups (91 Type 1 and 112 Type 2 diabetic patients vs 202 control subjects in the Hungarian study and 44 Type 1 diabetic and 44 Type 2 diabetic vs 125 control subjects in the Austrian study). There were also no significant apo(a) isoform frequency differences between both patient groups and control subjects in the two study groups. These data, obtained from two large ethnically different populations, provide no evidence of a contribution of Lp(a) to the increased risk for atherosclerosis in diabetes.

Adult↗
PubMed1992

Relation of the level of high-density lipoprotein subfractions to the presence and extent of coronary artery disease.

Plasma lipid profiles, including high-density lipoprotein (HDL) subfractions HDL2 and HDL3, were obtained in 115 men undergoing coronary angiography to assess the relation of lipid levels to coronary artery disease (CAD). CAD was present in 87 patients (76%) and absent in 28 (24%). The largest difference between the 2 groups were observed for HDL2 cholesterol, with a mean of 0.13 mmol/liter (5 mg/dl) in patients with CAD compared with 0.25 mmol/liter (10 mg/dl) in those without CAD (p less than 0.005). Smaller differences were found for HDL3 (1.02 mmol/liter [39 mg/dl] vs 1.19 mmol/liter [46 mg/dl]; p less than 0.005) and HDL (1.15 vs 1.42 mmol/liter [45 vs 55 mg/dl]; p less than 0.001) cholesterol, and apolipoprotein A-1 (1.37 vs 1.50 g/liter; p less than 0.01) and plasma triglycerides (1.79 vs 1.38 mmol/liter [159 vs 122 mg/dl]; p less than 0.05). No significant difference was found for plasma and low-density lipoprotein cholesterol, and apolipoprotein B levels. Simple regression analysis revealed that the most powerful independent variable associated with the extent of CAD was HDL2 cholesterol (Spearman rho = 0.311; p less than 0.001). Stepwise multiple regression analysis proved HDL2 cholesterol and age to be the strongest predictors of extent of CAD. The level of HDL2 cholesterol was reasonably well correlated with HDL cholesterol (r2 = 0.6; p less than 0.0001), but less so with plasma apolipoprotein A-1 (r2 = 0.4; p less than 0.0001). The data add to the growing body of information demonstrating an important association of HDL (and more specifically HDL2) with CAD in men.

Age Factors↗
PubMed1992

Low sensitivity of serum fructosamine as a screening parameter for gestational diabetes mellitus.

Oral glucose tolerance testing (OGTT) and quantification of serum fructosamine levels were performed in 190 asymptomatic women in weeks 24-28 of pregnancy. OGTT identified 10 of the 190 women as having gestational diabetes, but serum fructosamine quantification failed to do so because none of these 10 women exhibited levels exceeding the normal limit of 2.76 mmol/l. The mean fructosamine level in this group was 1.72 +/- 0.25 mmol/l compared to 1.60 +/- 0.15 mmol/l in the other 180 women without gestational diabetes. Fructosamine was found to correlate only with postload glucose values in excess of 180 mg/dl at 2 h (r = 0.87; p = 0.01), i.e. with the highest overall glucose values, but not with fasting glucose or milder postprandial hyperglycemia of under 180 mg/dl. We conclude that quantification of fructosamine detects only the rather severe cases of gestational hyperglycemia, but is too insensitive to uncover mild asymptomatic gestational diabetes mellitus, and we do not consider fructosamine to be a useful parameter for the diagnosis of this condition.

Diabetes, Gestational↗
PubMed1992

[Postpartum diabetes screening: value of fructosamine determination].

After birth of an infant with a birthweight of 4000 g or more maternal glucose tolerance should be examined. We measured blood glucose values after a 100 g oral glucose challenge and compared them with serum fructosamine values of the same subjects. 40 women who had given birth to an infant with macrosomia (group I) were matched with 40 women who had delivered babies with normal birthweight (group II). Impaired glucose tolerance was found in 6 women (15%) of group I, and in one woman (2.5%) of group II. Fructosamine values were within the normal range in each of the seven women (1.74 + 0.2 mmol/l vs 1.73 + 0.2 mmol/l). Thus, fructosamine determination is not sensitive enough to detect impaired glucose tolerance in asymptomatic women post partum. It is not feasible to replace the oral glucose tolerance test in screening for gestational diabetes mellitus.

Birth Weight↗
PubMed1991

[Is regression of atherosclerosis by drugs possible?].

The development of atheromatous wall changes and local thrombotic complications in coronary arteries may be influenced by drug treatment. Calcium antagonists appear to reduce the progression of minimal coronary lesions only, while lipid lowering agents (colestipol, niacin, fibrates and HMG-CoA-reductase inhibitors) can retard the progression of established stenotic lesions or even produce a slight regression in 20-30% of patients within two to four years. In acute stages of coronary artery disease, however, treatment with platelet inhibitors, anti-coagulants and betablockers is required to prevent life-threatening complications. Hence the optimum strategy for secondary prevention in coronary artery disease depends on the clinical presentation in individual patients.

Adrenergic beta-Antagonists↗
PubMed1991

Long-term effect of intensified insulin treatment on lipid parameters in diabetes mellitus type I.

Premature atherosclerosis is often found in patients with diabetes mellitus (DM) type I, and alterations in lipid metabolism seem to play an important role in the development of this complication. Intensified insulin therapy improves glycemic control parameters significantly. To evaluate the effect of this optimized insulin treatment (OIT) not only on glycemic control, but also on plasma lipids, 24 patients with DM type I (19 men and 5 women, 18 to 61 years) were switched from a standard insulin therapy to a regimen of OIT which has been maintained for more than 3 years now. After 2 years on OIT a reduction of HbA1c values from 8.1% to 7.5% (p less than 0.01) was accompanied by an increase in HDL cholesterol from 52 to 67 mg/dl (p less than 0.05) and a decrease of triglyceride levels from 319 to 67 mg/dl (p less than 0.001). At the end of the second year on OIT some of the patients exhibited a reversal of the favorable trend in HbA1c and lipid values. Intensified instructions regarding the implementation of OIT were therefore repeated and resulted in a renewed improvement of overall HbA1c, HDL cholesterol and triglyceride levels to 6.43%, 67 mg/dl, and 78 mg/dl, respectively. Our findings underline the value of OIT not only for glycemic control, but also for the control of plasma lipids considered to be major risk factors for coronary artery disease.

Adolescent↗
PubMed1991

Long-term follow-up of glycaemic control and parameters of lipid transport after pancreas transplantation.

We report the long-term metabolic observations made on 37 patients after simultaneous pancreas and kidney transplantation. Plasma C-peptide levels were above the physiological range in all patients and there was no significant difference between patients undergoing delayed duct occlusion (n = 12) or those with drainage of exocrine secretion into the urinary bladder (n = 25). HbA1c was equally at the upper end of the normal range in both subsets of patients. Mean fasting cholesterol (237 mg/dl) and triglycerides (122 mg/dl) were normal, and HDL-cholesterol was above normal with an average concentration of 77 mg/dl. Two patients underwent an oral fat tolerance test and showed extremely low postprandial lipaemia and very high lipoprotein lipase activities. We conclude that patients with a functioning pancreas graft persistently demonstrate normoglycaemia, elevated C-peptide, and a very favourable lipid profile both in the fasting and the postprandial state.

Adult↗
PubMed1990

[The effect of hyperlipoproteinemia on serum fructosamine].

In 127 patients, we investigated the influence of hyperlipemia on observed fructosamine values. An in vitro influence of the lipids on the fructosamine reading could be excluded for cholesterol, HDL-cholesterol and triglycerides. However, in patients with type I diabetes, both, cholesterol and triglycerides significantly (p less than 0.05) correlated with fructosamine. This may be explained by in vivo effects of hyperglycemia on lipids or lipoproteins. For a given level of hyperglycemia, fructosamine is slightly more sensitive than HbA1c.

Blood Proteins↗
PubMed1989

[Lipid values in a rural community].

In 1987 the population of a rural community in Tyrol aged 20 to 74 years was screened for plasma lipids (cholesterol, HDL cholesterol and triglycerides). The mean cholesterol value was 205.8 mg/dl (5.31 mml/l) in men and 207.9 mg/dl (5.37 mmol/l) in women. These values seem to be the lowest so far recorded for population-based cholesterol values in Austria. This might be partly explained by an intensive risk factor intervention programme which has been implemented in this community throughout the past ten years. HDL cholesterol was significantly higher in women (63.7 mg/dl or 1.64 mmol/l) than in men (51.1 mg/dl or 1.32 mmol/l). The opposite was true for non-fasting triglycerides, with mean values of 186.3 mg/dl (2.1 mmol/l) in men, and 122.1 mg/dl (1.4 mmol/l) in women.

Adult↗
PubMed1989

Risk factors for coronary artery disease: a study comparing hypercholesterolaemia and hypertriglyceridaemia in angiographically characterized patients.

Fifty-two male patients undergoing coronary angiography were allocated to four groups each consisting of 13 subjects: group I had normal coronary arteries and patients in groups II-IV exhibited coronary artery disease. In group II, plasma cholesterol was below 250 mg dl-1 and triglycerides below 160 mg dl-1; in group III, cholesterol was above 270 mg dl-1 and triglycerides under 160 mg dl-1; and in group IV, cholesterol was under 270 mg dl-1 and triglycerides above 180 mg dl-1. The hypertriglyceridaemic group IV had the highest coronary score. In addition, it had lowest lipoprotein lipase activity, lowest HDL-cholesterol and lowest high-density lipoproteins-2 (HDL-2) levels, suggesting that this type of hypertriglyceridaemia is caused--at least in part--by lipoprotein lipase deficiency with impaired removal of the triglyceride-rich lipoproteins and increased catabolism of HDL-2. Our findings point towards a type of hypertriglyceridaemia strongly associated with coronary artery disease which should therefore be treated accordingly.

Adult↗