The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform

Peter Schwandt - One of the best experts on this subject based on the ideXlab platform.

  • Hemorrheologic abnormalities in defined primary dyslipoproteinemias with both high and low atherosclerotic risks.
    Metabolism: clinical and experimental, 2001
    Co-Authors: Carsten Otto, Werner O. Richter, Michael M. Ritter, Ralf Minkenberg, Peter Schwandt
    Abstract:

    Abstract Dyslipoproteinemias are associated with hemorrheologic abnormalities (elevated fibrinogen concentration, higher viscosity of plasma and blood). Epidemiologic data suggest that not only elevated lipoprotein concentrations (eg, low-density lipoprotein [LDL] cholesterol), but also hemorrheologic abnormalities could causally be involved in the atherosclerotic process. To elucidate potential effects of hemorrheological disturbances, we investigated patients suffering from primary hyperlipoproteinemias with both low (Familial Hypertriglyceridemia, n = 25) and high (type III hyperlipoproteinemia, n = 21; Familial hypercholesterolemia, n = 19; mixed hyperlipoproteinemia, n = 19) atherosclerotic risk, as well as healthy controls (n = 49) in a cross-sectional design. Dyslipoproteinemias were classified by lipoprotein measurements (using ultracentrifugation), family history, and apolipoprotein E phenotype. Hemorrheology was characterized by the measurement of fibrinogen concentration, viscosity of plasma and blood at different shear rates, and red cell aggregation (RCA) at stasis and low shear. Fibrinogen concentration was lower in controls (2.38 ± 0.09 g/L) compared with Familial hypercholesterolemia (3.19 ± 0.19 g/L), to type III hyperlipoproteinemia (3.02 ± 0.12 g/L), to Familial Hypertriglyceridemia (2.95 ± 0.21 g/L) and to mixed hyperlipoproteinemia (3.01 ± 0.12 g/L) ( P P P

  • Postprandial hemorrheology and apolipoprotein B metabolism in patients with Familial Hypertriglyceridemia.
    Metabolism: clinical and experimental, 1997
    Co-Authors: Carsten Otto, Peter Schwandt, Andreas C. Soennichsen, Volkhard Pschierer, Werner O. Richter
    Abstract:

    Abstract Impaired postprandial lipoprotein metabolim has been found to be related to the extent of coronary artery disease. Moreover, since dyslipoproteinemias are associated with impaired hemorrheology, we investigated the effect of postprandial Hypertriglyceridemia on hemorrheological parameters before and after triglyceride-lowering therapy. Triglyceride-rich lipoproteins (TRLs) separated by ultracentrifugation (d P P P v 19.0 ± 7.6 to 33.0 ± 12.5 mg/dL before therapy, P P

  • Effects of n-3 fatty acids and fenofibrate on lipid and hemorrheological parameters in Familial dysbetalipoproteinemia and Familial Hypertriglyceridemia.
    Metabolism: clinical and experimental, 1996
    Co-Authors: Carsten Otto, Peter Schwandt, Michael M. Ritter, Andreas C. Soennichsen, Werner O. Richter
    Abstract:

    There is increasing evidence that hemorrheological abnormalities are associated with an enhanced risk of atherosclerosis. The n-3 fatty acids (n-3-FA) have been shown to have beneficial effects on atherosclerosis in patients with dyslipoproteinemias. We studied 23 patients with elevated plasma triglycerides to evaluate the influence of fish oil and fenofibrate therapy on hemorrheological parameters (15 patients with Familial Hypertriglyceridemia [FHTG] and eight with Familial dysbetalipoproteinemia [FDL]). The patients (one woman and 22 men aged 45.7 ± 2.0 years) were treated with increasing doses of n-3-FA (1.8 to 3.6 g/d: 0.9 to 1.8 g eicosapentaenoic acid and 0.6 to 1.2 g docosahexaenoic acid) for 8 weeks. Lipid parameters, whole-blood viscosity at different shear rates, plasma viscosity, fibrinogen concentration, and red blood cell aggregation (RCA) were measured at baseline and at weeks 2, 4, 8 (end of n-3-FA therapy), and 12. Compliance was ensured by measuring plasma concentrations of eicosapentaenoic acid and docosahexaenoic acid. After 12 weeks, patients began treatment with fenofibrate (250 mg daily); investigations were performed again at week 20. Total triglycerides (from 6.90 ± 1.70 to 3.61 ± 0.78 mmol/L in FDL and 7.44 ± 1.50 to 4.15 ± 0.55 in FHTG), very-low-density lipoprotein (VLDL) triglycerides, and VLDL cholesterol were significantly decreased with n-3-FA therapy in both groups (P < .05). In FHTG, low-density lipoprotein (LDL) cholesterol increased significantly (from 2.75 ± 0.28 to 3.97 ± 0.35 mmol/L, P < .01); in FDL, total cholesterol decreased (from 9.76 ± 1.32 to 7.34 ± 1.07 mmol/L, P < .05). No significant changes were observed in hemorrheological parameters, except for reduced RCA with 3.6 g n-3-FA in FHTG. However, with fenofibrate therapy, in addition to comparable lipoprotein changes seen with fish oil, fibrinogen levels and plasma and blood viscosity decreased in patients with FDL. We conclude that n-3-FA and fenofibrate have comparable effects on lipid parameters in patients with FDL and FHTG. Because of additional beneficial effects on hemorrheological parameters, fenofibrate may be preferred for the treatment of FDL.

  • Primary chylomicronemia in patients with severe Familial Hypertriglyceridemia responds to long-term treatment with (n-3) fatty acids.
    The Journal of nutrition, 1995
    Co-Authors: Volkhard Pschierer, Werner O. Richter, Peter Schwandt
    Abstract:

    Because it disturbs microcirculation, chylomicronemia can cause severe clinical complications such as acute pancreatitis. Dietary measures are very important in the prevention and treatment of this condition. Dietary supplementation with (n-3) fatty acids has been shown to be of benefit in short-term treatment of chylomicronemia. To evaluate the long-term efficacy of (n-3) fatty acids we added 2.16 or 4.32 g/d (for 3 mo) and 3.24 g/d (for a further 8 mo after 1 mo of no treatment) (n-3) fatty acids to the diet of eight patients with primary chylomicronemia. Serum triglycerides decreased significantly from 15.0 ± 2.5 to 9.9 ± 2.8 mmol/L (P < 0.01) after 11 mo of treatment, and VLDL triglycerides decreased from 12.3 ± 2.8 to 9.0 ± 2.4 mmol/L (P < 0.01) ; resulting in a significant decrease of plasma viscosity from 1.56 ± 0.17 mPa-s to 1.47 ± 0.12 mPa-s (P < 0.01). Total cholesterol, HDL and LDL cholesterol as well as lipoprotein (a) and fibrinogen concentrations were not affected by fish oil treatment. The presence of chylomicrons and chylomicron remnants (apolipoprotein B 48 concentration in the lipoprotein fraction with a density lower than 1.006 kg/L) was significantly reduced from 4.82 ± 1.08 to 1.06 ± 0.38 mg/L (P < 0.01). Body weight increased significantly from 71.0 ± 4.6 kg to 75.2 ± 5.3 kg after 11 mo of treatment with (n-3) fatty acids. These data indicate that despite an increase in body weight, long-term supplementation of a diet with (n-3) fatty acids results in a persistent decrease of serum triglyceride concentrations, a pronounced reduction in the number of chylomicrons present in the fasting state, and an improvement in plasma viscosity.

  • Treatment of primary chylomicronemia due to Familial Hypertriglyceridemia by ω-3 fatty acids
    Metabolism: clinical and experimental, 1992
    Co-Authors: Werner O. Richter, Bernd G. Jacob, Michael M. Ritter, Peter Schwandt
    Abstract:

    Abstract Primary Familial forms of chylomicronemia can lead to acute life-threatening complications, especially acute pancreatitis. The main aim of therapy is to avoid this so-called chylomicronemia syndrome. In 12 patients with primary chylomicronemia due to Familial Hypertriglyceridemia, the addition of 2.16 g ω-3 fatty acids over 4 weeks and 4.32 g for 8 weeks resulted in a decrease of serum triglyceride levels from 1,624 ± 333 to 894 ± 241 mg/dL after 12 weeks. Cholesterol and triglyceride levels in the chylomicron fraction were reduced concomitantly, the apolipoprotein B-100 B-48 ratio increased, very-low-density lipoprotein (VLDL) triglycerides, VLDL cholesterol, and total cholesterol levels decreased, and low-density lipoprotein (LDL) cholesterol showed a tendency to increase, but this finding did not reach significance. High-density lipoprotein (HDL) cholesterol levels remained unchanged, as did the levels of apolipoproteins A-I, A-II, and E, and lipoprotein(a). Apolipoprotein B levels decreased significantly. The decrease of triglyceride levels to still-elevated concentrations was accompanied by a substantial decrease in plasma and whole-blood viscosity and erythrocyte aggregation, which reached normal values. As in chylomicronemia, complications usually occur at triglyceride levels higher than 1,500 mg/dL; patients can still profit from treatment with ω-3 fatty acids, even though triglyceride levels are still substantially elevated. No clinically relevant side effects occurred, with the exception of the manifestation of diabetes mellitus in one patient, which could be reversed after discontinuation of treatment.

Werner O. Richter - One of the best experts on this subject based on the ideXlab platform.

  • Hemorrheologic abnormalities in defined primary dyslipoproteinemias with both high and low atherosclerotic risks.
    Metabolism: clinical and experimental, 2001
    Co-Authors: Carsten Otto, Werner O. Richter, Michael M. Ritter, Ralf Minkenberg, Peter Schwandt
    Abstract:

    Abstract Dyslipoproteinemias are associated with hemorrheologic abnormalities (elevated fibrinogen concentration, higher viscosity of plasma and blood). Epidemiologic data suggest that not only elevated lipoprotein concentrations (eg, low-density lipoprotein [LDL] cholesterol), but also hemorrheologic abnormalities could causally be involved in the atherosclerotic process. To elucidate potential effects of hemorrheological disturbances, we investigated patients suffering from primary hyperlipoproteinemias with both low (Familial Hypertriglyceridemia, n = 25) and high (type III hyperlipoproteinemia, n = 21; Familial hypercholesterolemia, n = 19; mixed hyperlipoproteinemia, n = 19) atherosclerotic risk, as well as healthy controls (n = 49) in a cross-sectional design. Dyslipoproteinemias were classified by lipoprotein measurements (using ultracentrifugation), family history, and apolipoprotein E phenotype. Hemorrheology was characterized by the measurement of fibrinogen concentration, viscosity of plasma and blood at different shear rates, and red cell aggregation (RCA) at stasis and low shear. Fibrinogen concentration was lower in controls (2.38 ± 0.09 g/L) compared with Familial hypercholesterolemia (3.19 ± 0.19 g/L), to type III hyperlipoproteinemia (3.02 ± 0.12 g/L), to Familial Hypertriglyceridemia (2.95 ± 0.21 g/L) and to mixed hyperlipoproteinemia (3.01 ± 0.12 g/L) ( P P P

  • Postprandial hemorrheology and apolipoprotein B metabolism in patients with Familial Hypertriglyceridemia.
    Metabolism: clinical and experimental, 1997
    Co-Authors: Carsten Otto, Peter Schwandt, Andreas C. Soennichsen, Volkhard Pschierer, Werner O. Richter
    Abstract:

    Abstract Impaired postprandial lipoprotein metabolim has been found to be related to the extent of coronary artery disease. Moreover, since dyslipoproteinemias are associated with impaired hemorrheology, we investigated the effect of postprandial Hypertriglyceridemia on hemorrheological parameters before and after triglyceride-lowering therapy. Triglyceride-rich lipoproteins (TRLs) separated by ultracentrifugation (d P P P v 19.0 ± 7.6 to 33.0 ± 12.5 mg/dL before therapy, P P

  • Effects of n-3 fatty acids and fenofibrate on lipid and hemorrheological parameters in Familial dysbetalipoproteinemia and Familial Hypertriglyceridemia.
    Metabolism: clinical and experimental, 1996
    Co-Authors: Carsten Otto, Peter Schwandt, Michael M. Ritter, Andreas C. Soennichsen, Werner O. Richter
    Abstract:

    There is increasing evidence that hemorrheological abnormalities are associated with an enhanced risk of atherosclerosis. The n-3 fatty acids (n-3-FA) have been shown to have beneficial effects on atherosclerosis in patients with dyslipoproteinemias. We studied 23 patients with elevated plasma triglycerides to evaluate the influence of fish oil and fenofibrate therapy on hemorrheological parameters (15 patients with Familial Hypertriglyceridemia [FHTG] and eight with Familial dysbetalipoproteinemia [FDL]). The patients (one woman and 22 men aged 45.7 ± 2.0 years) were treated with increasing doses of n-3-FA (1.8 to 3.6 g/d: 0.9 to 1.8 g eicosapentaenoic acid and 0.6 to 1.2 g docosahexaenoic acid) for 8 weeks. Lipid parameters, whole-blood viscosity at different shear rates, plasma viscosity, fibrinogen concentration, and red blood cell aggregation (RCA) were measured at baseline and at weeks 2, 4, 8 (end of n-3-FA therapy), and 12. Compliance was ensured by measuring plasma concentrations of eicosapentaenoic acid and docosahexaenoic acid. After 12 weeks, patients began treatment with fenofibrate (250 mg daily); investigations were performed again at week 20. Total triglycerides (from 6.90 ± 1.70 to 3.61 ± 0.78 mmol/L in FDL and 7.44 ± 1.50 to 4.15 ± 0.55 in FHTG), very-low-density lipoprotein (VLDL) triglycerides, and VLDL cholesterol were significantly decreased with n-3-FA therapy in both groups (P < .05). In FHTG, low-density lipoprotein (LDL) cholesterol increased significantly (from 2.75 ± 0.28 to 3.97 ± 0.35 mmol/L, P < .01); in FDL, total cholesterol decreased (from 9.76 ± 1.32 to 7.34 ± 1.07 mmol/L, P < .05). No significant changes were observed in hemorrheological parameters, except for reduced RCA with 3.6 g n-3-FA in FHTG. However, with fenofibrate therapy, in addition to comparable lipoprotein changes seen with fish oil, fibrinogen levels and plasma and blood viscosity decreased in patients with FDL. We conclude that n-3-FA and fenofibrate have comparable effects on lipid parameters in patients with FDL and FHTG. Because of additional beneficial effects on hemorrheological parameters, fenofibrate may be preferred for the treatment of FDL.

  • Primary chylomicronemia in patients with severe Familial Hypertriglyceridemia responds to long-term treatment with (n-3) fatty acids.
    The Journal of nutrition, 1995
    Co-Authors: Volkhard Pschierer, Werner O. Richter, Peter Schwandt
    Abstract:

    Because it disturbs microcirculation, chylomicronemia can cause severe clinical complications such as acute pancreatitis. Dietary measures are very important in the prevention and treatment of this condition. Dietary supplementation with (n-3) fatty acids has been shown to be of benefit in short-term treatment of chylomicronemia. To evaluate the long-term efficacy of (n-3) fatty acids we added 2.16 or 4.32 g/d (for 3 mo) and 3.24 g/d (for a further 8 mo after 1 mo of no treatment) (n-3) fatty acids to the diet of eight patients with primary chylomicronemia. Serum triglycerides decreased significantly from 15.0 ± 2.5 to 9.9 ± 2.8 mmol/L (P < 0.01) after 11 mo of treatment, and VLDL triglycerides decreased from 12.3 ± 2.8 to 9.0 ± 2.4 mmol/L (P < 0.01) ; resulting in a significant decrease of plasma viscosity from 1.56 ± 0.17 mPa-s to 1.47 ± 0.12 mPa-s (P < 0.01). Total cholesterol, HDL and LDL cholesterol as well as lipoprotein (a) and fibrinogen concentrations were not affected by fish oil treatment. The presence of chylomicrons and chylomicron remnants (apolipoprotein B 48 concentration in the lipoprotein fraction with a density lower than 1.006 kg/L) was significantly reduced from 4.82 ± 1.08 to 1.06 ± 0.38 mg/L (P < 0.01). Body weight increased significantly from 71.0 ± 4.6 kg to 75.2 ± 5.3 kg after 11 mo of treatment with (n-3) fatty acids. These data indicate that despite an increase in body weight, long-term supplementation of a diet with (n-3) fatty acids results in a persistent decrease of serum triglyceride concentrations, a pronounced reduction in the number of chylomicrons present in the fasting state, and an improvement in plasma viscosity.

  • Treatment of primary chylomicronemia due to Familial Hypertriglyceridemia by ω-3 fatty acids
    Metabolism: clinical and experimental, 1992
    Co-Authors: Werner O. Richter, Bernd G. Jacob, Michael M. Ritter, Peter Schwandt
    Abstract:

    Abstract Primary Familial forms of chylomicronemia can lead to acute life-threatening complications, especially acute pancreatitis. The main aim of therapy is to avoid this so-called chylomicronemia syndrome. In 12 patients with primary chylomicronemia due to Familial Hypertriglyceridemia, the addition of 2.16 g ω-3 fatty acids over 4 weeks and 4.32 g for 8 weeks resulted in a decrease of serum triglyceride levels from 1,624 ± 333 to 894 ± 241 mg/dL after 12 weeks. Cholesterol and triglyceride levels in the chylomicron fraction were reduced concomitantly, the apolipoprotein B-100 B-48 ratio increased, very-low-density lipoprotein (VLDL) triglycerides, VLDL cholesterol, and total cholesterol levels decreased, and low-density lipoprotein (LDL) cholesterol showed a tendency to increase, but this finding did not reach significance. High-density lipoprotein (HDL) cholesterol levels remained unchanged, as did the levels of apolipoproteins A-I, A-II, and E, and lipoprotein(a). Apolipoprotein B levels decreased significantly. The decrease of triglyceride levels to still-elevated concentrations was accompanied by a substantial decrease in plasma and whole-blood viscosity and erythrocyte aggregation, which reached normal values. As in chylomicronemia, complications usually occur at triglyceride levels higher than 1,500 mg/dL; patients can still profit from treatment with ω-3 fatty acids, even though triglyceride levels are still substantially elevated. No clinically relevant side effects occurred, with the exception of the manifestation of diabetes mellitus in one patient, which could be reversed after discontinuation of treatment.

Melissa A. Austin - One of the best experts on this subject based on the ideXlab platform.

  • Genome-wide scan for quantitative trait loci influencing LDL size and plasma triglyceride in Familial Hypertriglyceridemia.
    Journal of lipid research, 2003
    Co-Authors: Melissa A. Austin, John D. Brunzell, Karen L. Edwards, Stephanie A. Monks, Kent M. Koprowicz, Arno G. Motulsky, Michael C. Mahaney, James E. Hixson
    Abstract:

    Small, dense LDLs and Hypertriglyceridemia, two highly correlated and genetically influenced risk factors, are known to predict for risk of coronary heart disease. The ob- jective of this study was to perform a whole-genome scan for linkage to LDL size and triglyceride (TG) levels in 26 kindreds with Familial Hypertriglyceridemia (FHTG). LDL size was estimated using gradient gel electrophoresis, and genotyping was performed for 355 autosomal markers with an average heterozygosity of 76% and an average spacing of 10.2 centimorgans (cMs). Using variance components link- age analysis, one possible linkage was found for LDL size (logarithm of odds (LOD) � 2.1) on chromosome 6, peak at 140 cM distal to marker F13A1 (closest marker D6S2436). With adjustment for TG and/or HDL cholesterol, the LOD scores were reduced, but remained in exactly the same loca- tion. For TG, LOD scores of 2.56 and 2.44 were observed at two locations on chromosome 15, with peaks at 29 and 61 cM distal to marker D15S822 (closest markers D15S643 and D15S211, respectively). These peaks were retained with ad- justment for LDL size and/or HDL cholesterol. These findings, if confirmed, suggest that LDL particle size and plasma TG levels could be caused by two different genetic loci in FHTG. —Austin, M. A., K. L. Edwards, S. A. Monks, K. M. Koprowicz, J. D. Brunzell, A. G. Motulsky, M. C. Maha- ney, and J. E. Hixson. Genome-wide scan for quantitative trait loci influencing LDL size and plasma triglyceride in fa- milial Hypertriglyceridemia. J. Lipid Res. 2003. 44: 2161-2168.

  • Lipoprotein(a) as a risk factor for maternal cardiovascular disease mortality in kindreds with Familial combined hyperlipidemia or Familial Hypertriglyceridemia.
    Clinical genetics, 2002
    Co-Authors: Helen Kim, Karen L. Edwards, Arno G. Motulsky, Barbara Mcknight, Cynthia M. Bradley, Marguerite J. Mcneely, Bruce M. Psaty, Santica M. Marcovina, Melissa A. Austin
    Abstract:

    Most but not all epidemiologic studies have shown that lipoprotein(a) [Lp(a)] is a risk factor for cardiovascular disease (CVD). Lp(a) levels are also strongly genetically influenced. The purpose of this study was to evaluate the association between Lp(a) levels in adult offspring and parental CVD mortality in 61 kindreds with Familial forms of hyperlipidemia. The study sample consisted of offspring-parent pairs in which offspring had fasting Lp(a) measurements and parents had 20-year vital status data and standardized cause-of-death classification if deceased. Linear regression analyses, using a robust variance estimator, were performed separately for 241 offspring with known maternal history (114 mothers) and 194 offspring with known paternal history (93 fathers). Maternal history of CVD mortality was significantly (p=0.004) associated with 2.4-fold higher median Lp(a) levels in offspring compared with those with no maternal history, independent of diabetes, lipid-lowering medications and hormone use. No association was observed between paternal CVD mortality and offspring Lp(a) levels (p=0.505). Adjusting for apolipoprotein(a) kringle 4 number did not alter these parent-specific associations. In conclusion, Lp(a) levels in offspring may be associated with maternal but not paternal history of CVD mortality. This parent-specific finding needs to be confirmed in other samples of high-risk families.

  • Cardiovascular Disease Mortality in Familial Forms of Hypertriglyceridemia: A 20-Year Prospective Study
    Circulation, 2000
    Co-Authors: Melissa A. Austin, John D. Brunzell, Karen L. Edwards, Barbara Mcknight, Cynthia M. Bradley, Marguerite J. Mcneely, Bruce M. Psaty, Arno G. Motulsky
    Abstract:

    Background—Familial combined hyperlipidemia (FCHL) and Familial Hypertriglyceridemia (FHTG) are 2 of the most common Familial forms of hyperlipidemia. There is a paucity of prospective data concerning the risk of cardiovascular disease (CVD) in such families. The purposes of this study were to estimate 20-year total and CVD mortality risk among relatives in these families and to evaluate plasma triglyceride as a predictor of death. Methods and Results—The study was based on lipid and medical history data from 101 families ascertained in 2 studies conducted in the early 1970s. Vital status and cause of death was determined during 1993 to 1997 for 685 family members, including first-degree relatives of the probands and spouse control subjects. Compared with spouse control subjects, 20-year CVD mortality risk was increased among siblings and offspring in FCHL (relative risk 1.7, P=0.02) after adjustment for baseline covariates. In FHTG families, the relative risk was also 1.7 but was not statistically signif...

  • Triglyceride, small, dense low-density lipoprotein, and the atherogenic lipoprotein phenotype
    Current Atherosclerosis Reports, 2000
    Co-Authors: Melissa A. Austin
    Abstract:

    This review provides an overview of the recent data evaluating triglyceride and low-density lipoprotein (LDL) size, two highly interrelated, genetically influenced, risk factors for cardiovascular disease (CVD). An examination of new epidemiologic studies continues to demonstrate that plasma triglyceride levels predict CVD. The first prospective study of the Familial forms of Hypertriglyceridemia has shown that relatives in Familial-combined hyperlipidemia families are at increased risk for CVD mortality and that triglyceride levels predicted 20-year, CVD mortality among relatives in Familial Hypertriglyceridemia families. A meta-analysis of three, large-scale, prospective studies in men, and the first study to examine the correlation of LDL particle size distribution and vascular changes measured by B-mode ultrasound, add to growing evidence that small, dense LDL is atherogenic. Quantitative genetic analysis has recently shown substantial pleiotropic (common) genetic effects on triglyceride and LDL size. At least part of this may be explained by variation at the cholesterol ester transfer protein locus on chromosome 16, possibly through its role in reverse cholesterol transport. Taken together, these data provide new insights into the importance of triglyceride and LDL particle size for understanding genetic susceptibility to cardiovascular disease and its prevention.

Michael M. Ritter - One of the best experts on this subject based on the ideXlab platform.

  • Hemorrheologic abnormalities in defined primary dyslipoproteinemias with both high and low atherosclerotic risks.
    Metabolism: clinical and experimental, 2001
    Co-Authors: Carsten Otto, Werner O. Richter, Michael M. Ritter, Ralf Minkenberg, Peter Schwandt
    Abstract:

    Abstract Dyslipoproteinemias are associated with hemorrheologic abnormalities (elevated fibrinogen concentration, higher viscosity of plasma and blood). Epidemiologic data suggest that not only elevated lipoprotein concentrations (eg, low-density lipoprotein [LDL] cholesterol), but also hemorrheologic abnormalities could causally be involved in the atherosclerotic process. To elucidate potential effects of hemorrheological disturbances, we investigated patients suffering from primary hyperlipoproteinemias with both low (Familial Hypertriglyceridemia, n = 25) and high (type III hyperlipoproteinemia, n = 21; Familial hypercholesterolemia, n = 19; mixed hyperlipoproteinemia, n = 19) atherosclerotic risk, as well as healthy controls (n = 49) in a cross-sectional design. Dyslipoproteinemias were classified by lipoprotein measurements (using ultracentrifugation), family history, and apolipoprotein E phenotype. Hemorrheology was characterized by the measurement of fibrinogen concentration, viscosity of plasma and blood at different shear rates, and red cell aggregation (RCA) at stasis and low shear. Fibrinogen concentration was lower in controls (2.38 ± 0.09 g/L) compared with Familial hypercholesterolemia (3.19 ± 0.19 g/L), to type III hyperlipoproteinemia (3.02 ± 0.12 g/L), to Familial Hypertriglyceridemia (2.95 ± 0.21 g/L) and to mixed hyperlipoproteinemia (3.01 ± 0.12 g/L) ( P P P

  • Effects of n-3 fatty acids and fenofibrate on lipid and hemorrheological parameters in Familial dysbetalipoproteinemia and Familial Hypertriglyceridemia.
    Metabolism: clinical and experimental, 1996
    Co-Authors: Carsten Otto, Peter Schwandt, Michael M. Ritter, Andreas C. Soennichsen, Werner O. Richter
    Abstract:

    There is increasing evidence that hemorrheological abnormalities are associated with an enhanced risk of atherosclerosis. The n-3 fatty acids (n-3-FA) have been shown to have beneficial effects on atherosclerosis in patients with dyslipoproteinemias. We studied 23 patients with elevated plasma triglycerides to evaluate the influence of fish oil and fenofibrate therapy on hemorrheological parameters (15 patients with Familial Hypertriglyceridemia [FHTG] and eight with Familial dysbetalipoproteinemia [FDL]). The patients (one woman and 22 men aged 45.7 ± 2.0 years) were treated with increasing doses of n-3-FA (1.8 to 3.6 g/d: 0.9 to 1.8 g eicosapentaenoic acid and 0.6 to 1.2 g docosahexaenoic acid) for 8 weeks. Lipid parameters, whole-blood viscosity at different shear rates, plasma viscosity, fibrinogen concentration, and red blood cell aggregation (RCA) were measured at baseline and at weeks 2, 4, 8 (end of n-3-FA therapy), and 12. Compliance was ensured by measuring plasma concentrations of eicosapentaenoic acid and docosahexaenoic acid. After 12 weeks, patients began treatment with fenofibrate (250 mg daily); investigations were performed again at week 20. Total triglycerides (from 6.90 ± 1.70 to 3.61 ± 0.78 mmol/L in FDL and 7.44 ± 1.50 to 4.15 ± 0.55 in FHTG), very-low-density lipoprotein (VLDL) triglycerides, and VLDL cholesterol were significantly decreased with n-3-FA therapy in both groups (P < .05). In FHTG, low-density lipoprotein (LDL) cholesterol increased significantly (from 2.75 ± 0.28 to 3.97 ± 0.35 mmol/L, P < .01); in FDL, total cholesterol decreased (from 9.76 ± 1.32 to 7.34 ± 1.07 mmol/L, P < .05). No significant changes were observed in hemorrheological parameters, except for reduced RCA with 3.6 g n-3-FA in FHTG. However, with fenofibrate therapy, in addition to comparable lipoprotein changes seen with fish oil, fibrinogen levels and plasma and blood viscosity decreased in patients with FDL. We conclude that n-3-FA and fenofibrate have comparable effects on lipid parameters in patients with FDL and FHTG. Because of additional beneficial effects on hemorrheological parameters, fenofibrate may be preferred for the treatment of FDL.

  • Treatment of primary chylomicronemia due to Familial Hypertriglyceridemia by ω-3 fatty acids
    Metabolism: clinical and experimental, 1992
    Co-Authors: Werner O. Richter, Bernd G. Jacob, Michael M. Ritter, Peter Schwandt
    Abstract:

    Abstract Primary Familial forms of chylomicronemia can lead to acute life-threatening complications, especially acute pancreatitis. The main aim of therapy is to avoid this so-called chylomicronemia syndrome. In 12 patients with primary chylomicronemia due to Familial Hypertriglyceridemia, the addition of 2.16 g ω-3 fatty acids over 4 weeks and 4.32 g for 8 weeks resulted in a decrease of serum triglyceride levels from 1,624 ± 333 to 894 ± 241 mg/dL after 12 weeks. Cholesterol and triglyceride levels in the chylomicron fraction were reduced concomitantly, the apolipoprotein B-100 B-48 ratio increased, very-low-density lipoprotein (VLDL) triglycerides, VLDL cholesterol, and total cholesterol levels decreased, and low-density lipoprotein (LDL) cholesterol showed a tendency to increase, but this finding did not reach significance. High-density lipoprotein (HDL) cholesterol levels remained unchanged, as did the levels of apolipoproteins A-I, A-II, and E, and lipoprotein(a). Apolipoprotein B levels decreased significantly. The decrease of triglyceride levels to still-elevated concentrations was accompanied by a substantial decrease in plasma and whole-blood viscosity and erythrocyte aggregation, which reached normal values. As in chylomicronemia, complications usually occur at triglyceride levels higher than 1,500 mg/dL; patients can still profit from treatment with ω-3 fatty acids, even though triglyceride levels are still substantially elevated. No clinically relevant side effects occurred, with the exception of the manifestation of diabetes mellitus in one patient, which could be reversed after discontinuation of treatment.

Christine Fischer - One of the best experts on this subject based on the ideXlab platform.

  • Genetics of type III hyperlipoproteinemia.
    Genetic epidemiology, 1997
    Co-Authors: Giso Feussner, Susanne Piesch, Jürgen M Dobmeyer, Christine Fischer
    Abstract:

    One hundred forty-seven relatives of 43 patients with “classical” type III hyperlipoproteinemia (HLP) having the apolipoprotein (apo) E2/2 phenotype were studied to determine the occurrence of hyperlipidemia and the presence of further possible genes for lipoprotein disorders in these families. In 12 pedigrees primary dyslipidemia was prevalent among patients and respective blood-relatives. In these kindreds the coexistent presence of genes for Familial combined hyperlipidemia (n = 6), Familial Hypertriglyceridemia (n = 5), and Familial hypercholesterolemia (n = 1), respectively, was supposed. Our results, therefore, confirm and extend previous data on the multifactorial genesis of the diseases. Besides homozygosity for a receptor binding-defective isoform of apo E (apo E2), additional genes for Familial lipoprotein disorders might operate in the pathogenesis of type III HLP. This is the largest family study performed so far in this primary lipoprotein disorder. Genet. Epidemiol. 14:283–297,1997. © 1997 Wiley-Liss, Inc.