LDL-Apheresis in Hypercholesterolemic Patients: Technical and Clinical Aspects

Borberg, H.; Bode, C.; Mattele, L.; Oette, K.; Tauchert, M.; Stoffel, Wilhelm

doi:10.1159/000409403

Cited by 10 publications

(6 citation statements)

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“…After LDL apheresis, the cholesterol and apo B content in the serum was markedly decreased in all patients. As reported previously, 18 in LDL apheresis treatment a dilution of the patient's plasma of about 20% cannot be avoided. Therefore, a decrease of the albumin concentration during apheresis was also found ( Table 1).…”

Section: Resultsmentioning

confidence: 85%

Low density lipoproteins inhibit endotoxin activation of monocytes.

Weinstock

Ullrich

et al. 1992

Arterioscler Thromb

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Human serum and low density lipoproteins (LDLs) were shown to inactivate endotoxin (lipopolysaccharide [IPS]) by testing the effect of LPS interactions with serum or LDL on the activation of human monocytes. Sera and LDL preparations from four patients with familial hypercholesterolemia were used to demonstrate the inhibition of LPS from inducing interleukin-1 release. Before LDL removal by immunoapheresis, the patients' sera were able to inactivate approximately fivefold more LPS than after LDL removal. The LPS-inactivating capacity lost during apheresis could essentially be retrieved in the LDL-rich eluate from the immunoadsorption columns. Because patients were treated frequently with immunoapheresis, their LDL levels before LDL removal were not markedly elevated. These patients' sera before LDL removal were shown to inactivate amounts of LPS comparable to those inactivated by the sera from three healthy volunteers. LDL prepared by ultracentrifugation showed similar LPS inactivation as LDL prepared by immunoapheresis. We conclude that the inhibition of LPS-induced monocyte activation by human serum is dependent to a large extent on the LDL fraction. LDLs were demonstrated to inhibit LPS from inducing interleukin-1 release by human monocytes. ( 1 -3 Lipoproteins were recently shown to diminish the biologic activity of LPS with respect to human monokine release. -5 In humans, low density lipoproteins (LDLs) may bind more LPS than do high density lipoproteins.6 It was not known whether changes in the lipoprotein content of serum would influence the inhibitory effect of serum on LPSinduced monokine release and the extent of LDL involvement.In patients with familial hypercholesterolemia, the excessive content of LDL in serum is caused by defective LDL receptors. The LDL particles themselves, however, are not aberrant.7 Because marked changes in This study was undertaken to investigate the effect of changes in LDL content of human serum on LPS inactivation. In addition, human LDLs could be tested for their participation in LPS inactivation with regard to human monokine release. Methods PatientsThree female (25, 43, and 51 years old) and one male (48 years old) patient were studied, all having heterozygous familial hypercholesterolemia with hyperlipoproteinemia type Ila. Diagnoses were established in adulthood in all patients. The patients were treated once a week with LDL apheresis 1011 for 1-3 years, using immunoadsorption columns carrying anti-apolipoprotein (apo) B antibody (LDL-Therasorb, Baxter, Munich, FRG) to reduce serum cholesterol levels to 3.9 mmol/1 or less after treatment. For this study, an additional 20 ml of blood was drawn from the patients before and after LDL apheresis, but no changes in the procedure of the LDL apheresis therapy were made. Informed consent was obtained in accordance with regulations set by the ethics commission of the medical faculty of the University of

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Section: Resultsmentioning

confidence: 85%

Low density lipoproteins inhibit endotoxin activation of monocytes.

Weinstock

Ullrich

et al. 1992

Arterioscler Thromb

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“…Other techniques of plasmapheresis for plasma cholesterol removal, including absorbents such as anti-LDL, dextran sulfate bound to beads, or membrane filtration techniques, have been developed in order to overcome the disadvantages of plasma product substitutional fluids. These sorbents have been studied in animal models and FH patients [16,17]. Membrane filtration has also been applied because of the significant size difference of the HDL and (VLDL + LDL) fractions [ 181.…”

Section: Resultsmentioning

confidence: 99%

Selective removal of cholesterol by plasmapheresis and the progression of atherosclerosis

Nomura

et al. 1992

J of Clinical Apheresis

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There is a strong correlation of plasma cholesterol levels with the risk of coronary heart diseases as shown by epidemiologic studies. This study was undertaken to evaluate the effect of plasma cholesterol lowering on the progression of atherosclerosis in the homozygous Watanabe heritable hyperlipidemic (WHHL) rabbit. The effect of cholesterol lowering, which was accomplished by thermofiltration (on-line plasma separation with plasma filtration at 39 degrees C) was evaluated by comparison between treated and untreated control groups. Thermofiltration reduced significantly the mean plasma level of total cholesterol (284 vs. 655 mg/dl, P = 0.0005) and the percent aortic area occupied by atherosclerotic plaque (15.0 vs. 44.2%, P = 0.0003). The total lipid and cholesterol contents in the aortas in the treated group were also significantly lower than those in the control group. Microscopically, thickness measurements of the lesions showed that the mean thickness of the fibrous cap and the ratio of the thickness of the intima to that of the media were smaller for the treated group than the control group. This study demonstrated the slowing or stopping of the progression of atherosclerosis by lowering the plasma total cholesterol level in WHHL rabbits.

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“…Stoffel et al (8)(9)(10)(11) developed an immunoadsorbent for the removal of low density lipoproteins (LDL) from plasma. The group of Yamawaki (12) reported the use of binders for rheumatoid factors.…”

Section: Specific Adsorptionmentioning

confidence: 99%

“…For this plasma fractionating, methods using cascade filtration or special membrane filters (28) as well as LDL precipitation by means of dextran sulfate (29) or heparin (30) have been developed. Up to the present time two kinds of LDL removal by adsorption have been reported: 1) the specific or immune adsorption (8)(9)(10)(11), 2) the selective binding by carriers of polyanionic groups. The first type of LDL adsorbents (mentioned already above, see 2.1) consists of sepharose beads joined with sheep antibodies against the LDL apoproteins.…”

Section: Adsorbents For Low Density Lipoproteins (Ldl)mentioning

confidence: 99%