Changes in C‐reactive Protein Plasma Levels During Low‐density Lipoprotein Apheresis

Kojima, Sunao; Shida, Mikio; Yokoyama, Hiroyuki

doi:10.1046/j.1526-0968.2003.00080.x

Cited by 33 publications

(22 citation statements)

References 20 publications

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“…Kobayashi et al performed LDL apheresis in patients with peripheral artery disease and found a nonsignificant increase in MCP-1 after treatment with the LA-15 column [15], in line with our findings. Kojima et al noted a 70% increase in IL-6 during dextran-sulfate LDL apheresis even if hs-CRP was reduced [19]. We found less changes in IL-6 than Kojima, with a 10, 40, and 210% differences in IL-6 levels with columns DL-75, LA-15, and EC-50W, respectively.…”

Section: Cytokinescontrasting

confidence: 49%

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Different inflammatory responses induced by three LDL‐lowering apheresis columns

Hovland

Hardersen

Sexton

et al. 2009

J of Clinical Apheresis

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Low-density lipoprotein (LDL) apheresis is well-established in selected patients with uncontrolled LDL levels. As such treatment affects biomarkers important in atherosclerosis and acute coronary syndromes, we systematically compared the inflammatory response induced by three LDL apheresis columns. Three patients with heterozygous familial hypercholesterolemia participated in a cross-over study with six consecutive treatments with three different LDL apheresis columns: DL-75 (whole blood adsorption), LA-15 (plasma adsorption), and EC-50W (plasma filtration). Biochemical parameters and inflammatory biomarkers, including complement activation products and 27 cytokines, chemokines, and growth factors were measured before and after treatment. Complement was activated through the alternative pathway. The final end product sC5b-9 increased significantly (P < 0.01) and equally with all devices, whereas the anaphylatoxins C3a and C5a were lower by use of the adsorption columns. Hs-CRP was reduced by 77% (DL-75), 72% (LA-15), and 43% (EC-50W). The cytokines were consistently either increased (IL-1ra, IP-10, MCP-1), decreased (IFN-gamma, TNF-alpha, RANTES, PDGF, VEGF), or hardly changed (including IL-6, IL8, MIP-1alphabeta) during treatment. The changes were in general less pronounced with the adsorption columns. All columns reduced LDL significantly and to the same extent. In conclusion, three LDL-apheresis devices with equal cholesterol-lowering effect differed significantly with respect to the inflammatory response.

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Section: Cytokinescontrasting

confidence: 49%

“…It is based on electrostatic binding between positively charged Apo B and the negative charges of dextran [19].…”

Section: Ldl Apheresismentioning

confidence: 99%

Different inflammatory responses induced by three LDL‐lowering apheresis columns

Hovland

Hardersen

Sexton

et al. 2009

J of Clinical Apheresis

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“…In this study, we demonstrated short-term reductions of the LDL, MDA-LDL, oxidized LDL, CRP, and fibrinogen concentrations during a single apheresis, consistent with the results of previous studies. 5,20,21 More importantly, our results disclosed a long-term reduction of oxidized LDL, CRP, and fibrinogen specifically until the 10th apheresis in the responders. Although LDL apheresis did not cause a sustained decrease in LDL cholesterol in the responders or the nonresponders, the long-term therapeutic effects of LDL apheresis were related to the relatively sustained decrease in oxidized LDL, which is a marker of lipid peroxidation.…”

Section: Discussionmentioning

confidence: 51%

“…13,15,17,19 Previous studies demonstrated that a single LDL apheresis decreased not only the total LDL cholesterol but also the oxidized LDL, CRP, and fibrinogen concentrations as short-term effects. 5,20,21 Although previous studies reported that LDL apheresis may induce long-term reduction of the CRP and fibrinogen concentration, 21,22 there has been no report of the long-term effects of LDL apheresis on lipid-related oxidative stress. In this study, we demonstrated short-term reductions of the LDL, MDA-LDL, oxidized LDL, CRP, and fibrinogen concentrations during a single apheresis, consistent with the results of previous studies.…”

Section: Discussionmentioning

confidence: 99%

Sustained Inhibition of Oxidized Low-Density Lipoprotein Is Involved in the Long-Term Therapeutic Effects of Apheresis in Dialysis Patients

Tsurumi‐Ikeya

Tamura

Azuma

et al. 2010

ATVB

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Objective-Low-density lipoprotein (LDL) apheresis is a potential therapy for conventional therapy-resistant peripheral artery disease. In the present study, we examined the chronic effects of LDL apheresis on clinical parameters in vivo and endothelial cell functions in vitro in hemodialysis patients who had the complication of peripheral artery disease. Methods and Results-Twenty-five patients were enrolled, and the responses of 19 patients to LDL apheresis were analyzed. Patients were classified into 2 groups according to change in ankle-brachial pressure index (ABI) after treatment: patients with improved ABI (responders, nϭ10) and patients with worsened ABI (nonresponders, nϭ9). In the responders, apheresis resulted in a long-term reduction of circulating levels of oxidized LDL, C-reactive protein, and fibrinogen. In human umbilical vein endothelial cells (HUVECs), the serum from the responders increased expression of activated endothelial nitric oxide synthase protein and proliferative activity. Key Words: atherosclerosis Ⅲ endothelium Ⅲ nitric oxide synthase Ⅲ oxidized lipids Ⅲ peripheral arterial disease Ⅲ lipoproteins Ⅲ oxidative stress C ardiovascular disease is the primary cause of death in patients with end-stage renal disease. Patients on dialysis are reported to have a 10 -20-fold greater risk of cardiovascular disease-associated mortality than the general population after stratification for age, gender, race, and the presence or absence of diabetes. Patients undergoing dialysis have many of the risk factors for atherosclerosis, such as hypertension, dyslipidemia, and disturbed calcium-phosphate metabolism, and, indeed, they commonly experience severe atherosclerosis, including peripheral artery disease (PAD). Low-density lipoprotein (LDL) apheresis is a potentially useful treatment for conventional therapy-resistant hypercholesterolemic patients with coronary artery disease and PAD. 1,2 Previously, it was shown that a single LDL apheresis session enhanced the peripheral microcirculation, probably by increasing the production of nitric oxide (NO) and bradykinin, 3 reducing blood viscosity and adhesion molecules, 4 and inducing endothelium-dependent vasodilatation. 5 However, the precise molecular mechanism of the long-term effects of LDL apheresis on the improvement of the peripheral circulation remains unclear and warrants further investigation.We undertook the present study to investigate the shortand long-term effects of LDL apheresis on clinical and laboratory parameters in vivo and vascular endothelial cell function in vitro, in hemodialysis patients with PAD, and to identify factors related to the improvement of the peripheral circulation by LDL apheresis. Methods Patients and Study DesignThe study protocol was approved by the Human Ethics Committee of Yokohama City University Hospital. A total of 25 consecutive hemodialysis patients with leg impairments and ankle-

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“…It is based on electrostatic binding between positively charged Apo B and the negative charges of dextran [23].…”

Section: Ldl Apheresismentioning

confidence: 99%

Hematologic and hemostatic changes induced by different columns during LDL apheresis

Hovland

Hardersen

Mollnes

et al. 2010

J of Clinical Apheresis

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Low density lipoprotein (LDL) apheresis is a long-term treatment and its impact on risk factors other than lipoproteins could be of importance. Three patients with familial hypercholesterolemia participated in six consecutive treatments with three different LDL apheresis columns in random order: DL-75, LA-15, and EC-50W. We compared treatment effects on hemoglobin, leukocytes, platelets, fibrinogen, thrombin-antithrombin complexes (TAT), plasminogen activator inhibitor-1 (PAI-1), and homocysteine. Hemoglobin, leukocytes and platelets decreased significantly with DL-75 (P < 0.05). Hemoglobin and leukocytes increased significantly with LA-15 and EC-50W (P < 0.05). Platelets were unchanged. The DL-75 column was statistically different from LA-15 and EC-50W regarding these parameters. With the columns DL-75, LA-15, and EC-50W fibrinogen decreased significantly by 28%, 32%, and 42%, PAI-1 decreased significantly by 72%, 58%, and 30% while TAT increased significantly by 138%, 3%, and 251%, respectively (P < 0.05 for all). When comparing the columns there were significant differences between all of them regarding fibrinogen, no differences regarding TAT and a difference between DL-75 and EC-50W regarding PAI-1. With the columns DL-75, LA-15 and EC-50W homocysteine decreased 22%, 9%, and 13%, respectively, but there were no inter column differences. In conclusion, the three LDL apheresis columns affected important hematological and hemostatic risk factors differently.

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Changes in C‐reactive Protein Plasma Levels During Low‐density Lipoprotein Apheresis

Cited by 33 publications

References 20 publications

Different inflammatory responses induced by three LDL‐lowering apheresis columns

Different inflammatory responses induced by three LDL‐lowering apheresis columns

Sustained Inhibition of Oxidized Low-Density Lipoprotein Is Involved in the Long-Term Therapeutic Effects of Apheresis in Dialysis Patients

Hematologic and hemostatic changes induced by different columns during LDL apheresis

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